[
  {
    "Id": 1,
    "Name": "Cataract surgery",
    "Body": "\u003Cp class=\u0022MsoListParagraphCxSpFirst\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: 15.6933px; text-indent: -18pt;\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: Calibri, sans-serif; letter-spacing: normal;\u0022\u003ERegarding intraoperative management of astigmatism during cataract surgery, which of the following statements is most\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: Calibri, sans-serif; letter-spacing: normal; text-indent: -18pt;\u0022\u003Elikely to be true?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cp class=\u0022MsoListParagraphCxSpFirst\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: 15.6933px; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022 style=\u0022font-family: Symbol;\u0022\u003E\u00B7\u003Cspan style=\u0022font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; font-size: 7pt; line-height: normal; font-family: \u0026quot;Times New Roman\u0026quot;;\u0022\u003E\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003Cspan dir=\u0022LTR\u0022\u003E\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022\u003EIt is prudent to make reference marks\u003C/span\u003E\u003C/span\u003E\u003Cspan lang=\u0022EN-US\u0022\u003E, using a surgical marking pen, with the patient sitting up, preferably at the slit lamp. Marking with the patient in this position avoids reference-mark error due to cyclotorsion of the eyes. Studies have demonstrated that up to 15\u00B0 of cyclotorsion can occur when patients move from an upright to a supine position.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpFirst\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: 15.6933px; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpMiddle\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: 15.6933px; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022 style=\u0022font-family: Symbol;\u0022\u003E\u00B7\u003Cspan style=\u0022font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; font-size: 7pt; line-height: normal; font-family: \u0026quot;Times New Roman\u0026quot;;\u0022\u003E\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003Cspan dir=\u0022LTR\u0022\u003E\u003C/span\u003E\u003Cspan lang=\u0022EN-US\u0022\u003EWith increased age the majority of the population develop ATR astigmatism. Hence, a temporally placed incision may reduce or neutralise this astigmatism.\u0026nbsp;\u0026nbsp;Although it is generally preferable to undercorrect pre-existing astigmatism and avoid large swings of axis, WTR astigmatism is considered normal in younger individuals and may confer some optical advantage\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpMiddle\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: 15.6933px; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpLast\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: normal; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022 style=\u0022font-family: Symbol;\u0022\u003E\u00B7\u003Cspan style=\u0022font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; font-size: 7pt; line-height: normal; font-family: \u0026quot;Times New Roman\u0026quot;;\u0022\u003E\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003Cspan dir=\u0022LTR\u0022\u003E\u003C/span\u003E\u003Cspan lang=\u0022EN-US\u0022\u003EA toric IOL is appropriate for patients with regular corneal astigmatism,\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003Ecurrently up to 4.00 D\u003C/span\u003E\u0026nbsp;at the corneal plane (United States). Patients with astigmatism exceeding the upper correction limits require additional measures to obtain full correction\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpLast\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: normal; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022MsoListParagraphCxSpLast\u0022 style=\u0022margin: 0cm 0cm 0cm 36pt; line-height: normal; font-size: 11pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal; text-indent: -18pt;\u0022\u003E\u003Cspan lang=\u0022EN-US\u0022\u003E\u003Cimg src=\u0022http://blazorcss.somee.com/upload-2025-02-26-83b22e73-8a3c-4a68-9b5e-1a3db75ee6e5.png\u0022\u003E\u003Cbr\u003E\u003Cbr\u003E\u003Cimg src=\u0022/upload-2025-02-27-3c6debe9-4774-4b14-a62f-cc04808cda3d.png\u0022 width=\u00221000\u0022 height=\u0022500\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 2,
    "Name": "Cataract surgery",
    "Body": "\u003Cspan style=\u0022font-weight: bold; font-size: large;\u0022\u003ESystematic review of studies comparing mono-focal lens implants with multifocal lens implants showed:\u003C/span\u003E",
    "Explanation": "Patients with Multifocal IOLs are more likely to have significant glare, halos, and ghosting than those with monofocal, toric, or accommodating IOLs. These issues stem from various etiologies, including residual refractive error, ocular surface disease, or intrinsic IOL problems.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003EThe reports of halos intrinsically related to the IOL tend to subside over several months, perhaps from the patient\u0027s neural adaptation, but they may be persistent.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EBecause of a reduction in contrast sensitivity, the subjective quality of vision after MF-IOL insertion may not be as good as after monofocal IOL implantation.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EWith MF-IOLS, intermediate vision may be less clear than distance or near acuity.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EMF-IOLs compared to standard IOLs or monovision result in better uncorrected near vision and a higher proportion of patients who achieve spectacle independence, but a greater risk of unwanted visual phenomena.\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 3,
    "Name": "PXF",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EWhich of the following is characteristic of pseudo-exfoliation?\u003Co:p\u003E\u003C/o:p\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "PXF has no clear inheritance pattern. It is more common in females and those of Scandinavian ancestry. It causes chronic open angle glaucoma in about 15% at 10 years.",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 4,
    "Name": "Rieger\u0027s syndrome",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA patient has short stature, aortic stenosis, and mental retardation. On examination, the optic discs show glaucomatous cupping. What is the most likely diagnosis?\u003Co:p\u003E\u003C/o:p\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\u003Cbr\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 5,
    "Name": "Diabetic Retinopathy",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EWhich of the following is LEAST appropriate when performing focal argon laser for diabetic macular oedema?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "When performing focal argon laser treatment for diabetic macular oedema, the general recommended parameters are:\u0026nbsp;\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E\u2022\t\u003Cspan style=\u0022font-weight: bold;\u0022\u003ESpot size:\u003C/span\u003E typically 50\u2013100 microns\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\t\u003Cspan style=\u0022font-weight: bold;\u0022\u003EExposure time:\u003C/span\u003E short burns around 0.05\u20130.1 seconds, certainly not exceeding 0.2 seconds, to avoid excessive thermal diffusion\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\t\u003Cspan style=\u0022font-weight: bold;\u0022\u003EInitial power:\u003C/span\u003E generally less than 200 mW is reasonable to titrate a barely visible burn\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\t\u003Cspan style=\u0022font-weight: bold;\u0022\u003ETreatment area:\u003C/span\u003E apply burns to leaking microaneurysms between 500 and 3000 microns from the centre of the fovea. Lesions as near as 300 microns to the fovea may be treated, provided this would not be within the foveal avascular zone\u0026nbsp;\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Using laser burns longer than 0.2 seconds would cause excessive heat diffusion, damaging surrounding retina and retinal pigment epithelium beyond the intended treatment area, making this the least appropriate choice.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 6,
    "Name": "Nyctalopia",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA 54 year old female underwent bariatric surgery two years previously to try and control her weight. She is now complaining of nyctalopia. Which of these vitamins is the MOST likely therapy the patient requires?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Nyctalopia (night blindness) is classically caused by \u003Cspan style=\u0022font-weight: bold;\u0022\u003Evitamin A deficiency\u003C/span\u003E, which can occur after bariatric surgery due to fat-soluble vitamin malabsorption. Vitamin A is essential for rhodopsin regeneration in the retina, critical for night vision.\u0026nbsp;\u003Cdiv\u003E\u0026nbsp;Therefore, vitamin A supplementation is the most appropriate therapy.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 7,
    "Name": "Immune-suppresives",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA 55 year old patient with granulomatosis polyangiitis is being prescribed cyclophosphamide. Which of these side effects are they MOST likely to experience?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Cyclophosphamide is an alkylating agent with significant myelotoxicity, making bone marrow suppression the most common and dose-limiting side effect.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Other side effects (like hemorrhagic cystitis, due to acrolein metabolite) can also occur but are less frequent with proper feeding and hydration protocols. Hirsutism and osteoporosis are more associated with long-term steroid therapy, not cyclophosphamide.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThe BNF Lists myelosuppression as the most common and dose-limiting toxicity of cyclophosphamide.\u003C/span\u003E\n\n\nTherefore, marrow suppression is the most likely side effect.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 8,
    "Name": "Immune-suppresives",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EWhich of the following statements is MOST likely to be correct concerning Adalimumab?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "\u2022\tAdalimumab is a fully human monoclonal anti-TNF-\u03B1 antibody.\u0026nbsp;\u003Cdiv\u003E\u2022\tIt is typically used \u003Cspan style=\u0022font-weight: bold;\u0022\u003Esubcutaneously\u003C/span\u003E (so option D is incorrect).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tIn JIA-associated uveitis (iridocyclitis), it is indicated as second-line treatment if methotrexate fails, in accordance with uveitis guidelines.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tIt is \u003Cspan style=\u0022font-weight: bold;\u0022\u003Enot\u003C/span\u003E first line in sarcoid uveitis (option B incorrect).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tInfliximab (not adalimumab) is a chimeric antibody (option A incorrect).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 9,
    "Name": "Peads Cataract",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003ECataracts are MOST commonly associated with which ONE of the following collections of systemic abnormalities?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "This triad is characteristic of \u003Cspan style=\u0022font-weight: bold;\u0022\u003ELowe syndrome (oculocerebrorenal syndrome)\u003C/span\u003E, which is well known for causing congenital cataracts along with:\u0026nbsp;\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E\u2022\tlearning difficulties (cerebral involvement)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\thypotonia\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tproximal renal tubular acidosis\u0026nbsp;\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ERegarding the other choices:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EA: Biliary cirrhosis, muscle rigidity, muscle weakness\n\u2192 These features point more toward primary biliary cirrhosis or mitochondrial disorders like primary biliary cholangitis with myopathy \u2014 but these do not classically associate with cataracts.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;B: Hypodontia, mandibular hypoplasia, hypertelorism\n\u2192 Suggestive of orofacial-digital syndromes or other craniofacial dysplasias, which are not strongly linked with congenital cataracts.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;D: Mid-facial hypoplasia, epiphyseal dysplasia, deafness\n\u2192 Points toward conditions like Stickler syndrome or Treacher Collins, involving skeletal and facial anomalies and hearing loss, but cataracts are not their hallmark (Stickler is more linked with high myopia and retinal detachment).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 10,
    "Name": "Fuch\u2019s Endothelial dystrophy",
    "Body": "\u003Cp class=\u0022p1\u0022 style=\u0022margin-right: 0cm; margin-left: 0cm; font-size: 12pt; font-family: \u0026quot;Times New Roman\u0026quot;, serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn patients with Stage 1 Fuch\u2019s endothelial corneal dystrophy, which of the following is MOST likely to be true?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Stages of Fuchs\u2019 Endothelial Dystrophy (clinical):\u0026nbsp;\u003Cdiv\u003E\u2705 Stage 1 (Early):\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tFormation of central corneal guttae\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tNo stromal or epithelial edema\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u2705 Stage 2 (Edematous):\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tProgressive endothelial decompensation\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tStromal edema visible on slit-lamp\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tDescemet\u2019s folds may appear\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u2705 Stage 3 (Bullous keratopathy):\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tEpithelial edema with microcystic bullae\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tPain from ruptured bullae\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u2705 Stage 4 (Late / Scarring):\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tSubepithelial fibrosis\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tStromal scarring\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tPersistent edema\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1836/11034696/c80102a036d7/TJO-14-15-g002.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EAlgorithms for treating FECD.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E(a) Currently, only few conservative therapies could be tried. Surgery is the only definitive treatment for FECD.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E(b) As more novel therapeutic approaches are becoming available, a stepwise algorithm for treating FECD will substitute current surgery-centred manner. For patients with mild FECD, pharmacology-associated treatments should be used as the first line. Cell therapy-associated treatments are minimally invasive, being good candidates as second-line treatments. Surgery is reserved for patients with severe, refractory FECD. In addition to single treatment, the combination of different therapeutic methods should also be considered*\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; font-size: x-small;\u0022\u003E\u0026nbsp;*Liu, Jia-Xin \u0026amp; Chiang, Tung-Lin \u0026amp; Hung, Kai-Feng \u0026amp; Sun, Yi-Chen. (2024). Therapeutic future of Fuchs endothelial corneal dystrophy: An ongoing way to explore. Taiwan Journal of Ophthalmology. 14. 10.4103/tjo.TJO-D-23-00115.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; font-style: italic; text-decoration-line: underline;\u0022\u003ESources:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022\tKrachmer JH, Mannis MJ, Holland EJ. Cornea, 4th Edition. Elsevier; 2017.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tEye Bank Association of America Medical Standards (latest revision)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tEghrari AO, Riazuddin SA, Gottsch JD. Fuchs Corneal Dystrophy. Ophthalmology. 2015;122(12):2341-2349. doi:10.1016/j.ophtha.2015.08.017\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tAmerican Academy of Ophthalmology (AAO) EyeWiki: Fuchs Endothelial Corneal Dystrophy\u0026nbsp;\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 11,
    "Name": "OHT",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EIn the Ocular Hypertension Treatment Study (OHTS), which ONE of the following was found to be a risk factor for conversion to glaucoma?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "The Ocular Hypertension Treatment Study (OHTS) identified several significant risk factors for progression from ocular hypertension to primary open-angle glaucoma, including:\u0026nbsp;\u003Cdiv\u003E\u2022\tLarge vertical cup-disc ratio\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tThin central corneal thickness (not increased)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tHigher intraocular pressure\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tOlder age\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tAfrican ancestry\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Large vertical cup-disc ratio suggests existing structural vulnerability of the optic nerve head, making it a strong predictor of conversion.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-size: x-small;\u0022\u003ESource:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u2022\tKass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701\u2013713.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline; color: rgb(255, 0, 0);\u0022\u003E\u0026nbsp;Remember: OHT outcomes:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003EThe five-year risk of developing POAG from ocular hypertension was reduced ~50% with topical medications.\nHowever, the risk of conversion to glaucoma remained low in both groups at five years (4.4% treated vs. 9.5% untreated).\u003C/li\u003E\u003Cli\u003E66.4% of originally abnormal VFs were within normal limits on follow-up testing.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 12,
    "Name": "DVLA",
    "Body": "\u003Ch2 style=\u0022margin: 8pt 0cm 4pt; break-after: avoid; font-family: \u0026quot;Aptos Display\u0026quot;, sans-serif; font-weight: normal; letter-spacing: normal;\u0022\u003E\u003Cspan style=\u0022font-size: medium; color: rgb(6, 6, 6);\u0022\u003EAccording to UK law, which of these patients would NOT be legally able to drive within their category?\u003C/span\u003E\u003Cspan style=\u0022color: rgb(15, 71, 97); font-size: 16pt;\u0022\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/h2\u003E",
    "Explanation": "According to DVLA (Driver and Vehicle Licensing Agency) guidance, anyone who has experienced \u003Cspan style=\u0022font-weight: bold;\u0022\u003Etransient monocular vision loss (amaurosis fugax) \u003C/span\u003Emust stop driving for \u003Cspan style=\u0022text-decoration-line: underline;\u0022\u003Eat least one month\u003C/span\u003E and notify the DVLA if there is a risk of recurrence, due to potential underlying vascular risk (e.g., carotid disease). Three weeks is insufficient to resume driving safely without further assessment.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tDVLA rules allow Group 1 drivers to have minor defects as long as there are no significant defects within a 20\u00B0 radius around fixation.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tMonocular vision is acceptable for Group 1 driving as long as they meet the acuity standard and adapt to monocularity. Patching to control diplopia is permissible.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tGroup 2 (lorry/bus drivers) require at least 6/7.5 in their better eye and at least 6/12 in the other eye, with spectacle correction up to \u002B8.0D acceptable.\u0026nbsp;\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 13,
    "Name": "Glaucoma treatment",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003E\u003Cspan lang=\u0022EN-US\u0022\u003EWhich of the following glaucoma drops decreases aqueous production AND increases aqueous outflow?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "Alpha-2-adrenergic agonists such as brimonidine work by dual mechanism, decreasing aqueous production and increasing outflow.\u0026nbsp;",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 14,
    "Name": "CPEO",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EWhich of the following is the LEAST likely eye related manifestation associated with mitochondrial dysfunction?\u003Co:p\u003E\u003C/o:p\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "Mitochondrial diseases commonly affect high-energy-demand tissues like the optic nerve, retina, and extraocular muscles.\u0026nbsp;\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ETypical ophthalmic manifestations include:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022\tProgressive external ophthalmoplegia (eye movement limitation with or without ptosis)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tPtosis\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tOptic neuropathy (e.g., Leber hereditary optic neuropathy)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tPigmentary retinopathy\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EIn Kearns-Sayre syndrome\u003C/span\u003E for example, Motility restrictions vary with the stage of the disease and worsen as disease progresses and can limit eye excursions to 10% of normal in advanced cases. Because of symmetric limitation of motility, diplopia is reported in only 1/3 to 2/3 of patients with CPEO. Most patients exhibit exotropias (seen in up to 90% of patients) and 50% of patients develop suppression scotomas and remain asymptomatic.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EHowever, retro-chiasmal visual pathway lesions (causing visual field defects from cortical or retrochiasmal damage) are not typical features of mitochondrial disorders, since \u003Cspan style=\u0022font-weight: bold;\u0022\u003Emitochondria-related dysfunction tends to involve peripheral visual structures rather than the retrochiasmal visual pathways.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003ETherefore the least likely is:\u0026nbsp; Visual field defect from retrochiasmal visual pathway damage\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; font-size: x-small;\u0022\u003E\u2022\tSource: Arnold AC, \u201CMitochondrial optic neuropathies.\u201D J Neuroophthalmol. 2003;23(4):271\u2013279.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; font-size: x-small;\u0022\u003E\u2022\tSource: Sadun AA, \u201CMitochondrial optic neuropathies.\u201D Eye. 2003;17: 1003\u20131008.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 15,
    "Name": "Lid Tumors",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EWhich of these is the LEAST likely mechanism of action of propranolol when prescribed for management of lid haemangiomas?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Propranolol\u2019s primary mechanisms in infantile hemangiomas include:\u0026nbsp;\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E\u2022\t\u03B2-receptor blockade \u2192 promotes vasoconstriction\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tdownregulates VEGF (vascular endothelial growth factor)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tincreases apoptosis of capillary endothelial cells\u0026nbsp;\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EWhile propranolol can cause systemic bradycardia as a side effect, this is \u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003Enot\u003C/span\u003E the therapeutic mechanism responsible for hemangioma involution. \u003Cspan style=\u0022font-weight: bold;\u0022\u003EIts bradycardia does not selectively reduce tumor blood flow.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 16,
    "Name": "Esotropia",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA 2 year old child was seen by their GP out ouf hours and referred to your emergency clinic. The mother has recently noticed a large esotropia in the child. She reports a recent viral illness. The child is otherwise well. On examination the child will fix either eye but does prefer the right. Eye movements are difficult to ascertain but there is abduction in either eye past the midline. Fundus exam is completed under duress with no clear evidence of papilloedema. Which of the following is MOST likely to influence the management?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022text-decoration-line: underline;\u0022\u003EKey clues:\u0026nbsp;\u003C/span\u003E\u003Cdiv\u003E\u2022\tSudden-onset large esotropia in a 2-year-old\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tRecent viral illness\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tEye movements difficult to assess but some abduction preserved\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tFundoscopy not clearly showing papilloedema (but done under duress, so could miss subtle papilloedema)\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tOtherwise well\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;This scenario is highly suspicious for acquired sixth nerve palsy after a viral illness (post-viral cranial neuropathy). However, in a 2-year-old with acute-onset esotropia, you \u003Cspan style=\u0022font-weight: bold;\u0022\u003Emust exclude raised intracranial pressure\u003C/span\u003E (e.g., a posterior fossa tumor) as a cause of sixth nerve palsy, especially since fundoscopy was incomplete.\n\nTherefore, cranial imaging (usually MRI) is the investigation most likely to influence management, to rule out a serious intracranial lesion before assuming it is benign post-viral palsy.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 17,
    "Name": "Alphabet Patterns",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA 6 year old child presented to clinic with a complaint of intermittent left exotropia that is present 70% of daytime hours, according to his parents. Visual acuities are 6/6 in both eyes. Prism cover test shows an alternating exotropia of 40 prism dioptres base-in for distance and an exophoria of 25 prism dioptres for near, which does not change after half an hour of monocular patching in clinic. There is also a large \u2018V\u2019 pattern but no inferior oblique overaction. If you are considering surgery, which of these procedures would be the MOST appropriate?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "For both A and V patterns, the acronym \u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EMALE\u003C/span\u003E identifies the direction of vertical translation: \u003Cspan style=\u0022font-weight: bold;\u0022\u003EMR to Apex, LR to Ends\u0026nbsp;\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tA V-pattern exotropia means the exotropia is larger in upgaze than downgaze.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tThe appropriate surgery is to recess the \u003Cspan style=\u0022font-weight: bold;\u0022\u003Elateral rectus muscles \u003C/span\u003E(because it is an exotropia), with \u003Cspan style=\u0022font-weight: bold;\u0022\u003Edown-shift\u003C/span\u003E of the insertions to weaken their effect in upgaze, thereby collapsing the V pattern.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tUp-shifting the lateral rectus would be for an A-pattern exotropia (more exotropia in downgaze).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EV pattern is the most common type of pattern in strabismus. The V-pattern is considered to be significant if the difference in horizontal deviation between the up and down gazes is \u2265 15 prism diopters.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-10-f48fbae1-e302-465b-a100-96a36d960537.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EPhoto from: The American Academy Books: Paediatric Ophthalmology and Strabismus \u2013 Chapter 9 \u2013 Pattern Strabismus\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2021 and 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 18,
    "Name": "Sensitivity",
    "Body": "\u003Cp style=\u0022margin: 8pt 0cm 4pt; break-after: avoid; font-family: \u0026quot;Aptos Display\u0026quot;, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold; color: rgb(9, 9, 9);\u0022\u003EAccording to research on Anterior Ischaemic Optic Neuropathy (AION), around 20% of AION patients were found to have Giant Cell Arteritis (GCA) confirmed through temporal artery biopsy (TAB). Of those with positive TAB results, 70% showed elevated ESR levels, whereas only 5% of patients with negative TAB findings had a raised ESR. Based on these figures, what would be the approximate sensitivity of ESR for detecting GCA?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "The question is asking for the \u003Cspan style=\u0022font-weight: bold;\u0022\u003Esensitivity\u003C/span\u003E of ESR to detect GCA in biopsy-positive patients.\u0026nbsp;\u003Cdiv\u003ESensitivity = proportion of true positives detected:\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tAmong patients with biopsy-proven GCA (the \u201Cdisease positives\u201D), 70% had a high ESR.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Therefore, the sensitivity of ESR in this group is 70%.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://thosenerdygirls.org/wp-content/uploads/2022/05/Sarah-1.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EImage Source: https://thosenerdygirls.org/sensitivity-and-specificity/\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 19,
    "Name": "Glaucoma",
    "Body": "Primary congenital glaucoma is usually:",
    "Explanation": "Most cases of primary congenital glaucoma are sporadic. About 10% are inherited as autosomal recessive with incomplete penetrance.",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 20,
    "Name": "Infectious Uveitis",
    "Body": "\u003Cp style=\u0022margin: 8pt 0cm 4pt; break-after: avoid; font-family: \u0026quot;Aptos Display\u0026quot;, sans-serif; color: rgb(15, 71, 97); font-weight: normal; letter-spacing: normal;\u0022\u003E\u003Cstrong style=\u0022font-size: medium;\u0022\u003EIn patients who have recovered from infection with Ebola, and whose serological tests are negative, which ocular tissues / fluids are MOST likely to harbor active viral agents?\u003C/strong\u003E\u003C/p\u003E",
    "Explanation": "Studies have shown that Ebola virus can persist in immune-privileged sites such as the eye even after patients are serologically negative.\u0026nbsp;\u003Cdiv\u003EViral persistence has been demonstrated most notably in the aqueous humour, posing a risk of transmission during intraocular procedures.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;Therefore, the aqueous humour is the most likely ocular site to harbor active viral particles in survivors.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u0026nbsp;Source: Varkey JB, Shantha JG, Crozier I, et al.\nPersistence of Ebola Virus in Ocular Fluid during Convalescence.\nNew England Journal of Medicine. 2015;372(25):2423\u20132427.\nDOI: 10.1056/NEJMoa1500306\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in FRCOphth part 2 written exam in 2022.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 21,
    "Name": "Infectious Uveitis",
    "Body": "\u003Cp style=\u0022margin: 8pt 0cm 4pt; break-after: avoid; font-family: \u0026quot;Aptos Display\u0026quot;, sans-serif; color: rgb(15, 71, 97); letter-spacing: normal;\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EA 45-year-old man is complaining of floaters and reduced vision in one eye. On examination, he has vitritis and a pale lesion near the optic disc. Which of these conditions is the MOST likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u2022\tToxoplasma retinochoroiditis is the \u003Cspan style=\u0022font-weight: bold;\u0022\u003Emost common cause of posterior uveitis worldwide.\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u2022\tIt typically presents with focal retinitis (pale lesion) adjacent to an old pigmented scar, and significant vitritis (\u201C\u003Cspan style=\u0022font-weight: bold;\u0022\u003Eheadlight in the fog\u003C/span\u003E\u201D appearance).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tLesions often occur near the optic disc (juxtapapillary).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther choices are less typical:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022\tAPMPPE usually presents bilaterally with multiple placoid lesions\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tAcute retinal necrosis has more peripheral retinal involvement with severe retinal vasculitis\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tBirdshot chorioretinopathy is bilateral, with cream-colored spots and little vitritis\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Therefore, the most likely diagnosis is toxoplasmosis.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://webeye.ophth.uiowa.edu/eyeforum/atlas/photos/toxoplasmosis/toxoplasma-1-LRG.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003EActive lesions have a classic \u0022headlight in fog\u0022 appearance with a focal, white, fluffy lesion adjacent to an old scar visible through the associated granulomatous uveitis and vitritis\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 22,
    "Name": "Lid Tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA 76 year old man presented to your clinic with a hyperkeratotic lesion on the right upper eyelid. The excisional biopsy histopathology report shows a papillomatous tumor with surface keratin arising from dysplastic epidermis. It has an irregular outline and invades the underlying dermis. Which one of the following is the MOST likely diagnosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\u2022\tHistology describes dysplastic epidermis with invasion into the dermis \u2192 hallmark of carcinoma (malignancy).\u0026nbsp;\u003Cdiv\u003E\u2022\tThe presence of surface keratin and papillomatous growth is consistent with squamous differentiation.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tBasal cell papilloma and squamous cell papilloma are benign lesions without dermal invasion.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tKeratoacanthoma can look similar but typically shows rapid growth, central keratin plug, and may spontaneously regress \u2014 histology would not typically describe persistent dermal invasion from dysplastic epidermis in the same way as SCC.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ETherefore, squamous cell carcinoma is the most likely diagnosis.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ETreatment:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003EWide local excision may be achieved by Mohs\u2019 micrographical technique or by excisional biopsy with histological (e.g. paraffin or frozen section) control. This is usually curative for early lesions. Orbital involvement may require exenteration. SCCs in situ may be treated surgically or with cryotherapy, imiquimod cream, fluorouracil (5-FU), mitomycin, or PDT.*\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ESource: Oxford Handbook of Ophthalmology - Fourth Edition.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 23,
    "Name": "Anti-TB",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of these ophthalmic abnormalities is MOST likely to present in a patient being treated for tuberculosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEthambutol\u003C/b\u003E\u003C/span\u003E, a first-line drug in tuberculosis treatment, is well known for causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etoxic optic neuropathy\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt presents with decreased visual acuity, central or cecocentral scotomas, and red-green colour vision defects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERisk increases with high doses, prolonged use, and renal impairment.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther choices:\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBull\u2019s eye maculopathy \u2192 classically linked to hydroxychloroquine toxicity\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPigmentary retinopathy \u2192 linked to drugs like phenothiazines\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVortex keratopathy \u2192 linked to amiodarone, chloroquine, and some other drugs\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore, optic neuropathy is the most likely ocular side effect in TB treatment.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium; color: rgb(255, 0, 0); text-decoration-line: underline;\u0022\u003ERemember these common side effects:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-10-01b7aefd-0191-450c-90a2-4273dcd8ed32.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 24,
    "Name": "Visual Field",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EOn reading a Humphreys visual field printout, which of the following parameters is MOST likely to indicate an inaccurate visual field?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFalse positive errors\u003C/b\u003E\u003C/span\u003E occur when the patient responds when no stimulus is given, often due to over-anticipation or poor test understanding. High false positive rates can make the field appear \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebetter than it really is\u003C/b\u003E\u003C/span\u003E, leading to unreliable results.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFalse negatives\u003C/b\u003E\u003C/span\u003E (patient fails to respond to bright stimuli) can occur in true disease or fatigue, but are less indicative of an \u003Ci\u003Eunreliable\u003C/i\u003E field compared to high false positives.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFixation losses\u003C/b\u003E\u003C/span\u003E of 2/11 are acceptable (\u0026lt;20%).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMean deviation\u003C/b\u003E\u003C/span\u003E of -2.82 dB is within mild loss range and does not itself indicate unreliability.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EKey point:\u003C/b\u003E\u003C/span\u003E In reliability indices, \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Efalse positives are the biggest red flag\u003C/b\u003E\u003C/span\u003E for an inaccurate Humphrey visual field.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 25,
    "Name": "Cross-linking",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECollagen cross linking works by increasing cornea\u2019s rigidity with the release of oxygen free radical as a result of the combination of which of the following vitamins?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorneal collagen cross-linking\u003C/b\u003E\u003C/span\u003E is used to strengthen the cornea, most often in keratoconus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe standard (\u201CDresden\u201D) protocol uses \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eriboflavin (vitamin B2)\u003C/b\u003E\u003C/span\u003E applied to the cornea, followed by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUVA irradiation\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERiboflavin absorbs UVA and generates reactive oxygen species, which induce covalent cross-links between collagen fibers, increasing corneal rigidity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUVB is not used because it is more harmful to the corneal endothelium and deeper ocular structures.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVitamin B6 is not involved in this process.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 26,
    "Name": "Fourth Nerve Palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhat abnormal head position (AHP) would you expect to see in the presence of a LEFT superior oblique palsy?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleft superior oblique palsy\u003C/b\u003E\u003C/span\u003E causes vertical diplopia that worsens on looking down and in.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatients tilt their head \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaway from the affected side\u003C/b\u003E\u003C/span\u003E (right tilt in this case) to reduce the vertical deviation (Bielschowsky head tilt test).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThey may also turn their face \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etowards the side of the affected muscle\u003C/b\u003E\u003C/span\u003E (left face turn) to optimise binocular single vision in primary gaze.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESo the typical abnormal head posture for left SO palsy is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright head tilt with left face turn\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 27,
    "Name": "Field defect",
    "Body": "\u003Cbr\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EThis is the result of the neuro-imaging tests you ordered for your patient, What is the MOST likely visual field defect they were complaining of?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-10-4bbd366f-f484-4deb-83b4-87026035c178.png\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003E\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EFrom the MRI brain (left) and MR angiogram (right), the key abnormality is an infarct in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleft occipital lobe\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe occipital lobe contains the primary visual cortex, which processes visual information from the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econtralateral visual field\u003C/b\u003E\u003C/span\u003E of both eyes.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003ELesion Location and Effect\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELeft occipital lobe\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E damage \u2192 affects \u003C/span\u003E\u003Cb\u003Eright visual fields\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of both eyes.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis produces a \u003C/span\u003E\u003Cb\u003Eright homonymous hemianopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 28,
    "Name": "CMO",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 62 year old gentleman, a known diabetic for 10 years, underwent phacoemulsification with intraoperative posterior capsular rupture, anterior vitrectomy with implantation of anterior chamber intraocular lens. At the one-month post-operative review, he had a best corrected visual acuity of 6/6 with a normal macular appearance. However, at 8 weeks postoperatively, he presented with blurring and deterioration of vision 6/18. His intraocular pressure was within normal limits.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFundus examination was normal apart from a dull foveal reflex. Macular OCT scans showed cystoid macular oedema. Which of the following is the LEAST correct management option?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe OCT shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecystoid macular oedema (CMO)\u003C/b\u003E\u003C/span\u003E \u2014 a common complication after cataract surgery, especially with intraoperative complications like posterior capsular rupture and anterior vitrectomy. This is most likely \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIrvine\u2013Gass syndrome\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETypical management options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFirst line:\u003C/b\u003E\u003C/span\u003E Topical NSAIDs (e.g., nepafenac) and topical corticosteroids (prednisolone)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESecond line:\u003C/b\u003E\u003C/span\u003E Periocular or intravitreal corticosteroids (triamcinolone, dexamethasone implant)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnti-VEGF agents like \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebevacizumab\u003C/b\u003E\u003C/span\u003E are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E standard for post-surgical CMO unless there is coexistent macular oedema due to diabetic retinopathy or vein occlusion.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleast likely correct\u003C/b\u003E\u003C/span\u003E option here is:\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;Intravitreal injection Avastin (Bevacizumab 1.25 mg/0.05 ml)\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 29,
    "Name": "OCT",
    "Body": "\u003Cimg src=\u0022https://www.eyedocs.co.uk/images/eyeq/spectral_OCT.jpg\u0022\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn the spectral domain OCT image above, what is the layer labelled A?\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003Cimg src=\u0022https://www.eyedocs.co.uk/images/eyeq/OCT_01a.jpg\u0022\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 30,
    "Name": "Congenital Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 38 year old man presents with raised intraocular pressure, posterior embryotoxon, corectopia and hypodontia. Which of the following genetic mutations is MOST likely to be associated with his condition?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe features described \u2014 \u003C/span\u003E\u003Cb\u003Eposterior embryotoxon\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Ecorectopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Ehypodontia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eraised IOP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2014 are classic for \u003C/span\u003E\u003Cb\u003EAxenfeld\u2013Rieger syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAxenfeld\u2013Rieger syndrome is caused by mutations in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPITX2\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFOXC1\u003C/b\u003E\u003C/span\u003E genes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFOXC1 mutations are strongly associated with anterior segment dysgenesis, abnormal iris development, and systemic features like dental anomalies.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECYP450\u003C/b\u003E\u003C/span\u003E \u2014 unrelated to this syndrome; involved in drug metabolism.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMYOC\u003C/b\u003E\u003C/span\u003E \u2014 linked to juvenile open-angle glaucoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOPTN\u003C/b\u003E\u003C/span\u003E \u2014 linked to normal-tension glaucoma.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 31,
    "Name": "CSCR",
    "Body": "\u003Cimg src=\u0022https://www.eyedocs.co.uk/images/eyeq/OCT_001.jpg\u0022\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EBased on the OCT image shown, What is the most likely diagnosis?\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "The OCT shows a localised neurosensory detachment of the retina at the fovea. These findings are most consistent with central serous chorioretinopathy.\u003Cdiv\u003EIn neovascular Age related macular degeneration, neurosensory detachment can occur but it is usually associated with cystic retinal changes, drusen, and RPE changes.\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 32,
    "Name": "OHT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; color: rgb(14, 14, 14);\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold; font-family: Arial;\u0022\u003EBased on findings from the Ocular Hypertension Treatment Study (OHTS), which of the following options is the least accurate regarding baseline demographic and clinical factors that predict the likelihood of developing primary open-angle glaucoma (POAG)?\u003C/span\u003E\u003C/blockquote\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003Erom the \u003C/span\u003E\u003Cb\u003EOcular Hypertension Treatment Study (OHTS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the key baseline predictors for conversion to \u003C/span\u003E\u003Cb\u003Eprimary open-angle glaucoma (POAG)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E were:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOlder age\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAfrican American race\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELarger vertical cup-to-disc ratio\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigher IOP\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThinner central corneal thickness\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGreater pattern standard deviation on visual field testing\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EMigraine\u003C/b\u003E\u003C/span\u003E was \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E identified as a significant risk factor in OHTS, making option \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EC\u003C/b\u003E\u003C/span\u003E the least correct.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 33,
    "Name": "Retrobulbar Hemorrhage",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAn elderly man presents to A\u0026amp;E in the afternoon after undergoing bilateral lower lid blepharoplasties in the morning. He reports pain and sudden loss of vision in his right eye. The resident doctor measures an intraocular pressure of 40 mmHg. Which of the following is MOST likely to be an appropriate part of the IMMEDIATE management?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis presentation is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretrobulbar haemorrhage\u003C/b\u003E\u003C/span\u003E after eyelid surgery, causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorbital compartment syndrome\u003C/b\u003E\u003C/span\u003E with a dangerously high intraocular pressure and threat to optic nerve perfusion.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EImmediate sight-saving management\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELateral canthotomy and cantholysis\u003C/b\u003E\u003C/span\u003E (disinsertion of lids from the lateral canthus) to rapidly decompress the orbit\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMedical therapy (acetazolamide, mannitol, etc.) may follow, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esurgical decompression should not be delayed\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOther choices:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcetazolamide\u003C/b\u003E\u003C/span\u003E (A) helps lower IOP but is too slow alone in this acute compartment syndrome.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-dose corticosteroids\u003C/b\u003E\u003C/span\u003E (C) are not first-line in this scenario.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOpening surgical wounds\u003C/b\u003E\u003C/span\u003E (D) does not adequately decompress the orbit.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 34,
    "Name": "Cellulitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following is the MOST common organism in preseptal cellulitis associated with trauma in the majority of cases?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPreseptal cellulitis\u003C/b\u003E\u003C/span\u003E following trauma is most often caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eskin flora\u003C/b\u003E\u003C/span\u003E entering through the wound.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe most common organism is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStaphylococcus aureus\u003C/b\u003E\u003C/span\u003E, including MRSA in some regions.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBacillus cereus\u003C/b\u003E\u003C/span\u003E \u2014 more associated with penetrating ocular trauma involving organic material (e.g., soil, plant matter).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHaemophilus influenzae\u003C/b\u003E\u003C/span\u003E \u2014 historically common in children before Hib vaccination.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStreptococcus pneumoniae\u003C/b\u003E\u003C/span\u003E \u2014 can be a cause but is less common in trauma-related cases compared to S. aureus.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 35,
    "Name": "AMD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EAll of the following carotenoids are important for macular function EXCEPT:\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe macular pigment is composed mainly of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elutein\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ezeaxanthin\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emeso-zeaxanthin\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese carotenoids act as antioxidants and filter harmful blue light, supporting macular health and visual function.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIonones\u003C/b\u003E\u003C/span\u003E are aromatic compounds derived from carotenoids but are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E part of the macular pigment and do not contribute directly to macular function.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ERemember:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003Ein AREDS, vitamin supplements containing high-dose antioxidants and minerals (vitamins C and E, \u03B1-carotene, and zinc) delayed AMD progression from intermediate to advanced stages (particularly those in category 4 with neovascular AMD already in one eye).\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u03B2 -carotene may lead to an increased incidence of lung cancer in former smokers\u003C/li\u003E\u003Cli\u003Ethe results of AREDS2 suggest that lutein \u002B zeaxanthin may be an appropriate carotenoid substitute.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ENumerous supplements are commercially available, including: Bausch \u0026amp; Lomb\u2019s PreserVision\u00AE  (AREDS and AREDS2 formulations) and Alcon\u2019s I-Caps\u00AE .\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 Written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 36,
    "Name": "Phakomatosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich ONE of the following statements is MOST likely to be correct in regards to Neurofibromatosis NF2?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENF2\u003C/b\u003E\u003C/span\u003E is characterised by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral vestibular schwannomas\u003C/b\u003E\u003C/span\u003E, often leading to hearing loss, tinnitus, imbalance, and cranial nerve deficits.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELoss of the corneal reflex can occur due to involvement of the trigeminal nerve (CN V) by tumours.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKyphoscoliosis\u003C/b\u003E\u003C/span\u003E (A) and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELisch nodules\u003C/b\u003E\u003C/span\u003E (B) are features of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENF1\u003C/b\u003E\u003C/span\u003E, not NF2.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENF2\u003C/b\u003E\u003C/span\u003E is caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENF2 gene\u003C/b\u003E\u003C/span\u003E on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echromosome 22\u003C/b\u003E\u003C/span\u003E, not chromosome 17 (D). Chromosome 17 is linked to NF1.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 37,
    "Name": "DVLA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich one of the following conditions would be MOST LIKELY to cause a United Kingdom Group 1 driving licence to be revoked?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDVLA standards for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGroup 1 drivers\u003C/b\u003E\u003C/span\u003E require a horizontal visual field of at least \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E120 degrees\u003C/b\u003E\u003C/span\u003E with no significant defect within the central 20 degrees.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EComplete homonymous hemianopia\u003C/b\u003E\u003C/span\u003E causes a large central field defect, meaning the driver cannot meet visual field standards, leading to licence revocation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EColour blindness\u003C/b\u003E\u003C/span\u003E (A) is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E a bar to driving in the UK.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGlaucoma\u003C/b\u003E\u003C/span\u003E (C) is only disqualifying if it causes field loss below standards \u2014 ocular hypertension alone does not.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoconus\u003C/b\u003E\u003C/span\u003E (D) is acceptable if vision with correction meets the required standard (6/12 or better in both eyes together).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 38,
    "Name": "Non-infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 48 year old man with a history of recurrent red eyes for 15 years presented to your clinic. His red eyes were usually treated with topical lubricants and antibiotics. On examination, you noted that he has a peripheral corneal infiltrate with inferonasal corneal vascularisation in his right eye. Which of the following is the MOST likely diagnosis?\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERosacea keratitis\u003C/b\u003E\u003C/span\u003E is associated with chronic ocular surface inflammation, recurrent redness, and peripheral corneal vascularisation, often infero-nasal or inferior.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt can cause peripheral corneal infiltrates, thinning, and vascularisation due to chronic eyelid margin disease and meibomian gland dysfunction linked to rosacea.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther choices:\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDisciform keratitis\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is usually due to herpes simplex virus and presents as stromal oedema with an intact epithelium.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMarginal keratitis\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is typically a hypersensitivity reaction to staphylococcal antigens, presenting with small peripheral infiltrates near the limbus.\u0026nbsp;A perilimbal clear zone of cornea is preserved.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripheral ulcerative keratitis\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is often associated with systemic autoimmune diseases such as rheumatoid arthritis, presenting with peripheral stromal thinning and ulceration.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 39,
    "Name": "Physiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following BEST describes the sequence of changes in visual photopigments after light exposure?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evisual cycle\u003C/b\u003E\u003C/span\u003E, light converts \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E11-cis retinal\u003C/b\u003E\u003C/span\u003E (bound to opsin in rhodopsin) into \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eall-trans retinal\u003C/b\u003E\u003C/span\u003E \u2192 triggers a conformational change in opsin and initiates phototransduction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAll-trans retinal\u003C/b\u003E\u003C/span\u003E is then reduced to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eall-trans retinol\u003C/b\u003E\u003C/span\u003E in the photoreceptor.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis is transported to the retinal pigment epithelium (RPE), where it is converted back to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E11-cis retinol\u003C/b\u003E\u003C/span\u003E, and then oxidised to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E11-cis retinal\u003C/b\u003E\u003C/span\u003E, ready to recombine with opsin.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThis is a very common question in FRCOphth written exams.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 40,
    "Name": "Retrobulbar Hemorrhage",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EYou were called to see a 68 year old man in the emergency department. He gives a history of being on Warfarin, and had tripped over a step in his house. On examination, there is tense proptosis of the left eye with peri-orbital bruising, subconjunctival hemorrhage, restricted ocular motility, visual acuity of counting fingers, and a relative afferent pupillary defect. You could not examine the fundus. What is the MOST appropriate immediate management for this patient?\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis presentation is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorbital compartment syndrome\u003C/b\u003E\u003C/span\u003E due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretrobulbar haemorrhage\u003C/b\u003E\u003C/span\u003E, with sight-threatening optic nerve compression.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey signs: acute proptosis, tense orbit, severe vision drop, RAPD, restricted motility, and high-risk history (warfarin use, trauma).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EImmediate management\u003C/b\u003E\u003C/span\u003E: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELateral canthotomy and cantholysis\u003C/b\u003E\u003C/span\u003E at the bedside to decompress the orbit and restore optic nerve perfusion \u2014 this is sight-saving.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAcetazolamide lowers intraocular pressure but is too slow as the primary intervention.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOrbital wall decompression is a surgical procedure for chronic proptosis, not acute haemorrhage.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVitamin K addresses anticoagulation but does not relieve the immediate orbital pressure.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 41,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of these is the MOST appropriate prophylactic treatment for the prevention of recurrent herpes simplex keratitis?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprophylaxis\u003C/b\u003E\u003C/span\u003E against recurrent herpes simplex keratitis, the standard regimen is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoral aciclovir 400 mg twice daily\u003C/b\u003E\u003C/span\u003E for at least 6\u201312 months, as shown in the Herpetic Eye Disease Study (HEDS).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigher doses\u003C/b\u003E\u003C/span\u003E (800 mg 5\u00D7 daily) are used for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eactive treatment\u003C/b\u003E\u003C/span\u003E of herpes simplex infections, not prophylaxis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELower doses\u003C/b\u003E\u003C/span\u003E (200 mg bd) are subtherapeutic for prevention.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E800 mg bd\u003C/b\u003E\u003C/span\u003E is not a standard prophylactic dose and increases side effect risk unnecessarily.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 42,
    "Name": "Keratoconus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following is LEAST likely to be a sign suggestive of keratoconus?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKeratoconus signs on corneal topography\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInferior steepening relative to superior cornea\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESkewed radial axes (non-orthogonal bow tie)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAbnormal curvature progression (greater in downgaze/upgaze)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWavefront analysis\u003C/b\u003E\u003C/span\u003E: Vertical coma is the most characteristic higher-order aberration in keratoconus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAsymmetrical bow tie pattern with high angle kappa\u003C/b\u003E\u003C/span\u003E may mimic keratoconus but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E truly diagnostic or suggestive of keratoconus.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn keratoconus, the cone is often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einferiorly displaced\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhen you measure the corneal curvature in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edowngaze\u003C/b\u003E\u003C/span\u003E, the cone comes into the measurement zone \u2192 readings become \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esteeper\u003C/b\u003E\u003C/span\u003E than in primary gaze.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis is sometimes referred to as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cgaze-dependent keratometric change\u201D\u003C/b\u003E\u003C/span\u003E, and it helps distinguish keratoconus from normal corneas or regular astigmatism.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 43,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of these drugs is LEAST likely to be helpful in the management of a patient with diabetic macular oedema?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDapagliflozin\u003C/b\u003E\u003C/span\u003E \u2013 An SGLT2 inhibitor, improves glycaemic control, may reduce fluid overload, and has shown some promise in protecting against diabetic retinopathy progression.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFenofibrate\u003C/b\u003E\u003C/span\u003E \u2013 Supported by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFIELD\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EACCORD-Eye\u003C/b\u003E\u003C/span\u003E trials: reduces progression of diabetic retinopathy independent of lipid-lowering effects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPioglitazone\u003C/b\u003E\u003C/span\u003E \u2013 A thiazolidinedione. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAdverse effect\u003C/b\u003E\u003C/span\u003E: fluid retention and increased risk of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eworsening macular oedema\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERosuvastatin\u003C/b\u003E\u003C/span\u003E \u2013 Statins help improve endothelial function, lower lipid leakage, and some studies suggest reduced risk of diabetic retinopathy progression.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 44,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following is LEAST likely to be a manifestation of herpes zoster keratitis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHerpes Zoster Ophthalmicus (HZO)\u003C/b\u003E\u003C/span\u003E can present with a variety of corneal manifestations:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpithelial keratitis\u003C/b\u003E\u003C/span\u003E: Early lesions present as \u003Ci\u003Epunctate epithelial keratitis\u003C/i\u003E, which may progress to pseudodendrites (unlike the true dendrites of HSV).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStromal keratitis\u003C/b\u003E\u003C/span\u003E: May be nummular or diffuse; occurs due to immune-mediated inflammation after viral reactivation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEndotheliitis\u003C/b\u003E\u003C/span\u003E: Inflammation of the corneal endothelium, often with keratic precipitates and stromal edema, is a recognized complication of HZO.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\uD83D\uDC49 \u003C/span\u003E\u003Cb\u003EThickened corneal nerves\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, however, is \u003C/span\u003E\u003Cb\u003Enot a feature of herpes zoster keratitis\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThis finding is more typically associated with \u003C/span\u003E\u003Cb\u003Eherpes simplex keratitis (HSK)\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E or systemic conditions such as \u003C/span\u003E\u003Cb\u003Emultiple endocrine neoplasia (MEN), leprosy, or neurofibromatosis\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cimg src=\u0022https://eyewiki.org/w/images/a/ae/Corneal_Nerves.jpg?20221007230607\u0022 class=\u0022\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022 style=\u0022text-align: left;\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold; font-style: italic;\u0022\u003ECorneal nerves visible on slit lamp photograph\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022 style=\u0022text-align: left;\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold; font-style: italic;\u0022\u003ESource:\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Ehttps://eyewiki.org/File:Corneal_Nerves.jpg\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022 style=\u0022text-align: left;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022 style=\u0022text-align: left;\u0022\u003E\u003Cspan class=\u0022s3\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
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    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
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  },
  {
    "Id": 45,
    "Name": "Tests",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn Right Monofixation syndrome, what is the MOST likely response to Worth 4 dot test at near (33 cm)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMonofixation syndrome = small-angle deviation with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral fusion\u003C/b\u003E\u003C/span\u003E and a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecentral suppression scotoma\u003C/b\u003E\u003C/span\u003E in the non\u2011fixating eye (here, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright\u003C/b\u003E\u003C/span\u003E eye).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWorth 4\u2011dot at near (33 cm)\u003C/b\u003E\u003C/span\u003E the target subtends a larger visual angle, engaging \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral fusion\u003C/b\u003E\u003C/span\u003E and lying largely outside the small central scotoma \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efusion (4 dots)\u003C/b\u003E\u003C/span\u003E is the most typical response.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edistance Worth (6 m)\u003C/b\u003E\u003C/span\u003E the target is much smaller and falls within the central scotoma, so patients often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuppress the right eye\u003C/b\u003E\u003C/span\u003E and report \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethree green dots\u003C/b\u003E\u003C/span\u003E (since the white dot is seen only by the left/green eye).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EHence the expected \u003Ci\u003Enear\u003C/i\u003E response is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efour dots with fusion\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EReferences (standard texts):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVon Noorden \u0026amp; Campos. \u003Ci\u003EBinocular Vision and Ocular Motility\u003C/i\u003E, Monofixation syndrome and Worth 4\u2011dot testing.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWright \u0026amp; Strube. \u003Ci\u003EPediatric Ophthalmology and Strabismus\u003C/i\u003E, Worth test interpretation in monofixation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHolmes JM et\u202Fal. Monofixation syndrome\u2014clinical characteristics and sensory findings.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 46,
    "Name": "Chemical injury",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EWhich of the following statements is MOST likely to be correct regarding chemical eye injury?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAlkaline injury\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlkalis (e.g., ammonia, lye, lime) penetrate rapidly due to saponification of cell membrane lipids.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThey cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehydrophilic and lipophobic degeneration\u003C/b\u003E\u003C/span\u003E, allowing deep penetration into ocular tissues (stroma, anterior chamber).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMuch more severe than acid burns (which typically cause coagulative necrosis, forming a barrier).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDiphoterine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDiphoterine is indeed a chelating amphoteric solution used in Europe for chemical burns, but its \u003Ci\u003Eproven\u003C/i\u003E superiority over copious water/normal saline irrigation is still debated in clinical practice.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFirst-degree burn\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn dermatology, \u003C/span\u003E\u003Cb\u003Efirst-degree burns involve only the epidermis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (not dermis). Dermis is affected in \u003C/span\u003E\u003Cb\u003Esecond-degree burns\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDua classification\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDua classification\u003C/b\u003E\u003C/span\u003E (2001) has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E6 grades\u003C/b\u003E\u003C/span\u003E, based on limbal involvement (clock hours) and conjunctival involvement (%).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESo, the statement of \u201C4 levels\u201D is incorrect.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDCDA Sources:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDua HS et al. \u003Ci\u003EA new classification of ocular surface burns\u003C/i\u003E. Br J Ophthalmol. 2001.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EKuckelkorn R et al. \u003Ci\u003EChemical and thermal eye burns: emergency and clinical management\u003C/i\u003E. Ophthalmologe. 2002.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAmerican Academy of Ophthalmology (AAO): \u003Ci\u003EOcular Trauma \u2013 Chemical Injuries\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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  },
  {
    "Id": 47,
    "Name": "Trauma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA 28 year old man presented with blurred vision in both eyes after regaining consciousness following a head injury with a left fronto-parietal skull fracture. On examination, his vision was No Perception of Light\u0026nbsp; in the left eye and 6/9 in the right with a right temporal visual field defect. Ocular examination, and eye movements were normal with normal lids. The left pupil shows an afferent pupillary defect, and both optic discs appear atrophic; left more than right. From these signs, what is the MOST likely location of injury to the visual pathways?\u0026nbsp;\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey findings\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeft eye\u003C/b\u003E\u003C/span\u003E: No perception of light (severe optic nerve damage).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERight eye\u003C/b\u003E\u003C/span\u003E: Visual acuity 6/9 but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etemporal field defect\u003C/b\u003E\u003C/span\u003E (indicating involvement of nasal retinal fibers crossing in the chiasm).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERelative afferent pupillary defect (RAPD) in left eye\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: confirms more severe left optic nerve damage.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBilateral optic atrophy (left \u0026gt; right)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: chronic optic nerve/chiasmal injury.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhy not the other options?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOccipital infarct\u003C/b\u003E\u003C/span\u003E \u2192 would cause homonymous hemianopia, not monocular blindness \u002B contralateral temporal field loss.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptic nerve avulsion\u003C/b\u003E\u003C/span\u003E \u2192 usually unilateral, would not explain contralateral temporal hemianopia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetrobulbar haemorrhage\u003C/b\u003E\u003C/span\u003E \u2192 acute vision loss from orbital compartment syndrome, but would not selectively cause chiasmal field defects.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ED: Traumatic optic neuropathy with chiasmal involvement\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETrauma can damage both the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic nerve\u003C/b\u003E\u003C/span\u003E (left side severe) and the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic chiasm\u003C/b\u003E\u003C/span\u003E (affecting crossing nasal fibers \u2192 temporal field loss in right eye).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis explains the combination: unilateral blindness \u002B contralateral temporal field defect \u002B disc pallor.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDCDA Supporting sources:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMiller NR, Newman NJ. \u003Ci\u003EWalsh \u0026amp; Hoyt\u2019s Clinical Neuro-ophthalmology\u003C/i\u003E, 6th ed.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAmerican Academy of Ophthalmology (AAO) \u2013 \u003Ci\u003ENeuro-ophthalmology: Optic Neuropathies after Trauma\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": true,
    "CategoryId": 13,
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  },
  {
    "Id": 48,
    "Name": "Intra-ocular tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 63 year old woman presents with a pigmented lesion in the periphery of her right iris. Which of the following characteristics would make you MOST suspicious of a ciliary body melanoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECiliary body melanoma\u003C/b\u003E\u003C/span\u003E is a uveal melanoma, and often not visible on initial presentation because the ciliary body is posterior to the iris root.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EClues suggesting malignancy include\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProminent sentinel episcleral vessel\u003C/b\u003E\u003C/span\u003E \u2192 a dilated, tortuous episcleral vessel in the same quadrant as the tumor. This is considered one of the most important clinical signs of an underlying ciliary body melanoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIris distortion or corectopia (irregular pupil) may occur, but are less specific.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u201CSatellite lesions\u201D are more suggestive of conjunctival melanoma rather than intraocular (ciliary body) melanoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EConjunctival vessels are not typically associated with ciliary body tumors, but episcleral \u201Csentinel\u201D vessels are.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDCDA Supporting sources:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EShields JA, Shields CL. \u003Ci\u003EIntraocular Tumors: An Atlas and Textbook\u003C/i\u003E, 3rd ed.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAmerican Academy of Ophthalmology (AAO) \u2013 \u003Ci\u003EOcular Oncology and Pathology\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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  },
  {
    "Id": 49,
    "Name": "Fourth Nerve Palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following is LEAST likely to be a feature of a bilateral IV nerve palsy?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBilateral trochlear (IV) nerve palsy\u003C/b\u003E\u003C/span\u003E \u2192 affects both superior oblique muscles.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETypical clinical features include:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVertical diplopia\u003C/b\u003E\u003C/span\u003E (worse on downgaze, such as reading or going downstairs).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESmall hypertropia in primary gaze.\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPositive Bielschowski head tilt test to both sides:\u003C/b\u003E\u003C/span\u003E\u0026nbsp;hypertropia increases when head tilts to either shoulder.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReversing vertical diplopia with horizontal gaze:\u003C/b\u003E\u003C/span\u003E\u0026nbsp;the higher eye switches depending on the direction of gaze (right vs left).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EHead posture in bilateral IV palsy\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatients usually adopt a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echin-down\u003C/b\u003E\u003C/span\u003E posture to reduce diplopia (to avoid using downgaze where diplopia is worst).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChin-up posture\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is not typical and therefore is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleast likely\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 50,
    "Name": "Microbiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWith regard to routine media used in bacteriology, which statement is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMacConkey agar\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESelective and differential medium.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInhibits gram-positive organisms (due to bile salts and crystal violet).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ESpecifically supports growth of \u003C/span\u003E\u003Cb\u003Egram-negative rods (enteric bacteria, e.g., E. coli, Klebsiella)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDifferentiates \u003C/span\u003E\u003Cb\u003Elactose fermenters (pink colonies)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E from \u003C/span\u003E\u003Cb\u003Enon-fermenters (colorless colonies)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EChocolate agar\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEnriched medium (lysed blood cells release growth factors).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUsed for \u003C/span\u003E\u003Cb\u003Efastidious organisms\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E like \u003Ci\u003ENeisseria\u003C/i\u003E and \u003Ci\u003EHaemophilus influenzae\u003C/i\u003E, \u003C/span\u003E\u003Cb\u003Enot anaerobes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMeat broth\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEnrichment medium for cultivating \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanaerobic bacteria\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot acanthamoeba\u003C/b\u003E\u003C/span\u003E (acanthamoeba is typically cultured on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-nutrient agar with E. coli overlay\u003C/b\u003E\u003C/span\u003E).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENutrient agar\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGeneral-purpose medium for non-fastidious organisms.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot selective for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egram-negative cocci\u003C/b\u003E\u003C/span\u003E (which are fastidious and grow better on chocolate agar).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 51,
    "Name": "Microbiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ERegarding the microscopic examination of a preparation suspected of containing Acanthamoeba, which of the following preparations would be LEAST likely to be useful?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba\u003C/b\u003E\u003C/span\u003E is a free-living amoeba causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba keratitis\u003C/b\u003E\u003C/span\u003E and granulomatous amoebic encephalitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUseful diagnostic preparations\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECalcofluor white\u003C/b\u003E\u003C/span\u003E: Binds to cellulose and chitin in cyst walls \u2192 fluoresces under UV.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGiemsa stain\u003C/b\u003E\u003C/span\u003E: Demonstrates trophozoites and cysts.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKOH wet mount\u003C/b\u003E\u003C/span\u003E: Dissolves keratinous tissue and debris, making cysts visible.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcid-fast stain\u003C/b\u003E\u003C/span\u003E: Designed for organisms with mycolic acid in their cell wall (e.g., \u003Ci\u003EMycobacterium\u003C/i\u003E). \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba does not stain acid-fast\u003C/b\u003E\u003C/span\u003E, so this is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleast useful preparation\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-20-d3ef375a-8f1b-4f9a-ad9f-24423e033c67.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 52,
    "Name": "Vitrectomy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 73-year-old woman is undergoing phacovitrectomy for a stage 4 macular hole with good vision in the fellow eye and problems with postoperative posturing. Which intravitreal gas is the MOST appropriate to use as a retinal tamponade in this situation?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal tamponade gases\u003C/b\u003E\u003C/span\u003E are used to close macular holes by providing internal pressure.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe choice depends on \u003C/span\u003E\u003Cb\u003Eduration of tamponade\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Epatient compliance with posturing\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EGas options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESF6 (Sulphur hexafluoride):\u003C/b\u003E\u003C/span\u003E Short-acting (1\u20132 weeks). Expansion 2x. Used at 20% concentration.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC3F8 (Perfluoropropane):\u003C/b\u003E\u003C/span\u003E Long-acting (up to 6\u20138 weeks). Expansion 4x. Used at 12\u201314% concentration.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAir:\u003C/b\u003E\u003C/span\u003E Lasts only a few days, sometimes used in compliant patients.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022color: rgb(88, 0, 255);\u0022\u003E\u003Cb\u003E\u201CShort Six, Prolonged Propane\u0022\u0026nbsp;\u003C/b\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003ESF6 \u2192 Short (1\u20132 weeks),\u0026nbsp;\u003C/b\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EC3F8 \u2192 Prolonged (6\u20138 weeks)\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022text-decoration-line: underline;\u0022\u003EWhy 12% C3F8 here?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatient has difficulty posturing \u2192 requires a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elong-acting tamponade\u003C/b\u003E\u003C/span\u003E to keep the hole closed despite suboptimal compliance.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E12% C3F8\u003C/b\u003E\u003C/span\u003E provides prolonged support and is the standard choice for macular hole surgery in such cases.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigher concentrations (36% C3F8, 80% SF6) are dangerous because they expand excessively \u2192 risk of raised IOP and ischemia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E5% SF6 is too low to be effective (wrong concentration).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 53,
    "Name": "Demyelinating diseases",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 21-year-old lady presents complaining of acute unilateral visual loss. Her visual acuity is OD 6/6 and OS 6/60. The right optic nerve appears pale and the left optic nerve is oedematous. Colour vision is reduced in both eyes. She had a brief febrile illness when she was 8 associated with cognitive changes and seizures but recovered fully and there is no other past medical history of note. Which of the following results would MOST likely be positive?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis is a \u003C/span\u003E\u003Cb\u003Eclassic presentation of demyelinating optic neuritis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, commonly linked with \u003C/span\u003E\u003Cb\u003EMultiple Sclerosis (MS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFeatures supporting MS-related optic neuritis:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EYoung woman (20 years old)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 typical age group.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcute unilateral visual loss\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Ereduced colour vision\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOptic disc: one side pale (old optic neuritis), other swollen (acute episode).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHistory of a prior \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneurological episode\u003C/b\u003E\u003C/span\u003E (febrile illness with seizures/cognitive changes may have been a prior demyelinating attack).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EAnswer choices in context:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAQP4 antibody\u003C/b\u003E\u003C/span\u003E \u2192 suggests \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENeuromyelitis Optica (NMO)\u003C/b\u003E\u003C/span\u003E. Typically more severe, bilateral simultaneous optic neuritis, associated with longitudinally extensive transverse myelitis. Not the best fit here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBorrelia serology\u003C/b\u003E\u003C/span\u003E \u2192 would be relevant if Lyme disease suspected (tick bite, systemic features). Not consistent with this case.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECSF oligoclonal bands\u003C/b\u003E\u003C/span\u003E \u2192 Seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E85\u201395% of MS patients\u003C/b\u003E\u003C/span\u003E; the most likely positive test in this scenario.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMOG antibody\u003C/b\u003E\u003C/span\u003E \u2192 Associated with MOG-associated disease (MOGAD). Often presents in younger patients and children, more likely bilateral or recurrent optic neuritis with disc swelling. Less likely here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 54,
    "Name": "Intra-ocular tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ELooking at the image below, which of the following groups of factors are MOST associated with an increased risk of lesion growth?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-20-25ee3753-4099-4ed7-b147-c3dec1565b37.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe lesion in the fundus photo is suggestive of a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoroidal nevus\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003ERisk factors for transformation into \u003C/span\u003E\u003Cb\u003Echoroidal melanoma\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E have been well studied in the \u003C/span\u003E\u003Cb\u003ECOMS (Collaborative Ocular Melanoma Study)\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E and \u003C/span\u003E\u003Cb\u003EShields\u2019 mnemonic \u201CTo Find Small Ocular Melanoma Using Helpful Hints Daily\u201D\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ET\u003C/b\u003E\u003C/span\u003E: Thickness \u0026gt; 2 mm\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EF\u003C/b\u003E\u003C/span\u003E: Subretinal Fluid\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ES\u003C/b\u003E\u003C/span\u003E: Symptoms (e.g., vision loss, photopsia)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EO\u003C/b\u003E\u003C/span\u003E: Orange pigment (lipofuscin)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EM\u003C/b\u003E\u003C/span\u003E: Margin within 3 mm of optic disc\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUH\u003C/b\u003E\u003C/span\u003E: Ultrasonographic Hollowness\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EH\u003C/b\u003E\u003C/span\u003E: Absence of halo\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ED\u003C/b\u003E\u003C/span\u003E: Absence of drusen\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsence of drusen\u003C/b\u003E\u003C/span\u003E (which suggest chronic, stable lesion) increases the risk that the lesion is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eactive\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe presence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubretinal fluid\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethickness \u0026gt; 2 mm\u003C/b\u003E\u003C/span\u003E are major risk factors for growth.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-20-cd528ecf-460c-4ed5-80bf-528d70d2c931.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 55,
    "Name": "Supra-nuclear palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWith regard to ataxia telangiectasia, which of these statements is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAtaxia-telangiectasia (A-T)\u003C/b\u003E\u003C/span\u003E is a rare, autosomal recessive neurodegenerative disorder caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EATM gene\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey features:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOnset:\u003C/b\u003E\u003C/span\u003E Early childhood (usually before age 5, not in teenage years).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular:\u003C/b\u003E\u003C/span\u003E Oculomotor apraxia (difficulty initiating voluntary eye movements), but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evertical eye movements are not specifically affected early\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EImmune system:\u003C/b\u003E\u003C/span\u003E Patients have \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eimmune deficiency\u003C/b\u003E\u003C/span\u003E (especially IgA and IgG2 deficiency), leading to recurrent sinopulmonary infections.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBiochemical marker:\u003C/b\u003E\u003C/span\u003E \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERaised alpha-fetoprotein (AFP)\u003C/b\u003E\u003C/span\u003E is a classic laboratory finding, seen in \u0026gt;90% of patients.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E----\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline; color: rgb(255, 0, 0);\u0022\u003ESupra-Nuclear Palsy:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E1. Dorsal Midbrain Syndrome\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;2. Progressive Supranuclear palsy (PSP) - Steele Richardson Olszweski\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;3. Parkinsonism\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;4. Louis-Bar Syndrome (Ataxia Telangiectasia)\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; color: rgb(255, 0, 0); text-decoration-line: underline;\u0022\u003EAtaxia Telangectasia:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003EReduced volitional eye movements but intact oculocephalic manoeuvre\u0026nbsp;\u003C/li\u003E\u003Cli\u003ECutaneous and conjunctival telangiectasia (age of 3)\u0026nbsp;\u003C/li\u003E\u003Cli\u003EDiffuse cerebral atrophy\u0026nbsp;\u003C/li\u003E\u003Cli\u003EThymic aplasia = deficient T cell function (could have Thymic lymphoma)\u0026nbsp;\u003C/li\u003E\u003Cli\u003ER\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eecurrent sinopulmonary infection due to IgA deficiency\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 56,
    "Name": "Exotropia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following MOST accurately describes the general surgical aims of squint surgery for exotropia?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe aim of strabismus surgery depends on whether \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efusion potential\u003C/b\u003E\u003C/span\u003E exists:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIf fusion is possible (good sensory potential, e.g., intermittent exotropia):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAim for a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmall overcorrection\u003C/b\u003E\u003C/span\u003E (slight esotropia postoperatively).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EReason: Exotropia has a natural tendency to drift back outward (exodrift). A small overcorrection initially often results in long-term alignment close to orthotropia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIf fusion is absent (e.g., long-standing sensory exotropia, no binocularity):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECosmetic alignment is the goal.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOvercorrection should be avoided, as patients without fusion cannot adapt to diplopia \u2192 aim for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorthotropia or small undercorrection\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ol\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Col start=\u00221\u0022\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 57,
    "Name": "Confidence",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following is the MOST appropriate estimate of the reliability of the average final refractive outcome from the results of a study assessing the success of cataract surgery?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStandard deviation (SD):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMeasures variability of individual data points around the mean.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDescribes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espread\u003C/b\u003E\u003C/span\u003E, not reliability of the mean.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConfidence interval (CI):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGives a range within which the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrue population mean\u003C/b\u003E\u003C/span\u003E is likely to fall.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EReflects the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprecision and reliability\u003C/b\u003E\u003C/span\u003E of the mean estimate.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENarrow CI \u2192 higher reliability, Wide CI \u2192 lower reliability.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, best answer for reliability of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaverage final refractive outcome\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStudent\u2019s t test:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsed to compare means between two groups, not to measure reliability of one mean.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAnalysis of variance (ANOVA):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsed to compare means across more than two groups, not to estimate reliability of a mean.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: calc(1.3rem \u002B 0.6vw); letter-spacing: 0.14994px;\u0022\u003EKey Point:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETo judge \u003C/span\u003E\u003Cb\u003Evariability of data\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 use \u003C/span\u003E\u003Cb\u003ESD\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETo judge \u003C/span\u003E\u003Cb\u003Ereliability of the mean estimate\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 use \u003C/span\u003E\u003Cb\u003EConfidence Interval (CI)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 58,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements is MOST likely to be correct in Lattice Corneal Dystrophy Type II?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELattice Corneal Dystrophy (LCD) Type II\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAlso known as \u003C/span\u003E\u003Cb\u003EMeretoja syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECaused by \u003C/span\u003E\u003Cb\u003Emutations in Gelsolin gene (GSN)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESystemic disease with corneal lattice lines, cranial neuropathies, and cutis laxa.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHistology:\u003C/b\u003E\u003C/span\u003E Shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eamyloid deposits\u003C/b\u003E\u003C/span\u003E (not hyaline) in corneal stroma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInheritance:\u003C/b\u003E\u003C/span\u003E Autosomal \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edominant\u003C/b\u003E\u003C/span\u003E (not recessive).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOnset:\u003C/b\u003E\u003C/span\u003E Usually around the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethird decade\u003C/b\u003E\u003C/span\u003E, not as late as the fifth.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EIncorrect options:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHyaline deposits with Masson trichrome \u2192 seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGranular corneal dystrophy\u003C/b\u003E\u003C/span\u003E, not lattice.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInheritance is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E, not recessive.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOnset is usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eearlier (3rd decade)\u003C/b\u003E\u003C/span\u003E, not typically delayed to the fifth.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 59,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following are LEAST likely to be associated with Optociliary Collaterals?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptociliary collaterals\u003C/b\u003E\u003C/span\u003E = dilated pre-existing venous channels on the optic disc that act as shunts between retinal and choroidal circulation when normal venous outflow is obstructed.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThey are classically associated with:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECentral Retinal Vein Occlusion (CRVO)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 most common cause.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptic Nerve Glioma\u003C/b\u003E\u003C/span\u003E \u2192 causes venous outflow obstruction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIdiopathic Intracranial Hypertension (IIH)\u003C/b\u003E\u003C/span\u003E \u2192 chronic papilledema can lead to collateral vessel formation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003ENOT associated with:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EProliferative Diabetic Retinopathy (PDR):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn PDR, the hallmark is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneovascularization\u003C/b\u003E\u003C/span\u003E (new abnormal vessels on disc or elsewhere), not collateral/shunt vessels.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathogenesis: due to ischemia-induced VEGF release, not venous obstruction.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMnemonic\u003C/b\u003E\u003C/span\u003E to remember:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201CCollaterals = Clean\u201D\u003C/b\u003E\u003C/span\u003E \u2192 mature, non-leaking, smooth.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201CNeovascularization = New and Nasty\u201D\u003C/b\u003E\u003C/span\u003E \u2192 fragile, leaky, sight-threatening.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-20-0a79cada-d93b-4bb6-9774-dfec25259708.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 60,
    "Name": "Anaesthetics",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich local anaesthetic has the longest duration of action?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBupivacaine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVery \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elong-acting\u003C/b\u003E\u003C/span\u003E amide local anaesthetic.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDuration: \u003C/span\u003E\u003Cb\u003E4\u20138 hours (or longer with epinephrine)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECommonly used where prolonged postoperative analgesia is desired (e.g., nerve blocks, epidurals).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELidocaine (with epinephrine)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIntermediate duration\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (90\u2013180 min).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEpinephrine prolongs effect by vasoconstriction, but still shorter than bupivacaine.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMepivacaine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIntermediate acting\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (2\u20133 hrs).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESlightly longer than plain lidocaine, but less than bupivacaine.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPrilocaine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAlso \u003C/span\u003E\u003Cb\u003Eintermediate acting\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (1.5\u20133 hrs).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EShorter than bupivacaine.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\uD83D\uDCCC \u003C/span\u003E\u003Cb\u003EMnemonic to remember duration (short \u2192 long):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EL\u003C/b\u003E\u003C/span\u003Eidocaine \u2192 \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EM\u003C/b\u003E\u003C/span\u003Eepivacaine \u2192 \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EP\u003C/b\u003E\u003C/span\u003Erilocaine \u2192 \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EB\u003C/b\u003E\u003C/span\u003Eupivacaine\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\uD83D\uDC49 \u201C\u003C/span\u003E\u003Cb\u003ELittle Mice Play Briefly\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E\u201D\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 61,
    "Name": "CCF",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following is LEAST likely to be associated with a Carotico-cavernous fistula?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecarotico-cavernous fistula (CCF)\u003C/b\u003E\u003C/span\u003E is an abnormal arteriovenous communication between the carotid artery and cavernous sinus. The high-pressure shunt causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evenous congestion in the orbit\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETypical features include:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEngorged conjunctival/episcleral vessels\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (\u201Cred eye with corkscrew vessels\u201D).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProptosis\u003C/b\u003E\u003C/span\u003E (due to venous engorgement).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERaised intraocular pressure\u003C/b\u003E\u003C/span\u003E (from impaired aqueous drainage via congested episcleral veins).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital bruit or pulsatile exophthalmos\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESecondary retinal venous stasis and venous engorgement\u003C/b\u003E\u003C/span\u003E \u2192 can lead to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emacular oedema\u003C/b\u003E\u003C/span\u003E, disc swelling, and retinal haemorrhages.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAnterior segment ischemia in the direct CCF.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitreous haemorrhage, however, is NOT a common feature\u003C/b\u003E\u003C/span\u003E of CCF. It is more typically seen in proliferative diabetic retinopathy, retinal vein occlusion, trauma, etc.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; color: rgb(0, 165, 255); text-decoration-line: underline;\u0022\u003ERemember, The raised\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eepiscleral venous pressure causing a secondary open-angle glaucoma, can also cause:\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cul\u003E\u003Cli\u003E80% of patients with CCF develop ocular hypertension\u0026nbsp;\u003C/li\u003E\u003Cli\u003E25% develop optic disc cupping\u0026nbsp;\u003C/li\u003E\u003Cli\u003E20% visual field defects.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 62,
    "Name": "VMT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhat is the MOST likely diagnosis accounting for the Optical Coherence Tomogram (OCT) appearance shown?\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-20-8ff1f5f7-2753-4713-9555-7a2bbef30483.gif\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe OCT image shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFoveal elevation with cystic spaces\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in the inner retina.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efocal foveal detachment\u003C/b\u003E\u003C/span\u003E with vitreomacular traction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis is an \u003C/span\u003E\u003Cb\u003Eimpending (Stage 1) macular hole\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: medium;\u0022\u003EOther options:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECystoid macular oedema\u003C/b\u003E\u003C/span\u003E \u2192 would show multiple cystic hyporeflective spaces in a petaloid pattern, often involving the parafovea (not just central foveal detachment).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpiretinal membrane\u003C/b\u003E\u003C/span\u003E \u2192 OCT would show a hyperreflective membrane on the inner retinal surface with surface wrinkling (not present here).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWet AMD\u003C/b\u003E\u003C/span\u003E \u2192 would show subretinal/intraretinal fluid, pigment epithelial detachment, or subretinal neovascular membrane (not seen here).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EAlthough a diagnosis of vitreomacular traction is the most suitable for this scan, among the choices provided, an impending macular hole is the most likely.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 63,
    "Name": "Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following features are MOST likely to be associated with retinoschisis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinoschisis\u003C/b\u003E\u003C/span\u003E is a splitting of the retinal layers, usually between the outer plexiform and inner nuclear layers.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIt is typically \u003C/span\u003E\u003Cb\u003Ebilateral, inferotemporal, and seen in hypermetropic patients\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EWhy not the others?\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDemarcation line\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 seen in \u003C/span\u003E\u003Cb\u003Elongstanding rhegmatogenous retinal detachment (RRD)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not retinoschisis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal haemorrhage\u003C/b\u003E\u003C/span\u003E \u2192 uncommon in retinoschisis; haemorrhage is more linked to vascular disease (e.g., diabetic retinopathy, CRVO).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShaffer\u2019s sign (tobacco dust in vitreous)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 a hallmark of \u003C/span\u003E\u003Cb\u003Erhegmatogenous retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not retinoschisis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EKey Points for Exams:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinoschisis\u003C/b\u003E\u003C/span\u003E = Hypermetropia \u002B Inferotemporal \u002B Smooth dome-shaped elevation \u002B Absolute scotoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal detachment\u003C/b\u003E\u003C/span\u003E = Myopia \u002B Flashes/floaters \u002B Shaffer\u2019s sign \u002B Demarcation line.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 64,
    "Name": "Vitrectomy",
    "Body": "\u003Cspan style=\u0022font-weight: 700; letter-spacing: 0.14994px; font-size: medium;\u0022\u003EWhich of the following BEST describes the MOST common effect of intravitreal silicone oil on the refraction of a phakic eye?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESilicone oil\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E has a \u003C/span\u003E\u003Cb\u003Ehigher refractive index (\u22481.405)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E compared to the vitreous (\u22481.336).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephakic eyes\u003C/b\u003E\u003C/span\u003E, this change in refractive index alters the optics:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior surface of the lens\u003C/b\u003E\u003C/span\u003E now interfaces with silicone oil rather than vitreous.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis creates a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigher converging power\u003C/b\u003E\u003C/span\u003E, shifting refraction toward \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopia\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe magnitude of induced myopia depends on lens thickness and curvature (often 3\u20135D).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EWhy not the others?\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAstigmatic power is reduced\u003C/b\u003E\u003C/span\u003E \u2192 Incorrect. Silicone oil induces \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espherical change\u003C/b\u003E\u003C/span\u003E, not selective astigmatic changes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMyopic refractive error is reduced\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Opposite effect; oil \u003C/span\u003E\u003Cb\u003Einduces myopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in phakic eyes.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo change in spherical refractive error\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Incorrect, as a \u003C/span\u003E\u003Cb\u003Esignificant myopic shift\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is clinically well-documented.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cb\u003EKey memory aid:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003E\u201CSilicone oil sinks eyes into myopia.\u201D\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
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    "HighYield": true,
    "CategoryId": 2,
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  },
  {
    "Id": 65,
    "Name": "Congenital optic disc anomalies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich ONE of the following is NOT a recognised association of optic nerve hypoplasia?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EOptic nerve hypoplasia (ONH) is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econgenital anomaly\u003C/b\u003E\u003C/span\u003E characterized by a small optic disc and reduced number of axons. It is often associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emidline brain abnormalities\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eendocrine dysfunctions\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ERecognized associations of ONH:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESepto-optic dysplasia (de Morsier syndrome):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHypoplasia of the corpus callosum\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAbsence of septum pellucidum\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPituitary hypoplasia \u2192 leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eendocrine dysfunctions\u003C/b\u003E\u003C/span\u003E (e.g., diabetes insipidus, growth hormone deficiency, hypopituitarism).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular features:\u003C/b\u003E\u003C/span\u003E Nystagmus, strabismus, reduced visual acuity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMaternal associations:\u003C/b\u003E\u003C/span\u003E More common in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyoung maternal age (\u0026lt;20 years)\u003C/b\u003E\u003C/span\u003E, especially teenage pregnancies, and maternal risk factors such as alcohol, drugs, and diabetes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\u0026nbsp;\u003Cspan style=\u0022font-size: large;\u0022\u003EThe options:\u003C/span\u003E\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiabetes Insipidus\u003C/b\u003E\u003C/span\u003E \u2192 True. ONH often involves pituitary dysfunction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHypoplasia of the corpus callosum\u003C/b\u003E\u003C/span\u003E \u2192 True. Seen in septo-optic dysplasia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENystagmus\u003C/b\u003E\u003C/span\u003E \u2192 True. Common presenting ocular feature.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMaternal age \u0026gt;30 years\u003C/b\u003E\u003C/span\u003E \u2192\u0026nbsp; Incorrect. The known risk is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyoung maternal age (\u0026lt;20 years)\u003C/b\u003E\u003C/span\u003E, not advanced maternal age.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 66,
    "Name": "Artery Occlusion",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EIn the management of a patient with an acute Cilio-Retinal artery occlusion, which statement is LEAST likely to be correct?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECilio-retinal artery occlusion\u003C/b\u003E\u003C/span\u003E is a retinal vascular emergency.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EManagement focuses on:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EExcluding \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egiant cell arteritis (GCA)\u003C/b\u003E\u003C/span\u003E if over age 50 \u2192 check ESR, CRP, temporal artery biopsy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIdentifying \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecardioembolic and carotid sources\u003C/b\u003E\u003C/span\u003E \u2192 echocardiography and carotid Doppler are standard.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EConsidering \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eocular ischaemic syndrome\u003C/b\u003E\u003C/span\u003E if widespread mid-peripheral hemorrhages are seen (due to severe carotid stenosis).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ENote:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELowering systemic blood pressure is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econtraindicated in the acute setting\u003C/b\u003E\u003C/span\u003E, because ocular perfusion pressure may already be critically low.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFurther lowering BP risks worsening retinal ischaemia and infarction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInstead, maintaining or even slightly supporting perfusion pressure is preferred.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EOther options:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB: Carotid Doppler \u002B Echocardiogram\u003C/b\u003E\u003C/span\u003E \u2192 True, essential to rule out embolic sources.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC: Raised inflammatory markers \u2192 GCA\u003C/b\u003E\u003C/span\u003E \u2192 True, must be excluded urgently in elderly.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ED: Retinal haemorrhages \u2192 ocular ischaemic syndrome\u003C/b\u003E\u003C/span\u003E \u2192 True, classically seen with severe carotid stenosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": true,
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  },
  {
    "Id": 67,
    "Name": "Cataract Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA 69-year-old gentleman presents 12 hours after an uneventful cataract surgery. He is worried that his vision has dropped quite suddenly, but he does not report any pain. On examination, there is no lid swelling or discharge. On examination, Vision is 6/60 in the affected eye, and the cornea is diffusely oedematous. The intraocular pressure is 35 mmHg, and there is mild anterior chamber activity. The pupil is unreactive. On B scan, there is no vitritis. Which of the following statements is MOST likely to be correct?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis patient most likely has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute postoperative raised intraocular pressure (IOP)\u003C/b\u003E\u003C/span\u003E after cataract surgery (secondary acute glaucoma or early Toxic Anterior Segment Syndrome (TASS) vs. retained viscoelastic).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EKey features here:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEarly onset (12 hrs post-op)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPainless loss of vision\u003C/b\u003E\u003C/span\u003E (endophthalmitis usually causes pain \u002B hypopyon \u002B vitritis, which are absent here)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiffuse corneal oedema\u003C/b\u003E\u003C/span\u003E due to endothelial pump failure from high IOP\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP 35 mmHg\u003C/b\u003E\u003C/span\u003E \u2192 elevated\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUnreactive pupil\u003C/b\u003E\u003C/span\u003E (secondary to iris ischaemia from high IOP)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EIf untreated, \u003C/span\u003E\u003Cb\u003Esustained raised IOP\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003Eirreversible corneal endothelial decompensation\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E \u2192 permanent corneal oedema and vision loss.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EThe other options:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnterior chamber washout\u003C/b\u003E\u003C/span\u003E \u2192 This may be useful if viscoelastic retention is suspected, but the immediate issue is high IOP; medical management (acetazolamide, topical IOP-lowering agents) is first-line. Washout is not the most likely correct general statement.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EExplantation of IOL and capsular bag\u003C/b\u003E\u003C/span\u003E \u2192 This is a very late salvage option (e.g., chronic TASS, intractable inflammation). Not relevant in the acute 12-hour presentation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopical steroids with caution\u003C/b\u003E\u003C/span\u003E \u2192 In fact, topical steroids are often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eindicated\u003C/b\u003E\u003C/span\u003E in TASS to reduce inflammation. The caution applies in fungal keratitis, not here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 68,
    "Name": "GCA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EConcerning giant cell arteritis (GCA), which of these statements is LEAST likely to be correct?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECRP is raised\u003C/b\u003E\u003C/span\u003E \u2192 Correct. Both \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EESR and CRP are usually elevated\u003C/b\u003E\u003C/span\u003E in GCA and are highly sensitive markers for diagnosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFemales are more susceptible\u003C/b\u003E\u003C/span\u003E \u2192 Correct. GCA occurs more commonly in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eelderly women\u003C/b\u003E\u003C/span\u003E, particularly of Northern European descent.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHistological diagnosis is based on fragmentation of the internal elastic lamina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Correct. The biopsy shows \u003C/span\u003E\u003Cb\u003Egranulomatous inflammation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, typically with \u003C/span\u003E\u003Cb\u003Edisruption/fragmentation of the internal elastic lamina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPresence of giant cells required for diagnosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Incorrect. Despite the name, \u003C/span\u003E\u003Cb\u003Egiant cells are not always present\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on biopsy. The key diagnostic feature is \u003C/span\u003E\u003Cb\u003Egranulomatous inflammation with disruption of the internal elastic lamina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Absence of giant cells does \u003C/span\u003E\u003Cb\u003Enot\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E rule out GCA.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMnemonic for biopsy features of GCA \u2192 \u201CFIGS\u201D:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EF\u003C/b\u003E\u003C/span\u003E: Fragmentation of internal elastic lamina\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EI\u003C/b\u003E\u003C/span\u003E: Inflammatory infiltrate (granulomatous, lymphocytes, macrophages)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EG\u003C/b\u003E\u003C/span\u003E: Giant cells (sometimes, but not always present)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ES\u003C/b\u003E\u003C/span\u003E: Skip lesions (patchy involvement)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 69,
    "Name": "Hereditaty vitreoretinopathies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 12-month-old developmentally delayed boy with hearing impairment is referred. Examination findings include hand movements vision and bilateral white retrolental masses. The child\u2019s skin is normal. Which of these is the MOST likely diagnosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENorrie disease\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked recessive\u003C/b\u003E\u003C/span\u003E disorder caused by mutations in the \u003Ci\u003ENDP gene\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EClassic triad: \u003C/span\u003E\u003Cb\u003Econgenital/infantile blindness (retrolental masses, leukocoria)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Esensorineural deafness\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Edevelopmental delay/mental retardation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESkin is typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enormal\u003C/b\u003E\u003C/span\u003E, which helps differentiate it from other conditions.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EStrong match to the vignette.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECongenital rubella infection\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAssociated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etriad\u003C/b\u003E\u003C/span\u003E: cataract, deafness, congenital heart disease (PDA).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetrolental \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewhite masses\u003C/b\u003E\u003C/span\u003E are not typical; rather, cataracts are seen.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIncontinentia pigmentii\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked dominant\u003C/b\u003E\u003C/span\u003E (lethal in males).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFeatures: skin lesions (vesicular \u2192 verrucous \u2192 hyperpigmented \u2192 atrophic), dental anomalies, CNS issues, and retinal vascular disease.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENormal skin\u003C/b\u003E\u003C/span\u003E here rules this out.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinoblastoma\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELeukocoria is typical, but usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral (can be bilateral)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDoes not usually present with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehearing loss or developmental delay\u003C/b\u003E\u003C/span\u003E, so not the best fit.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENorrie disease = Blindness \u002B Deafness \u002B Developmental delay (boys, X-linked) =\u0026nbsp;\u003C/b\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EDoesn\u2019t see, doesn\u2019t hear, doesn\u2019t understand\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThink of \u003C/span\u003E\u003Cb\u003ENDP gene mutation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Ebilateral retrolental masses\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E as the hallmark.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 70,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EIn which ONE of the following dystrophies does the central cornea show grey-white, fine round and polygonal opacities in Bowman\u2019s layer?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EReis-Buckler dystrophy (RBCD)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESite\u003C/b\u003E\u003C/span\u003E: Bowman\u2019s layer (primary pathology).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFindings\u003C/b\u003E\u003C/span\u003E: Grey-white, fine round and polygonal opacities in the central cornea.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese opacities coalesce over time, causing recurrent erosions and progressive visual loss.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAutosomal dominant, mutation in \u003Ci\u003ETGFBI gene\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA: Granular dystrophy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHyaline deposits in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estroma\u003C/b\u003E\u003C/span\u003E (bread-crumb like, discrete opacities).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot in Bowman\u2019s layer.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EB: Macular dystrophy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAutosomal recessive\u003C/b\u003E\u003C/span\u003E, deposits of glycosaminoglycans.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiffuse stromal haze\u003C/b\u003E\u003C/span\u003E involving full thickness of cornea.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot restricted to Bowman\u2019s.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EC: Meesmann dystrophy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETiny intraepithelial vesicles (microcysts), especially in interpalpebral zone.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpithelial dystrophy\u003C/b\u003E\u003C/span\u003E, not Bowman\u2019s layer.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIf \u003C/span\u003E\u003Cb\u003EBowman\u2019s layer\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is involved \u2192 think \u003C/span\u003E\u003Cb\u003EReis-Buckler dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EReis-Buckler\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003E\u201CRB = Rigid Bowman\u201D\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 opacities sit in \u003C/span\u003E\u003Cb\u003EBowman\u2019s layer\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 71,
    "Name": "MG",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA 47-year-old patient who has rheumatoid arthritis complains of variable double vision. On examination, you noted a mild ptosis with fatigueability and limited depression of the left eye. Which of the following drugs is MOST likely to be the cause?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe patient has \u003C/span\u003E\u003Cb\u003Evariable diplopia, ptosis, and fatigability\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 classical features of \u003C/span\u003E\u003Cb\u003Emyasthenia gravis (MG)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDrug-induced myasthenia\u003C/b\u003E\u003C/span\u003E is a recognized phenomenon.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022text-decoration-line: underline;\u0022\u003EPenicillamine\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECan induce a \u003C/span\u003E\u003Cb\u003Emyasthenia gravis-like syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in \u003C/span\u003E\u003Cb\u003E0.1\u20131%\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of patients.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMechanism: autoimmune cross-reaction leading to acetylcholine receptor (AChR) antibodies.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOnset: may occur \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eweeks to years\u003C/b\u003E\u003C/span\u003E after starting therapy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUsually \u003C/span\u003E\u003Cb\u003Eresolves after withdrawal\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of the drug.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOther options\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMethotrexate\u003C/b\u003E\u003C/span\u003E \u2192 causes hepatotoxicity, cytopenias, lung fibrosis, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot MG\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPrednisolone\u003C/b\u003E\u003C/span\u003E \u2192 immunosuppressive, often used to treat MG, not cause it.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESodium aurothiomalate (gold therapy)\u003C/b\u003E\u003C/span\u003E \u2192 can cause dermatitis, nephropathy, cytopenias, but not MG.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 72,
    "Name": "Physiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following is MOST likely correct regarding the mechanism for the pathogenesis of Type 2 diabetes?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe pathogenesis of \u003C/span\u003E\u003Cb\u003EType 2 Diabetes Mellitus (T2DM)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E involves:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInsulin resistance\u003C/b\u003E\u003C/span\u003E \u2192 in skeletal muscle, liver, and adipose tissue.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMuscle: \u2193 glucose uptake.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELiver: \u2191 hepatic glucose production (not decreased).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFat: \u2191 lipolysis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProgressive Beta-cell dysfunction\u003C/b\u003E\u003C/span\u003E \u2192 the pancreas cannot compensate with enough insulin, leading to hyperglycemia.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInitially, there may be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperinsulinemia\u003C/b\u003E\u003C/span\u003E (not excessive insulin secretion long-term).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOver time, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebeta-cell failure\u003C/b\u003E\u003C/span\u003E is the hallmark of progression.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGlucose uptake\u003C/b\u003E\u003C/span\u003E \u2192 is decreased in skeletal muscle, not increased.\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 73,
    "Name": "Secondary Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 29-year-old lady presents after being punched in her left eye. On examination, her visual acuity is 6/6 right and 6/18 left. The left eye has a deep anterior chamber with dispersed red blood cells, and fundus examination is normal. She is given no treatment.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E5 months later, she presented with an intraocular pressure of 32 mmHg in the left eye. Her visual acuity is 6/9 with no refractive error and there is no anterior chamber activity. Which of the following is the MOST likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlunt trauma\u003C/b\u003E\u003C/span\u003E with early hyphema/RBCs followed by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edelayed IOP rise months later\u003C/b\u003E\u003C/span\u003E is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eangle\u2011recession glaucoma\u003C/b\u003E\u003C/span\u003E (tear between longitudinal and circular fibers of the ciliary muscle \u2192 trabecular dysfunction).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAqueous misdirection (malignant glaucoma)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E presents with \u003C/span\u003E\u003Cb\u003Eshallow AC\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and high IOP, typically \u003C/span\u003E\u003Cb\u003Epost\u2011intraocular surgery\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not trauma.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGhost cell glaucoma\u003C/b\u003E\u003C/span\u003E occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eweeks\u003C/b\u003E\u003C/span\u003E after a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreous hemorrhage\u003C/b\u003E\u003C/span\u003E (or vitrectomy) when degenerated RBCs enter the AC; history here lacks VH and timing is longer.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELens dislocation\u003C/b\u003E\u003C/span\u003E would usually cause refractive shift/iridodonesis or lens decentration\u2014absent here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ESo the delayed ocular hypertension after blunt trauma fits \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eangle recession\u003C/b\u003E\u003C/span\u003E best.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 74,
    "Name": "Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of these is the MOST likely retinal pathology in a patient presenting with an absolute peripheral field defect?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinoschisis\u003C/b\u003E\u003C/span\u003E = splitting of retinal layers \u2192 produces a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmooth, immobile, dome-shaped elevation\u003C/b\u003E\u003C/span\u003E of retina.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOn visual fields, this corresponds to an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsolute scotoma\u003C/b\u003E\u003C/span\u003E (no light perception in that area) because there is a disruption in the connections between the retinal layers, so the visual stimulus is not properly transmitted to the visual pathways.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis is in contrast to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal detachment\u003C/b\u003E\u003C/span\u003E, which produces a relative scotoma, as despite the presence of a separation between the photoreceptors and the RPE, the visual pathway connections remain intact.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGiant retinal tear\u003C/b\u003E\u003C/span\u003E \u2192 causes risk of retinal detachment and relative field loss, not usually absolute.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPavingstone degeneration\u003C/b\u003E\u003C/span\u003E \u2192 benign, asymptomatic, no field defects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESnail track degeneration\u003C/b\u003E\u003C/span\u003E \u2192 predisposes to tears but does not itself cause absolute peripheral defects.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-21-a645b406-1406-46d1-a02d-0d8f7ca04d06.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThis table from Oxford Handbook is really important for both written and oral exams.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 75,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA gentleman presenting to you for left cataract surgery has a corrected acuity of 6/18 and the following refractive error and keratometry readings in the same eye:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E-0.75 / \u002B1.50 \u00D7 110 and keratometry 41.28 D @ 170 degrees and 44.54 D @ 80 degrees.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of these options is MOST likely to give the best refractive outcome?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERefractive error given\u003C/b\u003E\u003C/span\u003E: -0.75 / \u002B1.50 \u00D7 110 \u2192 Indicates significant \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eastigmatism\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKeratometry readings\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E41.28 D @ 170\u00B0 (flat meridian)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E44.54 D @ 80\u00B0 (steep meridian)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECylinder \u2248 \u003C/span\u003E\u003Cb\u003E3.26 D corneal astigmatism\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EThis is \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Ecorneal (regular) astigmatism\u003C/b\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E, best corrected by a \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Etoric IOL\u003C/b\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhy not the other options?\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003Estandard IOL with incision placement:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECorneal incisions can induce only ~0.5\u20131.0 D of astigmatism correction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInsufficient for a patient with \u0026gt;3 D of astigmatism.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003Etoric correction based on refractive error:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERefractive error includes both corneal and lenticular astigmatism.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOnce cataract (lens) is removed, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erefractive astigmatism changes\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECorrect calculation must be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebased on corneal keratometry\u003C/b\u003E\u003C/span\u003E, not spectacle refraction.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 76,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 68-year-old gentleman presents with blurring of vision in his right eye specially when looking upwards for the past 1 month. His visual acuity was 6/9 in the right eye and 6/6 in the left eye. The refraction was right -2D Cylinder @ 90 which improved vision to 6/6 and left plano. Slit lamp examination reveals an in-the-bag subluxated intraocular lens displaced inferiorly and nasally. Dilated fundus examination was normal. What is the MOST appropriate next step in management?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPatient has \u003C/span\u003E\u003Cb\u003Egood visual acuity (6/6 with refraction)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E despite IOL subluxation.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESubluxated IOL is stable and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot causing major visual disability or complications\u003C/b\u003E\u003C/span\u003E (e.g., corneal touch, glaucoma, CME).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EImmediate surgical intervention\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is not necessary unless vision is poor, lens is unstable, or complications occur.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDischarging to optician\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is inappropriate \u2014 the patient needs ophthalmology follow-up.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUltrasound biomicroscopy\u003C/b\u003E\u003C/span\u003E\u0026nbsp;may be useful in long-term monitoring, but the immediate next step is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espectacle correction and review\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003ERemember:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStable subluxated IOL \u002B good corrected vision \u2192 Conservative management with glasses and monitoring.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESurgery is indicated\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E if:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPoor visual outcome with correction\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELens instability progressing\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESecondary complications (glaucoma, corneal decompensation, CME).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
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  },
  {
    "Id": 77,
    "Name": "Investigations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhen doing a B-scan ultrasound of the eye using an ultrasound probe, which of the following is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe probe beam is usually directed \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperpendicular\u003C/b\u003E\u003C/span\u003E to structures for optimal imaging, not oblique.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EToo high a gain causes excessive noise and reduces clarity. Gain should be adjusted appropriately to balance resolution and contrast.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELowering gray scale reduces detail; instead, optimal contrast should be maintained.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewhite marker (or notch)\u003C/b\u003E\u003C/span\u003E on the probe is a standard convention in ultrasonography. It denotes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebeam orientation\u003C/b\u003E\u003C/span\u003E, allowing correlation between the patient\u2019s anatomy and the display (top of screen corresponds to marker side).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
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  },
  {
    "Id": 78,
    "Name": "Cataract",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EThe most frequent ocular association in most of the affected males in Alport\u2019s Syndrome includes:\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAlport\u2019s syndrome\u003C/b\u003E\u003C/span\u003E = a genetic condition caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emutations in type IV collagen\u003C/b\u003E\u003C/span\u003E \u2192 affects kidneys (hematuria, progressive renal failure), ears (sensorineural deafness), and eyes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eclassic ocular finding\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003E\u003Cb\u003EAnterior Lenticonus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (pathognomonic).\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe lens bulges forward due to weak capsule \u2192 causes progressive myopia and irregular astigmatism.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDot-and-fleck retinopathy\u003C/b\u003E\u003C/span\u003E is also common but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless frequent\u003C/b\u003E\u003C/span\u003E than anterior lenticonus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior lenticonus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 usually seen in \u003C/span\u003E\u003Cb\u003Econgenital cataracts\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not Alport\u2019s.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior polymorphous corneal dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E can also happen in Alport\u0027s syndrome but not as pathognomonic/common as Anterior lenticonus.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 79,
    "Name": "Keratoconus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich ONE of the following is LEAST likely to be correct for corneal cross linking in the treatment of keratoconus?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECorneal cross-linking (CXL):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMain aim = \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehalt progression\u003C/b\u003E\u003C/span\u003E of keratoconus by stiffening the cornea with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eriboflavin \u002B UV-A light\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETraditionally thought \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot to improve VA\u003C/b\u003E\u003C/span\u003E, but studies show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emany patients do gain lines of BCVA\u003C/b\u003E\u003C/span\u003E due to corneal regularisation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIndications (true):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDocumented progression of keratoconus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntolerance to rigid contact lenses.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThin corneas with risk of further ectasia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMore effective after epithelial removal (epi-off CXL):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBecause riboflavin penetrates deeper.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEpi-on is less effective but safer.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETakes about 1 hour:\u003C/b\u003E\u003C/span\u003E True \u2014 ~30 min riboflavin soak \u002B 30 min UV exposure.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 80,
    "Name": "Studies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 53\u2011year\u2011old lady with hypermetropia is referred to your clinic with suspected glaucoma. Her IOP is 30\u202FmmHg in both eyes, with no cataract, C/D ratio 0.6 OD and 0.7 OS. Gonioscopy grading: Shaffer grade 1 OU with heavily pigmented trabecular meshwork and no PAS. Automated perimetry shows bilateral visual field defects.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following studies could best guide your management?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe clinical findings (very narrow angles, IOP 30, VF loss) fit \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprimary angle\u2011closure glaucoma (PACG)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEAGLE\u003C/b\u003E\u003C/span\u003E trial compared \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclear\u2011lens extraction vs LPI/medical therapy\u003C/b\u003E\u003C/span\u003E in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPAC/PACG with IOP \u226530 mmHg\u003C/b\u003E\u003C/span\u003E and showed lens extraction had better IOP control, fewer procedures, and improved quality of life\u2014directly applicable.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECIGTS\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEMGT\u003C/b\u003E\u003C/span\u003E address \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eopen\u2011angle glaucoma\u003C/b\u003E\u003C/span\u003E (surgery vs meds; treatment vs observation), not angle\u2011closure.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EZAP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E studied \u003C/span\u003E\u003Cb\u003Eprophylactic LPI in angle\u2011closure suspects (PACS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E without glaucoma\u2014doesn\u2019t match this case.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 81,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EOn examining patients in the post-operative trabeculectomy clinic, which of the following clinical signs is MOST suggestive of sub-optimal function of the surgery?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHealthy bleb\u003C/b\u003E\u003C/span\u003E: Usually diffuse, slightly elevated, with microcysts (indicating filtration).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAvascular/thin bleb\u003C/b\u003E\u003C/span\u003E: Risk of leaks/infection but not necessarily poor function.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMicrocysts\u003C/b\u003E\u003C/span\u003E: Sign of \u003Ci\u003Egood filtration\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorkscrew/tortuous vessels\u003C/b\u003E\u003C/span\u003E: Classic early warning sign of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebleb failure\u003C/b\u003E\u003C/span\u003E due to subconjunctival fibrosis and vascularisation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 82,
    "Name": "Thryoid",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following is LEAST likely to be correct regarding Thyroid associated orbitopathy (TAO)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMost cases of TAO\u003C/b\u003E\u003C/span\u003E: associated with hyperthyroidism, but ~5\u201310% are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eeuthyroid\u003C/b\u003E\u003C/span\u003E\u0026nbsp;\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDysthyroid optic neuropathy (DON)\u003C/b\u003E\u003C/span\u003E: occurs due to apical crowding by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eenlarged extraocular muscles\u003C/b\u003E\u003C/span\u003E (muscle-predominant disease), \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot fat-predominant\u003C/b\u003E\u003C/span\u003E\u0026nbsp;\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETeprotumumab\u003C/b\u003E\u003C/span\u003E: is a monoclonal antibody against \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIGF-1 receptor\u003C/b\u003E\u003C/span\u003E, used in active TAO.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThy-1\u002B fibroblasts\u003C/b\u003E\u003C/span\u003E: differentiate into myofibroblasts, driving fibrosis in late/chronic TAO.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 83,
    "Name": "NNT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn the Early Treatment Diabetic Retinopathy Study (ETDRS) for laser treatment of diabetic macular oedema, moderate visual loss occurred in 12% of treated eyes compared to 24% of untreated eyes in three years. Which of these is MOST likely to be the approximate value of numbers needed to treat in this study?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAbsolute risk reduction (ARR)\u003C/b\u003E\u003C/span\u003E = Control event rate \u2013 Treatment event rate\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E= 24% \u2013 12%\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E= \u003C/span\u003E\u003Cb\u003E12% (0.12)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENumber Needed to Treat (NNT)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E = 1 \u00F7 ARR\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E= 1 \u00F7 0.12\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u2248 \u003C/span\u003E\u003Cb\u003E8.3 \u2192 round up = 9\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ESo about 9 patients need to be treated with laser to prevent 1 case of moderate visual loss over 3 years.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 84,
    "Name": "MMP",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWith regards to mucous membrane pemphigoid, which of the following is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMucous membrane pemphigoid (MMP)\u003C/b\u003E\u003C/span\u003E = chronic autoimmune blistering disease mainly affecting mucous membranes (conjunctiva, oral cavity, pharynx, larynx, genital mucosa).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESkin involvement\u003C/b\u003E\u003C/span\u003E: possible but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunusual\u003C/b\u003E\u003C/span\u003E, seen in \u0026lt;30% of cases.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPathology\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESubepithelial blistering (not intra-epithelial bullae).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIgG and C3 most commonly implicated (not IgA/IgM ).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDiagnosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDirect immunofluorescence (DIF)\u003C/b\u003E\u003C/span\u003E of conjunctival/skin biopsy is gold standard, showing linear deposition of IgG and C3 at basement membrane.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIndirect immunofluorescence (IIF) is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless sensitive\u003C/b\u003E\u003C/span\u003E \u2192 not definitive.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 85,
    "Name": "MH",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn idiopathic full-thickness macular holes, which preoperative factor is MOST likely to indicate a post-operative better visual prognosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPrognosis in macular hole surgery\u003C/b\u003E\u003C/span\u003E depends mainly on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esize\u003C/b\u003E\u003C/span\u003E and associated findings.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESmall holes (\u0026lt;250\u2013300 \u00B5m)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E have \u003C/span\u003E\u003Cb\u003Emuch better surgical and visual outcomes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELarger holes (\u0026gt;400 \u00B5m) have poorer prognosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPersistent vitreomacular traction (VMT)\u003C/b\u003E\u003C/span\u003E in small holes may be beneficial \u2192 once released surgically, the hole can close more effectively.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENegative prognostic factors:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELarge size (\u0026gt;400\u2013500 \u00B5m).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPresence of operculum.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntraretinal cystic changes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EChronicity and RPE changes/deposits.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 86,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ERegarding Mitomycin C used in glaucoma drainage surgery, which of of the following statements is MOST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMitomycin C (MMC):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPotent antimetabolite (DNA cross-linker).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsed intraoperatively in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrabeculectomy and glaucoma drainage devices\u003C/b\u003E\u003C/span\u003E to reduce fibroblast proliferation \u2192 prevents bleb scarring.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESide effects:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELimbal stem cell deficiency\u003C/b\u003E\u003C/span\u003E \u2192 MMC can damage limbal stem cells when applied near the limbus \u2192 leads to persistent epithelial defects, corneal vascularization, and vision loss.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThin, avascular blebs \u2192 predisposition to leaks and infection.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther options explained:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMMC is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore potent\u003C/b\u003E\u003C/span\u003E than 5-FU at therapeutic levels.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMMC is commonly used at \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.02% (0.2 mg/mL)\u003C/b\u003E\u003C/span\u003E, not 0.2% (which would be 10\u00D7 stronger and toxic).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Eits main action is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einhibition of fibroblast proliferation\u003C/b\u003E\u003C/span\u003E, not mast cells.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 87,
    "Name": "Lid Tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following is the MOST likely diagnosis in an elderly patient presenting with a rapidly growing and well-demarcated bluish-purple upper lid lesion?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMerkel cell carcinoma (MCC):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERare, highly malignant neuroendocrine tumor of the skin.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EClassically affects \u003C/span\u003E\u003Cb\u003Eelderly, immunosuppressed, or sun-exposed individuals\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAppears as a \u003C/span\u003E\u003Cb\u003Erapidly growing, painless, firm, red-to-violaceous nodule\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOn eyelid \u2192 often well-demarcated, bluish-purple, mimicking vascular or hematologic lesions.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAggressive \u2192 high risk of local recurrence and metastasis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBasal cell carcinoma:\u003C/b\u003E\u003C/span\u003E Most common eyelid malignancy, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eslow-growing\u003C/b\u003E\u003C/span\u003E, pearly edges, telangiectasia, rarely bluish-purple.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELymphoma:\u003C/b\u003E\u003C/span\u003E Usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esalmon-pink patch\u003C/b\u003E\u003C/span\u003E in conjunctiva, not a purple nodule.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESebaceous carcinoma:\u003C/b\u003E\u003C/span\u003E Typically arises from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emeibomian glands\u003C/b\u003E\u003C/span\u003E, masquerades as recurrent chalazion, yellowish not purple.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 88,
    "Name": "White Dot syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following findings is LEAST likely to occur in multiple evanescent white dot syndrome (MEWDS)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMEWDS (Multiple Evanescent White Dot Syndrome):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAcute, unilateral visual loss in young women.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECharacterized by \u003C/span\u003E\u003Cb\u003Emultiple small white dots at the RPE/outer retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETypically self-limiting.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EImaging findings:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOCT:\u003C/b\u003E\u003C/span\u003E Disruption of the ellipsoid zone (IS/OS junction).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFFA:\u003C/b\u003E\u003C/span\u003E Early punctate hyperfluorescence in a \u201Cwreath-like pattern.\u201D\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAutofluorescence:\u003C/b\u003E\u003C/span\u003E Hyperautofluorescent lesions corresponding to white dots.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EICG:\u003C/b\u003E\u003C/span\u003E \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHypo\u003C/b\u003E\u003C/span\u003Ecyanescence (not hyper) corresponding to lesions.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETherefore, \u003C/span\u003E\u003Cb\u003Ehypercyanescence on ICG\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003E\u003Cb\u003Enot a feature\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 89,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements regarding idiopathic tonic pupil (Adie syndrome / pupil) is MOST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAdie\u2019s tonic pupil\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003C/span\u003E at presentation (can become bilateral later, ~20%).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMost often occurs in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyoung women\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPupil is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edilated and poorly reactive to light\u003C/b\u003E\u003C/span\u003E, but better to near (light-near dissociation).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOver years, the affected pupil \u003C/span\u003E\u003Cb\u003Egradually becomes smaller (miotic)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2014 called \u201C\u003C/span\u003E\u003Cb\u003Elittle old Adie\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u201D\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther Options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDiagnosis is confirmed with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edilute pilocarpine (0.125%)\u003C/b\u003E\u003C/span\u003E, not phenylephrine.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAssociated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperopia\u003C/b\u003E\u003C/span\u003E, not myopia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003C/span\u003E at onset, not bilateral.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOver time, pupil becomes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogressively more miotic\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 90,
    "Name": "Congenital optic disc anomalies",
    "Body": "\u003Cbr\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 23-year-old student is referred because of the incidental finding of an abnormal optic disc (see image). What is the abnormality shown?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022https://imagebank.asrs.org/tmp/asrs-rib-image-26420.jpg/image-full;max$643,0.ImageHandler\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe image shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebright, autofluorescent deposits\u003C/b\u003E\u003C/span\u003E at the optic nerve head.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic disc drusen\u003C/b\u003E\u003C/span\u003E: calcified hyaline bodies within the optic nerve head.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOn \u003C/span\u003E\u003Cb\u003Efundus autofluorescence (FAF)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E imaging \u2192 they appear \u003C/span\u003E\u003Cb\u003Ebright white due to their autofluorescence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOther options:\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPapilloedema:\u003C/b\u003E\u003C/span\u003E Causes disc swelling, but would not autofluoresce.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHamartoma:\u003C/b\u003E\u003C/span\u003E Usually pigmented or irregular mass, not bright autoflurescent deposits.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal emboli:\u003C/b\u003E\u003C/span\u003E Appear as refractile intravascular bodies, not disc-centered autofluorescence.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThis is a very common question in the FRCOphth written exams.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 91,
    "Name": "Medicolegal",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn which of the following cases did the Supreme Court affirm that a doctor \u003Cspan style=\u0022font-style: italic;\u0022\u003E\u201Chas a duty to take reasonable care to ensure that the patient is aware of any material risks involved in any recommended treatment, and of any reasonable alternative or variant treatments\u201D\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMontgomery v Lanarkshire (2015)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ELandmark case in \u003C/span\u003E\u003Cb\u003Emedical consent law\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe UK Supreme Court ruled that doctors must:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInform patients of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ematerial risks\u003C/b\u003E\u003C/span\u003E of treatment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDiscuss \u003C/span\u003E\u003Cb\u003Ereasonable alternatives\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EEnsure \u003C/span\u003E\u003Cb\u003Eshared decision-making\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EShifted standard from the \u003C/span\u003E\u003Cb\u003Edoctor-centred Bolam test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 to \u003C/span\u003E\u003Cb\u003Epatient-centred standard\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EOther cases in context:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBolam v Friern (1957):\u003C/b\u003E\u003C/span\u003E Established the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBolam test\u003C/b\u003E\u003C/span\u003E \u2192 a doctor is not negligent if acting in accordance with a responsible body of medical opinion.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBarnett v Chelsea (1968):\u003C/b\u003E\u003C/span\u003E Case on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecausation\u003C/b\u003E\u003C/span\u003E, not consent. (Failure to diagnose arsenic poisoning but death was unavoidable).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWilsher v Essex (1988):\u003C/b\u003E\u003C/span\u003E Case on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecausation\u003C/b\u003E\u003C/span\u003E in a premature infant with retinopathy of prematurity.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 92,
    "Name": "Laser",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EComparing Argon laser trabeculoplasty to selective laser trabeculoplasty, which of the following statements is LEAST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EArgon Laser Trabeculoplasty (ALT):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUses thermal energy \u2192 causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecoagulative burns\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Escarring\u003C/b\u003E\u003C/span\u003E in the trabecular meshwork.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWorks by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etissue contraction\u003C/b\u003E\u003C/span\u003E and increasing aqueous outflow.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECauses an \u003C/span\u003E\u003Cb\u003Einflammatory reaction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESelective Laser Trabeculoplasty (SLT):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUses a Q-switched, frequency-doubled Nd:YAG (532 nm).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEnergy is selectively absorbed by pigmented trabecular cells.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECauses \u003C/span\u003E\u003Cb\u003Ebiological stimulation (cellular and cytokine-mediated response)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E rather than thermal damage.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMinimal inflammation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E compared to ALT.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
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  },
  {
    "Id": 93,
    "Name": "Exotropia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EConcerning consecutive exotropia, which of the following is MOST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt may appear immediately post-op or years later.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EKey associations:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECommonly linked to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eovercorrection\u003C/b\u003E\u003C/span\u003E of esotropia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elimitation of adduction\u003C/b\u003E\u003C/span\u003E due to scarring or slipped/over-recessed medial rectus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMay also be linked with amblyopia, anisometropia, or poor binocular fusion.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EOption breakdown:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEven in amblyopic eyes, post-op diplopia can still occur (though suppression reduces risk).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMore commonly seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehypermetropes\u003C/b\u003E\u003C/span\u003E (due to accommodative esotropia surgery).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdduction limitation is a classic feature due to medial rectus weakening.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u0026nbsp;Orthoptic exercises rarely help; surgical re-correction is often needed.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 94,
    "Name": "Disc Oedema",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EAn asymptomatic 63-year-old lady is referred by her optician with a unilateral swollen optic disc and an arcuate field defect. Which of the following is the MOST appropriate initial investigation?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral swollen optic disc\u003C/b\u003E\u003C/span\u003E with a corresponding \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efield defect\u003C/b\u003E\u003C/span\u003E raises suspicion for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompressive optic neuropathy\u003C/b\u003E\u003C/span\u003E (e.g., optic nerve sheath meningioma, orbital or intracranial mass).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe patient is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Easymptomatic\u003C/b\u003E\u003C/span\u003E (no acute pain or systemic signs), making causes like optic neuritis or papilloedema less likely.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EOption breakdown:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB-scan ultrasound\u003C/b\u003E\u003C/span\u003E \u2192 Useful for optic disc drusen, but less sensitive for ruling out compressive causes. Not appropriate as first-line here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECT brain\u003C/b\u003E\u003C/span\u003E \u2192 Can detect large intracranial masses, but MRI with contrast is more sensitive for orbital/optic nerve pathology.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFluorescein angiography\u003C/b\u003E\u003C/span\u003E \u2192 Helpful for vascular or retinal conditions, not for optic nerve compression.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMRI of orbit with gadolinium contrast\u003C/b\u003E\u003C/span\u003E \u2192 Best first-line test for unilateral disc swelling with field defect. Detects compressive, infiltrative, and demyelinating lesions.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 95,
    "Name": "Tests",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhen measuring stereopsis, which of the following is LEAST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENormal stereoacuity\u003C/b\u003E\u003C/span\u003E in humans is far finer than 100 seconds of arc:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBest stereoacuity \u2248 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E20\u201340 seconds of arc\u003C/b\u003E\u003C/span\u003E (sometimes even 10 sec of arc in young adults with excellent binocular vision).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E100 seconds of arc indicates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereduced stereoacuity\u003C/b\u003E\u003C/span\u003E, not the physiological limit.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EOption breakdown:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPanum\u2019s fusional area = small disparity range where fusion is possible.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENormal stereoacuity is ~20\u201340 arc seconds, not 100.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERandot uses random dot patterns, eliminating monocular cues.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA stereoscope indeed measures convergence required to fuse dissimilar images.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 96,
    "Name": "Disc Oedema",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 54-year-old lady notices blurred vision in her left eye without any pain or discomfort. On examination:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EVA: 6/12\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIshihara: 8/17 correct\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ELeft RAPD\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EVisual fields: central scotoma\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E5.5 mm axial proptosis, normal eyelids and motility\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFundus: swollen left optic disc\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ERight eye: normal\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFour months later vision deteriorates to PL only, but fundus remains unchanged.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat type of pathological process is MOST likely to be the problem?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey features pointing to compression:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGradual onset \u0026amp; progression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (over months).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProptosis\u003C/b\u003E\u003C/span\u003E (5.5 mm axial displacement suggests orbital mass/lesion).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptic disc swelling without pain\u003C/b\u003E\u003C/span\u003E \u2192 typical for compression (not neuritis).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteady deterioration to PL\u003C/b\u003E\u003C/span\u003E \u2192 compressive lesions cause progressive irreversible loss.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFundus unchanged despite worsening vision\u003C/b\u003E\u003C/span\u003E \u2192 \u201Coptic atrophy\u201D lagging behind functional decline, seen in compressive causes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhy not the others?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDemyelinating optic neuritis\u003C/b\u003E\u003C/span\u003E \u2192 usually acute painful visual loss, recovers partially, common in younger patients.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGranulomatous optic neuritis\u003C/b\u003E\u003C/span\u003E (e.g., sarcoid, TB) \u2192 would cause inflammation, often painful, with systemic features.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPost-infective optic neuritis\u003C/b\u003E\u003C/span\u003E \u2192 acute/subacute, typically self-limiting, not progressive deterioration over months.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 97,
    "Name": "Tests",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA four-prism diopter base-out test is used to evaluate which of the following?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFour Prism Diopter Base Out (4\u0394 BO) Test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUsed to detect \u003C/span\u003E\u003Cb\u003Emicrostrabismus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E or \u003C/span\u003E\u003Cb\u003Ecentral suppression scotoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA 4\u0394 BO prism is placed in front of one eye.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn a normal patient:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe eye under prism makes a refixation movement.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe fellow eye makes a fusional movement.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn a patient with \u003C/span\u003E\u003Cb\u003Ecentral suppression scotoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe refixation movement occurs, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethe fellow eye does not move\u003C/b\u003E\u003C/span\u003E, because the image falls into the suppression scotoma.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EWhy not the others?\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDistance stereoacuity\u003C/b\u003E\u003C/span\u003E \u2192 Tested with stereotests like Frisby, Randot, TNO.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMicrotropia without identity\u003C/b\u003E\u003C/span\u003E \u2192 Can be suspected with this test, but the 4\u0394 BO specifically targets \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecentral suppression\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripheral binocular vision\u003C/b\u003E\u003C/span\u003E \u2192 Assessed with synoptophore, Worth 4-dot, not this test.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 98,
    "Name": "GCA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 79-year-old woman presents with right-sided unilateral headache and a complete right pupil-sparing third nerve palsy. Which of the following is the most important initial investigation to order?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey clinical features:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EElderly patient (78 years old)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENew-onset \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eheadache\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EComplete third nerve palsy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but \u003C/span\u003E\u003Cb\u003Epupil-sparing\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHigh suspicion for \u003C/span\u003E\u003Cb\u003Egiant cell arteritis (GCA)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn older patients, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupil-sparing third nerve palsy\u003C/b\u003E\u003C/span\u003E is usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eischemic (microvascular)\u003C/b\u003E\u003C/span\u003E, but the presence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eheadache\u003C/b\u003E\u003C/span\u003E raises concern for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGCA\u003C/b\u003E\u003C/span\u003E, a medical emergency.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Emost important initial test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003E\u003Cb\u003EESR (or CRP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E to urgently check for GCA.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDelay in diagnosis can lead to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eirreversible blindness\u003C/b\u003E\u003C/span\u003E due to anterior ischemic optic neuropathy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIf ESR/CRP are raised \u2192 immediate high-dose corticosteroid therapy should be started.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EOther Options:\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECT head\u003C/b\u003E\u003C/span\u003E \u2192 May help rule out compressive causes, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGCA must be excluded first\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPlasma glucose\u003C/b\u003E\u003C/span\u003E \u2192 Relevant for vascular palsies (diabetes-related), but less urgent than excluding GCA.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMR/CT angiography\u003C/b\u003E\u003C/span\u003E \u2192 Needed if a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupil-involving third nerve palsy\u003C/b\u003E\u003C/span\u003E is present (to exclude posterior communicating artery aneurysm). But here the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupil is spared\u003C/b\u003E\u003C/span\u003E. Some clinicians advocate for ordering MRA for all 3rd nerve palsies, however, ESR seems like the more logical \u0022first\u0022 investigation in this case.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 99,
    "Name": "SO",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn a patient with sympathetic ophthalmia, which of the following is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESympathetic ophthalmia (SO):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ERare, \u003C/span\u003E\u003Cb\u003Ebilateral granulomatous panuveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E that follows \u003C/span\u003E\u003Cb\u003Epenetrating trauma or intraocular surgery\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in one eye.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt occurs due to an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautoimmune reaction\u003C/b\u003E\u003C/span\u003E against retinal antigens.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey features:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESymptoms usually appear \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eweeks to months\u003C/b\u003E\u003C/span\u003E after injury (not within 5 days \u2192 rules out option C).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EExudative retinal detachment is common\u003C/b\u003E\u003C/span\u003E because of severe choroidal inflammation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDalen-Fuchs nodules\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E are not polymorphonuclear \u2192 they are \u003C/span\u003E\u003Cb\u003Ecollections of epithelioid cells (macrophages) between RPE and Bruch\u2019s membrane\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (rules out option A).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEnucleation of the severely injured eye may be considered \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewithin 10\u201314 days\u003C/b\u003E\u003C/span\u003E if there is no visual potential, to reduce risk of SO (so option D is misleading).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EOther options:\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDalen-Fuchs nodules are granulomatous (epithelioid histiocytes), not polymorphonuclear.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOnset usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2 weeks to months\u003C/b\u003E\u003C/span\u003E after injury, not within 5 days.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe injured eye may need \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eenucleation\u003C/b\u003E\u003C/span\u003E if unsalvageable, to protect the sympathizing eye.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in FRCOphth part 2 written exam in 2022.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 100,
    "Name": "Sarcoidosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 6-year-old boy with a history of an upper respiratory tract infection presented to you with a rash on his legs, that is lumpy. His ocular examination showed bilateral anterior uveitis, granulomatous keratic precipitates, with marked flare and 2\u002B cells. His posterior segment examination was normal. Which of the following diagnoses is MOST likely to be True?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey clinical clues from the stem:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAge:\u003C/b\u003E\u003C/span\u003E child (5 years)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESystemic:\u003C/b\u003E\u003C/span\u003E recent URTI \u002B \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elumpy rash on legs\u003C/b\u003E\u003C/span\u003E (erythema nodosum is classic in sarcoidosis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOcular:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u003C/span\u003E\u003Cb\u003Ebilateral granulomatous anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with keratic precipitates and flare\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFundus normal\u003C/b\u003E\u003C/span\u003E (so posterior involvement less likely at this stage)\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p4\u0022\u003EThis combination strongly suggests \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Esarcoidosis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther Options:\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EJuvenile idiopathic arthritis (JIA):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECauses \u003C/span\u003E\u003Cb\u003Echronic, non-granulomatous anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (fine KPs, not granulomatous).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERash is not typical.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELymphoma:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERare in this age, and usually involves \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior segment masquerade syndromes\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMetastatic endophthalmitis:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWould cause a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epainful red eye\u003C/b\u003E\u003C/span\u003E with hypopyon, vitreous involvement and abnormal fundus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis child has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Equiet fundi\u003C/b\u003E\u003C/span\u003E and granulomatous inflammation, so not endophthalmitis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: medium; color: rgb(64, 0, 255);\u0022\u003ESarcoidosis:\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: medium; color: rgb(64, 0, 255);\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ERare in children but should be suspected when \u003C/span\u003E\u003Cb\u003Euveitis \u002B systemic features (rash, lymphadenopathy, arthritis, lung involvement)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOcular involvement is often \u003C/span\u003E\u003Cb\u003Egranulomatous anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESkin manifestations like \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eerythema nodosum\u003C/b\u003E\u003C/span\u003E are common.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 101,
    "Name": "Anatomy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following nerves is a cranial nerve that supplies the contralateral side?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECranial Nerve IV (Trochlear nerve):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eonly cranial nerve that decussates (crosses) completely\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in the brainstem (at the dorsal midbrain).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIt then innervates the \u003C/span\u003E\u003Cb\u003Econtralateral superior oblique muscle\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis makes it unique: all other cranial nerves supply ipsilateral structures.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ERemember:\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\uD83D\uDC49 \u201C\u003C/span\u003E\u003Cb\u003ETrochlear Turns\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u201D \u2192 Trochlear nerve \u003C/span\u003E\u003Cb\u003Ecrosses and turns\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E to supply the \u003C/span\u003E\u003Cb\u003Econtralateral superior oblique\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 102,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 26-year-old gentleman presents to you with a hyperacute conjunctivitis in his right eye. On examination, the cornea has a 3 mm ulcer with significant thinning. You ordered a gram film. Which one of the following is MOST likely to be shown?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperacute conjunctivitis\u003C/b\u003E\u003C/span\u003E with rapid corneal involvement and ulceration strongly suggests \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENeisseria gonorrhoeae\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENeisseria gonorrhoeae\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003ENeisseria meningitidis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E appear as \u003C/span\u003E\u003Cb\u003EGram-negative diplococci\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on gram stain.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGonococcal keratoconjunctivitis is an ophthalmic emergency as it can \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erapidly cause corneal perforation\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOther options:\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGram negative rods\u003C/b\u003E\u003C/span\u003E \u2192 e.g., Pseudomonas \u2192 typically seen in contact lens\u2013related keratitis, not hyperacute conjunctivitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGram positive diplococci\u003C/b\u003E\u003C/span\u003E \u2192 e.g., Streptococcus pneumoniae \u2192 can cause keratitis but not this hyperacute picture.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGram positive rods\u003C/b\u003E\u003C/span\u003E \u2192 e.g., Listeria, Corynebacterium \u2192 rare ocular pathogens, not the likely cause here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 103,
    "Name": "Torch",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EYou are asked to see an infant who has history of intrauterine growth retardation. The infant suffers from deafness, a patent ductus arteriosus, and bilateral cataract. Which of these diagnoses is MOST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EExplanation:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis infant presents with the \u003C/span\u003E\u003Cb\u003Eclassic triad of congenital rubella syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESensorineural deafness\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital cataracts\u003C/b\u003E\u003C/span\u003E (or other ocular abnormalities such as pigmentary retinopathy)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital heart disease\u003C/b\u003E\u003C/span\u003E (commonly patent ductus arteriosus or pulmonary artery stenosis).\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECytomegalovirus\u003C/b\u003E\u003C/span\u003E: Causes microcephaly, periventricular calcifications, chorioretinitis \u2014 not classically PDA and cataracts.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGalactosaemia\u003C/b\u003E\u003C/span\u003E: Can cause cataracts, but usually associated with hepatomegaly, hypoglycaemia, jaundice \u2014 not PDA or deafness.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELowe syndrome\u003C/b\u003E\u003C/span\u003E: Presents with congenital cataracts, hypotonia, and renal tubular dysfunction \u2014 not PDA and deafness.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThus, the findings here are \u003C/span\u003E\u003Cb\u003Emost consistent with maternal rubella infection during pregnancy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 104,
    "Name": "Nystagmus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following statements\u0026nbsp;\u003C/b\u003E\u003Cspan style=\u0022font-size: medium; font-weight: 700; letter-spacing: 0.14994px;\u0022\u003Eis LEAST likely to be true\u0026nbsp;\u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: medium;\u0022\u003Eregarding Congenital Nystagmus (infantile nystagmus syndrome)?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital/infantile nystagmus\u003C/b\u003E\u003C/span\u003E is usually \u003Ci\u003Enot associated with oscillopsia\u003C/i\u003E, because the visual cortex adapts.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatients often adopt a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enull point\u003C/b\u003E\u003C/span\u003E (head turn/tilt) to reduce the amplitude of nystagmus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConvergence typically dampens\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E congenital nystagmus.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUnlike acquired forms, \u003C/span\u003E\u003Cb\u003Efixation tends to increase nystagmus intensity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not decrease it\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003ESo\u0026nbsp;\u003Cb\u003ECorrect Answer: It is typically decreased by attempted fixation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb style=\u0022color: rgb(255, 0, 0); text-decoration-line: underline;\u0022\u003EMnemonic for CONGENITAL Nystagmus:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EC\u003C/span\u003Eonvergence and eye closure dampen the nystagmus\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EO\u003C/span\u003Epen eyes\u003Cspan style=\u0022font-weight: bold;\u0022\u003E - \u003C/span\u003Eso absent during sleep\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EN\u003C/span\u003Eull zone is present\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EG\u003C/span\u003Eaze position stable: so gaze position does \u003Cspan style=\u0022font-weight: bold;\u0022\u003Enot\u003C/span\u003E change the direction of nystagmus;\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EE\u003C/span\u003Equal amplitude and frequency of nystagmus in each eye\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EN\u003C/span\u003Eear acuity is good because convergence dampens the nystagmus\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EI\u003C/span\u003Enversion of optokinetic nystagmus occurs\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ET\u003C/span\u003Eurning of head or abnormal head posture to allow eyes to enter a null zone leads to better visual acuity\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA\u003C/span\u003Ebsent Oscillopsia as the brain adapts at a young age.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EL\u003C/span\u003Eatent nystagmus occurs.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 105,
    "Name": "Hereditaty vitreoretinopathies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 53-year-old asymptomatic woman is referred by her optometrist after detection of peripheral retinal haemorrhages in both eyes. Visual acuity and anterior segment examination are normal, and there is no relevant family history. The fluorescein angiogram shown demonstrates the retinal findings. What is the MOST likely diagnosis?\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-27-0b246267-5fbf-4fa8-9fc0-705b6ade4553.png\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe fluorescein angiogram shows \u003C/span\u003E\u003Cb\u003Eperipheral avascular retina with neovascularisation at the junction between perfused and non-perfused retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis is characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efamilial exudative vitreoretinopathy (FEVR)\u003C/b\u003E\u003C/span\u003E, an inherited condition (often autosomal dominant) where retinal vascular development is incomplete.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey differentiators:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECoat\u2019s disease\u003C/b\u003E\u003C/span\u003E \u2192 usually unilateral, telangiectatic vessels with exudation (not seen here).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIncontinentia pigmenti\u003C/b\u003E\u003C/span\u003E \u2192 X-linked dominant, presents in infancy with skin changes, not in a healthy 53-year-old.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201CRetinal angiogenesis\u201D\u003C/b\u003E\u003C/span\u003E is a process, not a diagnosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThus, the most likely diagnosis here is \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EFEVR\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 106,
    "Name": "Phakomatosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 45-year-old woman is referred for retinal screening following successful removal of a cerebral tumour. Based on the retinal appearance and fluorescein angiography findings, what is the abnormality and its associated heredo-familial syndrome?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-27-087a5655-c41d-4116-a582-a33df993bce6.png\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe image shows a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal capillary haemangioblastoma (retinal angioma)\u003C/b\u003E\u003C/span\u003E \u2014 a vascular lesion with feeder vessels that demonstrates hyperfluorescence and leakage on fluorescein angiography.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis lesion is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echaracteristically associated with von Hippel\u2013Lindau (VHL) disease\u003C/b\u003E\u003C/span\u003E, an autosomal dominant condition due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVHL gene mutation\u003C/b\u003E\u003C/span\u003E (chromosome 3p25\u201326). Patients are predisposed to retinal angiomas, cerebellar and spinal haemangioblastomas, renal cell carcinoma, and pheochromocytoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhy not the others?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E(NF1):\u003C/b\u003E\u003C/span\u003E Associated with optic gliomas and Lisch nodules, not retinal angiomas.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E(Tuberous sclerosis):\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E Associated with \u003C/span\u003E\u003Cb\u003Eastrocytic hamartomas\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not vascular angiomas.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E(NF2):\u003C/b\u003E\u003C/span\u003E Associated with bilateral vestibular schwannomas and retinal hamartomas, not angiomas.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u003Cb\u003ESupporting Evidence:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: x-small;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003ESingh AD, Shields CL, Shields JA. \u003Ci\u003EVon Hippel\u2013Lindau disease.\u003C/i\u003E Surv Ophthalmol. 2001;46(2):117\u2013142.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EAmerican Academy of Ophthalmology, BCSC Retina section, VHL chapter.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cbr\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 107,
    "Name": "Non-infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following dermatological conditions is most likely to be associated with marginal keratitis?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMarginal keratitis\u003C/b\u003E\u003C/span\u003E is a peripheral corneal inflammation classically associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estaphylococcal lid disease\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eocular rosacea\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular rosacea\u003C/b\u003E\u003C/span\u003E is a chronic inflammatory condition that affects the meibomian glands and eyelids, leading to chronic blepharitis, meibomian gland dysfunction, and secondary marginal keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhy not the others?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E(Acne vulgaris):\u003C/b\u003E\u003C/span\u003E While acne can affect sebaceous glands, it is not associated with marginal keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E(Dermatitis herpetiformis):\u003C/b\u003E\u003C/span\u003E Linked with gluten sensitivity, not ocular keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E(Pompholyx):\u003C/b\u003E\u003C/span\u003E A vesicular hand eczema, no ocular link.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u003Cb\u003ESupporting Evidence:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: x-small;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EAmerican Academy of Ophthalmology (AAO) BCSC: External Disease and Cornea (Ocular Rosacea section).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EO\u2019Donnell B, Morrow GL. \u003Ci\u003EOcular rosacea: Epidemiology, pathogenesis and treatment.\u003C/i\u003E Am J Clin Dermatol. 2012;13(6):421\u2013430.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 108,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cb\u003EA patient is reviewed after right-eye cataract surgery. Pre-operative refraction was R \u22125.00 D and L \u22121.00 D. The left eye remains phakic, and the operated right eye now sees 6/6 unaided. Since surgery the patient reports eyestrain (asthenopic symptoms), having had no pre-op symptoms apart from blur in the right eye. What is the MOST likely cause of these symptoms?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EUnilateral cataract surgery has converted a \u22125.00 D myopic eye to emmetropia while the fellow eye remains \u22121.00 D, creating \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epost-operative anisometropia\u003C/b\u003E\u003C/span\u003E. The resulting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einterocular image-size disparity (aniseikonia)\u003C/b\u003E\u003C/span\u003E commonly causes asthenopic symptoms (eyestrain, discomfort) even when acuity is excellent. Differences as small as ~2\u20133 D can be symptomatic; larger differences increase the likelihood of aniseikonia.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EFaulty biometry or a wrong-power IOL would more likely reduce unaided acuity rather than produce isolated asthenopia with 6/6 vision. Induced astigmatism presents with blur/ghosting and isn\u2019t suggested by the data provided.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\uD83D\uDCD6 AAO BCSC: Refractive Management \u0026amp; Cataract Surgery\u2014anisometropia/aniseikonia after unilateral pseudophakia; Grosvenor T. \u003Ci\u003EPrimary Care Optometry\u003C/i\u003E, 5th ed.\u2014clinical effects and thresholds for symptomatic aniseikonia.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 109,
    "Name": "Intra-ocular tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWith respect to choroidal osteoma, which of the following statements is LEAST accurate?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EChoroidal osteoma is a benign ossifying choristoma, typically located in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipapillary or macular region\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDecalcified areas\u003C/b\u003E\u003C/span\u003E are more prone to choroidal neovascularisation (CNV), which can threaten central vision.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathologically, it is indeed a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoristoma\u003C/b\u003E\u003C/span\u003E (normal tissue in an abnormal location).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELesions often occur near the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic nerve or macula\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EImportantly, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanti-VEGF agents are not contraindicated\u003C/b\u003E\u003C/span\u003E; instead, they are an established treatment for secondary CNV associated with choroidal osteoma, improving or stabilising vision.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-Shields CL, Shields JA. \u003Ci\u003EChoroidal Osteoma: Clinical Features and Update on Diagnosis and Management\u003C/i\u003E. Int Ophthalmol Clin. 2006;46(1):171-179.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-BCSC Retina \u0026amp; Vitreous (2022\u201323): management of CNV in choroidal osteoma includes intravitreal anti-VEGF therapy.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 110,
    "Name": "Study types",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhen evaluating a case\u2013control study, which factor is MOST likely to enhance the level of evidence?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe strength of a case\u2013control study depends heavily on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emethodological rigour\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EClearly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edefined and objective outcomes\u003C/b\u003E\u003C/span\u003E reduce misclassification bias and improve internal validity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHistorical controls\u003C/b\u003E\u003C/span\u003E introduce recall and selection bias, lowering evidence strength.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDifferent populations\u003C/b\u003E\u003C/span\u003E reduce comparability and increase confounding.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProxies for outcome\u003C/b\u003E\u003C/span\u003E are less reliable than direct measures, reducing validity.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThus, the use of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprecise and predefined outcomes\u003C/b\u003E\u003C/span\u003E enhances the credibility and evidence level of case\u2013control studies.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-Grimes DA, Schulz KF. \u003Ci\u003EBias and causal associations in observational research\u003C/i\u003E. Lancet. 2002;359(9302):248\u2013252.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-BCSC Section on Fundamentals \u0026amp; Principles of Ophthalmology (2022\u201323): emphasis on outcome definition in study design.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: x-small;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 111,
    "Name": "Trauma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EAccording to the Ocular Trauma Score, which of the following specific clinical findings directly influences the patient\u2019s score and predicted visual outcome?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular Trauma Score (OTS)\u003C/b\u003E\u003C/span\u003E is a validated system used to predict final visual outcomes following ocular trauma. It is calculated from:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInitial visual acuity, and\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDeductions for the presence of specific severe ocular findings.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Efive factors that reduce the OTS score\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E are:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGlobe rupture\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEndophthalmitis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPerforating injury\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinal detachment\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERelative afferent pupillary defect (RAPD)\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther findings, such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh intraocular pressure\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eophthalmoplegia\u003C/b\u003E\u003C/span\u003E, are not included in the OTS calculation. A \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretained intraocular foreign body\u003C/b\u003E\u003C/span\u003E affects prognosis but is not part of the OTS scoring system itself.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EKuhn F, Maisiak R, Mann L, Mester V, Morris R, Witherspoon CD. \u003Ci\u003EThe Ocular Trauma Score (OTS)\u003C/i\u003E. Ophthalmol Clin North Am. 2002 Jun;15(2):163\u2013165.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EBCSC Section 5: Neuro-Ophthalmology and Ocular Trauma (2022\u201323).\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 112,
    "Name": "Non-infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 23-year-old woman presents with recurrent ocular redness, episcleritis, a peripheral corneal ulcer, saddle-nose deformity, and aortic valve involvement. Based on these findings, what is the most likely diagnosis?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ERelapsing polychondritis is a rare autoimmune disorder characterized by recurrent inflammation of cartilaginous and connective tissue structures.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey diagnostic clues in this case include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular involvement\u003C/b\u003E\u003C/span\u003E: episcleritis, scleritis, keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENasal cartilage involvement\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: saddle-nose deformity.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECardiovascular involvement\u003C/b\u003E\u003C/span\u003E: aortic valve disease (common complication).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESystemic inflammation\u003C/b\u003E\u003C/span\u003E: elevated ESR, anemia of chronic disease.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe combination of ocular, nasal, and cardiovascular features is \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ehighly characteristic of relapsing polychondritis\u003C/b\u003E\u003C/span\u003E and not typical of dermatomyositis, Kawasaki disease, or rheumatoid arthritis.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-Kent A, Michet CJ. \u003Ci\u003ERelapsing Polychondritis: Clinical Features and Diagnosis\u003C/i\u003E. Rheumatology (Oxford). 2019.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-BCSC Section 9: Uveitis and Ocular Inflammation (2022\u201323).\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 113,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EAccording to UK national diabetic retinopathy screening guidelines, if R3 (active proliferative) retinopathy is identified at screening, within what timeframe should the patient be referred to the Hospital Eye Service (HES)?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EUK diabetic eye screening guidelines state that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esight-threatening diabetic retinopathy (R3, proliferative retinopathy)\u003C/b\u003E\u003C/span\u003E requires \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eurgent referral to the Hospital Eye Service (HES) within 2 weeks\u003C/b\u003E\u003C/span\u003E. This ensures that patients at high risk of severe visual loss are promptly assessed for treatment such as panretinal photocoagulation (PRP) or intravitreal therapy.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 114,
    "Name": "Genetics",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhen considering colour vision deficiency, which of the following statements is MOST likely to be correct?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMost common congenital red-green colour vision defects are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked recessive\u003C/b\u003E\u003C/span\u003E. This means:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMales (XY) with the defective gene are affected.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDaughters of affected males (who inherit the defective X) are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eobligate heterozygous carriers\u003C/b\u003E\u003C/span\u003E, unless the mother also carries the gene.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESons of an affected male will not inherit the condition (since they receive the father\u2019s Y chromosome).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther points from the options:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EProtanomaly is not the most common defect\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E; the most frequent is \u003C/span\u003E\u003Cb\u003Edeuteranomaly\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPseudo-isochromatic plates (Ishihara)\u003C/b\u003E\u003C/span\u003E can detect red-green deficiency but cannot reliably distinguish protanomaly from deuteranomaly.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe prevalence of red-green colour deficiency in UK males is ~8%, not 2%.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E-Birch J. \u003Ci\u003EWorldwide prevalence of red-green colour deficiency\u003C/i\u003E. J Opt Soc Am A. 2012.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E-NHS Genomics Education Programme \u2013 Colour Vision Deficiency Genetics.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 115,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EYou review a patient 1 week after left trabeculectomy with Mitomycin-C. They present with IOP 45 mmHg, a flat bleb with no leak, and a uniformly shallow anterior chamber. The retina is unremarkable. What is the most appropriate management plan?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis presentation is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaqueous misdirection (malignant glaucoma)\u003C/b\u003E\u003C/span\u003E after trabeculectomy:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigh IOP despite a flat bleb (so the bleb is not functioning).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUniformly shallow anterior chamber in all quadrants (not peripheral shallowing as in pupillary block).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAbsence of choroidal effusion or suprachoroidal haemorrhage.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInitial management\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecycloplegia (atropine) and aqueous suppression\u003C/b\u003E\u003C/span\u003E, to move the lens-iris diaphragm posteriorly and reduce aqueous misdirection. Hyperosmotic agents may also help.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EArgon laser suture lysis\u003C/b\u003E\u003C/span\u003E is inappropriate because the IOP is already high with a flat bleb (not under-filtration).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBleb massage\u003C/b\u003E\u003C/span\u003E will not help, as aqueous misdirection is the cause, not flap resistance.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERe-forming the anterior chamber with viscoelastic\u003C/b\u003E\u003C/span\u003E is temporary and does not address the pathophysiology.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 116,
    "Name": "Tests",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EInvestigators are comparing two independent groups of subjects for a continuous variable that is not normally distributed (skewed data). Which is the most appropriate statistical test?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFor \u003C/span\u003E\u003Cb\u003Econtinuous variables with skewed distribution\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (non-parametric data):\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMann-Whitney U test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is used to compare \u003C/span\u003E\u003Cb\u003Etwo independent groups\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUnpaired t test\u003C/b\u003E\u003C/span\u003E assumes normal distribution, so inappropriate here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPaired t test\u003C/b\u003E\u003C/span\u003E is for matched/paired data, not independent groups.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWilcoxon signed rank test\u003C/b\u003E\u003C/span\u003E is also for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epaired data\u003C/b\u003E\u003C/span\u003E, not independent groups.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EThus, \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EMann-Whitney U test\u003C/b\u003E\u003C/span\u003E is the correct choice when comparing two separate groups with skewed data.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 117,
    "Name": "Physiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following statements about intraocular pressure is correct?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENormal \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaqueous humor production\u003C/b\u003E\u003C/span\u003E is about \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2\u20133 \u03BCl/min\u003C/b\u003E\u003C/span\u003E, primarily by the ciliary body.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntraocular pressure (IOP) is determined by the balance between aqueous humor \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eproduction and outflow\u003C/b\u003E\u003C/span\u003E (via trabecular meshwork and uveoscleral pathways).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot directly proportional to systemic blood pressure\u003C/b\u003E\u003C/span\u003E or cerebrospinal fluid pressure, though extreme systemic changes may have minor effects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe statement about reforming anterior and posterior chambers in 1000 min is physiologically incorrect.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 118,
    "Name": "Consent",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWith regard to disclosure of personal information without a patient\u2019s consent, which statement is the most accurate?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDoctors \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eowe a duty of confidentiality\u003C/b\u003E\u003C/span\u003E to their patients, but this is not absolute.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBoth the \u003C/span\u003E\u003Cb\u003EGMC (General Medical Council) guidance\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and the \u003C/span\u003E\u003Cb\u003EData Protection Act / GDPR framework\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E recognise exceptions.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDisclosure \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewithout consent\u003C/b\u003E\u003C/span\u003E is justified where there is a risk of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eserious harm or death\u003C/b\u003E\u003C/span\u003E to others, e.g. risk of violence, terrorism, or serious communicable disease.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA multidisciplinary team discussion is good practice but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot a legal prerequisite\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E- GMC Confidentiality Guidance (2020).\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E- NHS Digital \u2013 Data Protection and Confidentiality.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E- UK GDPR Article 9(2)(i): \u201Cprocessing necessary for reasons of public interest in the area of public health.\u201D\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 119,
    "Name": "CSCR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich statement best reflects current understanding of central serous chorioretinopathy (CSR)?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECSR is associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eincreased corticosteroid levels\u003C/b\u003E\u003C/span\u003E, whether exogenous (steroid therapy) or endogenous (stress, Cushing\u2019s syndrome, pregnancy).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPregnancy, especially in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethird trimester\u003C/b\u003E\u003C/span\u003E, is a recognised risk factor for CSR, and cases often resolve spontaneously after delivery.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathogenesis is linked to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoroidal vascular hyperpermeability\u003C/b\u003E\u003C/span\u003E and RPE dysfunction, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot VEGF\u003C/b\u003E\u003C/span\u003E (unlike neovascular AMD).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe presence of fibrin within CSR is not a favourable prognostic sign; in fact, it can be associated with poorer outcomes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 120,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA 25-year-old man with slowly progressive central visual difficulties undergoes fundus photography and fluorescein angiography. He has no relevant ocular family history. Based on the clinical and imaging findings, what is the most likely diagnosis?\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-27-9e13dd07-fc60-4d6b-a3ef-3ea66ee1d4ca.png\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EStargardt disease is the most common inherited macular dystrophy, typically presenting in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efirst to third decade of life\u003C/b\u003E\u003C/span\u003E with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogressive central vision loss\u003C/b\u003E\u003C/span\u003E and difficulty with tasks such as reading fine print. Fundus findings show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyellow-white pisciform flecks\u003C/b\u003E\u003C/span\u003E and a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cbeaten bronze\u201D macula\u003C/b\u003E\u003C/span\u003E. On fluorescein angiography, a characteristic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cdark choroid\u201D sign\u003C/b\u003E\u003C/span\u003E is often observed due to lipofuscin accumulation in the RPE blocking background choroidal fluorescence.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcute multifocal placoid pigment epitheliopathy (APMPPE):\u003C/b\u003E\u003C/span\u003E presents acutely with multiple creamy placoid lesions post-viral illness, not gradual deterioration.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDominant drusen:\u003C/b\u003E\u003C/span\u003E usually strong family history with drusen scattered at posterior pole, not pisciform flecks.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAdult Best disease:\u003C/b\u003E\u003C/span\u003E shows vitelliform lesions at the macula, usually with family history (autosomal dominant BEST1 mutations).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-Lambertus S, et al. \u003Ci\u003EProg Retin Eye Res\u003C/i\u003E 2017 \u2014 Stargardt disease pathophysiology and clinical features.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E-BCSC Retina \u2014 description of flecks, dark choroid, and distinguishing features from Best disease and drusen.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: x-small;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 121,
    "Name": "Nystagmus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following conditions is least likely to cause downbeat nystagmus?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDownbeat nystagmus is a \u003C/span\u003E\u003Cb\u003Epathological ocular motor sign\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E typically associated with lesions at the \u003C/span\u003E\u003Cb\u003Ecervicomedullary junction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (such as Arnold\u2013Chiari malformation), \u003C/span\u003E\u003Cb\u003Ebrainstem stroke\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, or \u003C/span\u003E\u003Cb\u003Ecerebellar disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It may also be induced by certain \u003C/span\u003E\u003Cb\u003Emedications (e.g., anticonvulsants such as phenytoin or carbamazepine)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBy contrast, \u003C/span\u003E\u003Cb\u003EParkinson\u2019s disease does not cause downbeat nystagmus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Instead, Parkinson\u2019s is primarily associated with abnormalities of \u003C/span\u003E\u003Cb\u003Esaccades, smooth pursuit, and fixation instability (e.g., square wave jerks)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but not vertical downbeat nystagmus.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ESo to summarise:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECommon causes\u003C/b\u003E\u003C/span\u003E \u2192 \u003Ci\u003EChiari malformation, brainstem stroke, cerebellar disease, anticonvulsants\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENOT a cause\u003C/b\u003E\u003C/span\u003E \u2192 \u003Ci\u003EParkinson\u2019s disease\u003C/i\u003E (causes other eye movement problems, not downbeat nystagmus)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EMnemonic:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u201CDownbeat is CBA (Chiari, Brainstem, Anticonvulsants)\u201D\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2013 not Parkinson\u2019s.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 122,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhat is the most accurate statement regarding HbA1C targets in adults with type 2 diabetes mellitus?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENICE guidelines (NG17) recommend \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E53 mmol/mol (7.0%)\u003C/b\u003E\u003C/span\u003E as the general target.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis applies especially when the treatment carries a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erisk of hypoglycaemia\u003C/b\u003E\u003C/span\u003E, as tighter control (e.g. 48 mmol/mol / 6.5%) may not be safe.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA slightly higher target (58 mmol/mol / 7.5%) can be considered if managed only with lifestyle/diet or if treatment burden is high.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EKey point for revision:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHypo-risk drugs \u2192 HbA1c 53 (7.0%)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo hypo-risk drug \u2192 can aim lower (48 / 6.5%)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELifestyle only \u2192 relax to 58 (7.5%)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 123,
    "Name": "Hereditaty vitreoretinopathies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn Stickler syndrome Type I, which genetic and inheritance pattern is correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EStickler syndrome Type I is due to \u003C/span\u003E\u003Cb\u003Emutations in type II collagen (COL2A1 gene)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and is inherited in an \u003C/span\u003E\u003Cb\u003Eautosomal dominant pattern with complete penetrance\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EStickler syndrome is a connective tissue disorder affecting the eye, joints, and face.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EType I Stickler\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 caused by \u003C/span\u003E\u003Cb\u003ECOL2A1 gene mutation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (type II collagen).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common subtype\u003C/b\u003E\u003C/span\u003E and is inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E fashion.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EComplete penetrance means that all individuals with the mutation will show clinical features, though severity may vary.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 124,
    "Name": "Keratoconus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhat is the MOST likely diagnosis based upon this topography image?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-28-d438413d-d022-43fb-9138-52de298786e4.jpg\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe map shows \u003C/span\u003E\u003Cb\u003Einferior peripheral steepening with central/paracentral relative flattening\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, creating a \u003C/span\u003E\u003Cb\u003E\u201Ccrab-claw/kissing-dove\u201D\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E bow-tie pattern\u2014classic for \u003C/span\u003E\u003Cb\u003EPMD\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPMD is a \u003C/span\u003E\u003Cb\u003Eperipheral inferior thinning disorder (typically 4\u20138 o\u2019clock, near the limbus)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E that produces \u003C/span\u003E\u003Cb\u003Ehigh against-the-rule astigmatism\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and the above topographic signature.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKeratoconus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E usually has a \u003C/span\u003E\u003Cb\u003Eparacentral cone with localized inferior steepening and skewed radial axes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not the peripheral band of steepening seen in PMD.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPost-LASIK\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E corneas for myopia show \u003C/span\u003E\u003Cb\u003Ecentral flattening with a peripheral ring of relative steepening\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, rather than an inferior claw.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPost-ECCE astigmatism\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E gives a \u003C/span\u003E\u003Cb\u003Eregular bow-tie aligned with the incision axis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, lacking the inferior claw appearance.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 125,
    "Name": "Visual Field",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EWhich type of visual field defect is LEAST commonly linked to glaucoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETypical glaucomatous field defects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENasal step\u003C/b\u003E\u003C/span\u003E (due to arcuate bundle damage)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EParacentral scotoma\u003C/b\u003E\u003C/span\u003E (early damage near fixation)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EArcuate scotoma\u003C/b\u003E\u003C/span\u003E (Bjerrum scotoma, following RNFL loss)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETemporal wedge defects\u003C/b\u003E\u003C/span\u003E are \u003Ci\u003Enot characteristic of glaucoma\u003C/i\u003E. Instead, they are more commonly associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic nerve or chiasmal disease\u003C/b\u003E\u003C/span\u003E (e.g., compressive lesions).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 126,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EYou\u0027re examining a 38-year-old man who presents with a 2-day history of pain and redness in his right eye. Slit-lamp examination reveals a dendritic corneal ulcer with terminal bulbs, but there is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno evidence of stromal oedema, vascularisation, or keratic precipitates\u003C/b\u003E\u003C/span\u003E, and the anterior chamber remains deep and quiet. He reports having had \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etwo previous similar episodes of herpetic epithelial keratitis in the past year\u003C/b\u003E\u003C/span\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhat is the most appropriate treatment plan for managing this current episode and reducing the risk of further recurrences?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis patient has \u003C/span\u003E\u003Cb\u003Euncomplicated recurrent epithelial herpes simplex keratitis (HSK)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2014 presenting with a dendritic ulcer and \u003C/span\u003E\u003Cb\u003Eno stromal involvement or anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Therefore, the treatment is:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETopical aciclovir 3% ointment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E 5\u00D7/day for 10\u201314 days\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u00B1 epithelial debridement\u003C/b\u003E\u003C/span\u003E, which can reduce viral load and speed epithelial healing in some cases\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteroids are contraindicated\u003C/b\u003E\u003C/span\u003E in epithelial disease alone\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOral prophylaxis (400 mg BD)\u003C/b\u003E\u003C/span\u003E is considered only \u003Ci\u003Eafter resolution\u003C/i\u003E in select recurrent cases, but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot part of acute management\u003C/b\u003E\u003C/span\u003E for isolated epithelial disease\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EHEDS Trial \u2013 Key Findings (Epithelial Arm):\u003C/b\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003EHEDS-Epithelial Keratitis Trial\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E showed that:\u003C/span\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003EAdding oral aciclovir to topical treatment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E did \u003C/span\u003E\u003Cb\u003Enot significantly improve resolution or reduce recurrence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of epithelial HSK during an active episode.\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETherefore, topical antiviral alone remains first-line therapy for epithelial disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, even in recurrent cases.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p5\u0022\u003E-- Oral aciclovir \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003E400 mg twice daily for 12 months\u003C/b\u003E\u003C/span\u003E (from the HEDS-Acyclovir Prevention Trial) \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eis only for prophylaxis\u003C/b\u003E\u003C/span\u003E, not acute treatment \u2014 and is more relevant in stromal or uveitic disease or frequent recurrences.\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 127,
    "Name": "MMP",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements regarding the diagnosis of \u003Cspan class=\u0022s1\u0022\u003Eocular cicatricial pemphigoid (OCP)\u003C/span\u003E is MOST accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EOcular cicatricial pemphigoid (OCP) is a chronic autoimmune subepithelial blistering disorder affecting mucous membranes including the conjunctiva. Diagnosis relies heavily on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edirect immunofluorescence (DIF)\u003C/b\u003E\u003C/span\u003E of a conjunctival biopsy.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\uD83D\uDD2C \u003C/span\u003E\u003Cb\u003EKey points based on evidence and clinical guidelines:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor best results, the biopsy should be taken from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless inflamed, non-ulcerated conjunctiva\u003C/b\u003E\u003C/span\u003E, ideally 2\u20133 mm from the limbus. Severely inflamed areas often yield false negatives due to immune complex degradation.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u21B3 \u003Ci\u003EReference: Mondino BJ et al. Diagnosis and management of ocular cicatricial pemphigoid. Ophthalmology. 1992.\u003C/i\u003E\u003C/span\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe hallmark finding on DIF is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elinear deposition of IgG, IgA, or C3\u003C/b\u003E\u003C/span\u003E (not typically IgE) along the epithelial basement membrane. IgE is not a diagnostic feature.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u21B3 \u003Ci\u003EReference: American Academy of Ophthalmology (AAO) Basic and Clinical Science Course; Cornea.\u003C/i\u003E\u003C/span\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUp to \u003C/span\u003E\u003Cb\u003E40% of biopsy specimens may be negative\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially if taken from inflamed tissue. Therefore, a \u003C/span\u003E\u003Cb\u003Enegative DIF does not exclude\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E OCP.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u21B3 \u003Ci\u003EReference: Tauber J et al., 1992; Watson PG et al., 1986.\u003C/i\u003E\u003C/span\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFormalin destroys antigenicity\u003C/b\u003E\u003C/span\u003E needed for immunofluorescence. The specimen must be transported in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMichel\u2019s transport medium\u003C/b\u003E\u003C/span\u003E or similar. Formalin is used for standard histopathology, not DIF.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u21B3 \u003Ci\u003EReference: American Society for Clinical Pathology guidelines.\u003C/i\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDD11\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/b\u003E\u003Cb style=\u0022font-size: calc(1.3rem \u002B 0.6vw); letter-spacing: 0.14994px;\u0022\u003ENote for Revision:\u003C/b\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EIn suspected OCP, conjunctival biopsy for direct immunofluorescence should be taken from minimally inflamed tissue and placed in Michel\u2019s medium\u2014not formalin. A negative DIF does not exclude the diagnosis.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
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    "CategoryId": 6,
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  },
  {
    "Id": 128,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich histopathological stain is most useful for confirming the diagnosis of \u003Cspan class=\u0022s1\u0022\u003EAvellino corneal dystrophy\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAvellino corneal dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, also known as \u003C/span\u003E\u003Cb\u003Egranular-lattice corneal dystrophy (or granular corneal dystrophy type II)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, is characterised by a combination of:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHyaline deposits\u003C/b\u003E\u003C/span\u003E (as seen in granular dystrophy type I)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmyloid deposits\u003C/b\u003E\u003C/span\u003E (as seen in lattice dystrophy)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\uD83E\uDDEA \u003C/span\u003E\u003Cb\u003EStaining characteristics:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EH\u0026amp;E stain\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost useful and practical\u003C/b\u003E\u003C/span\u003E routine stain for detecting both granular (hyaline) and lattice (amyloid-like) deposits. It shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEosinophilic hyaline material in the anterior stroma (granular)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFaint or refractile linear deposits (lattice component)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAlcian blue\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Highlights \u003C/span\u003E\u003Cb\u003Emucin\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E; useful in \u003C/span\u003E\u003Cb\u003Emacular corneal dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not Avellino.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongo red\u003C/b\u003E\u003C/span\u003E: Used for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eamyloid\u003C/b\u003E\u003C/span\u003E, but Avellino\u2019s amyloid deposits are usually minimal and not always Congo red-positive.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOil Red O\u003C/b\u003E\u003C/span\u003E: Stains \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elipids\u003C/b\u003E\u003C/span\u003E; useful in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elipid keratopathy\u003C/b\u003E\u003C/span\u003E, not relevant here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\uD83D\uDD2C Although Congo red may detect amyloid in some lattice dystrophies, the \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Ecombined features of Avellino dystrophy are best demonstrated with H\u0026amp;E\u003C/b\u003E\u003C/span\u003E, making it the \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Emost useful single stain\u003C/b\u003E\u003C/span\u003E for diagnosis.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003EUsually, the exams direct the questions to the common corneal dystrophies, as remembered by this mnemonic:\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u0022\u003Cspan style=\u0022font-weight: bolder; color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EMarylin Monroe Always Gets Her Men in L. A. County\u0022\u003C/span\u003E\u003C/p\u003E\u003Cul style=\u0022margin-top: 0.3em; margin-bottom: 0px; margin-left: 1.6em; padding-left: 0px; list-style-position: outside; list-style-image: url(\u0026quot;data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAAYAAAAJCAYAAAARml2dAAAABHNCSVQICAgIfAhkiAAAAAlwSFlzAAAN1wAADdcBQiibeAAAABl0RVh0U29mdHdhcmUAd3d3Lmlua3NjYXBlLm9yZ5vuPBoAAABUSURBVAiZdY4xDsAgFELB2J0DdnbwQI5OHvDfgC62SY0yvhAetI1dWEq5JN0kKwDYbhEx8oT9a5JdEtLb/M2QNW0FAJLttkLbLUfEkIRVztPdo\u002BMBm8UkW9Zxc20AAAAASUVORK5CYII=\u0026quot;); color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EM\u003C/span\u003Eacular dystrophy -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EM\u003C/span\u003Eucopolysaccharide -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EA\u003C/span\u003Elcian blue\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EG\u003C/span\u003Eranular dystrophy -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EH\u003C/span\u003Eyaline materials -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EM\u003C/span\u003Easson trichrome\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EL\u003C/span\u003Eattice dystrophy -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EA\u003C/span\u003Emyloid -\u0026nbsp;\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EC\u003C/span\u003Eongo red\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 129,
    "Name": "Chemical injury",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn a patient with a chemical eye injury, which of the following features, in addition to limbal ischaemia, is associated with a \u003Cspan class=\u0022s1\u0022\u003Epoor visual prognosis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: small; font-weight: normal;\u0022\u003EThe key difference between Dua\u2019s classification and the Roper-Hall classification is that Dua\u2019s includes limbal epithelial involvement (rather than limbal ischaemia) and conjunctival involvement. These support the clinical relevance of conjunctival tissue in contributing to corneal re-epithelialisation in cases of limbal stem cell deficiency.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: small; font-weight: normal;\u0022\u003ELimbal involvement, assessed via fluorescein staining, offers a more objective and reproducible measure compared to limbal ischaemia, which can be highly subjective.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: small; font-weight: normal;\u0022\u003EThe degree of conjunctival involvement serves as an important indicator of conjunctival stem cell loss, which is critical in severe injuries where limbal stem cells are compromised.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003E\uD83D\uDD2C\u003Cspan style=\u0022font-size: medium;\u0022\u003EKey prognostic indicators (per\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003C/b\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EDua Classification\u0026nbsp;\u003C/b\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Eand literature):\u003C/b\u003E\u003C/span\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELimbal ischaemia\u003C/b\u003E\u003C/span\u003E is the most important predictor of long-term epithelial healing and stem cell deficiency.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESevere conjunctival involvement\u003C/b\u003E\u003C/span\u003E (\u0026gt;80%) is also associated with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor prognosis\u003C/b\u003E\u003C/span\u003E due to its impact on mucin-producing goblet cells and overall ocular surface healing.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAnterior chamber cells \u0026gt;2\u002B\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E indicate inflammation but are \u003C/span\u003E\u003Cb\u003Enot independently predictive\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of poor outcome.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP of 28 mmHg\u003C/b\u003E\u003C/span\u003E is not itself prognostic unless \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epersistent\u003C/b\u003E\u003C/span\u003E, and is more of a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomplication to manage\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELarge epithelial defects\u003C/b\u003E\u003C/span\u003E are expected in early phases but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal opacification and stromal haze\u003C/b\u003E\u003C/span\u003E are more prognostic than the size of the epithelial defect alone.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\uD83D\uDCD6 \u003C/span\u003E\u003Cb\u003EReferences:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDua HS et al. \u003Ci\u003EA new classification of ocular surface burns\u003C/i\u003E. Br J Ophthalmol. 2001;85(11):1379-1383.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHolland EJ et al. \u003Ci\u003EManagement of ocular surface chemical injuries\u003C/i\u003E. Int Ophthalmol Clin. 1997;37(4):105-122.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://eyewiki.org/w/images/1/1b/Burnlegend2.JPG?20121201015301\u0022\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 130,
    "Name": "OSSN",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Eocular surface squamous neoplasia (OSSN)\u003C/span\u003E is MOST likely to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular surface squamous neoplasia (OSSN)\u003C/b\u003E\u003C/span\u003E includes a spectrum of dysplastic lesions of the conjunctival and corneal epithelium, from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econjunctival intraepithelial neoplasia (CIN)\u003C/b\u003E\u003C/span\u003E to invasive \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esquamous cell carcinoma\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThere is a strong and well-documented association between OSSN and HIV infection.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn regions with high HIV prevalence (especially sub-Saharan Africa), OSSN is significantly more common and more aggressive.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAs a result, \u003C/span\u003E\u003Cb\u003Escreening for HIV/AIDS is recommended in all newly diagnosed OSSN patients\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially in younger or atypical presentations.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\uD83D\uDD17 \u003Ci\u003EReference: Shields CL et al. Ocular surface squamous neoplasia: review of epidemiology and pathophysiology. Surv Ophthalmol. 2002;47(6):481\u2013502.\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe incidence of OSSN in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECaucasian populations\u003C/b\u003E\u003C/span\u003E is much \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elower\u003C/b\u003E\u003C/span\u003E, estimated at \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.03\u20130.2 per 100,000/year\u003C/b\u003E\u003C/span\u003E, not per 10,000.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOSSN usually presents at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elimbus\u003C/b\u003E\u003C/span\u003E, particularly the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einterpalpebral nasal conjunctiva\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E the inferior fornix.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBowen\u2019s disease (a term used in skin pathology) is \u003C/span\u003E\u003Cb\u003Eequivalent to conjunctival intraepithelial neoplasia (CIN)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2014 a \u003C/span\u003E\u003Cb\u003Enon-invasive lesion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It \u003C/span\u003E\u003Cb\u003Edoes not breach the basement membrane\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDD11\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;Remember:\u003C/span\u003E\u003C/b\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p5\u0022\u003E\u003Cb\u003EAll patients with OSSN should undergo HIV screening, as\u0026nbsp;\u003C/b\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Eimmunosuppression is a major risk factor and may influence the lesion\u2019s behaviour and management.\u003C/b\u003E\u003C/p\u003E\n\n\n\n\n\n\n\n",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 131,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following organisms is capable of penetrating an \u003Cspan class=\u0022s1\u0022\u003Eintact corneal epithelium and is more common in current Ophthalmic practice?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EOnly a select group of organisms are known to have the ability to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einvade the cornea through an intact epithelial surface\u003C/b\u003E\u003C/span\u003E, bypassing the usual epithelial barrier.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ENeisseria gonorrhoeae\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ENeisseria meningitidis\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci style=\u0022font-weight: bold;\u0022\u003ECorynebacterium diphtheriae\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EListeria monocytogenes\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EHaemophilus influenzae\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Ci\u003EPseudomonas aeruginosa\u003C/i\u003E\u003C/b\u003E\u003Cb\u003E\u003Ci\u003E\u003C/i\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EShigella\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u2705 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPseudomonas aeruginosa\u003C/b\u003E\u003C/span\u003E is a highly virulent, opportunistic gram-negative organism. It can adhere to intact epithelium, secrete proteases, and cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erapid corneal ulceration\u003C/b\u003E\u003C/span\u003E, especially in contact lens wearers.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorynebacterium diphtheriae\u003C/b\u003E\u003C/span\u003E: Can penetrate intact epithelium \u2014 but \u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003Enot \u003Cspan class=\u0022s1\u0022\u003Ecommonly\u003C/span\u003E seen in modern ophthalmic infections due to vaccination\u003C/span\u003E. Still a correct choice in other contexts, but not the best answer here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGroup A Streptococcus\u003C/b\u003E\u003C/span\u003E: Requires \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompromised epithelium\u003C/b\u003E\u003C/span\u003E (e.g., trauma) to infect the cornea.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMoraxella lacunata\u003C/b\u003E\u003C/span\u003E: Low virulence, typically affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompromised\u003C/b\u003E\u003C/span\u003E ocular surfaces, not intact epithelium.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\uD83D\uDD17 \u003Ci\u003EReference: Krachmer JH, Mannis MJ, Holland EJ. Cornea (4th ed). Elsevier.\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\uD83D\uDD17 \u003Ci\u003EAAO BCSC Cornea, Section 8 (latest edition)\u003C/i\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 132,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 32-year-old lady presents with a 6-month history of photophobia and reduced vision in the right eye following a chemical injury. Her visual acuity is 6/36. Slit-lamp examination reveals \u003Cspan class=\u0022s1\u0022\u003E3 clock hours of peripheral corneal conjunctivalisation\u003C/span\u003E extending centrally towards the visual axis, along with \u003Cspan class=\u0022s1\u0022\u003Estippled fluorescein staining\u003C/span\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhat is the MOST appropriate initial management for this case?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis patient has \u003C/span\u003E\u003Cb\u003Epartial limbal stem cell deficiency (LSCD)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2014 evidenced by:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPrior chemical injury (a common cause)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConjunctivalisation of the cornea\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (3 clock hours)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInvolvement of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evisual axis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStippled fluorescein staining\u003C/b\u003E\u003C/span\u003E, indicating abnormal, unstable epithelium\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESuboptimal vision (6/36)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EIn \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Epartial LSCD\u003C/b\u003E\u003C/span\u003E, especially with limited involvement (e.g., \u22643 clock hours), the preferred first-line approach is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Esequential sector conjunctival epitheliectomy (SSCE) \u002B amniotic membrane graft\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\uD83D\uDD0D \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003ESSCE\u003C/b\u003E\u003C/span\u003E involves:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMechanical removal of conjunctivalised epithelium from the corneal surface\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAllowing the remaining healthy limbus to repopulate the cornea with normal epithelium\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften performed under topical anaesthesia as a minor outpatient procedure\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHas good outcomes in \u003C/span\u003E\u003Cb\u003Eearly or localised disease\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmniotic membrane transplant\u003C/b\u003E\u003C/span\u003E: Helpful for promoting epithelial healing in acute injuries or non-healing epithelial defects, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot sufficient alone\u003C/b\u003E\u003C/span\u003E for LSCD with central visual axis involvement.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnterior lamellar keratoplasty\u003C/b\u003E\u003C/span\u003E: Addresses \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estromal scarring\u003C/b\u003E\u003C/span\u003E, but does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot correct the epithelial abnormality\u003C/b\u003E\u003C/span\u003E or LSCD \u2014 not suitable unless the epithelium has first been restored.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAutologous limbal stem cell transplant\u003C/b\u003E\u003C/span\u003E: This is reserved for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etotal or bilateral LSCD\u003C/b\u003E\u003C/span\u003E or when SSCE fails. Not first-line in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epartial\u003C/b\u003E\u003C/span\u003E LSCD with remaining healthy limbal tissue.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\uD83D\uDD11\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;Remember:\u003C/span\u003E\u003C/b\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThis table from Oxford Handbook - Fourth Edition:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-08-29-8716bb6d-d923-4366-a858-03a893647132.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 133,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following corneal dystrophies is caused by a mutation in a gene \u003Cspan class=\u0022s1\u0022\u003Edifferent\u003C/span\u003E from the others?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMost corneal dystrophies are classified by the affected \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elayer of the cornea\u003C/b\u003E\u003C/span\u003E and their \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emolecular genetics\u003C/b\u003E\u003C/span\u003E.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMeesmann corneal dystrophy\u003C/b\u003E\u003C/span\u003E is genetically distinct, it involves \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ekeratin gene mutations\u003C/b\u003E\u003C/span\u003E (\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKRT3/KRT12\u003C/b\u003E\u003C/span\u003E) affecting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal epithelium\u003C/b\u003E\u003C/span\u003E, whereas the others\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eare all caused by mutations in the BIGH3 gene, or known as transforming growth factor \u03B2-induced\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003ETGFBI\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E mutations affecting \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003EBowman\u2019s layer and/or stroma\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bolder; color: rgb(255, 0, 0); border-radius: 0px !important; text-decoration-line: underline;\u0022\u003ERemember:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bolder; border-radius: 0px !important;\u0022\u003EBIG is LARGE:\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EBIGH3gene defect in\u003C/span\u003E\u003C/p\u003E\u003Cul style=\u0022margin-top: 0.3em; margin-bottom: 0px; margin-left: 1.6em; padding-left: 0px; list-style-position: outside; list-style-image: url(\u0026quot;data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAAYAAAAJCAYAAAARml2dAAAABHNCSVQICAgIfAhkiAAAAAlwSFlzAAAN1wAADdcBQiibeAAAABl0RVh0U29mdHdhcmUAd3d3Lmlua3NjYXBlLm9yZ5vuPBoAAABUSURBVAiZdY4xDsAgFELB2J0DdnbwQI5OHvDfgC62SY0yvhAetI1dWEq5JN0kKwDYbhEx8oT9a5JdEtLb/M2QNW0FAJLttkLbLUfEkIRVztPdo\u002BMBm8UkW9Zxc20AAAAASUVORK5CYII=\u0026quot;); color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EL\u003C/span\u003Eattice\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EA\u003C/span\u003Evellino\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003ER\u003C/span\u003Eeis-Buckler\u0027s\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EG\u003C/span\u003Eranular\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bolder; border-radius: 0px !important;\u0022\u003EE\u003C/span\u003Empty\u003C/li\u003E\u003C/ul\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMeesmann corneal dystrophy is caused by mutations in keratin genes (KRT3 or KRT12), making it genetically distinct from granular, Thiel\u2013Behnke, and many EBMD cases, which involve TGFBI mutations.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 134,
    "Name": "LSCD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following findings on \u003C/span\u003Ecorneal impression cytology\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003Emost suggestive of limbal stem cell deficiency (LSCD)?\u003C/span\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorneal impression cytology\u003C/b\u003E\u003C/span\u003E is a non-invasive diagnostic tool used to evaluate the cellular composition of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal surface\u003C/b\u003E\u003C/span\u003E \u2014 particularly useful in diagnosing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elimbal stem cell deficiency (LSCD)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn LSCD, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econjunctival epithelial cells\u003C/b\u003E\u003C/span\u003E migrate onto the corneal surface, replacing the normal corneal epithelium. This results in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econjunctivalisation\u003C/b\u003E\u003C/span\u003E of the cornea, including:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPresence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egoblet cells\u003C/b\u003E\u003C/span\u003E (normally absent on the cornea)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EExpression of \u003C/span\u003E\u003Cb\u003Econjunctival markers\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E like \u003C/span\u003E\u003Cb\u003ECK19\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003ECK13\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ELoss of normal \u003C/span\u003E\u003Cb\u003Ecorneal epithelial markers\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, including \u003C/span\u003E\u003Cb\u003ECK3\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003ECK12\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-29-44d86f34-6ab1-413e-8527-0039634088c1.png\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 135,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EA 28-year-old gentleman undergoes an uncomplicated penetrating keratoplasty for keratoconus. On the first post-operative day, they complain of a \u003Cspan class=\u0022s1\u0022\u003Eheadache\u003C/span\u003E and have a \u003Cspan class=\u0022s1\u0022\u003Efixed dilated pupil\u003C/span\u003E in the operated eye. The anterior chamber is deep and quiet. The dilated pupil \u003Cspan class=\u0022s1\u0022\u003Edoes not constrict with 2% pilocarpine\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003Eptosis is absent\u003C/span\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhat is the most appropriate next step in management?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis is a classic presentation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUrrets-Zavalia syndrome\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EDiagnosis: Urrets-Zavalia Syndrome\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EKey Clinical Features Recap:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOccurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eafter penetrating keratoplasty\u003C/b\u003E\u003C/span\u003E (especially in keratoconus patients)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPresents with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efixed dilated pupil\u003C/b\u003E\u003C/span\u003E postoperatively\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDeep and quiet anterior chamber\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMay be associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eheadache or discomfort\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo response to pilocarpine 2%\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, due to \u003C/span\u003E\u003Cb\u003Eiris sphincter ischaemia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo ptosis or ocular motility deficit \u2192 rules out 3rd nerve palsy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften associated with a \u003C/span\u003E\u003Cb\u003Esignificant rise in intraocular pressure (IOP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E early post-op\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EUrrets-Zavalia syndrome is thought to result from:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcute postoperative IOP spike\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ELeading to \u003C/span\u003E\u003Cb\u003Eiris ischemia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and subsequent \u003C/span\u003E\u003Cb\u003Esphincter paralysis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe result is a \u003C/span\u003E\u003Cb\u003Epermanent, non-reactive mydriasis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe condition is more likely in \u003C/span\u003E\u003Cb\u003Eyoung keratoconus patients\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Etight peripheral iridectomy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E or when \u003C/span\u003E\u003Cb\u003Eair/gas is used in the anterior chamber\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EManagement Approach:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMeasure and control IOP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E immediately\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInitiate \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP-lowering therapy\u003C/b\u003E\u003C/span\u003E if pressure is elevated\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMonitor for resolution \u2014 but pupil often remains \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epermanently dilated\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELater, if symptomatic (e.g. glare, photophobia), options include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPhotochromic lenses\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECosmetic contact lenses\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESurgical options\u003C/b\u003E\u003C/span\u003E (e.g., artificial iris or pupiloplasty in select cases)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ol\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ESo c\u003Cb style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;Helvetica Neue\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Ehecking the patient\u2019s IOP\u0026nbsp;\u003C/b\u003E\u003Cspan style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Eis the best \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Einitial\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E next step \u2014 because elevated IOP is \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Ecausal and potentially reversible\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E if treated early.\u003C/span\u003E\u003C/div\u003E\u003Col start=\u00221\u0022\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 136,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 79-year-old patient presents with a \u003Cspan class=\u0022s1\u0022\u003Evesicular rash\u003C/span\u003E affecting the \u003Cspan class=\u0022s1\u0022\u003Eright forehead, scalp, and nasal tip\u003C/span\u003E, respecting the facial midline. On examination, there are \u003Cspan class=\u0022s1\u0022\u003Epseudodendritic lesions\u003C/span\u003E on the cornea and \u003Cspan class=\u0022s1\u0022\u003Emild anterior chamber inflammation\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following statements is most accurate regarding this presentation?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis patient has \u003C/span\u003E\u003Cb\u003Eherpes zoster ophthalmicus (HZO)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, given:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDermatomal rash in \u003C/span\u003E\u003Cb\u003Eophthalmic division of trigeminal nerve (V1)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInvolvement of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enasociliary branch\u003C/b\u003E\u003C/span\u003E (Hutchinson\u2019s sign \u2014 tip of nose)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAssociated \u003C/span\u003E\u003Cb\u003Epseudodendritic keratitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Eanterior uveitis\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EHZO:\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHZO affects the \u003C/span\u003E\u003Cb\u003Enasociliary nerve\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which innervates the \u003C/span\u003E\u003Cb\u003Ecornea, ciliary body, and iris\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPatients are at \u003C/span\u003E\u003Cb\u003Ehigh risk of corneal denervation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, leading to:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENeurotrophic keratopathy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPersistent epithelial defects\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECorneal melt or perforation in severe cases\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECorneal sensation must be monitored regularly\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EAntivirals such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoral aciclovir are still beneficial\u003C/b\u003E\u003C/span\u003E even if started \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eafter 72 hours\u003C/b\u003E\u003C/span\u003E, especially if new vesicles or ocular involvement are present\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u21B3 Starting antivirals up to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E7 days\u003C/b\u003E\u003C/span\u003E after onset may reduce complications\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETopical aciclovir is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot routinely indicated\u003C/b\u003E\u003C/span\u003E in HZO keratitis; systemic treatment is preferred unless epithelial disease is severe\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u21B3 Most HZO pseudodendrites respond well to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoral antivirals\u003C/b\u003E\u003C/span\u003E and supportive therapy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBilateral periorbital swelling is caused by\ngravitational oedema instead of spreading of infection; therefore, antibiotic is not warranted.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 137,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 49-year-old man presents with a 3-day history of photophobia and mildly reduced vision in the right eye, one year after undergoing penetrating keratoplasty. He recently recovered from a viral illness. On slit-lamp examination, the eye is minimally injected, with mild papillary conjunctival reaction and \u003Cspan class=\u0022s1\u0022\u003Emultiple subepithelial infiltrates within the graft\u003C/span\u003E. There is \u003Cspan class=\u0022s1\u0022\u003Eno epithelial defect, stromal oedema, keratic precipitates, or anterior chamber inflammation\u003C/span\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhat is the most appropriate management in this case?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EDiagnosis: Subepithelial Rejection\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EFollowing penetrating keratoplasty, this patient has developed \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Emultiple subepithelial opacities\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E within the graft after a \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eviral illness\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, with:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo epithelial defect\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo stromal oedema\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo keratic precipitates\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo AC activity\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EThe incidence of this type of stromal rejection ranges between 2% and 5%.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p3\u0022\u003EThis is consistent with \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Esubepithelial immune rejection\u003C/b\u003E\u003C/span\u003E, sometimes an early or isolated manifestation.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003ETreatment:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\n\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESubepithelial rejection can precede or co-exist with more severe endothelial rejection.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPrompt use of \u003C/span\u003E\u003Cb\u003Efrequent topical corticosteroids\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E can \u003C/span\u003E\u003Cb\u003Ereverse inflammation and prevent progression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDexamethasone 0.1%\u003C/b\u003E\u003C/span\u003E QID\u20136\u00D7/day is an appropriate and standard regimen.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA short follow-up interval (within 2\u20133 days) is critical to assess treatment response and detect progression.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELubricants\u003C/b\u003E\u003C/span\u003E \u2013 Not sufficient for immune-mediated inflammation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChloramphenicol\u003C/b\u003E\u003C/span\u003E \u2013 There is no infection.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPrednisolone 0.5% BID\u003C/b\u003E\u003C/span\u003E \u2013 Too mild a dose and frequency for subepithelial rejection. Also, weaker than dexamethasone 0.1%.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 138,
    "Name": "Degenerations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Ecorneal arcus\u003C/span\u003E is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003EArcus is a common bilateral degeneration, 2\u00B0 to progressive deposition of lipid in the peripheral stroma. It is usually age-related but may be associated with hyperlipidaemia.\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ECauses:\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003EMost bilateral cases have no systemic association, but hyperlipidaemia (notably type II) should be ruled out in those presenting at a young age (arcus juvenilis).\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022color: rgb(255, 0, 0);\u0022\u003EUnilateral\u003C/span\u003E\u0026nbsp;arcus is rare and may signify\u0026nbsp;\u003Cspan style=\u0022color: rgb(255, 0, 0);\u0022\u003Econtralateral carotid\u003C/span\u003E\u0026nbsp;compromise or previous ocular hypotony.\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EClinical features:\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003EProgressive peripheral opacity starts (and remains thickest) superiorly and inferiorly but spreads circumferentially to form a complete ring of around 1mm thickness\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003Etypically, the central margin is blurred, but the peripheral margin is sharp, leaving a zone of clear perilimbal cornea (which may show thinning).\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003ESource: Oxford Handbook of Ophthalmology - Fourth Edition\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 139,
    "Name": "Degenerations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003EWilson\u2019s disease\u003C/span\u003E, copper deposition in the cornea leads to the formation of a \u003Cspan class=\u0022s1\u0022\u003EKayser\u2013Fleischer ring\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich corneal layer is primarily involved in this deposition?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKayser\u2013Fleischer ring\u003C/b\u003E\u003C/span\u003E seen in Wilson\u2019s disease is caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecopper accumulation\u003C/b\u003E\u003C/span\u003E at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral cornea\u003C/b\u003E\u003C/span\u003E, visible as a golden-brown or greenish ring.\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECopper is deposited at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elevel of Descemet\u2019s membrane\u003C/b\u003E\u003C/span\u003E, typically beginning at \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E12 and 6 o\u2019clock\u003C/b\u003E\u003C/span\u003E, then progressing circumferentially.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe deposition occurs due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eimpaired hepatic copper metabolism\u003C/b\u003E\u003C/span\u003E, resulting in systemic copper overload.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EWilson\u0027s disease:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cul\u003E\u003Cli\u003EThe diagnosis can be made by increased serum and urinary copper levels, reduced serum caeruloplasmin\u003C/li\u003E\u003Cli\u003EMRI brain of the basal ganglia showing increased intensity on T2 scan (\u2018face of giant panda\u2019)\u003C/li\u003E\u003Cli\u003Eliver biopsy is the gold standard.\u003C/li\u003E\u003Cli\u003ESerum ceruloplasmin \u0026lt; 20mg/dL in 90% of all patients with Wilson disease.\u0026nbsp;\u003C/li\u003E\u003Cli\u003ESystemic Treatment with Penicillamine can lead to the disappearance of the ring.\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003Ekayser-fleischer rings DD:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cul\u003E\u003Cli\u003EPrimary biliary cirrhosis\u003C/li\u003E\u003Cli\u003ECholestasis\u003C/li\u003E\u003Cli\u003ECirrhosis\u003C/li\u003E\u003Cli\u003EChronic copper poisoning\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://eyewiki.org/w/images/thumb/7/7e/Kayser_Fleischer_ring_seen_on_parallelopiped_slitlamp_illumination.jpg/900px-Kayser_Fleischer_ring_seen_on_parallelopiped_slitlamp_illumination.jpg?20250531112658\u0022\u003E\u003C/div\u003E\u003C/p\u003E\n\n\n\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 140,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following corneal conditions is associated with \u003Cspan class=\u0022s1\u0022\u003E\u2018curly fibres\u2019 in Bowman\u2019s layer\u003C/span\u003E on histopathologic examination?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThiel\u2013Behnke corneal dystrophy\u003C/b\u003E\u003C/span\u003E is a type of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBowman\u2019s layer dystrophy\u003C/b\u003E\u003C/span\u003E and is often confused clinically with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReis\u2013Bucklers dystrophy\u003C/b\u003E\u003C/span\u003E \u2014 both present with recurrent corneal erosions and subepithelial opacities.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003EKey Histopathological Feature:\u003C/b\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThiel\u2013Behnke dystrophy shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Ccurly fibres\u201D\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Csaw-tooth\u201D pattern\u003C/b\u003E\u003C/span\u003E within a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edisrupted Bowman\u2019s layer\u003C/b\u003E\u003C/span\u003E, which is pathognomonic for this dystrophy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese curly fibres consist of abnormal collagen fibrils on electron microscopy.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMeesmann dystrophy\u003C/b\u003E\u003C/span\u003E: Intraepithelial cysts; mutation in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKRT12/KRT3\u003C/b\u003E\u003C/span\u003E, not Bowman\u2019s layer.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReis\u2013Bucklers\u003C/b\u003E\u003C/span\u003E: Bowman\u2019s layer is replaced by fibrous connective tissue, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno curly fibres\u003C/b\u003E\u003C/span\u003E \u2014 instead, dense, rod-shaped bodies are seen.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchnyder dystrophy\u003C/b\u003E\u003C/span\u003E: Characterised by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elipid/crystal deposits in the stroma\u003C/b\u003E\u003C/span\u003E, not Bowman\u2019s layer, and no curly fibres.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 141,
    "Name": "Keratoconus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements regarding \u003Cspan class=\u0022s1\u0022\u003Ekeratoconus\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003ELEAST likely to be correct\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHistopathologically, keratoconus is characterised by:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThinning of the corneal stroma\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBreaks in Bowman\u2019s layer\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIron deposition (Fleischer ring)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIrregular epithelial thickening\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosterior keratoconus\u003C/b\u003E\u003C/span\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E entity, distinct from keratoconus:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften \u003C/span\u003E\u003Cb\u003Econgenital\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFrequently \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELocalised thinning of the posterior corneal surface with no ectasia anteriorly\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior corneal steepening\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is often \u003C/span\u003E\u003Cb\u003Eone of the earliest detectable changes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in keratoconus.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdvanced corneal imaging (e.g., Scheimpflug tomography) detects early \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior elevation\u003C/b\u003E\u003C/span\u003E and steepening \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebefore anterior surface changes are obvious\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003EBelin Ambrosio Enhanced Ectasia Display\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E (see below) \u003C/span\u003E\u003Cb\u003Erelies heavily on posterior curvature changes\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E to detect subclinical keratoconus.\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBelin Ambrosio Display\u003C/b\u003E\u003C/span\u003E (on Pentacam) integrates:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAnterior \u0026amp; posterior elevation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPachymetric progression\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECorneal thickness profile\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u2192 To detect \u003C/span\u003E\u003Cb\u003Eforme fruste\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E or \u003C/span\u003E\u003Cb\u003Esubclinical keratoconus\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 142,
    "Name": "Anterior segment",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements regarding\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003EPeters anomaly\u003C/span\u003E is MOST likely to be\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003Ecorrect\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EPeters anomaly is a type of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior segment dysgenesis\u003C/b\u003E\u003C/span\u003E, often presenting at birth with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECentral corneal opacity\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior corneal defect (absence of Descemet\u2019s membrane and endothelium)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIris\u2013cornea adhesions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (Type I)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELens\u2013cornea adhesions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (Type II)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPeters anomaly may be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eisolated\u003C/b\u003E\u003C/span\u003E, but it can also be part of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esyndromic conditions\u003C/b\u003E\u003C/span\u003E such as:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPeters Plus Syndrome\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhich includes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECardiac defects\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECNS abnormalities (e.g., hydrocephalus)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDevelopmental delay\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShort stature and craniofacial abnormalities\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETIMP3 gene\u003C/b\u003E\u003C/span\u003E mutations are associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESorsby fundus dystrophy\u003C/b\u003E\u003C/span\u003E, not Peters anomaly.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPeters anomaly has been associated with mutations in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPAX6\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPITX2\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFOXC1\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB3GALTL\u003C/b\u003E\u003C/span\u003E (especially in Peters Plus syndrome).\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGlaucoma develops in up to 50\u201370% of patients\u003C/b\u003E\u003C/span\u003E with Peters anomaly, particularly in more severe forms (Type II).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESo the stated figure of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E20%\u003C/b\u003E\u003C/span\u003E significantly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunderestimates the true prevalence\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eprimary defect is in the posterior cornea\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (i.e., \u003C/span\u003E\u003Cb\u003EDescemet\u2019s membrane and endothelium\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is not primarily a stromal developmental defect.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 143,
    "Name": "Conjunctival lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 14-year-old girl presents with a slowly enlarging lesion on the white of her eye. On examination, there is a \u003Cspan class=\u0022s1\u0022\u003Eminimally elevated pigmented conjunctival lesion\u003C/span\u003E near the \u003Cspan class=\u0022s1\u0022\u003Elimbus\u003C/span\u003E, showing \u003Cspan class=\u0022s1\u0022\u003Ecystic changes\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003Eno vascularisation\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003Eno epithelial defect\u003C/span\u003E. Her mother states the lesion has been present for \u003Cspan class=\u0022s1\u0022\u003Emany years\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EConjunctival naevus:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMost common\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E conjunctival tumour in \u003C/span\u003E\u003Cb\u003Echildren and adolescents\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETypically located near the \u003C/span\u003E\u003Cb\u003Elimbus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E or in the \u003C/span\u003E\u003Cb\u003Einterpalpebral bulbar conjunctiva\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPigmented\u003C/b\u003E\u003C/span\u003E, but may be amelanotic\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECystic spaces\u003C/b\u003E\u003C/span\u003E within the lesion are common (and helpful in diagnosis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ELesion is usually \u003C/span\u003E\u003Cb\u003Estable\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but \u003C/span\u003E\u003Cb\u003Ecan enlarge slightly during puberty\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo feeder vessels\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, no epithelial defect, and \u003C/span\u003E\u003Cb\u003Eno signs of malignancy\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; text-decoration-line: underline;\u0022\u003EConjunctival melanoma\u003C/b\u003E\u003Cbr\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERare in this age group (more common in middle-aged or older adults)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften arises \u003C/span\u003E\u003Cb\u003Ede novo or from primary acquired melanosis (PAM)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETypically \u003C/span\u003E\u003Cb\u003Erapidly growing\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, may be \u003C/span\u003E\u003Cb\u003Enon-cystic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and often shows \u003C/span\u003E\u003Cb\u003Efeeder vessels or nodularity\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; text-decoration-line: underline;\u0022\u003EConjunctival melanosis\u003C/b\u003E\u003Cbr\u003E\u003Cul style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsually refers to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPAM\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eracial melanosis\u003C/b\u003E\u003C/span\u003E, which presents as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eflat\u003C/b\u003E\u003C/span\u003E pigmentation with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno elevation or cysts\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot typically described as a \u201Clesion\u201D enlarging with time\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; text-decoration-line: underline;\u0022\u003EConjunctival papilloma\u003C/b\u003E\u003Cbr\u003E\u003Cul style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften \u003C/span\u003E\u003Cb\u003Enon-pigmented\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Efleshy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and has a \u003C/span\u003E\u003Cb\u003Evascularised, lobulated or frond-like\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E appearance\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EMay be \u003C/span\u003E\u003Cb\u003Eassociated with HPV\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003ETypically lacks cystic features\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://www.aao.org/image.axd?id=30a703a5-291a-4f0e-9aed-fb6c767d4877\u0026amp;t=635565060124270000\u0022\u003E\u003C/div\u003E\u003Cp class=\u0022p2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 144,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following statements regarding the \u003C/span\u003Euse of topical corticosteroids in bacterial keratitis\u003Cspan class=\u0022s1\u0022\u003E is MOST likely to be\u0026nbsp;\u003C/span\u003Etrue\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis question is based on data from the landmark \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteroids for Corneal Ulcers Trial (SCUT)\u003C/b\u003E\u003C/span\u003E \u2014 a large, NIH-funded, randomized controlled trial designed to evaluate the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esafety and efficacy of adjunctive topical corticosteroids in bacterial keratitis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large; text-decoration-line: underline;\u0022\u003EKey SCUT Trial Findings (2004\u20132011):\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPrimary outcome\u003C/b\u003E\u003C/span\u003E: Best spectacle-corrected visual acuity (BSCVA) at 3 months\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EResult\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: \u003C/span\u003E\u003Cb\u003ENo significant difference overall\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E between steroid and placebo groups\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EHowever, in subgroup analysis:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPatients with \u003C/span\u003E\u003Cb\u003Eworse vision at presentation (\u22646/60)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E had a \u003C/span\u003E\u003Cb\u003Estatistically significant improvement in visual outcomes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with the use of \u003C/span\u003E\u003Cb\u003Eadjunctive topical steroids\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESteroids hasten healing time\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003EIncorrect\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESCUT showed \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno difference in epithelial healing time\u003C/b\u003E\u003C/span\u003E between steroid and placebo groups\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESteroids increase perforation risk\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003EIncorrect\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESCUT showed no increased risk\u003C/b\u003E\u003C/span\u003E of corneal perforation in the steroid group\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhen used appropriately (i.e., after organism sensitivity confirmed), steroids are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esafe\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESteroids improve outcomes in Nocardia keratitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003EIncorrect\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESCUT subgroup data showed that patients with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENocardia keratitis had worse outcomes\u003C/b\u003E\u003C/span\u003E when treated with topical steroids\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHence, steroids are \u003C/span\u003E\u003Cb\u003Econtraindicated\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in \u003C/span\u003E\u003Cb\u003ENocardia infections\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 145,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich statement about Schnyder corneal dystrophy is least likely to be accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ESchnyder corneal dystrophy is a \u003C/span\u003E\u003Cb\u003Erare autosomal dominant disorder\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E characterized by \u003C/span\u003E\u003Cb\u003Eprogressive corneal opacification due to lipid deposition\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKey features:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Earcus lipoides\u003C/b\u003E\u003C/span\u003E (correct).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUsually begins in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efirst or second decade\u003C/b\u003E\u003C/span\u003E (correct).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPrimarily affects the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estroma and epithelium\u003C/b\u003E\u003C/span\u003E, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot the endothelium\u0026nbsp;\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003EMost important point:\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003ECorneal crystals are not universal\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u2014 only about \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003E50% of patients\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E show visible crystals. The rest show haze without crystals.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-family: Arial; font-size: small;\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 29, 53); letter-spacing: normal;\u0022\u003EThe condition was reclassified from \u0022Schnyder crystalline corneal dystrophy\u0022 to \u0022Schnyder corneal dystrophy\u0022 to reflect this variable presentation, which can delay diagnosis in affected individuals.\u003C/span\u003E\u003Cspan jscontroller=\u0022JHnpme\u0022 class=\u0022pjBG2e\u0022 data-cid=\u0022c840db4c-8fce-4994-abbc-9b347044b8cf\u0022 jsaction=\u0022rcuQ6b:npT2md\u0022 style=\u0022color: rgb(0, 29, 53); letter-spacing: normal;\u0022\u003E\u003Cspan class=\u0022UV3uM\u0022 style=\u0022text-wrap-mode: nowrap;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EAnterior segment OCT has \u0022shown diffuse high reflectivity in the epithelium, anterior, mid, and posterior stroma, which correspond to the hyperreflective deposits observed with IVCM and FF-OCT at the same level. Presence of epithelial hyperreflectivity was consistent with the presence of areas of thick and irregular epithelium on epithelial mapping.\u0022\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 146,
    "Name": "Patterns",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhat is the correct definition of A-pattern and V-pattern ocular deviations?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPattern strabismus\u003C/b\u003E\u003C/span\u003E describes changes in the horizontal deviation between upgaze and downgaze.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EA-pattern\u003C/b\u003E\u003C/span\u003E: more \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eesotropia in downgaze\u003C/b\u003E\u003C/span\u003E (resembles the shape of the letter \u201CA\u201D).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDefined when difference is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026gt;10 prism diopters\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EV-pattern\u003C/b\u003E\u003C/span\u003E: more \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eesotropia in upgaze\u003C/b\u003E\u003C/span\u003E (resembles the shape of \u201CV\u201D).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDefined when difference is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026gt;15 prism diopters\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese definitions are based on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estandard strabismus diagnostic criteria\u003C/b\u003E\u003C/span\u003E (Burian \u0026amp; Miller classification).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\uD83E\uDDE0 \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EMemory aid:\u003C/b\u003E\u003C/span\u003E \u003Ci\u003EA = 10, V = 15\u003C/i\u003E \u2192 \u201CA comes before V, so the cut-off is smaller.\u201D\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 147,
    "Name": "Posterior Uveitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 29-year-old man presents with a painful, photophobic, red right eye with reduced vision. On examination, he has both anterior chamber and vitreous cells as well as an extensive white patch in the peripheral retina. What is the MOST likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcute retinal necrosis (ARN):\u003C/b\u003E\u003C/span\u003E Caused by herpes viruses (VZV, HSV).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFeatures: painful red eye, anterior uveitis \u002B vitritis, peripheral necrotising retinitis (white patch).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERapid progression, high risk of retinal detachment.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPars planitis:\u003C/b\u003E\u003C/span\u003E Chronic, painless, usually bilateral with snowbanking, not acute.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosterior scleritis:\u003C/b\u003E\u003C/span\u003E Causes pain, thickened sclera, T-sign on ultrasound, but not necrotising retinitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERecurrent toxoplasma:\u003C/b\u003E\u003C/span\u003E Classically causes focal retinochoroiditis adjacent to an old scar, not widespread peripheral white patches.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022 style=\u0022text-align: center; \u0022\u003E\u003Cimg src=\u0022https://journal.opted.org/wp-content/uploads/2020/10/F20.P3.Fig1_.png\u0022 class=\u0022rz-state-selected\u0022\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 148,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich statement about preoperative cataract surgery biometry is the most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAfter myopic LASIK/PRK:\u003C/b\u003E\u003C/span\u003E The cornea is flattened, but keratometry still assumes a normal anterior/posterior corneal curvature ratio.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunderestimation of corneal power\u003C/b\u003E\u003C/span\u003E \u2192 IOL power calculation error \u2192 patient ends up \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore hypermetropic than planned\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESpecial formulae\u003C/b\u003E\u003C/span\u003E (e.g. Barrett True-K, Haigis-L) or historical refractive data should be used.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E1D keratometry error \u2248 1D IOL error, not 1.25D.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003EO\u003C/span\u003Eptical biometry is actually more accurate than ultrasound unless dense cataract blocks signal.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESRK/T tends to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunderestimate\u003C/b\u003E\u003C/span\u003E IOL power in short eyes, not overestimate.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\uD83E\uDDE0 \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EMemory hook:\u003C/b\u003E\u003C/span\u003E \u003Ci\u003EPost-myopic LASIK = \u201Cflat cornea trap\u201D \u2192 routine K underestimates power \u2192 hyperopic surprise.\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 149,
    "Name": "Nystagmus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhat is the most important initial step when managing a child with nystagmus?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efirst step in childhood nystagmus\u003C/b\u003E\u003C/span\u003E is always a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomprehensive clinical exam\u003C/b\u003E\u003C/span\u003E (history, refraction, anterior and posterior segment assessment, ocular motility).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis identifies treatable causes like \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunrecognised refractive error, media opacity, or ocular pathology\u003C/b\u003E\u003C/span\u003E (albinism, aniridia, achromatopsia, retinal dystrophies).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdditional tests (ERG, VEP, MRI, genetics) are important but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eguided by clinical findings\u003C/b\u003E\u003C/span\u003E \u2014 not the first step.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 150,
    "Name": "RD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 26-year-old emmetropic male with a history of blunt trauma presents with superior visual field loss. He is found to have an inferior retinal detachment caused by a large retinal dialysis spanning 3 clock hours. What is the most appropriate treatment?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinal dialysis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a common cause of \u003C/span\u003E\u003Cb\u003Etraumatic retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, usually in \u003C/span\u003E\u003Cb\u003Eyoung phakic patients\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe standard treatment is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Escleral buckling with cryotherapy\u003C/b\u003E\u003C/span\u003E, often combined with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edrainage of subretinal fluid\u003C/b\u003E\u003C/span\u003E for large dialyses.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERadial buckles\u003C/b\u003E\u003C/span\u003E may be used for small anterior dialyses, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecircumferential or segmental buckles with drainage\u003C/b\u003E\u003C/span\u003E are preferred for large ones.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitrectomy\u003C/b\u003E\u003C/span\u003E is generally reserved for more complex detachments (e.g., posterior breaks, vitreous haemorrhage, proliferative vitreoretinopathy).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 151,
    "Name": "Entropion",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 79-year-old patient presents with discomfort from involutional entropion. On examination, there is moderate lid laxity. Which surgical treatment is most likely to have the lowest recurrence rate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInvolutional entropion\u003C/b\u003E\u003C/span\u003E is usually due to a combination of:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHorizontal lid laxity\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOverriding of preseptal orbicularis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDisinsertion/weakness of lower lid retractors\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEverting sutures\u003C/b\u003E\u003C/span\u003E (Quickert sutures) are simple but have a high recurrence rate, especially with lid laxity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdding \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elateral lid tightening\u003C/b\u003E\u003C/span\u003E reduces recurrence but does not address orbicularis override.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELid tightening \u002B excision of overriding preseptal orbicularis\u003C/b\u003E\u003C/span\u003E is the most comprehensive approach \u2192 it corrects all the key mechanisms and therefore has the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elowest recurrence rate\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInferior retractor plication\u003C/b\u003E\u003C/span\u003E can help but is less effective if orbicularis override is not corrected.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 152,
    "Name": "VKC",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhen distinguishing between Atopic Keratoconjunctivitis (AKC) and Vernal Keratoconjunctivitis (VKC), which statement is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAKC\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EChronic, affects young adults (often late teens to 30s).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAssociated with atopic dermatitis, asthma, eczema.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAffects \u003C/span\u003E\u003Cb\u003Eboth sexes equally\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EMore risk of \u003C/span\u003E\u003Cb\u003Econjunctival and corneal scarring\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E than VKC.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVKC\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETypically begins in \u003C/span\u003E\u003Cb\u003Echildhood (first decade of life)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EStrong male predominance.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESeasonal, self-limiting by late teens.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECharacterised by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egiant papillae and thick ropy discharge\u003C/b\u003E\u003C/span\u003E, but less risk of scarring compared to AKC.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 153,
    "Name": "AMD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EAccording to the latest NICE guidelines for age-related macular degeneration (AMD), which of the following is \u003Cspan class=\u0022s1\u0022\u003ENOT\u003C/span\u003E considered a treatment eligibility criterion?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ENICE criteria for \u003C/span\u003E\u003Cb\u003Eanti-VEGF treatment in wet AMD\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBest-corrected vision \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebetween 6/12 and 6/96\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo permanent structural damage\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E to the fovea\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESigns of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edisease progression\u003C/b\u003E\u003C/span\u003E (e.g., recent visual deterioration or leakage on imaging)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECentral macular thickness\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E part of the NICE eligibility requirements (it is used in diabetic macular oedema, not AMD).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 154,
    "Name": "GPA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements most accurately describes the clinical features of granulomatosis with polyangiitis (Wegener\u2019s granulomatosis)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOcular involvement in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egranulomatosis with polyangiitis (GPA)\u003C/b\u003E\u003C/span\u003E occurs in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~50% of cases\u003C/b\u003E\u003C/span\u003E, not \u0026lt;10% , and orbital involvement in up to 22%.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital inflammation with adjacent bony destruction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a well-recognised manifestation.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOrbital involvement \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecan occur independently\u003C/b\u003E\u003C/span\u003E of sinus disease.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERenal disease is common, often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubclinical in the early stages\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 155,
    "Name": "Anterior uveitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn an eye affected by Fuch\u2019s heterochromic uveitis, which of the following signs is least likely to be present?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFuch\u2019s heterochromic uveitis (FHU)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a \u003C/span\u003E\u003Cb\u003Echronic, low-grade anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EClassic signs include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFine, diffuse \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estellate KPs\u003C/b\u003E\u003C/span\u003E across the cornea.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIris atrophy\u003C/b\u003E\u003C/span\u003E leading to heterochromia and transillumination defects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELow-grade \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitritis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosterior synechiae are characteristically absent\u003C/b\u003E\u003C/span\u003E because the inflammation is mild and not sticky, unlike in other uveitides (e.g., HLA-B27).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 156,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements is least accurate regarding Descemet Membrane Endothelial Keratoplasty (DMEK)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDMEK\u003C/b\u003E\u003C/span\u003E is the most selective endothelial keratoplasty \u2014 only Descemet\u2019s membrane and endothelium are transplanted.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIt \u003C/span\u003E\u003Cb\u003Ecan be performed after failed PKP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E due to endothelial failure.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt also has the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elowest risk of immunological rejection\u003C/b\u003E\u003C/span\u003E among endothelial keratoplasties.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGlaucoma drainage tubes make surgery technically more challenging but are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot an absolute contraindication\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDonor selection:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E Studies show that \u003C/span\u003E\u003Cb\u003Eolder donor corneas (up to 75 years)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E perform equally well as younger ones in DMEK, so \u003C/span\u003E\u003Cb\u003Epreferring \u0026lt;40 years is incorrect\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 157,
    "Name": "LSCD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn a \u003Cspan class=\u0022s1\u0022\u003Eunilateral\u003C/span\u003E severe chemical injury with clinical and cytological evidence of \u003Cspan class=\u0022s1\u0022\u003Elimbal stem cell deficiency (LSCD)\u003C/span\u003E (loss of palisades, conjunctivalization with goblet cells), which intervention is the best next step?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFindings (loss of palisades of Vogt, vascularized scar, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egoblet cells on impression cytology\u003C/b\u003E\u003C/span\u003E) = \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econjunctivalization \u2192 LSCD\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral LSCD\u003C/b\u003E\u003C/span\u003E, the treatment of choice is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautologous limbal stem cell transplantation\u003C/b\u003E\u003C/span\u003E from the fellow eye (e.g., CLAU/SLET), often preceded by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperficial keratectomy\u003C/b\u003E\u003C/span\u003E to remove fibrovascular pannus. This restores the corneal epithelial stem cell population so the surface can re-epithelialize normally.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAmniotic membrane \u002B serum\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u0026nbsp;can support healing but \u003C/span\u003E\u003Cb\u003Edoes not replace missing limbal stem cells\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u2014insufficient for established LSCD.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPenetrating keratoplasty\u003C/b\u003E\u003C/span\u003E\u0026nbsp;fails without prior restoration of limbal stem cells (the graft epithelium will conjunctivalize).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoprosthesis\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is a salvage option, typically reserved for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral\u003C/b\u003E\u003C/span\u003E severe disease or multiple graft failures.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 158,
    "Name": "NNT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EA study reports a number needed to treat (NNT) of 3.13 for intravitreal ranibizumab (IVR) versus sham to prevent vision loss in neovascular AMD. Which statement best fits that result?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENNT = 3.13\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E means \u003C/span\u003E\u003Cb\u003Eabout 3 patients must be treated with IVR (instead of sham) for one additional patient to retain vision\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E who otherwise would not have.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOptions \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ED\u003C/b\u003E\u003C/span\u003E incorrectly interpret NNT as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erisk ratio/odds ratio\u003C/b\u003E\u003C/span\u003E (they are not).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOption \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EA\u003C/b\u003E\u003C/span\u003E is about \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etreatment allocation\u003C/b\u003E\u003C/span\u003E, not outcome.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile option \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB\u003C/b\u003E\u003C/span\u003E is phrased loosely, it most closely reflects the NNT concept (\u22483 treated \u2192 1 extra patient benefits compared with sham).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 159,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIn a patient with anisocoria that is more pronounced in bright light, which drug would be most helpful for assessment?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnisocoria \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eworse in bright light\u003C/b\u003E\u003C/span\u003E suggests the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elarger pupil is abnormal\u003C/b\u003E\u003C/span\u003E (likely due to parasympathetic denervation \u2192 possible Adie\u2019s pupil).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E0.1% pilocarpine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (dilute) is used as a \u003C/span\u003E\u003Cb\u003Ediagnostic test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAdie\u2019s tonic pupil\u003C/b\u003E\u003C/span\u003E (denervation hypersensitivity), the pupil \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econstricts\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA normal pupil does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot constrict\u003C/b\u003E\u003C/span\u003E with this dilute strength.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E1% pilocarpine\u003C/b\u003E\u003C/span\u003E would constrict both normal and abnormal pupils, so it\u2019s not diagnostic.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPhenylephrine 2.5%\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eapraclonidine\u003C/b\u003E\u003C/span\u003E are used for sympathetic pathway disorders (e.g., Horner\u2019s syndrome), not for this situation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 160,
    "Name": "Anti-histamines",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENedocromil sodium belongs to which class of drugs?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENedocromil sodium\u003C/b\u003E\u003C/span\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emast cell stabiliser\u003C/b\u003E\u003C/span\u003E, preventing degranulation and release of histamine and other mediators of allergy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUsed in \u003C/span\u003E\u003Cb\u003Eallergic conjunctivitis and asthma prophylaxis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E an antihistamine (which blocks histamine receptors), an NSAID (which inhibits cyclooxygenase), or a vasoconstrictor (which reduces redness via vascular action).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 161,
    "Name": "Investigations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following statements about optical coherence tomography (OCT) is MOST likely to be true?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOCT\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is excellent for detecting \u003C/span\u003E\u003Cb\u003Estructural changes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E such as \u003C/span\u003E\u003Cb\u003Eintraretinal cysts, vitreomacular traction, macular holes, and subretinal fluid\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreomacular traction\u003C/b\u003E\u003C/span\u003E, cystic spaces can appear on OCT, even though fluorescein angiography may show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno leakage\u003C/b\u003E\u003C/span\u003E \u2014 a key diagnostic distinction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOCT \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecannot reliably differentiate\u003C/b\u003E\u003C/span\u003E between active CNV and fibrosis (angiography or OCTA is required).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot used alone\u003C/b\u003E\u003C/span\u003E to decide on laser for DMO \u2014 clinical context and angiography are essential.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOCT \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecannot distinguish rhegmatogenous vs exudative RD\u003C/b\u003E\u003C/span\u003E \u2014 that requires clinical exam and other imaging.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 162,
    "Name": "Drops",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of the following is the MOST appropriate choice?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBrimonidine\u003C/b\u003E\u003C/span\u003E is contraindicated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETCAs\u003C/b\u003E\u003C/span\u003E \u2192 risk of reduced efficacy \u0026amp; systemic side effects.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDorzolamide\u003C/b\u003E\u003C/span\u003E is contraindicated in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esevere renal impairment\u003C/b\u003E\u003C/span\u003E (CrCl \u0026lt;30 ml/min).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETimolol\u003C/b\u003E\u003C/span\u003E contraindicated in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Easthma\u003C/b\u003E\u003C/span\u003E \u2192 risk of bronchospasm.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELatanoprost\u003C/b\u003E\u003C/span\u003E is generally safe in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econtact lens users\u003C/b\u003E\u003C/span\u003E, provided lenses are removed before instillation and reinserted after 15 minutes (to avoid preservative absorption).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 163,
    "Name": "Anti-biotics",
    "Body": "\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 25-year-old woman was prescribed oral antibiotics for an infection after attending the eye casualty 2 weeks earlier. She now presents with a skin rash after the use of a sunbed, and she attributes it to the drug. What is the most likely infection for which the patient was prescribed that drug?\u003C/span\u003E",
    "Explanation": "\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECommon ocular reason for doxycycline\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: \u003Ci\u003EChlamydia trachomatis\u003C/i\u003E conjunctivitis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBorrelia burgdorferi\u003C/b\u003E\u003C/span\u003E \u2192 Lyme disease, ocular involvement rare, not routine in UK ophthalmology clinics.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPropionibacterium (Cutibacterium) acnes\u003C/b\u003E\u003C/span\u003E \u2192 causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echronic post-cataract endophthalmitis\u003C/b\u003E\u003C/span\u003E, but that would be intraocular, not superficial; managed with intravitreal antibiotics/pars plana vitrectomy, not oral antibiotics.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETreponema pallidum\u003C/b\u003E\u003C/span\u003E \u2192 syphilis can involve the eye (uveitis, interstitial keratitis, scleritis), and is treated with systemic antibiotics (penicillin, doxycycline if allergic).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPhotosensitivity rash is \u003C/span\u003E\u003Cb\u003Eclassically associated with doxycycline\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDoxycycline is used for:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EChlamydia trachomatis (adult inclusion conjunctivitis)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOcular rosacea / meibomianitis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESyphilis (if penicillin allergic)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EBut only \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EChlamydia trachomatis\u003C/b\u003E\u003C/span\u003E is a common reason in an ophthalmology clinic to give oral tetracyclines (especially doxycycline).\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 164,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA 6-month-old baby is referred with anisocoria. The mother has noticed this for 3 months but is unsure if it was present before then. She comments that the pupils appear unequal most of the time but not always. Which factor would MOST strongly influence the decision to investigate further?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnisocoria in infants can often be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephysiological\u003C/b\u003E\u003C/span\u003E, especially if mild and stable.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ered flag\u003C/b\u003E\u003C/span\u003E is when anisocoria is associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eptosis\u003C/b\u003E\u003C/span\u003E, which raises suspicion for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHorner\u2019s syndrome\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHorner\u2019s syndrome in infants may be linked to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eserious underlying causes\u003C/b\u003E\u003C/span\u003E such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneuroblastoma or birth trauma\u003C/b\u003E\u003C/span\u003E \u2192 requires further urgent investigation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFamily history, pupil size alone, or variable history are less concerning compared to ptosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 165,
    "Name": "General",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EPatients with Body Dysmorphic Disorder (BDD) usually present with several characteristic features. Which of the following is the exception?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBDD is a psychiatric disorder\u003C/b\u003E\u003C/span\u003E, not a disorder of real cosmetic deformity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatients are preoccupied with an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eimagined or minimal flaw\u003C/b\u003E\u003C/span\u003E, often perceived as much worse than reality.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThey often have \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emultiple cosmetic procedures\u003C/b\u003E\u003C/span\u003E but remain dissatisfied.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFeatures such as \u003C/span\u003E\u003Cb\u003Etype-A personality traits\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Eunrealistic expectations\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E are common.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe key point: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThe defect is perceived, not real\u003C/b\u003E\u003C/span\u003E \u2192 therefore \u201Ccosmetic body defect\u201D is the exception.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 166,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich of these drugs is the most effective for inducing miosis during cataract surgery?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIntracameral acetylcholine (Miochol-E)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is routinely used in cataract surgery to \u003C/span\u003E\u003Cb\u003Eproduce rapid and complete miosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt acts \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edirectly on muscarinic receptors\u003C/b\u003E\u003C/span\u003E of the iris sphincter muscle.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMethacholine is not commonly used in surgery.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPhysostigmine is an acetylcholinesterase inhibitor, not a direct surgical miotic.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESuccinylcholine is a neuromuscular blocker for muscle relaxation, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot for intraocular miosis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore, acetylcholine is the drug of choice.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 167,
    "Name": "RVO",
    "Body": "\u003Cdiv\u003E\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Aptos, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\u003Cb\u003EA \u0026nbsp;68 yr old asian woman presented with decreased vision in her right eye that had occurred about 2 weeks previously on waking up. Examination shows relative afferent pupillary defect and a visual acuity of 4/60. After revieweing her macular scans, what would your management be as per the most recent RCOphth guidelines?\u003C/b\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E\u003C/div\u003E\u003Cimg src=\u0022https://www.mdpi.com/jcm/jcm-12-06710/article_deploy/html/images/jcm-12-06710-g005-550.jpg\u0022\u003E",
    "Explanation": "These features together fit ischemic central retinal vein occlusion (CRVO) with macular oedema.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u0026nbsp;According to RCOphth guidelines:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u2022\tFirst-line is an anti-VEGF trial (3 injections) for macular oedema secondary to CRVO,\u0026nbsp;\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u2022\tWith close monitoring for neovascular complications, including neovascular glaucoma, since the ischemic CRVO variant has high risk of anterior segment neovascularisation.\u0026nbsp;\u003C/div\u003E\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u0026nbsp;Image source:\nKurobe, R.; Hirano, Y.; Yuguchi, T.; Suzuki, N.; Yasukawa, T. Severe Macular Ischemia Is Associated with a Poor Visual Prognosis and Serious Complications in Eyes with Central Retinal Vein Occlusion. J. Clin. Med. 2023, 12, 6710. https://doi.org/10.3390/jcm12216710\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 168,
    "Name": "CIN",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following is the least appropriate treatment option for conjunctival intraepithelial neoplasia (CIN)?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EStandard treatments for CIN include \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esurgical excision with cryotherapy\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etopical chemotherapy\u003C/b\u003E\u003C/span\u003E (e.g., mitomycin C, 5-fluorouracil, or interferon \u03B12b).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese methods achieve good control and have fewer complications.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EExternal beam radiotherapy is not routinely used\u003C/b\u003E\u003C/span\u003E due to significant risks (limbal stem cell failure, dry eye, secondary malignancy).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore, external beam radiotherapy is the least appropriate option.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 169,
    "Name": "DR",
    "Body": "\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EYou are reviewing a 42-year-old Type I diabetic patient. His visual acuity in both eyes is 6/6. His latest HbA1c was 12% (107 mmol/mol). His OCT scan showed the following findings. Which of the following is the most appropriate treatment?\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-08-31-d9125af9-851d-4dfb-912b-336828384533.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003Cp\u003E\u003Cspan style=\u0022font-family: Arial;\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal;\u0022\u003EThe structural OCT shows NVEs presenting as homogenous hyperreflective loops breaching the ILM and protruding into the vitreous with posterior retinal shadowing.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal;\u0022\u003EUsing SD-OCT, NVEs have been proposed to develop in 3 stages:\u0026nbsp;\u003Cbr\u003E\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003EI\u2014disruption of ILM\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003EII\u2014horizontal growth along ILM\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003EIII\u2014multiple breach of PH and linear growth\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-family: Arial;\u0022\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal;\u0022\u003ENVEs were also classified according to location\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal;\u0022\u003Ebased on their intraretinal component\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal;\u0022\u003E:\u003Cbr\u003E\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003E(1) above the ILM\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003E(2) below the ILM types\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-family: Arial;\u0022\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022color: rgb(51, 51, 51); letter-spacing: normal; font-size: medium;\u0022\u003ENonetheless, most use the histopathology definition of NVE, where a breach of the ILM is a requisite.\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp\u003EOf course, the presence of NVE indicates that this is active proliferative diabetic retinopathy requiring Argon PRP laser treatment.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA Similar question appeared in a previous FRCOphth written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 170,
    "Name": "AMD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAccording to NICE guidance (2008, updated 2012) for wet AMD treatment, which of the following is least likely to be a valid criterion for anti-VEGF therapy?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENICE treatment criteria for wet AMD (anti-VEGF eligibility) include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBCVA 6/12\u20136/96\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAbsence of permanent foveal damage\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEvidence of recent progression\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELesion size restriction is no longer a criterion\u003C/b\u003E\u003C/span\u003E in NICE guidance, making it the least valid option here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore, the correct answer is: lesion size \u2264 4 disc areas.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 171,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich clinical finding is most consistent with aqueous misdirection one week after trabeculectomy with a patent peripheral iridotomy?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAqueous misdirection (malignant glaucoma)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E occurs when aqueous is misdirected posteriorly into/behind the vitreous, causing \u003C/span\u003E\u003Cb\u003Eforward displacement of the lens\u2013iris diaphragm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey clinical triad:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShallow or flat anterior chamber (generalized, not peripheral only)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENormal or mildly raised IOP (often ~15\u201320 mmHg, not severely high)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPatent iridotomy (rules out pupillary block)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis differentiates it from:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPupillary block\u003C/b\u003E\u003C/span\u003E \u2192 high IOP \u002B shallow peripheral AC \u002B closed angle\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChoroidal detachment\u003C/b\u003E\u003C/span\u003E \u2192 shallow AC \u002B choroidal elevation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESimple trabeculectomy failure\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 raised IOP \u002B deep AC\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ETherefore, the scenario with shallow anterior chamber and IOP of 18 mmHg best fits aqueous misdirection.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ENote:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn \u003C/span\u003E\u003Cb\u003Eaqueous misdirection (malignant glaucoma)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP is not always severely raised\u003C/b\u003E\u003C/span\u003E. Multiple authoritative sources (textbooks and reviews) describe it as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enormal to moderately elevated\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\uD83D\uDD39 \u003C/span\u003E\u003Cb\u003EAAO BCSC: Glaucoma (2023\u201324 edition)\u003C/b\u003E\u003C/p\u003E\u003Cblockquote style=\u0022margin: 0.0px 0.0px 0.0px 15.0px; font: 14.0px \u0027.AppleSystemUIFont\u0027; color: #0e0e0e\u0022\u003E\u201CAqueous misdirection is characterized by a uniformly shallow or flat anterior chamber, a patent iridotomy, and an IOP that may be normal or moderately elevated.\u201D\u003C/blockquote\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\uD83D\uDD39 \u003C/span\u003E\u003Cb\u003EYanoff \u0026amp; Duker, Ophthalmology (5th edition)\u003C/b\u003E\u003C/p\u003E\u003Cblockquote style=\u0022margin: 0.0px 0.0px 0.0px 15.0px; font: 14.0px \u0027.AppleSystemUIFont\u0027; color: #0e0e0e\u0022\u003E\u201CThe intraocular pressure is usually mildly elevated, though it may be normal in some cases. Marked elevation is not typical at presentation.\u201D\u003C/blockquote\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\uD83D\uDD39 \u003C/span\u003E\u003Cb\u003EReview: Malignant Glaucoma: A Review (Eye, 2012)\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u201CAlthough originally described as \u2018malignant\u2019 because of severe and refractory IOP rise, current descriptions emphasize that the pressure may be normal or only modestly raised, with the predominant sign being uniform shallowing of the anterior chamber.\u201D\u003C/blockquote\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 172,
    "Name": "Consent",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 15-year-old girl attends alone requesting squint surgery for a cosmetically troubling consecutive exotropia. According to GMC guidance, what is the most accurate statement regarding the consent process in this case?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn the UK, patients under 16 can legally consent to treatment if they are assessed as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGillick competent\u003C/b\u003E\u003C/span\u003E (able to understand the nature, purpose, risks, and benefits of the treatment).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGMC guidance emphasizes that even if a child is competent, it is good practice to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einvolve parents or carers\u003C/b\u003E\u003C/span\u003E, unless the young person objects and confidentiality needs to be respected.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBeing under 18 does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E automatically remove the right to consent if competence is established.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 173,
    "Name": "Lid Tumors",
    "Body": "\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 5 month old boy is brought to your clinic by his parents who noticed a \u0022lump on his eye\u0022. On examination, you see the lesion shown in the photo. What is the MOST likely diagnosis?\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://d31g6oeq0bzej7.cloudfront.net/Assets/ResizeImages/image/webp/__detail/3c6f257b-d1b3-4245-a6d0-ab07302561d5.webp\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003ECorneal dermoids are solid (not cystic) choristomas with surface epithelium resembling epidermis and dermis, often containing collagenous connective tissue, hair, skin, fat, and sebaceous glands on histology. Grossly, they are elevated, opaque, yellow-white masses often localized to the corneal limbus.\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EThe diagnosis of a corneal dermoid is largely clinical. Biopsy is generally not necessary. However, if surgical removal of the lesion is pursued, histopathology can confirm the diagnosis.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ch2 style=\u0022color: rgb(0, 0, 0); padding-top: 0.5em; padding-bottom: 0.17em; overflow: hidden; font-size: calc(1.2625rem \u002B 0.15vw); font-family: \u0026quot;Gotham SSm A\u0026quot;; letter-spacing: -0.5px; margin-bottom: 0px !important; border-style: initial !important; border-color: initial !important; border-image: initial !important; border-radius: 0px !important;\u0022\u003E\u003Cspan class=\u0022mw-headline\u0022 id=\u0022Risk_Factors_\u0026amp;_Associated_Conditions\u0022 style=\u0022border-radius: 0px !important;\u0022\u003EAssociated Conditions:\u003C/span\u003E\u003C/h2\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: \u0026quot;Gotham SSm A\u0026quot;; font-size: 1.125rem; letter-spacing: -0.5px;\u0022\u003EGoldenhar syndrome\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: \u0026quot;Gotham SSm A\u0026quot;; font-size: 1.125rem; letter-spacing: -0.5px;\u0022\u003ERing dermoid syndrome\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: \u0026quot;Gotham SSm A\u0026quot;; font-size: 1.125rem; letter-spacing: -0.5px;\u0022\u003EEpidermal nevus syndromes\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EIn the case of\u0026nbsp;\u003C/span\u003E\u003Ca href=\u0022https://eyewiki.org/Goldenhar_Syndrome\u0022 title=\u0022Goldenhar Syndrome\u0022 style=\u0022color: rgb(62, 135, 203); background-image: none; background-position: initial; background-size: initial; background-repeat: initial; background-attachment: initial; background-origin: initial; background-clip: initial; font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003EGoldenhar syndrome\u003C/a\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E, head and neck examination may reveal periauricular tragi, microtia or anotia of external ear, hearing loss, low implantation of the auricular pavilion, micrognathia, or mandibular hypoplasia. Vertebral anomalies are also common, such as scoliosis and hemivertebrae. Congenital heart disease and central nervous system abnormalities have also been reported.\u003C/span\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold; text-decoration-line: underline;\u0022\u003ECorneal dermoids have been traditionally classified into three grades:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EGrade I : superficial lesions \u0026lt;5mm and localized to the limbus.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EGrade II: larger lesions covering most of the cornea and extending deep into the stroma down to Descemet membrane without involving it.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EGrade III: large lesions covering the whole cornea and extending through the structures between the anterior surface of the eye and the pigmented epithelium of the iris.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EA comprehensive review of the literature by Pirouzian generated the following management recommendations:\u003C/span\u003E\u003C/p\u003E\u003Cul style=\u0022margin-top: 0.3em; margin-bottom: 0px; margin-left: 1.6em; padding-left: 0px; list-style-position: outside; list-style-image: url(\u0026quot;data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAAYAAAAJCAYAAAARml2dAAAABHNCSVQICAgIfAhkiAAAAAlwSFlzAAAN1wAADdcBQiibeAAAABl0RVh0U29mdHdhcmUAd3d3Lmlua3NjYXBlLm9yZ5vuPBoAAABUSURBVAiZdY4xDsAgFELB2J0DdnbwQI5OHvDfgC62SY0yvhAetI1dWEq5JN0kKwDYbhEx8oT9a5JdEtLb/M2QNW0FAJLttkLbLUfEkIRVztPdo\u002BMBm8UkW9Zxc20AAAAASUVORK5CYII=\u0026quot;); color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003EGrade I, \u0026lt;50 \u03BCm thickness and \u0026lt;1 mm diameter*: simple excision\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003EGrade I, \u0026lt;100 \u03BCm thickness and \u0026lt;1 mm diameter*: keratectomy \u002B amniotic membrane transplantation \u002B autologous limbal stem cell allograft\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003EGrade II and deeper Grade I: keratectomy \u002B amniotic membrane transplantation \u002B limbal stem cell allograft \u002B pericardial patch graft versus anterior or deep anterior lamellar keratoplasty \u00B1 amniotic membrane transplantation\u003C/li\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003EGrade III: total anterior segment reconstruction\u003C/li\u003E\u003C/ul\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E*Corneal dermoids of such small size were rarely observed in our clinical practice.\u003C/p\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003EAdditionally, optical iridectomy is frequently needed in staged surgical management to permit visual development in the absence of clear cornea.\u003C/p\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003ESource:\u0026nbsp;\u003Ca href=\u0022https://eyewiki.org/Corneal_Dermoid\u0022 style=\u0022font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EEyeWiki\u003C/a\u003E\u003C/p\u003E\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 174,
    "Name": "Intermediate uveitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 41-year-old woman with known sarcoidosis presents with vision of 6/24 in her right eye and clinical signs of intermediate uveitis. The left eye has normal vision (6/6) and appears normal on examination. What is the most likely cause of visual loss in her right eye?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn \u003C/span\u003E\u003Cb\u003Esarcoid-related intermediate uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the \u003C/span\u003E\u003Cb\u003Emost common cause of vision loss is cystoid macular oedema (CMO)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELess common causes include choroidal granulomas or CNV, but these are not the primary mechanisms of visual loss.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMacular ischaemia is also less typical in sarcoid compared to diabetic or vascular uveitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, macular oedema is the key complication to suspect when visual acuity drops.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 175,
    "Name": "Sarcoidosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 42-year-old woman with erythema nodosum, interstitial nephritis, bilateral lung nodules, and bilateral hilar lymphadenopathy presents with gradual visual loss and mild ocular pain for 2 months. Visual acuity is LogMAR 0.48 in the right eye and 0.30 in the left. Which of the following is \u003Cspan class=\u0022s1\u0022\u003Eleast likely\u003C/span\u003E to be an ocular feature of her systemic condition?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis case describes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esarcoidosis\u003C/b\u003E\u003C/span\u003E, which can affect multiple organs and cause ocular inflammation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETypical ocular features include \u003C/span\u003E\u003Cb\u003Egranulomatous anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Echorioretinal lesions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eoptic nerve or choroidal granulomas\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinal vasculitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E can occur in sarcoid, but it is usually \u003C/span\u003E\u003Cb\u003Evenous (phlebitis)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E rather than \u003C/span\u003E\u003Cb\u003Esevere retinal arteritis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESevere retinal arteritis is more characteristic of conditions like \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBeh\u00E7et\u2019s disease\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 176,
    "Name": "Scleritis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 64-year-old woman with rheumatoid arthritis on methotrexate presents to the Eye ED with severe pain and redness in her left eye for three days. She had a similar episode in the right eye 10 years ago. Examination reveals diffuse anterior scleritis in the left eye. Which is the most appropriate next step?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe patient already has a \u003C/span\u003E\u003Cb\u003Econfirmed diagnosis of rheumatoid arthritis (RA)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHer current presentation (scleritis) is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eknown complication of RA\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdditional autoimmune screening (ANCA, anti-dsDNA, RF) is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot necessary\u003C/b\u003E\u003C/span\u003E because the systemic cause is already established.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EManagement should focus on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etreating the scleritis\u003C/b\u003E\u003C/span\u003E (e.g., systemic immunosuppression if needed) rather than repeating investigations.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 177,
    "Name": "Anti-epileptics",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following medications is most commonly associated with binasal concentric visual field loss as a side effect?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVigabatrin (used in epilepsy, especially infantile spasms) can cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eirreversible concentric visual field constriction\u003C/b\u003E\u003C/span\u003E, often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebinasal in distribution\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe mechanism involves \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGABA toxicity to retinal cells\u003C/b\u003E\u003C/span\u003E, particularly affecting the nasal retina.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EChloroquine \u2192 macular \u201Cbull\u2019s eye\u201D retinopathy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EChlorpromazine \u2192 pigmentary retinopathy, corneal deposits.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETamoxifen \u2192 crystalline retinopathy, macular changes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 178,
    "Name": "Esotropia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 4-year-old boy has a 4-month history of a convergent squint. His unaided visual acuity is 0.00 LogMAR in the right eye and 0.12 in the left eye. Examination shows \u003Cspan class=\u0022s1\u0022\u003E40 prism dioptres of esotropia at near\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E20 prism dioptres at distance\u003C/span\u003E. Worth lights demonstrate left eye suppression. Cycloplegic refraction is \u002B4.75D in the right eye and \u002B5.00D in the left eye. Fundus is normal.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold; letter-spacing: 0.14994px;\u0022\u003EWhat is the MOST likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EChild is hypermetropic (\u002B4.75D, \u002B5.00D) \u2192 strong accommodative drive.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ESquint is \u003C/span\u003E\u003Cb\u003Egreater at near (40\u0394) than distance (20\u0394)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 typical of \u003C/span\u003E\u003Cb\u003Econvergence excess type\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESuppression in the left eye confirms reduced binocular control.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot non-accommodative esotropia (since refractive error explains it).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENot nystagmus blockage (no nystagmus mentioned).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 179,
    "Name": "Albinism",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn which way is oculocutaneous albinism MOST likely to be inherited?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOculocutaneous albinism (OCA)\u003C/b\u003E\u003C/span\u003E is caused by mutations in genes affecting melanin biosynthesis (e.g., TYR, OCA2, TYRP1, SLC45A2).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIt is \u003C/span\u003E\u003Cb\u003Emost commonly inherited in an autosomal recessive manner\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECarriers are asymptomatic, but when both parents pass on the defective gene, the child manifests OCA.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EX-linked inheritance patterns are associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eocular albinism\u003C/b\u003E\u003C/span\u003E, not oculocutaneous albinism.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 180,
    "Name": "Contracts",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EAt your first job plan as a consultant, the manager asks you to do 15 lists per year to cover colleagues\u2019 holidays on a flexible annual basis. What PA allocation should you receive in your contract?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn NHS consultant contracts, \u003C/span\u003E\u003Cb\u003E1 PA (Programmed Activity) = 4 hours of work per week\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, across the year.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA typical year has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E42 working weeks\u003C/b\u003E\u003C/span\u003E (allowing for leave).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETherefore, \u003C/span\u003E\u003Cb\u003E1 list/week = 42 lists/year = 1 PA\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFor \u003C/span\u003E\u003Cb\u003E15 lists/year \u2192 15 \u00F7 42 = 0.36 PA\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 181,
    "Name": "Fourth Nerve Palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following surgical techniques would be MOST appropriate when aiming to correct the torsional component of a bilateral IV (trochlear) nerve paresis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperior oblique muscle\u003C/b\u003E\u003C/span\u003E provides \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintorsion\u003C/b\u003E\u003C/span\u003E, especially through its anterior fibres.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral trochlear nerve palsy\u003C/b\u003E\u003C/span\u003E, patients often develop \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etorsional diplopia\u003C/b\u003E\u003C/span\u003E due to loss of intorsion.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESurgical correction aims to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erestore intorsional action\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdvancing the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior fibres\u003C/b\u003E\u003C/span\u003E of the superior oblique tendon specifically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eenhances intorsion\u003C/b\u003E\u003C/span\u003E without excessively affecting vertical action.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther listed procedures either weaken the wrong muscles or address vertical deviations rather than torsion.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 182,
    "Name": "Dystonias",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn patients with hemifacial spasm, which artery is the most common site of an aneurysm causing compression of the facial nerve root entry zone?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHemifacial spasm is most often due to \u003C/span\u003E\u003Cb\u003Evascular compression at the root entry zone of the facial nerve\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior inferior cerebellar artery (PICA)\u003C/b\u003E\u003C/span\u003E is the vessel most frequently responsible.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe anterior inferior cerebellar artery (AICA) can occasionally be involved, but other arteries such as the carotid or basilar tip are not typical causes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 183,
    "Name": "Dystonias",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements about hemifacial spasm (HFS) is true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHemifacial spasm is usually due to \u003C/span\u003E\u003Cb\u003Evascular compression of the facial nerve root entry zone\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe most frequent culprit is the \u003C/span\u003E\u003Cb\u003Eposterior inferior cerebellar artery (PICA)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore common in women\u003C/b\u003E\u003C/span\u003E (so option \u201Cmore common in men\u201D is incorrect).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt affects the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eipsilateral facial nerve\u003C/b\u003E\u003C/span\u003E, not the contralateral.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt often presents in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emiddle age\u003C/b\u003E\u003C/span\u003E, not just in the 70\u201380 age group.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 184,
    "Name": "RD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn the context of a giant retinal break, which statement is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EGiant retinal tears are \u003C/span\u003E\u003Cb\u003Efull-thickness circumferential retinal breaks\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E extending \u0026gt;90\u00B0.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe key feature is that the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreous is still attached to the posterior edge\u003C/b\u003E\u003C/span\u003E \u2192 this causes the retina to roll over and invert.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESatellite breaks are common\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (so \u201Cuncommon\u201D is wrong).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPVR develops but not always rapidly\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETrauma is a risk factor, but many are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espontaneous (e.g., in myopes, lattice degeneration)\u003C/b\u003E\u003C/span\u003E, so trauma is not the main cause.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 185,
    "Name": "Trauma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 40-year-old man sustained a right upper lid injury which was surgically repaired. Six weeks later, he presents with right-sided ptosis. His marginal reflex distance (MRD1) is 1 mm on the right (compared to 4 mm on the left). Levator function in the right eye is measured at 5 mm. What is the most appropriate next step in management?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis patient has \u003C/span\u003E\u003Cb\u003Etraumatic ptosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Efair levator function (5 mm)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESix weeks is still \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etoo early for definitive surgery\u003C/b\u003E\u003C/span\u003E \u2014 levator function may recover spontaneously over a few months.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOrbital imaging is not indicated unless there are atypical features (e.g., suspicion of fracture or foreign body).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELevator resection or brow suspension are surgical interventions, but only considered if the ptosis is persistent after a sufficient recovery period (usually \u22656 months).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 186,
    "Name": "White Dot syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 23-year-old myopic woman has 4 weeks of photopsia and 1 week of metamorphopsia in the right eye. Fundus shows multiple small round lesions (~\u2153 disc diameter) in the posterior pole. Fluorescein angiography reveals a choroidal neovascular membrane next to one lesion. What is the MOST likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPIC\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E classically affects \u003C/span\u003E\u003Cb\u003Eyoung myopic women\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Emultiple small (100\u2013300 \u03BCm) yellow-white lesions in the posterior pole\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and has a \u003C/span\u003E\u003Cb\u003Ehigh risk of CNV\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u2014fits the vignette.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBirdshot\u003C/b\u003E\u003C/span\u003E: middle-aged, HLA-A29\u002B, numerous cream spots in mid-periphery, not tiny posterior-pole dots.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAPMPPE\u003C/b\u003E\u003C/span\u003E: larger placoid RPE lesions, often after viral prodrome; CNV is uncommon.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EToxoplasma\u003C/b\u003E\u003C/span\u003E: focal retinochoroiditis with vitritis (\u201Cheadlight in fog\u201D) and old scars.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 187,
    "Name": "Hereditaty vitreoretinopathies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EAn 11-year-old boy presents with vision of 6/6 in the right eye and 6/18 in the left, plus intermittent left exotropia. On examination:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ESubtle peripheral vascular changes in the right eye\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ELeft eye: macula dragged inferotemporally, associated retinal fold, mild neovascularisation, and subretinal exudates\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003ERest of ocular exam normal\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhat is the MOST likely diagnosis?\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFEVR\u003C/b\u003E\u003C/span\u003E: Bilateral (though asymmetric) peripheral avascular retina, macular dragging, retinal folds, neovascularisation, and exudation in children/teens.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECoats disease\u003C/b\u003E\u003C/span\u003E: Usually unilateral, marked telangiectasia, heavy exudation, no macular dragging.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENorrie disease\u003C/b\u003E\u003C/span\u003E: Presents in infancy with congenital blindness, not at age 11 with useful vision.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPersistent fetal vasculature\u003C/b\u003E\u003C/span\u003E: Unilateral, microphthalmia, retrolental membrane\u2014present early in life.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 188,
    "Name": "Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following pathologic conditions is \u003Cspan class=\u0022s1\u0022\u003ELEAST likely\u003C/span\u003E to be associated with pathologic axial myopia?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathologic myopia often leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopic foveoschisis\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emacular holes\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreomacular traction\u003C/b\u003E\u003C/span\u003E due to progressive posterior staphyloma and vitreoretinal interface abnormalities.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripheral retinoschisis\u003C/b\u003E\u003C/span\u003E, however, is usually related to age-related vitreoretinal degeneration (common in older hyperopes), not high/pathologic myopia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 189,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich one of the following statements in regards to phacoemulsification machines is \u003Cspan class=\u0022s1\u0022\u003EMOST likely\u003C/span\u003E to be correct?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeristaltic system\u003C/b\u003E\u003C/span\u003E: Flow depends on pump speed, not infusion pressure.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVenturi system\u003C/b\u003E\u003C/span\u003E: Vacuum is present immediately (not only after occlusion).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPiezoelectric crystals\u003C/b\u003E\u003C/span\u003E: Vibrate with alternating current (AC), not DC.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPulse/burst mode\u003C/b\u003E\u003C/span\u003E: Reduces cumulative ultrasound energy, limiting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eheat generation\u003C/b\u003E\u003C/span\u003E in the anterior chamber and decreasing risk of corneal endothelial damage.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 190,
    "Name": "Congenital Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following statements \u003Cspan class=\u0022s1\u0022\u003EBEST\u003C/span\u003E describes the inheritance of primary congenital glaucoma in the UK?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn the UK, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprimary congenital glaucoma\u003C/b\u003E\u003C/span\u003E is usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esporadic\u003C/b\u003E\u003C/span\u003E, without a clear family history.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESome cases are inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal recessive\u003C/b\u003E\u003C/span\u003E pattern, often linked to CYP1B1 mutations, but this is more common in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econsanguineous populations\u003C/b\u003E\u003C/span\u003E (e.g., Middle East, South Asia).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAutosomal dominant inheritance is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EMost UK cases are sporadic.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 191,
    "Name": "Intra-ocular tumors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA tumour is reported histologically as being comprised of tubules and acini formed by proliferating multilayered small cells. The cells form a lace-like network within a mucoid stroma. Occasional rosette-like structures are also seen. What is the MOST likely histological diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMedulloepithelioma\u003C/b\u003E\u003C/span\u003E is a rare intraocular tumour (usually ciliary body) that shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETubules and acini lined by multilayered neuroepithelial cells\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elace-like network\u003C/b\u003E\u003C/span\u003E in a mucoid stroma\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPresence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erosette-like structures\u003C/b\u003E\u003C/span\u003E, which are neuroectodermal features\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinoblastoma also shows rosettes (Flexner-Wintersteiner, Homer Wright), but the description of tubules, acini, and mucoid stroma is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclassic for medulloepithelioma\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBasal cell carcinoma and sebaceous carcinoma do not show this histological pattern.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 192,
    "Name": "Studies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EWhich of the following statements is\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003ENOT\u003C/span\u003E a finding from the LIGHT study?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELIGHT trial\u003C/b\u003E\u003C/span\u003E (Laser in Glaucoma and Ocular Hypertension Trial) compared selective laser trabeculoplasty (SLT) with eye drops as first-line treatment for open-angle glaucoma and ocular hypertension.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey findings:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESLT was \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eas effective as drops\u003C/b\u003E\u003C/span\u003E in controlling IOP at 36 months (\u224895% laser vs \u224893% drops).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EQuality of life (EQ-5D)\u003C/b\u003E\u003C/span\u003E scores were similar between groups.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEvent rates\u003C/b\u003E\u003C/span\u003E (e.g., need for surgery, disease progression) were lower in the SLT group (4.19 vs 7.97 per 1000 eye-years).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHerpes simplex keratitis and uveitis\u003C/b\u003E\u003C/span\u003E were not reported outcomes in the LiGHT study \u2014 making this statement incorrect.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 193,
    "Name": "Endophthalmitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 67-year-old man with no other medical problems presents to the eye casualty with \u003Cspan class=\u0022s1\u0022\u003Eacute endophthalmitis. He underwent cataract surgery\u003C/span\u003E\u0026nbsp;four days ago, which was uneventful. His visual acuity on presentation is counting fingers. Which of these statements is \u003Cspan class=\u0022s1\u0022\u003EMOST likely to be correct\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEndophthalmitis Vitrectomy Study (EVS)\u003C/b\u003E\u003C/span\u003E is the landmark trial guiding management of postoperative acute endophthalmitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEVS found:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor patients with presenting VA of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehand movements or better\u003C/b\u003E\u003C/span\u003E, outcomes with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreous tap/inject\u003C/b\u003E\u003C/span\u003E were comparable to immediate vitrectomy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVitrectomy only showed benefit when presenting VA was \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elight perception\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EIn LP vision, vitrectomy produced a 3x increase in achieving 6/12 or better (33% vs 11%) \u0026amp; 50% decrease in severe visual loss (20% vs 47%) over TAP.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u03B2-haemolytic streptococci\u003C/b\u003E\u003C/span\u003E \u2192 poor prognosis, not good.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntravitreal steroids\u003C/b\u003E\u003C/span\u003E are \u003Ci\u003Enot\u003C/i\u003E routinely recommended.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPropionibacterium acnes (Cutibacterium acnes)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is linked to \u003C/span\u003E\u003Cb\u003Echronic delayed-onset endophthalmitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not acute cases.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 194,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich of the following features is \u003Cspan class=\u0022s1\u0022\u003EMOST likely to be true\u003C/span\u003E regarding a pupil affected by \u003Cspan class=\u0022s1\u0022\u003EHorner\u2019s syndrome\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHorner\u2019s syndrome \u2192 disruption of the sympathetic pathway \u2192 affected pupil is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmaller\u003C/b\u003E\u003C/span\u003E (miosis), especially in dim light.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWith chronic denervation, the iris dilator muscle develops \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edenervation hypersensitivity\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EApraclonidine\u003C/b\u003E\u003C/span\u003E (a weak alpha-1 agonist) usually has minimal effect in a normal pupil, but in Horner\u2019s it causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edilation\u003C/b\u003E\u003C/span\u003E due to upregulated alpha-1 receptors.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAnisocoria is greater in darkness\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not unchanged.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EApraclonidine causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edilation\u003C/b\u003E\u003C/span\u003E, not constriction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPhenylephrine 1% may dilate a Horner\u2019s pupil (denervation hypersensitivity), but this is not paradoxical.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 195,
    "Name": "AMD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 60-year-old diabetic female patient presents with 6/18 BCVA in her left eye. Fundus exam shows fine crystalline deposits and retinal pigment epithelium hyperplasia temporal to the fovea. A macular OCT is shown. Which of the following is \u003Cspan class=\u0022s1\u0022\u003Eyour next step in her management\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-09-06-bdcc809e-8e16-4b7f-aefb-6ca7920f174e.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EClassic MacTel features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBilateral parafoveal involvement (often asymmetric at presentation)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECrystalline deposits\u003C/b\u003E\u003C/span\u003E at the inner retina\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPigment hyperplasia temporal to the fovea\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOCT showing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyporeflective spaces (\u201Cpseudo-cysts\u201D)\u003C/b\u003E\u003C/span\u003E without true retinal thickening or leakage (unlike diabetic macular edema).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVisual acuity is often reduced (like 6/18 in this case).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe key giveaway is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecrystalline deposits \u002B temporal pigment changes\u003C/b\u003E\u003C/span\u003E \u2192 highly characteristic of MacTel.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EManagement:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EObservation\u003C/b\u003E\u003C/span\u003E if no neovascular proliferation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnti-VEGF\u003C/b\u003E\u003C/span\u003E only if subretinal neovascularization develops\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\uD83D\uDC49 In this vignette: The correct next step is \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EObservation\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 196,
    "Name": "Visual pathway",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn a right-handed individual with a glioma in the \u003Cspan class=\u0022s1\u0022\u003Eleft occipito-temporal region\u003C/span\u003E, which clinical feature would be most expected?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleft occipito-temporal region\u003C/b\u003E\u003C/span\u003E in a right-handed person corresponds to the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elanguage-dominant hemisphere\u003C/b\u003E\u003C/span\u003E (left hemisphere).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELesions here can disrupt the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evisual word form area\u003C/b\u003E\u003C/span\u003E \u2192 causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehemianopic alexia\u003C/b\u003E\u003C/span\u003E (also known as \u201Cpure alexia\u201D).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022color: rgb(71, 71, 71); font-family: Arial, sans-serif; letter-spacing: normal;\u0022\u003EThe visual word form area (VWFA) is\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold; color: rgb(118, 118, 118); font-family: Arial, sans-serif; letter-spacing: normal;\u0022\u003Ea functional region of the left fusiform gyrus and surrounding cortex\u003C/span\u003E\u003Cspan style=\u0022color: rgb(71, 71, 71); font-family: Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u0026nbsp;(right-hand side being part of the fusiform face area)\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe patient typically has a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright homonymous hemianopia\u003C/b\u003E\u003C/span\u003E but with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Especific inability to read\u003C/b\u003E\u003C/span\u003E, while other language functions remain intact.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options explained:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFixed dilated pupil\u003C/b\u003E\u003C/span\u003E \u2192 suggests CN III palsy, not occipito-temporal lesion.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeft homonymous hemianopia\u003C/b\u003E\u003C/span\u003E \u2192 incorrect side; lesion in left occipital lobe causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright homonymous hemianopia\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESee-saw nystagmus\u003C/b\u003E\u003C/span\u003E \u2192 associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediencephalic/chiasmal lesions\u003C/b\u003E\u003C/span\u003E, not occipito-temporal gliomas.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ENotes about hemianopic alexia:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cul\u003E\u003Cli\u003EHemianopic alexia is the most peripheral of the alexias and also the most common. It particularly affects patients with macular-splitting hemianopias.\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u0026nbsp;It is caused by a hemianopia that mildly interferes with single-word reading but has its main impact on upon text reading.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EThis is because the visuomotor system is robbed of visual information away from the point of fixation that it requires in order to plan efficient reading eye movements.\u0026nbsp;\u003C/li\u003E\u003Cli\u003Ereaders of left-to-right scripts, a right-sided hemianopia is more disabling than a left-sided one\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u0026nbsp;The Read-Right therapy consisted of reading laterally scrolling text (from right-to-left), to induce small-field OKN.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EMost cases of alexia without agraphia are due to cerebrovascular accidents from thromobotic or thromboembolic disease involving the left posterior cerebral artery (PCA), which results in an infarct of the left occipital cortex and the splenium of the corpus callosum\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 197,
    "Name": "Side effects",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is \u003Cspan class=\u0022s1\u0022\u003ENOT\u003C/span\u003E a recognised ocular side effect of systemic drug use?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBisphosphonates\u003C/b\u003E\u003C/span\u003E \u2192 can cause ocular inflammation (episcleritis, scleritis, uveitis).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopiramate\u003C/b\u003E\u003C/span\u003E \u2192 known to cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Euveal effusion\u003C/b\u003E\u003C/span\u003E, angle closure glaucoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitamin A\u003C/b\u003E\u003C/span\u003E (in excess) \u2192 can lead to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ekeratopathy\u003C/b\u003E\u003C/span\u003E and even papilloedema due to toxicity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMinocycline\u003C/b\u003E\u003C/span\u003E \u2192 associated with pigmentation (skin, sclera, conjunctiva), not papilloedema. Papilloedema is linked more to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etetracyclines like doxycycline\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitamin A derivatives (isotretinoin)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 198,
    "Name": "Anti-viral",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 73-year-old man with \u003Cspan class=\u0022s1\u0022\u003Eacute retinal necrosis\u003C/span\u003E is started on \u003Cspan class=\u0022s1\u0022\u003Ehigh-dose acyclovir\u003C/span\u003E. He is NPO and dehydrated before surgery, then quickly becomes unwell. \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EWhich renal complication is most likely?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-dose IV acyclovir \u002B dehydration\u003C/b\u003E\u003C/span\u003E \u2192 intratubular precipitation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacyclovir crystals\u003C/b\u003E\u003C/span\u003E \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute kidney injury\u003C/b\u003E\u003C/span\u003E within 24\u201348 h (crystal-induced acute tubular obstruction).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ERisk is highest with \u003C/span\u003E\u003Cb\u003Erapid infusion, inadequate hydration, pre-existing renal impairment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EManifests with a rapid rise in creatinine and reduced urine output; prevention is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eslow infusion and vigorous IV hydration\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMesangiocapillary nephritis and nephrotic syndrome are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot typical\u003C/b\u003E\u003C/span\u003E acute toxicities of acyclovir; UTI does not explain the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esudden\u003C/b\u003E\u003C/span\u003E decline immediately after high-dose therapy.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 199,
    "Name": "Conjunctival lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 40-year-old woman from Ethiopia presents with small (\u0026lt;1 mm) depressions at the peripheral cornea near the limbus, consistent with \u003Cspan class=\u0022s1\u0022\u003EHerbert\u2019s pits\u003C/span\u003E. Which microbiological description of the causative organism is most likely linked to this finding?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHerbert\u2019s pits are a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epathognomonic sign of trachoma\u003C/b\u003E\u003C/span\u003E, seen after resolution of limbal follicles.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETrachoma is caused by \u003C/span\u003E\u003Cb\u003EChlamydia trachomatis (serotypes A\u2013C)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOn histology, the hallmark is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebasophilic intra-cytoplasmic epithelial inclusion bodies\u003C/b\u003E\u003C/span\u003E (seen in conjunctival epithelial cells).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGram staining would not reveal typical cocci or rods because \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC. trachomatis is an obligate intracellular bacterium\u003C/b\u003E\u003C/span\u003E, not detectable by routine Gram stain.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 200,
    "Name": "Refractive",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium; font-weight: bold;\u0022\u003EA 28-year-old female patient, hours after a \u003Cspan class=\u0022s1\u0022\u003Ephakic IOL\u003C/span\u003E procedure for high myopia, presents with severe left-eye pain, CF vision, and \u003Cspan class=\u0022s1\u0022\u003EIOP 61 mmHg\u003C/span\u003E. What is the \u003Cspan class=\u0022s1\u0022\u003Ebest immediate\u003C/span\u003E treatment?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPhakic IOLs (e.g., ICL) can cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupillary-block acute angle closure\u003C/b\u003E\u003C/span\u003E soon after surgery.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHallmarks: sudden pain/blur, very \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh IOP\u003C/b\u003E\u003C/span\u003E, usually within hours.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENd:YAG peripheral iridotomy (PI)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E promptly bypasses the block and is the \u003C/span\u003E\u003Cb\u003Edefinitive immediate\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E step.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPilocarpine\u003C/b\u003E\u003C/span\u003E can worsen block or be ineffective in very high IOP.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECycloplegia\u003C/b\u003E\u003C/span\u003E is for aqueous misdirection, not pupillary block.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAC paracentesis\u003C/b\u003E\u003C/span\u003E only gives transient IOP reduction and does not treat the underlying block.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 201,
    "Name": "Ptosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich feature is \u003Cspan class=\u0022s1\u0022\u003Eleast commonly associated\u003C/span\u003E with congenital ptosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECongenital ptosis is due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elevator palpebrae superioris dysgenesis\u003C/b\u003E\u003C/span\u003E, not orbicularis weakness.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECommon associations:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAbsent lid crease\u003C/b\u003E\u003C/span\u003E (poor levator development).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAstigmatism\u003C/b\u003E\u003C/span\u003E (from lid pressure).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmblyopia\u003C/b\u003E\u003C/span\u003E (from visual axis obstruction or astigmatism).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOrbicularis oculi weakness\u003C/b\u003E\u003C/span\u003E is a feature of facial nerve palsy, not congenital ptosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 202,
    "Name": "Lacrimal",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EIn an external dacryocystorhinostomy (DCR), what is the correct anterior-to-posterior order of bones encountered?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn DCR, the bony pathway to the lacrimal sac follows a consistent order:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMaxilla\u003C/b\u003E\u003C/span\u003E (anterior wall of the lacrimal sac fossa).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELacrimal bone\u003C/b\u003E\u003C/span\u003E (thin bone, main surgical target to access sac).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEthmoid bone\u003C/b\u003E\u003C/span\u003E (posterior limit, sometimes exposed).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFrontal and nasal bones are not encountered in the routine anterior-posterior sequence.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 203,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOn OCT, which condition is most likely to show large intraretinal cystic spaces without evidence of leakage on fluorescein angiography (FFA)?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EX-linked juvenile retinoschisis shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esplitting of the retinal layers (schisis cavities)\u003C/b\u003E\u003C/span\u003E that appear cystic on OCT. These spaces are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot caused by vascular leakage\u003C/b\u003E\u003C/span\u003E, so FFA typically shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno leakage\u003C/b\u003E\u003C/span\u003E, unlike cystoid macular edema.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022https://eyewiki.org/w/images/8/8c/Optical_coherence_tomography_in_X-linked_retinoschisis.jpg?20220120222055\u0022\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 204,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EA 68-year-old woman develops ocular discomfort and blurred vision in her right eye two months after uncomplicated cataract surgery. Examination shows corneal edema with keratic precipitates, anterior chamber and vitreous inflammation, elevated IOP, and a posterior capsular plaque. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EPropionibacterium acnes endophthalmitis\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003ETiming:\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E Appears \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eweeks to months\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E after cataract surgery (vs. acute bacterial endophthalmitis which occurs within days).\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESigns:\u003C/b\u003E\u003C/span\u003E Mild-to-moderate anterior uveitis, keratic precipitates, vitritis, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclassic posterior capsular plaque\u003C/b\u003E\u003C/span\u003E (organism embedded in lens capsule).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECausative organism:\u003C/b\u003E\u003C/span\u003E \u003Ci\u003ECutibacterium (Propionibacterium) acnes\u003C/i\u003E \u2013 a slow-growing, low virulence organism.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDifferentiation:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETASS\u003C/b\u003E\u003C/span\u003E: Presents within \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E24\u201348 hrs\u003C/b\u003E\u003C/span\u003E post-op, sterile inflammation, no vitreous involvement, no posterior capsular plaque.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETB uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Possible given her history, but would not cause a \u003C/span\u003E\u003Cb\u003Elocalized posterior capsular plaque after cataract surgery\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcute post-op endophthalmitis\u003C/b\u003E\u003C/span\u003E: Rapid onset (within 1\u20132 weeks), pain, hypopyon, severe vision loss.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 205,
    "Name": "Physiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-size: medium;\u0022\u003EWhich vitamin supplement has the strongest evidence for providing neuroprotection in patients with glaucoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitamin B3 (Niacinamide):\u003C/b\u003E\u003C/span\u003E Animal and early clinical studies show it supports \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emitochondrial function\u003C/b\u003E\u003C/span\u003E and protects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal ganglion cells\u003C/b\u003E\u003C/span\u003E against glaucomatous damage. Considered the most promising neuroprotective supplement.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitamin B2 (Riboflavin):\u003C/b\u003E\u003C/span\u003E Important for corneal collagen cross-linking (keratoconus) but not proven as neuroprotective in glaucoma.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitamin B1 \u0026amp; B6:\u003C/b\u003E\u003C/span\u003E Essential vitamins, but no strong evidence for glaucoma neuroprotection.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFurther information:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENicotinamide \u002B Pyruvate Phase 2 Trial (De Moraes et al.)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERandomized, double-blind, placebo-controlled trial in open-angle glaucoma patients.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EShort-term visual field gains: the number of improving test points was higher in the treatment arm vs placebo.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESuggests nicotinamide may \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esupport inner retinal function\u003C/b\u003E\u003C/span\u003E when combined with IOP-lowering therapy.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThe Glaucoma Nicotinamide Trial (TGNT, NCT05275738)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOngoing prospective, double-masked, placebo-controlled trial of nicotinamide in open-angle glaucoma.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAims to test whether nicotinamide slows progression when added to standard IOP-lowering therapy.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOther Nicotinamide Trials\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA crossover randomized trial showed improvement in inner retinal electrophysiology (photopic negative response) with nicotinamide supplementation.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESeveral clinical trial listings exist investigating nicotinamide\u2019s neuroprotective role in glaucoma (e.g. NCT05405868).\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConcerns \u0026amp; Position Statements\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe American Glaucoma Society and AAO are developing a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposition statement on nicotinamide\u003C/b\u003E\u003C/span\u003E use in glaucoma, noting that it has promise but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot yet approved therapy\u003C/b\u003E\u003C/span\u003E.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESafety considerations include \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epossible liver toxicity\u003C/b\u003E\u003C/span\u003E, especially at high doses.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 206,
    "Name": "Pseudoexfoliation",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements is correct regarding Pseudoexfoliation?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EPseudo-exfoliation (PXF)\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: 700;\u0022\u003Edoes have genetic associations with\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003ELOXL1 gene variants\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;(G153D, R141L), but these polymorphisms have\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003Ehigh prevalence in the general population\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, so the inheritance is\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003Ecomplex, multifactorial\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, and influenced by environmental factors.\u0026nbsp;\u003C/span\u003ETherefore, it is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot considered a clearly inherited disease\u003C/b\u003E\u003C/span\u003E, despite known genetic risk alleles.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMost large epidemiological studies show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eequal or slightly increased prevalence in females\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EPXF prevalence is highest in \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003EScandinavian countries\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E (up to 20\u201330% in individuals over 60).\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003ELong-term cohort studies show\u0026nbsp;\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E~15% of patients with pseudo-exfoliation develop glaucoma over a 10-year period.\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EA similar question appeared in multiple previous FRCOphth exams.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
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    "Category": null,
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  },
  {
    "Id": 207,
    "Name": "Rieger\u0027s syndrome",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 22-year-old patient was referred to you from the optician as they suspected glaucoma. You notice that the patient has a short stature and has a history of aortic stenosis and intellectual disability. On ocular examination, you do find glaucomatous cupping. What is the most likely diagnosis?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAxenfeld\u2013Rieger syndrome (ARS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a \u003C/span\u003E\u003Cb\u003Edevelopmental disorder of the anterior segment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, characterised by abnormalities of the \u003C/span\u003E\u003Cb\u003ESchwalbe\u2019s line\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Eiris\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and various \u003C/span\u003E\u003Cb\u003Esystemic defects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It represents the spectrum of \u003C/span\u003E\u003Cb\u003EAxenfeld anomaly\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003ERieger anomaly\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and associated systemic features.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003EOcular Features\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosterior embryotoxon\u003C/b\u003E\u003C/span\u003E: anteriorly displaced and prominent Schwalbe\u2019s line.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften accompanied by \u003C/span\u003E\u003Cb\u003Eiridocorneal adhesions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Eiris stromal hypoplasia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGlaucoma develops in approximately 50% of patients\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, typically during childhood or early adulthood.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003ESystemic Features\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003ESystemic anomalies occur mainly when the condition is due to \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EPITX2\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EFOXC1\u003C/b\u003E\u003C/span\u003E mutations (true Axenfeld\u2013Rieger \u003Ci\u003Esyndrome\u003C/i\u003E). They include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003ECraniofacial anomalies\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHypertelorism\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETelecanthus\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMaxillary hypoplasia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBroad, flat nasal bridge\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EDental abnormalities\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHypodontia or oligodontia (most characteristic)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMicrodontia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EConical teeth\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EOther systemic manifestations\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHypospadias\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnal stenosis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUmbilical abnormalities\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPituitary dysfunction or growth retardation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECongenital heart defects (e.g., valvular anomalies)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://www.frontiersin.org/files/Articles/732170/fgene-12-732170-HTML/image_m/fgene-12-732170-g003.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003EOcular features and systemic manifestations in our patients with ARS.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(A)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;posterior embryotoxon indicated by white arrowheads.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(B)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;iris stromal hypoplasia and polycoria.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(C)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;irregular pupil and corectopia.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(D)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;iridocorneal adhesions across the anterior chamber angle indicated by white arrowheads.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(E)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;The ultrasound biomicroscopy (UBM) image\u0026nbsp; shows the iris strands bridging the iris to the posterior embryotoxon indicated by a white arrowhead.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(F\u2013H)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E. craniofacial abnormalities (a broad flat nasal root, maxillary hypoplasia, thin upper lip and everted lower lip)\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(F,G)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;and redundant periumbilical skin\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(H)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E(I)\u003C/strong\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;dental anomalies (hypodontia and microdontia).\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003ESource:\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EHeterogeneity of Axenfeld\u2013Rieger Syndrome: Molecular and Clinical Findings in Chinese Patients; Youjia Zhang et al\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022display: revert; color: rgb(40, 40, 40); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 12px; letter-spacing: normal; background-color: rgb(247, 247, 247);\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Ca class=\u0022ArticleLayoutHeader__info__doi\u0022 href=\u0022https://doi.org/10.3389/fgene.2021.732170\u0022 style=\u0022display: inline-block; cursor: revert; vertical-align: middle; text-wrap-mode: nowrap; font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; font-size: 12px; letter-spacing: normal; background-color: rgb(247, 247, 247);\u0022\u003Ehttps://doi.org/10.3389/fgene.2021.732170\u003C/a\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
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    "Category": null,
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  },
  {
    "Id": 208,
    "Name": "ICE syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIn Iridocorneal Endothelial (ICE) syndrome, which statement is FALSE?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EGlaucoma in ICE syndrome arises from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogressive synechial angle closure\u003C/b\u003E\u003C/span\u003E caused by contraction of the abnormal, proliferative corneal endothelium. These eyes have a high risk of surgical failure because the aggressive endothelial membrane often obstructs or scars filtering pathways.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EEven with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emitomycin C\u003C/b\u003E\u003C/span\u003E,\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EICE glaucoma is notoriously surgical-resistant and\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Etrabeculectomy frequently fails over time, with high rates of \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Ebleb fibrosis\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E and \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eprogressive peripheral anterior synechiae\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E. Modern data show that many patients ultimately require a \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eglaucoma drainage device\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E for long-term IOP control.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBroad PAS, corneal endothelial abnormalities (especially in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChandler syndrome\u003C/b\u003E\u003C/span\u003E), and a suspected \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eviral (HSV) association\u003C/b\u003E\u003C/span\u003E are all well-supported features of ICE syndrome.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EChandler subtype features the most marked endothelial dysfunction, leading to corneal oedema and the \u201Cbeaten metal\u201D endothelium.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a recent FRCOphth written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 209,
    "Name": "Drops",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich glaucoma medication both reduces aqueous humour production and enhances aqueous outflow?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBrimonidine\u003C/b\u003E\u003C/span\u003E, an \u03B12-adrenergic agonist, lowers intraocular pressure through a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edual mechanism\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EReduces aqueous production\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E at the ciliary body\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIncreases uveoscleral outflow\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther listed agents have single dominant actions:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBimatoprost\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (prostaglandin analogue): \u003C/span\u003E\u003Cb\u003E\u2191 uveoscleral outflow\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBetaxolol\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (\u03B21-selective blocker): \u003C/span\u003E\u003Cb\u003E\u2193 aqueous production\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDorzolamide\u003C/b\u003E\u003C/span\u003E (carbonic anhydrase inhibitor): \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u2193 aqueous production\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThus, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebrimonidine\u003C/b\u003E\u003C/span\u003E is the only option that provides both reduced aqueous formation and enhanced outflow.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 210,
    "Name": "Drops",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich medication is a direct cholinergic agonist that lowers intraocular pressure by enhancing conventional (trabecular meshwork) outflow?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPilocarpine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a \u003C/span\u003E\u003Cb\u003Edirect-acting muscarinic agonist\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E that contracts the ciliary muscle, opening the trabecular meshwork and \u003C/span\u003E\u003Cb\u003Eincreasing conventional aqueous outflow\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThe other options work via different mechanisms:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELatanoprost\u003C/b\u003E\u003C/span\u003E (prostaglandin analogue): \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u2191 uveoscleral outflow\u003C/b\u003E\u003C/span\u003E (the non-conventional pathway).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EApraclonidine\u003C/b\u003E\u003C/span\u003E (\u03B12 \u0026gt; \u03B11 adrenergic agonist): \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u2193 aqueous production\u003C/b\u003E\u003C/span\u003E, with minimal effect on outflow.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEchothiophate\u003C/b\u003E\u003C/span\u003E: an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eindirect\u003C/b\u003E\u003C/span\u003E cholinergic agonist that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eirreversibly inhibits acetylcholinesterase\u003C/b\u003E\u003C/span\u003E, thereby raising acetylcholine levels; it is not a direct receptor agonist.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 211,
    "Name": "Secondary Glaucoma",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 52-year-old lady with COPD attends a routine optician appointment. She is asymptomatic but is found to have bilateral IOPs of 32 mmHg on pneumatic tonometry. Which of his inhaled treatments is most likely responsible for this raised IOP?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EInhaled corticosteroids such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efluticasone\u003C/b\u003E\u003C/span\u003E can trigger a significant IOP rise in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esteroid responders;\u003C/b\u003E\u003C/span\u003E\u0026nbsp;a group that constitutes roughly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5% of the general population\u003C/b\u003E\u003C/span\u003E, and a higher proportion of glaucoma patients. A typical response is an IOP increase of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026gt;15 mmHg from baseline\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ESalbutamol (\u03B2-agonist) and ipratropium (anticholinergic) can occasionally precipitate \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute angle closure\u003C/b\u003E\u003C/span\u003E through mild mydriasis, but such episodes are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehighly symptomatic\u003C/b\u003E\u003C/span\u003E (pain, blurred vision, halos).\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EA saline nebuliser has no effect on IOP.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ERemember:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EChronic IOP rise \u2192 think STEROIDS first (any route).\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcute, painful, red eye \u2192 angle closure from anticholinergics, sympathomimetics, or sulfa-induced choroidal effusion.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETopiramate = bilateral, acute myopic shift \u002B angle closure (classical exam favourite).\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-02-31525531-d209-4633-a339-b76d89f4462c.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 212,
    "Name": "Inflammatory Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 31-year-old myopic man presents with blurred vision and moderate photophobia. His intraocular pressure is 50 mmHg. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosner-Schlossman syndrome\u003C/b\u003E\u003C/span\u003E is the most likely diagnosis:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUnilateral, recurrent episodes\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDisproportionately high IOP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (often 40\u201360 mmHg)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOnly \u003C/span\u003E\u003Cb\u003Emild anterior chamber inflammation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBlurred vision due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emild corneal oedema\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMinimal pain and no systemic symptoms\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThis pattern:\u0026nbsp;\u003C/span\u003E\u003Cb\u003Eyoung adult, very high IOP, mild photophobia, minimal inflammation =\u0026nbsp;\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003Eis classic for \u003C/span\u003E\u003Cb\u003Eglaucomatocyclitic crisis\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EAcute angle-closure glaucoma is very uncommon in a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyoung myope\u003C/b\u003E\u003C/span\u003E\u0026nbsp;and typically presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esevere ocular pain\u003C/b\u003E\u003C/span\u003E, headache, nausea, and a mid-dilated pupil; features not seen here.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\n\n\n\n\n\n\n\n\n\n\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EHerpetic keratitis and toxoplasma uveitis can elevate IOP, but they are usually associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esignificant anterior chamber inflammation\u003C/b\u003E\u003C/span\u003E, corneal epithelial disease (in HSV), keratic precipitates, or vitritis. It is unusual for either to produce an IOP of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E50 mmHg\u003C/b\u003E\u003C/span\u003E at first presentation without marked inflammation.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline; font-size: large;\u0022\u003ENote:\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold; font-size: large;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 126, 255);\u0022\u003EHLA-Bw54\u003C/span\u003E in Posner\u2013Schlossman Syndrome (PSS)\u003C/b\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESeveral Japanese studies (e.g., Yamamoto et al., 1993; Shimizu et al., 1982) reported that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~40\u201350% of Japanese patients with PSS\u003C/b\u003E\u003C/span\u003E are HLA-Bw54 positive.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis association is \u003C/span\u003E\u003Cb\u003Epopulation-specific\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Enot seen in Western cohorts\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo causal relationship has been proven; it is considered a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egenetic susceptibility marker\u003C/b\u003E\u003C/span\u003E rather than a diagnostic feature.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
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  },
  {
    "Id": 213,
    "Name": "Surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ETwo days after trabeculectomy, a patient presents with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eshallow anterior chamber\u003C/b\u003E\u003C/span\u003E and an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP of 18 mmHg\u003C/b\u003E\u003C/span\u003E. What is the most likely diagnosis?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eshallow anterior chamber with a normal or elevated IOP\u003C/b\u003E\u003C/span\u003E early after trabeculectomy is most characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaqueous misdirection\u003C/b\u003E\u003C/span\u003E (malignant glaucoma). In this condition, aqueous humour is diverted posteriorly into or behind the vitreous, pushing the lens-iris diaphragm forward. Typical features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShallow or flat anterior chamber\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERelatively high or \u201Cnormal\u201D IOP\u003C/b\u003E\u003C/span\u003E despite recent filtration surgery\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPoor/flat bleb\u003C/b\u003E\u003C/span\u003E due to lack of anterior aqueous flow\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn contrast:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBleb leak\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003Eshallow AC \u002B hypotony\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (low IOP)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECiliary body shutdown\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003Eshallow AC \u002B hypotony\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E due to reduced aqueous production\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUveitis alone\u003C/b\u003E\u003C/span\u003E does not typically cause significant chamber shallowing and would not explain an IOP of 18 mmHg soon after filtration surgery\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThus, the clinical picture strongly favours \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaqueous misdirection\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-02-803b6fe4-5d1a-4722-a852-333dda21ea55.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb\u003ETop Exam Pearls\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShallow AC \u002B normal/high IOP = think malignant glaucoma first\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E unless iris bombe suggests pupillary block.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShallow AC \u002B low IOP = leak or ciliary body shutdown.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDeep AC \u002B high IOP = blocked ostium or encapsulated bleb.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPainful, sudden deterioration post-op = rule out suprachoroidal haemorrhage.\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 214,
    "Name": "Allergy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcetazolamide is contraindicated in a patient with which drug allergy?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EAcetazolamide is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecarbonic anhydrase inhibitor\u003C/b\u003E\u003C/span\u003E and belongs to the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-antibiotic sulfonamide\u003C/b\u003E\u003C/span\u003E class. Although cross-reactivity between sulfonamide antibiotics and non-antibiotic sulfonamides is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless common than once believed\u003C/b\u003E\u003C/span\u003E, patients with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrue, severe sulfonamide antibiotic allergy\u003C/b\u003E\u003C/span\u003E (e.g., Stevens\u2013Johnson syndrome, anaphylaxis) are generally considered at \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigher risk\u003C/b\u003E\u003C/span\u003E and acetazolamide should be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eavoided\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ESulfamethoxazole is a classic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esulfonamide antibiotic\u003C/b\u003E\u003C/span\u003E, so a confirmed allergy to it is a contraindication.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIf the exam says \u201Csevere sulfa allergy\u201D \u2192 avoid acetazolamide.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIf the exam says \u201Cpenicillin / aminoglycoside / quinolone allergy\u201D \u2192 acetazolamide is safe.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopical CAIs (dorzolamide, brinzolamide)\u003C/b\u003E\u003C/span\u003E can also be avoided if the allergy was severe (SJS/TEN).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 215,
    "Name": "Laser",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following represents the most appropriate initial laser settings for argon laser trabeculoplasty (ALT)?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EALT uses a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmall spot size and short pulse duration\u003C/b\u003E\u003C/span\u003E to deliver relatively \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh-energy bursts\u003C/b\u003E\u003C/span\u003E to the trabecular meshwork. The goal is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emechanical (disruptive) effect\u003C/b\u003E\u003C/span\u003E, producing localized thermal expansion and tightening of the trabecular beams.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ETypical starting parameters for ALT are:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESpot size:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u003C/span\u003E\u003Cb\u003E50 \u00B5m\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDuration:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u003C/span\u003E\u003Cb\u003E0.1 seconds\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEnergy:\u003C/b\u003E\u003C/span\u003E\u0026nbsp;3\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E00\u20131000 mW\u003C/b\u003E\u003C/span\u003E, titrated to achieve \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emild blanching\u003C/b\u003E\u003C/span\u003E of the trabecular meshwork\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWrong combinations include:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E500 \u00B5m spot sizes\u003C/b\u003E\u003C/span\u003E \u2192 used in SLT or MicroPulse, never in ALT.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.5 second duration\u003C/b\u003E\u003C/span\u003E \u2192 too long; would cause excessive coagulative damage.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEnergy too low (200 mW)\u003C/b\u003E\u003C/span\u003E \u2192 insufficient for ALT endpoints.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 216,
    "Name": "Cataract",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements about posterior polar cataracts is TRUE?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EPosterior polar cataract is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edistinct congenital cataract subtype\u003C/b\u003E\u003C/span\u003E, not to be confused with posterior subcapsular cataract (a common \u003Ci\u003Eacquired\u003C/i\u003E opacity). Posterior polar cataracts arise from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edysplastic posterior lens fibres\u003C/b\u003E\u003C/span\u003E that form a characteristic central plaque \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eadherent to an extremely thin and fragile posterior capsule\u003C/b\u003E\u003C/span\u003E. This anatomical arrangement explains the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh risk of posterior capsule rupture\u003C/b\u003E\u003C/span\u003E during surgery.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EInheritance is most commonly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E (not recessive), though sporadic cases occur.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EMyotonic dystrophy is associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior cortical cataracts\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChristmas-tree cataracts\u003C/b\u003E\u003C/span\u003E, not posterior polar cataracts.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022https://eyewiki.org/w/images/9/92/Central_posterior_polar_cataract.jpeg?20170711035407\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003ESource of image: Eyewiki\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 217,
    "Name": "Secondary Cataract",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich statement about cataracts is most likely to be TRUE?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWilson\u2019s disease leads to the classic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esunflower cataract\u003C/b\u003E\u003C/span\u003E, caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecopper deposition beneath the anterior lens capsule\u003C/b\u003E\u003C/span\u003E. It is highly distinctive and often highlighted in exams.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cimg src=\u0022https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/qjmed/114/11/10.1093_qjmed_hcab226/1/m_hcab226f1.jpeg?Expires=1766033277\u0026amp;Signature=cmhtfQw7cpJdroKrlmUlrYLXBYCVefvJBUpGdvjn7h8sgbtx0bh03-pszcAMwajnjkfN5h8RZgDytbe0xX2Yj8hGburtt6y~Qn6F1x5Gu6ZN3TkYzAf6VLendL5DaNjKipFU8PoCbA7IeTfwavtkphqY6zODe-xjJQ7pWZvX72NDrOTv-GqQDt8TFNHgZiczSP1hwYHXqEn8Rx5zDLLKwGYnc-Ji4sahmVy8SAUkrHTMq120Cpztvo9VOr0ymPZDHv3G9fg4DDbatos-HFtTN6rWxFpPkPbflgCIe-1UHF~q7X0cpXVzT63xnHT1HFOjIBf7pLTzdgHWvgBOHlf08w__\u0026amp;Key-Pair-Id=APKAIE5G5CRDK6RD3PGA\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022color: rgb(42, 42, 42); font-family: \u0026quot;Source Sans Pro\u0026quot;, Helvetica, Arial, sans-serif; font-size: 15px; letter-spacing: normal; font-weight: bold;\u0022\u003EKayser\u2013Fleischer ring and sunflower cataract (arrows and arrowheads, respectively)\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022color: rgb(42, 42, 42); font-family: \u0026quot;Source Sans Pro\u0026quot;, Helvetica, Arial, sans-serif; font-size: 15px; letter-spacing: normal;\u0022\u003ESource:\u0026nbsp;\u003C/span\u003E\u003Ca href=\u0022https://doi.org/10.1093/qjmed/hcab226\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ET -Y Lin, I -C Liang, Y -H Chang, Kayser\u2013Fleischer ring and sunflower cataract in a patient with Wilson\u2019s disease, QJM: An International Journal of Medicine, Volume 114, Issue 11, November 2021, Pages 822\u2013823\u003C/a\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EThe other statements are incorrect:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOil-droplet cataracts\u003C/b\u003E\u003C/span\u003E occur in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egalactosaemia\u003C/b\u003E\u003C/span\u003E, which is characterised by the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epresence\u003C/b\u003E\u003C/span\u003E of reducing substances in the urine (galactose), not their absence.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMyotonic dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E typically causes a \u003C/span\u003E\u003Cb\u003EChristmas tree cataract\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and later a \u003C/span\u003E\u003Cb\u003Eposterior subcapsular cataract\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not an anterior cortical opacity.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteroids\u003C/b\u003E\u003C/span\u003E are strongly associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior subcapsular cataracts\u003C/b\u003E\u003C/span\u003E, not anterior subcapsular cataracts.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
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    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 218,
    "Name": "Refractive",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA phakic patient develops a retinal detachment with PVR [proliferative vitreoretinopathy] and undergoes vitrectomy with silicone oil fill, but \u003Cspan class=\u0022s1\u0022\u003Eno lens surgery\u003C/span\u003E is done. What postoperative refractive change is expected?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ESilicone oil changes the effective refractive index of the vitreous cavity.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephakic\u003C/b\u003E\u003C/span\u003E eye, silicone oil has a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elower refractive index than the natural vitreous\u003C/b\u003E\u003C/span\u003E, which effectively \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereduces the converging power\u003C/b\u003E\u003C/span\u003E of the posterior segment \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperopic shift\u003C/b\u003E\u003C/span\u003E (typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u002B5 to \u002B9D\u003C/b\u003E\u003C/span\u003E depending on axial length and oil viscosity).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn an \u003C/span\u003E\u003Cb\u003Eaphakic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E eye, silicone oil acts as a \u003C/span\u003E\u003Cb\u003Erefractive medium compensating for the missing lens\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, producing a \u003C/span\u003E\u003Cb\u003Emyopic shift\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 219,
    "Name": "Refractive",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA mildly myopic patient undergoes routine phacoemulsification with in-the-bag posterior chamber IOL implantation. Biometry was accurate and reproducible with a target of emmetropia. Postoperatively, the patient is \u22121.50 D.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EWhat is the most likely cause of this myopic refractive surprise?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA postoperative \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopic shift\u003C/b\u003E\u003C/span\u003E in an eye with accurate biometry and standard in-the-bag IOL placement is most commonly due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretained viscoelastic trapped behind the IOL optic\u003C/b\u003E\u003C/span\u003E, producing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecapsular bag distension syndrome\u003C/b\u003E\u003C/span\u003E. The viscoelastic pushes the IOL \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanteriorly\u003C/b\u003E\u003C/span\u003E, reducing the effective lens position and increasing its refractive power \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopia\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options are less likely:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECystoid macular oedema\u003C/b\u003E\u003C/span\u003E typically causes a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperopic shift\u003C/b\u003E\u003C/span\u003E due to macular thickening and flattening of the posterior pole.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior IOL dislocation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E moves the lens \u003Ci\u003Ebackward\u003C/i\u003E, reducing power \u2192 \u003C/span\u003E\u003Cb\u003Ehyperopic shift\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnterior IOL dislocation\u003C/b\u003E\u003C/span\u003E causing \u22121.50 D is very unlikely with an intact capsular bag and stable zonules.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch1\u003E\u003Cb style=\u0022font-size: x-large; color: rgb(0, 50, 255);\u0022\u003ETOP EXAM PEARLS\u003C/b\u003E\u003C/h1\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-size: x-large; color: rgb(0, 50, 255);\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEarly myopia post-phaco = think retained viscoelastic (CBDS).\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHyperopia after stable surgery = suspect IOL sitting posteriorly.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPosterior segment causes (CME) \u2192 hyperopic shift.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIncorrect biometry \u2192 direction depends on whether AL or K is wrong.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EToric IOL: every 30\u00B0 off = zero effect.\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 220,
    "Name": "Neuropathy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 69-year-old woman undergoes routine right cataract surgery. Her pre-operative VA was 6/18 (right) and 6/6 (left). At her 2-week post-operative review, her right VA remains 6/18. OCT macula is normal, but the right optic disc appears slightly pale.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EWhat is the most appropriate next investigation?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EPersistent reduced visual acuity after uncomplicated cataract surgery with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enormal OCT\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic disc pallor\u003C/b\u003E\u003C/span\u003E strongly suggests \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic neuropathy\u003C/b\u003E\u003C/span\u003E, not macular disease. The priority is to rule out \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompressive or inflammatory optic nerve pathology\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile visual fields can help document functional loss, they are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot the definitive next step\u003C/b\u003E\u003C/span\u003E when optic disc pallor is noted early post-operatively.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMRI of the brain and orbits with contrast\u003C/b\u003E\u003C/span\u003E is the most appropriate test because it can identify:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOptic nerve compression (meningioma, pituitary disease, orbital mass)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOptic neuritis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIschaemic or infiltrative optic neuropathies\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EFA is unnecessary with a normal OCT, and serum electrophoresis is for systemic paraproteinaemias, not acute optic disc pallor.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
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    "HighYield": true,
    "CategoryId": 8,
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  },
  {
    "Id": 221,
    "Name": "Ectopia Lentis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following is NOT typically associated with homocystinuria?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EHomocystinuria (usually due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecystathionine \u03B2-synthase deficiency\u003C/b\u003E\u003C/span\u003E) is an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal recessive\u003C/b\u003E\u003C/span\u003E metabolic disorder characterised by:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInferonasal lens dislocation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (downward displacement)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMarfanoid habitus\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigh risk of thromboembolic events\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMitral valve prolapse\u003C/b\u003E\u003C/span\u003E and other connective-tissue cardiac findings\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFair, lightly pigmented hair\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (often reddish or blonde)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe key distinguishing feature from Marfan syndrome is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edirection of lens displacement\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHomocystinuria \u2192 lens moves inferonasally\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMarfan syndrome \u2192 lens moves superotemporally\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003ETherefore, \u003C/span\u003E\u003Cb\u003Esuperior lens dislocation is NOT typical\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E of homocystinuria.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
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    "Category": null,
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  },
  {
    "Id": 222,
    "Name": "Lenticonus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient with \u003Cspan class=\u0022s1\u0022\u003E\u221214.00 D\u003C/span\u003E myopia in the right eye undergoes biometry before cataract surgery. Keratometry shows \u003Cspan class=\u0022s1\u0022\u003EK1 44.1 D\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003EK2 44.5 D\u003C/span\u003E, and the axial length is \u003Cspan class=\u0022s1\u0022\u003E23.8 mm\u003C/span\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cb\u003EWhat is the most likely diagnosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA refractive error of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u221214.00 D\u003C/b\u003E\u003C/span\u003E is very high, yet this patient\u2019s biometry shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENormal keratometry\u003C/b\u003E\u003C/span\u003E (\u224844 D \u2192 excludes keratoconus or steep cornea\u2013induced myopia)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENormal axial length\u003C/b\u003E\u003C/span\u003E (\u224823.8 mm \u2192 excludes axial myopia)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhen refractive error is disproportionately myopic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edespite normal axial length and corneal power\u003C/b\u003E\u003C/span\u003E, the remaining location of excess refractive power is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elens\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EPosterior lenticonus causes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELocalised posterior bulging of the lens\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIncreased lenticular power \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emarked myopia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften disproportionate to AL and K readings\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA classic \u201Cbiometry\u2013refraction mismatch\u201D\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIndex myopia from nuclear sclerosis can induce a myopic shift, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u221214 D is far too large\u003C/b\u003E\u003C/span\u003E to be explained purely by nuclear change\u2014especially if the patient was highly myopic even before cataract formation.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ESurgeons must be cautious during cataract extraction because posterior lenticonus is associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior capsule thinning or pre-existing dehiscence\u003C/b\u003E\u003C/span\u003E, increasing the risk of rupture.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
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    "HighYield": true,
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    "Category": null,
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  },
  {
    "Id": 223,
    "Name": "Secondary Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn uveitis\u2013glaucoma\u2013hyphaema (UGH) syndrome, which of the following statements is most likely to be TRUE?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EUGH syndrome occurs when an intraocular lens, typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emalpositioned\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erotated\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eloose\u003C/b\u003E\u003C/span\u003E, or with an exposed \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehaptic,\u0026nbsp;\u003C/b\u003E\u003C/span\u003Emechanically irritates the iris or ciliary body. This leads to:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003Erecurrent \u003C/span\u003E\u003Cb\u003Eanterior uveitis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003Ehyphaema\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Esecondary \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eglaucoma\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Echronic pain, photophobia, and fluctuating vision\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EAlthough \u003C/span\u003E\u003Cb\u003Emost classically associated with rigid anterior chamber IOLs\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, UGH can \u003C/span\u003E\u003Cb\u003Ealso\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E occur with:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Eposterior chamber IOLs (especially if a haptic protrudes into the sulcus or ciliary body)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Escleral- or iris-fixated lenses\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003Esubluxed/dialysed in-the-bag lenses\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe condition is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003C/span\u003E, painful, and symptomatic; not bilateral or silent!\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EUGH has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno association with dermatologic depigmentation\u003C/b\u003E\u003C/span\u003E (this distractor echoes Vogt\u2013Koyanagi\u2013Harada disease).\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 224,
    "Name": "Secondary Glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient has cataract surgery complicated by a posterior capsule rupture, and a posterior chamber IOL is placed in the \u003Cspan class=\u0022s1\u0022\u003Esulcus\u003C/span\u003E. 10 weeks later, the intraocular pressure was found to be 29 mmHg.\u0026nbsp;\u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely cause of this raised IOP?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA sulcus-placed IOL, especially if its haptics or optic edge rub against the posterior iris, can cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emechanical pigment release\u003C/b\u003E\u003C/span\u003E. This leads to trabecular meshwork obstruction and a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edelayed rise in IOP\u003C/b\u003E\u003C/span\u003E, typically weeks to months post-operatively.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey points supporting pigment dispersion:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOccurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eweeks to months\u003C/b\u003E\u003C/span\u003E after surgery (not immediately)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERelated to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eiris chafing\u003C/b\u003E\u003C/span\u003E from sulcus-fixated IOLs\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECauses gradual IOP elevation (often in the high 20s)\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Ca href=\u0022https://www.linkedin.com/posts/ahmed-omara-20713484_iris-chafing-syndrome-single-piece-iol-was-activity-7069029508959346688-Y_ck?utm_source=social_share_send\u0026amp;utm_medium=member_desktop_web\u0026amp;rcm=ACoAABwQJJsBaZhptdwPAib-jtOYs5OOIRqsr4w\u0022 style=\u0022color: rgb(0, 212, 255);\u0022\u003ESlit Lamp video showing Iris Chafing by Dr Ahmed Omara\u003C/a\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EThe other options are less likely:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUGH syndrome\u003C/b\u003E\u003C/span\u003E can occur in sulcus IOLs but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emuch less common with modern designs\u003C/b\u003E\u003C/span\u003E, and typically presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyphaema, pain, inflammation\u003C/b\u003E\u003C/span\u003E, \u003Cspan style=\u0022text-decoration-line: underline;\u0022\u003Enot isolated IOP rise.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAngle recession\u003C/b\u003E\u003C/span\u003E is associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrauma\u003C/b\u003E\u003C/span\u003E, not cataract surgery.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAqueous misdirection\u003C/b\u003E\u003C/span\u003E occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eearly\u003C/b\u003E\u003C/span\u003E post-op and produces \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ea shallow anterior chamber\u003C/b\u003E\u003C/span\u003E, not a normal AC with late-onset pressure rise.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThus, \u003C/span\u003E\u003Cb\u003Eiris pigment chafing from the sulcus IOL\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E is the most likely explanation.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
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  },
  {
    "Id": 225,
    "Name": "Cataract surgery",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA hypermetropic patient with an axial length of \u003Cspan class=\u0022s1\u0022\u003E21 mm\u003C/span\u003E undergoes routine cataract surgery. Four weeks later, he reports deteriorating vision to his optician, measured at \u003Cspan class=\u0022s1\u0022\u003E6/36\u003C/span\u003E. The optician notes \u003Ci\u003E\u201Cretinal swelling.\u201D\u0026nbsp;\u003C/i\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECystoid macular oedema\u003C/b\u003E\u003C/span\u003E (Irvine Gass syndrome) is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common retinal cause of reduced vision\u003C/b\u003E\u003C/span\u003E in the weeks following uncomplicated cataract surgery. It typically presents between \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E4 - 6 weeks post-operatively\u003C/b\u003E\u003C/span\u003E and appears as blurred or reduced central vision; OCT confirms the diagnosis.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe alternative diagnoses are much less likely:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUveal effusion syndrome\u003C/b\u003E\u003C/span\u003E is strongly associated with \u003Ci\u003Enanophthalmos\u003C/i\u003E (axial length \u2248 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u2264 16 mm\u003C/b\u003E\u003C/span\u003E). An axial length of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E21 mm\u003C/b\u003E\u003C/span\u003E is short but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot nanophthalmic\u003C/b\u003E\u003C/span\u003E, and uveal effusion after routine cataract surgery remains \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECiliary body detachment\u003C/b\u003E\u003C/span\u003E causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehypotony\u003C/b\u003E\u003C/span\u003E and often a shallow anterior chamber, not isolated \u201Cretinal swelling.\u201D\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERhegmatogenous retinal detachment\u003C/b\u003E\u003C/span\u003E reduces vision but typically presents with flashes, floaters, or a field defect rather than optician-described \u201Cretinal swelling.\u201D\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EGiven the timing, symptoms, and findings, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECMO is by far the most likely diagnosis.\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 226,
    "Name": "Glaucoma suspect",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient is referred by their community optometrist for possible glaucoma. On examination, the intraocular pressure (IOP) is \u003Cspan class=\u0022s1\u0022\u003E24 mmHg\u003C/span\u003E, the optic discs appear \u003Cspan class=\u0022s1\u0022\u003Enormal\u003C/span\u003E, and the\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003Evisual fields are normal\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most appropriate management plan?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAn IOP of \u003C/span\u003E\u003Cb\u003E24 mmHg\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Enormal discs\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Enormal visual fields\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E meets criteria for \u003C/span\u003E\u003Cb\u003Eocular hypertension only\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not glaucoma.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EAccording to NICE NG81 (Glaucoma: Diagnosis and Management):\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETreatment is NOT recommended\u003C/b\u003E\u003C/span\u003E for IOP \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026lt; 25 mmHg\u003C/b\u003E\u003C/span\u003E unless there is evidence of structural or functional damage.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIndividuals with IOP \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E22\u201324 mmHg\u003C/b\u003E\u003C/span\u003E, normal discs, and normal fields should be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereturned to community optometry\u003C/b\u003E\u003C/span\u003E for routine \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eannual surveillance\u003C/b\u003E\u003C/span\u003E, not hospital follow-up.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThere is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno indication\u003C/b\u003E\u003C/span\u003E for medication, as the risk of conversion to glaucoma at this IOP level is low.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-34424722-55ba-48aa-98fe-ccf9caae8916.png\u0022\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThus, the correct management is \u003C/span\u003E\u003Cb\u003Esafe discharge to community monitoring\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared recently in FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EIt is a very high-yield topic as it represents a recent [2022] change to the guidelines:\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Ca href=\u0022https://www.nice.org.uk/guidance/ng81/resources/glaucoma-diagnosis-and-management-pdf-1837689655237\u0022 style=\u0022color: rgb(0, 136, 255); text-decoration-line: underline;\u0022\u003EGlaucoma Management and Diagnosis - NICE guidelines\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 227,
    "Name": "CIN",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements about conjunctival intraepithelial neoplasia (CIN) is TRUE?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECIN represents \u003C/span\u003E\u003Cb\u003Ecarcinoma in situ\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on the spectrum of \u003C/span\u003E\u003Cb\u003Eocular surface squamous neoplasia (OSSN)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It typically presents as a \u003C/span\u003E\u003Cb\u003Emobile, gelatinous, leukoplakic, or papilliform limbal lesion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Eprominent feeder vessels\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Important risk factors include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUltraviolet light exposure\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFair complexion\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EImmunosuppression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially \u003C/span\u003E\u003Cb\u003EHIV infection\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHPV infection (particularly HPV-16/18)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECIN \u003C/span\u003E\u003Cb\u003Eresponds well to topical chemotherapeutic agents\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, including:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMitomycin C (MMC)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E5-fluorouracil (5-FU)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInterferon \u03B1-2b\u003C/b\u003E\u003C/span\u003E (excellent efficacy with best tolerability)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EThe tumour is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Enot fixed\u003C/b\u003E\u003C/span\u003E to the sclera; mobility helps distinguish it from invasive disease. CIN progresses to \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Esquamous cell carcinoma\u003C/b\u003E\u003C/span\u003E, \u003Ci\u003Enot\u003C/i\u003E basal cell carcinoma.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022https://eyerounds.org/atlas/pages/imgs/R_1cuBEeE9NvHsmvK_Screenshot2025.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022color: rgb(108, 117, 125); font-family: Roboto, sans-serif; font-size: 14.4px; letter-spacing: normal;\u0022\u003ESlit lamp photograph of the left eye in lateral gaze demonstrates a nasal, elevated, gelatinous, flesh-colored conjunctival lesion with leukoplakic areas extending approximately 1 mm onto the cornea, along with prominent nasal vessels.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003ESource:\u0026nbsp;\u003Ca href=\u0022https://eyerounds.org/atlas/pages/CIN-Conjunctival-intraepithelial-neoplasia.htm#gsc.tab=0\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EEyerounds - CIN\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ENotes on OSSN:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cul\u003E\u003Cli\u003EThe prevalence of OSSN is estimated to range from \u0026lt;0.2 cases/million/year (UK, 1996) to 35 cases/million/year (Uganda, 1992).\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u0026nbsp;In several series, CIN has been reported to be the most common conjunctival neoplasia, whereas SCC has been found to be the most common conjunctival malignancy.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EIn the western hemisphere, OSSN afflicts mainly Caucasian men in their 60s to 70s who live close to the equator.\nHowever in Africa and certain parts of Asia, OSSN afflicts younger patients and tends to be more clinically aggressive.\nA similar pattern has been observed in patients with the human immunodeficiency virus (HIV) and xeroderma pigmentosum.\u003C/li\u003E\u003Cli\u003EPunctal occlusion is recommended during topical cytotoxic therapy to minimise systemic absorption.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 228,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EYou receive a histopathology of an excised corneal button that shows the following findings:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThickened epithelial basement membrane\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EDuplication of the basement membrane\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFibrillar/granular material between the basement membrane and Bowman\u2019s layer\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EWhat is the most likely diagnosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe described histology is classic for \u003C/span\u003E\u003Cb\u003EMap\u2013dot\u2013fingerprint dystrophy (epithelial basement membrane dystrophy, EBMD)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Key features include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThickened and reduplicated epithelial basement membrane\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETrapped fibrillar and fibrogranular material\u003C/b\u003E\u003C/span\u003E between the basement membrane and Bowman\u2019s layer\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPoor epithelial adhesion due to abnormal hemidesmosomes\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EThese structural abnormalities create the characteristic \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Emap\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Edot\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Efingerprint lines\u003C/b\u003E\u003C/span\u003E seen clinically.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-893295d9-04d7-475e-9277-f3c1521d3371.png\u0022\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EThe other options have distinct pathology:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFuchs dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 endothelial guttae, Descemet\u2019s membrane thickening\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReis\u2013B\u00FCcklers dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 replacement of Bowman\u2019s layer with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efibrous scar tissue\u003C/b\u003E\u003C/span\u003E; \u201Choneycomb\u201D opacities\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMeesmann\u2019s dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 intraepithelial cysts filled with \u003C/span\u003E\u003Cb\u003EPAS-positive material\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThus, the histology described is \u003C/span\u003E\u003Cb\u003Etypical of EBMD / map\u2013dot\u2013fingerprint dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 229,
    "Name": "Rosacea Keratitis",
    "Body": "\u003Cspan style=\u0022font-size:11.0pt;line-height:115%;\nfont-family:\u0026quot;Cambria\u0026quot;,serif;mso-ascii-theme-font:minor-latin;mso-fareast-font-family:\n\u0026quot;MS Mincho\u0026quot;;mso-fareast-theme-font:minor-fareast;mso-hansi-theme-font:minor-latin;\nmso-bidi-font-family:Arial;mso-bidi-theme-font:minor-bidi;mso-ansi-language:\nEN-US;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003EYou are asked to see\na 50-year-old man with recurrent red eyes for 15\nyears, treated with topical lubricants and antibiotics. He has developed a\nperipheral corneal infiltrate with infero-nasal corneal vascularization. Which\nof these is the MOST likely diagnosis?\u003Cbr\u003E\n\u003Cbr\u003E\n\u003C!--[if !supportLineBreakNewLine]--\u003E\u003Cbr\u003E\n\u003C!--[endif]--\u003E\u003C/span\u003E",
    "Explanation": "Correct Answer: Rosacea keratitis.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003ERosacea keratitis typically affects middle-aged patients and presents with chronic ocular redness and peripheral corneal vascularization, often infero-nasal. It is associated with meibomian gland dysfunction and lid margin disease, and patients may have facial rosacea features such as telangiectasia.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EManagement includes lid hygiene, oral doxycycline, lubricants, and cautious use of topical steroids.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EIncorrect options: Disciform keratitis is linked to HSV and affects the central cornea. Marginal keratitis is acute, associated with staphylococcal blepharitis, and lacks chronic vascularization. Peripheral ulcerative keratitis is severe, linked to systemic autoimmune disease, and presents with crescent-shaped ulceration and thinning.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EMnemonic: Red, Rough, Rosacea \u2013 chronic red eyes, lid disease, peripheral corneal changes.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-03-4dc5d27b-f35a-4dc0-b59c-64cb8efaf6aa.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-8fca96cf-f324-4eab-9f91-3ad9016d6fc2.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-5ce2f594-cebd-48c9-a4bc-f2b366bb0f73.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-03-3bbe550b-3d2a-464b-a577-1a8057025c7a.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;list of pictures:\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E1-Rosacea keratitis.(https://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/rosacea/Rosacea-OD-LRG.jpg)\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E2-Marginal Keratitis.(\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Ehttps://www.sciencedirect.com/science/article/pii/S2214250922001640)\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E3-Disciform keratitis. (https://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/Disciform-keratitis/Disciform-keratitis.jpg)\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E4- PUK.(https://webeye.ophth.uiowa.edu/eyeforum/cases-i/case194/Fig1A-LRG.jpg)\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 230,
    "Name": "Leber\u2019s Hereditary Optic Neuropathy (LHON)",
    "Body": "In Leber\u2019s Hereditary Optic Neuropathy (LHON), which of the following statements is MOST likely to be correct?",
    "Explanation": "Correct Answer: A: A pathogenic mutation of mitochondrial DNA can be identified in approximately 90% of cases.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003ELHON is a maternally inherited optic neuropathy caused by mutations in mitochondrial DNA, most commonly affecting genes encoding complex I of the respiratory chain. The three primary mutations are ND4 (11778), ND1 (3460), and ND6 (14484), which account for the majority of cases.Genetic testing confirms the diagnosis in most patients.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EIncorrect options: LHON is transmitted exclusively through maternal inheritance, so symptomatic males do not pass the condition to their offspring. Spontaneous recovery of vision is uncommon but can occur, particularly in patients with the ND6 mutation (14484). Visual loss does not usually present as a gradual, symmetrical onset; instead, it typically begins in one eye and involves the fellow eye within weeks.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EMnemonic: LHON = Leber\u2019s Hereditary Optic Neuropathy \u2192 Mitochondrial mutation, Maternal inheritance.\u0026nbsp;\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-03-aaf7ddec-d21f-4d87-823b-a2d896f6abe5.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003Ehttps://eyewiki.org/Leber_Hereditary_Optic_Neuropathy\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 231,
    "Name": "Neonatal Retinal Haemorrhage",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003EA baby born by spontaneous vaginal delivery at 33 weeks has\ndot and blot retinal hemorrhages found shortly after birth. Which of the\nfollowing is the MOST likely diagnosis?\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Correct Answer: C: Normal finding.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003ERetinal hemorrhages detected shortly after birth in a premature infant delivered vaginally are considered a normal physiological occurrence. These hemorrhages result from mechanical compression and transient venous congestion during delivery and typically resolve within a few weeks without intervention. Their presence immediately after birth does not indicate pathology and should not be confused with conditions such as retinopathy of prematurity or trauma.\u003C/div\u003E\u003Cdiv\u003EThe other options are incorrect: An inherited disorder of coagulation would present with systemic bleeding tendencies and persistent hemorrhages rather than isolated retinal findings immediately after birth.\u003C/div\u003E\u003Cdiv\u003ENon-accidental injury is characterized by extensive, multilayered retinal hemorrhages often accompanied by other signs of trauma or neurological involvement, which are absent in this case.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003ERetinopathy of prematurity develops later in premature infants, particularly those exposed to supplemental oxygen, and does not manifest as dot and blot hemorrhages immediately after birth.\u0026nbsp;\u003Cimg src=\u0022/upload-2025-12-03-9b97bc91-98b1-4319-b6c2-4c4836e3bce8.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003Ehttps://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/non-accidental-trauma.htm\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 232,
    "Name": "DVLA Driving Standards",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003EAccording to UK law, which of these patients would NOT be\nlegally able to drive within their category?\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Correct Answer: C: A Group 1 driver who experienced a single episode of amaurosis fugax three weeks ago with no recurrence.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EDriving After a Cerebrovascular Event (DVLA Guidance)\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003EGroup 1 Drivers (Cars / Motorcycles\u003C/span\u003E)\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tMust stop driving for: 1 month [not 3 weeks] after a stroke or TIA.\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tMay resume driving if: Clinical recovery is satisfactory.\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tNotify DVLA?\no\tNot required unless neurological deficit persists beyond 1 month.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u2022\tMultiple TIAs within a short period:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp;o\tMust be attack-free for at least 3 months.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp;o\tDVLA must be notified.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u0026nbsp;Group 2 Drivers (Heavy goods vehicles / Buses)\u003C/span\u003E\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u2022\tLicense refused or revoked for: 1 year after stroke or TIA.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u2022\tRe-licensing possible if:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u0026nbsp; o\tNo residual deficits affecting safe driving.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u0026nbsp; o\tNo other significant risk factors.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-weight: bold;\u0022\u003EDefect affecting central area only (Esterman within 20 degree radius of fixation) for Group 1 car and motorcycle driving:\n\u003C/span\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003Ethe following are generally regarded as acceptable central loss\u003C/span\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\uF0A7\tscattered single missed points\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\uF0A7\ta single cluster of up to 3 adjoining points\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u0026nbsp;the following are generally regarded as unacceptable (\u2018significant\u2019) central loss:\u003C/span\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\uF0A7\ta cluster of 4 or more adjoining points that is either wholly or partly within the central 20\u00B0 area\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\uF0A7\tloss consisting of both a single cluster of 3 adjoining missed points up to and including 20\u00B0 from fixation, and any additional separate missed points within the central 20\u00B0 area\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\uF0A7\t any central loss that is an extension of hemianopia or quadrantanopia of size greater than 3 missed points.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhy Other Options Are Incorrect B: Controlled diplopia with a patch and good acuity is permitted for Group 1 driving.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EA: a cluster of 4 or more adjoining points that is either wholly or partly within the central 20\u00B0 area is considered unacceptable.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ED: A Group 2 driver with \u002B6.00 D correction and acuity of 6/6 and 6/12 meets DVLA standards because the prescription is within \u002B8.00 D and acuity thresholds are satisfied.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EReference:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003EDVLA Visual Disorders: Assessing Fitness to Drive \u2013 GOV.UK: https://www.gov.uk/guidance/visual-disorders-assessing-fitness-to-drive\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 233,
    "Name": "Stargardt Disease",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003EA 10-year-old girl presents with a recent history of\nproblems seeing at distance. She has 6/18 vision in both eyes, a normal\nrefraction, and subtle scattered sub-macular deposits. What is the MOST likely\ndiagnosis?\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "Correct Answer: D: Stargardt disease.\u0026nbsp;\u003Cdiv\u003EStargardt disease is the most common juvenile macular dystrophy, typically presenting in childhood or adolescence with progressive bilateral central vision loss. The hallmark features include normal refraction despite reduced visual acuity and the presence of subtle yellowish-white flecks or deposits at the posterior pole, often described as fundus flavimaculatus. Visual acuity of 6/18 in both eyes with normal refraction strongly supports a macular pathology rather than a refractive error. Stargardt disease is caused by mutations in the ABCA4 gene, leading to accumulation of lipofuscin in the retinal pigment epithelium.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EWhy Other Options Are Incorrect: A: Cone dystrophy: Usually presents with photophobia, color vision defects, and progressive loss of central vision, but the fundus changes differ and often include bull\u2019s-eye maculopathy rather than scattered flecks.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EB:Dominant drusen: Typically occurs later in life and is associated with drusen deposits in the macula and peripapillary region, not subtle flecks in a child.\u003C/div\u003E\u003Cdiv\u003EC: Fundus albipunctatus: Characterized by numerous small white dots throughout the retina and associated with night blindness, not isolated macular deposits or central vision loss in a child.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EClinical Pearls:\nMnemonic: \u2018Stargardt = Star flecks in macula\u2019 \u2192 Think of yellowish flecks and central vision loss in children.\nVisual acuity reduction with normal refraction in a child should raise suspicion for macular dystrophy.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EList of images:\u003C/div\u003E\u003Cdiv\u003E1-Stargard dystrophy.(https://webeye.ophth.uiowa.edu/eyeforum/atlas/photos/stargardt-13-OD.jpg )\u003C/div\u003E\u003Cdiv\u003E2-Cone dystrophy.(https://www.eyerounds.org/atlas/pages/cone-rod-dystrophy.htm)\u003C/div\u003E\u003Cdiv\u003E3-Dominant drusen (https://imagebank.asrs.org/file/26145/familial-dominant-drusen)\u003C/div\u003E\u003Cdiv\u003E4-Fundus albipunctatus. (https://endeavors.unc.edu/win2005/retina.php).\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-03-db982fba-e53a-4843-97ab-f97d51f78433.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2025-12-03-e34d7768-6e91-4c89-a33d-00df6e8bdbe2.jpg\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-79eb382f-fa94-4d35-888a-8177771ead5e.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-03-00e73f90-7e8e-443a-a8b2-6b6f5a2e66fb.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 234,
    "Name": "Dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EHistological examination of a corneal button demonstrates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongo red\u2013positive deposits within the corneal stroma\u003C/b\u003E\u003C/span\u003E.\u0026nbsp;\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongo red positivity\u003C/b\u003E\u003C/span\u003E indicates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eamyloid deposition\u003C/b\u003E\u003C/span\u003E, which is the hallmark histopathological feature of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elattice corneal dystrophy\u003C/b\u003E\u003C/span\u003E. The amyloid accumulates within the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal stroma\u003C/b\u003E\u003C/span\u003E, producing the characteristic branching, lattice-like lines seen clinically.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMacular corneal dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 stromal deposition of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eglycosaminoglycans\u003C/b\u003E\u003C/span\u003E (alcian blue\u2013positive)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGranular corneal dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyaline\u003C/b\u003E\u003C/span\u003E deposits (Masson trichrome\u2013positive)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReis\u2013B\u00FCcklers dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 fibrous replacement of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBowman\u2019s layer\u003C/b\u003E\u003C/span\u003E, not amyloid\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 235,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements about Acanthamoeba is TRUE?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EAcanthamoeba\u003C/i\u003E species are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efree-living protozoa\u003C/b\u003E\u003C/span\u003E widely distributed in the environment, including \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esoil, dust, air, freshwater, seawater, and swimming pools\u003C/b\u003E\u003C/span\u003E. Growth in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egarden soil\u003C/b\u003E\u003C/span\u003E is well recognised and underpins environmental exposure risk.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other statements are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EAcanthamoeba\u003C/i\u003E is \u003C/span\u003E\u003Cb\u003Enot easy to culture\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E; it requires \u003C/span\u003E\u003Cb\u003Enon-nutrient agar seeded with E. coli\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrophozoite\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eactive, replicating form\u003C/b\u003E\u003C/span\u003E, while the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecyst\u003C/b\u003E\u003C/span\u003E is the dormant, resistant stage.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe organism is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereadily identifiable on microscopy\u003C/b\u003E\u003C/span\u003E (especially cysts with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edouble-walled structure\u003C/b\u003E\u003C/span\u003E) using corneal scrapings, confocal microscopy, or histology.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
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  },
  {
    "Id": 236,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements about Candida species is FALSE?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ECandida\u003C/i\u003E species are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyeasts\u003C/b\u003E\u003C/span\u003E that have well-defined staining and culture characteristics:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPAS and GMS positive\u003C/b\u003E\u003C/span\u003E \u2192 highlights fungal cell walls\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGram-positive\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Ecalcofluor-white positive\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 binds to chitin and cellulose\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOptimal growth on Sabouraud dextrose agar\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, though growth also occurs on blood agar\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EHowever, \u003C/span\u003E\u003Cb\u003Emacroscopic colonies of Candida are typically creamy white\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E on agar.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EYellow-green colonies\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E are characteristic of \u003C/span\u003E\u003Cb\u003EAspergillus flavus\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, not \u003Ci\u003ECandida\u003C/i\u003E.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 237,
    "Name": "Conjunctival lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA man from \u003Cspan class=\u0022s1\u0022\u003EBotswana\u003C/span\u003E presents with a \u003Cspan class=\u0022s1\u0022\u003Ehaemorrhagic conjunctival lesion\u003C/span\u003E in the right eye.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKaposi sarcoma\u003C/b\u003E\u003C/span\u003E is strongly associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHIV infection\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHHV-8\u003C/b\u003E\u003C/span\u003E, and is particularly prevalent in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esub-Saharan Africa\u003C/b\u003E\u003C/span\u003E, including Botswana. Ocular involvement commonly presents as a:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERed\u2013purple or haemorrhagic conjunctival mass\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHighly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evascular\u003C/b\u003E\u003C/span\u003E, often mistaken for subconjunctival haemorrhage\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFrequently involves the \u003C/span\u003E\u003Cb\u003Einferior fornix or bulbar conjunctiva\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EConjunctival melanoma\u003C/b\u003E\u003C/span\u003E typically appears as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epigmented\u003C/b\u003E\u003C/span\u003E, non-haemorrhagic lesion.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConjunctival squamous cell carcinoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E presents as a \u003C/span\u003E\u003Cb\u003Efleshy, leukoplakic limbal mass\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often linked to UV exposure and HIV, but is \u003C/span\u003E\u003Cb\u003Enot typically haemorrhagic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn a patient from an HIV-endemic region with a haemorrhagic conjunctival lesion, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKaposi sarcoma is the most likely diagnosis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 238,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following antibiotics is least effective against Pseudomonas aeruginosa keratitis?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EPseudomonas aeruginosa\u003C/i\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGram-negative, aerobic organism\u003C/b\u003E\u003C/span\u003E with intrinsic resistance to several antibiotics.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChloramphenicol\u003C/b\u003E\u003C/span\u003E has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor activity against Pseudomonas\u003C/b\u003E\u003C/span\u003E and is therefore ineffective for pseudomonal keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGentamicin\u003C/b\u003E\u003C/span\u003E (aminoglycoside) has good anti-pseudomonal activity and is commonly used in severe keratitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOfloxacin\u003C/b\u003E\u003C/span\u003E (fluoroquinolone) provides effective Gram-negative coverage, including \u003Ci\u003EPseudomonas\u003C/i\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECefuroxime\u003C/b\u003E\u003C/span\u003E (a second-generation cephalosporin) has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elimited activity\u003C/b\u003E\u003C/span\u003E against \u003Ci\u003EPseudomonas\u003C/i\u003E, but still offers \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore coverage than chloramphenicol\u003C/b\u003E\u003C/span\u003E, which has essentially none.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThus, \u003C/span\u003E\u003Cb\u003Echloramphenicol\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E is the \u003C/span\u003E\u003Cb\u003Eleast effective\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E option.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 239,
    "Name": "Infectious Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the approximate \u003C/span\u003Epercentage reduction in recurrence of stromal herpes simplex keratitis (HSK)\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E6 months of oral acyclovir prophylaxis\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003EHerpetic Eye Disease Study II (HEDS II)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E demonstrated that \u003C/span\u003E\u003Cb\u003Eoral acyclovir 400 mg twice daily for 6 months\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E significantly reduces recurrences of ocular HSV disease.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EKey findings:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOverall ocular HSV recurrence:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E reduced by ~\u003C/span\u003E\u003Cb\u003E45%\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAcyclovir group: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E18%\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPlacebo group: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E30%\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStromal keratitis recurrence:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E14%\u003C/b\u003E\u003C/span\u003E with acyclovir vs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E28%\u003C/b\u003E\u003C/span\u003E with placebo \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~50% reduction\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEpithelial keratitis recurrence:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E9% vs 14% (modest reduction)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGreatest benefit\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E seen in patients with \u003C/span\u003E\u003Cb\u003Emultiple prior episodes\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo additional benefit\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E when oral acyclovir was added to \u003C/span\u003E\u003Cb\u003Etopical trifluridine\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EEffect consistent across \u003C/span\u003E\u003Cb\u003Eage, sex, and time since last episode\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThus, for stromal HSK, oral acyclovir halves the recurrence risk, making \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003E~50% reduction\u003C/b\u003E\u003C/span\u003E the best answer.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 240,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 14-year-old boy is noted to have \u003C/span\u003Escattered punctate white flecks at the left fovea\u003Cspan class=\u0022s1\u0022\u003E and a \u003C/span\u003Esub-foveal elevation in the right eye\u003Cspan class=\u0022s1\u0022\u003E. His father has similar ocular findings.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe clinical picture is characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBest vitelliform macular dystrophy\u003C/b\u003E\u003C/span\u003E, an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E condition caused by mutations in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBEST1\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey supporting features:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOnset in childhood or adolescence\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESub-foveal vitelliform (\u201Cegg-yolk\u201D) lesion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which may fragment into \u003C/span\u003E\u003Cb\u003Epunctate white flecks\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E as it evolves\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPositive family history\u003C/b\u003E\u003C/span\u003E consistent with autosomal dominant inheritance\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften, there is\u0026nbsp;\u003C/span\u003E\u003Cb\u003Erelatively preserved visual acuity early on\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, despite striking fundus changes\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEOG (reduced Arden ratio) is classically abnormal, even when VA is good.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhy the other options are less likely:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAutosomal dominant drusen\u003C/b\u003E\u003C/span\u003E \u2192 typically later onset, with radial drusen around the disc (\u201Choneycomb\u201D pattern)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFundus flavimaculatus\u003C/b\u003E\u003C/span\u003E \u2192 a form of Stargardt disease, usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal recessive\u003C/b\u003E\u003C/span\u003E, with widespread pisciform flecks\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENorth Carolina macular dystrophy\u003C/b\u003E\u003C/span\u003E \u2192 congenital, non-progressive, often present from birth rather than adolescence\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 241,
    "Name": "Retinal Detachment",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 64-year-old myopic woman presents with \u003Cspan class=\u0022s1\u0022\u003Esudden-onset flashes and floaters\u003C/span\u003E. The optician notes the presence of \u003Cspan class=\u0022s1\u0022\u003Etobacco dust\u003C/span\u003E in the vitreous.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETobacco dust\u003C/b\u003E\u003C/span\u003E (Shafer\u2019s sign) represents \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epigment cells in the vitreous\u003C/b\u003E\u003C/span\u003E, released from the retinal pigment epithelium. In the context of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute flashes and floaters\u003C/b\u003E\u003C/span\u003E, this finding is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehighly predictive of a retinal break\u003C/b\u003E\u003C/span\u003E and should be considered a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal tear until proven otherwise\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey points:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinal tears commonly occur following \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior vitreous detachment\u003C/b\u003E\u003C/span\u003E, especially in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopes\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erhegmatogenous retinal detachment\u003C/b\u003E\u003C/span\u003E may develop subsequently, but in the absence of a peripheral field defect or curtain-like visual loss, a tear is more likely at presentation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMigraine causes transient visual phenomena without vitreous pigment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinal vein occlusion presents with painless visual loss and fundoscopic haemorrhages, not flashes or tobacco dust.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EVideo showing Shafer\u0027s sign:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.youtube.com/watch?v=JHZqmlyVLW4\u0022 style=\u0022color: rgb(0, 29, 255);\u0022\u003ESchaffer\u2019 sign / Tobacco dust sign - Pigments in anterior Vitreous\u003C/a\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 242,
    "Name": "Viral retinitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhat is the most appropriate treatment for peripheral cytomegalovirus (CMV) retinitis?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOral ganciclovir,\u0026nbsp;\u003C/b\u003E\u003C/span\u003Emost commonly given as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evalganciclovir,\u0026nbsp;\u003C/b\u003E\u003C/span\u003Eis the preferred \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esystemic oral therapy\u003C/b\u003E\u003C/span\u003E for CMV retinitis, particularly when disease is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral and non-sight-threatening\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey points:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGanciclovir/valganciclovir\u003C/b\u003E\u003C/span\u003E are active against CMV and achieve adequate intraocular levels.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFoscarnet\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E has anti-CMV activity but is \u003C/span\u003E\u003Cb\u003Enot available orally\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E; it is given \u003C/span\u003E\u003Cb\u003Eintravenously or intravitreally\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EValacyclovir\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacyclovir\u003C/b\u003E\u003C/span\u003E are ineffective against CMV due to lack of viral thymidine kinase activity.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 243,
    "Name": "PCV",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ERegarding \u003C/span\u003Eidiopathic polypoidal choroidal vasculopathy (PCV)\u003Cspan class=\u0022s1\u0022\u003E, which of the following statements is \u003C/span\u003ETRUE\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPCV is an idiopathic choroidal vasculopathy characterised clinically by \u003C/span\u003E\u003Cb\u003Eserous pigment epithelial detachments (PEDs)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often associated with \u003C/span\u003E\u003Cb\u003Esubretinal fluid and recurrent subretinal or sub-RPE haemorrhage\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIndocyanine green angiography (ICG)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is diagnostic and shows:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebranching vascular network\u003C/b\u003E\u003C/span\u003E at the level of the choriocapillaris\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPolypoidal (aneurysmal) dilatations\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E at terminal vessels\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ELesions that \u003C/span\u003E\u003Cb\u003Efill slowly and then leak intensely\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EThe other statements are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERisk is increased in Asian populations\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not Scandinavian ancestry.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EICG does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E show occluded vessels; it demonstrates abnormal \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaneurysmal choroidal vasculature\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMacular involvement is most common\u003C/b\u003E\u003C/span\u003E; peripapillary lesions occur but account for only \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~20%\u003C/b\u003E\u003C/span\u003E of cases.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 244,
    "Name": "Stickler Syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements regarding Stickler syndrome is FALSE?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EStickler syndrome is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econnective tissue disorder\u003C/b\u003E\u003C/span\u003E most commonly inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E pattern. It is typically caused by mutations in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECOL2A1\u003C/b\u003E\u003C/span\u003E (type II collagen), though other collagen genes may also be involved.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey ophthalmic features include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigh congenital myopia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVitreoretinal degeneration\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigh risk of retinal detachment\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EStickler syndrome demonstrates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomplete penetrance\u003C/b\u003E\u003C/span\u003E, meaning affected individuals will show some features of the condition, but with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evariable expressivity\u003C/b\u003E\u003C/span\u003E, so the severity and combination of ocular, craniofacial, and musculoskeletal features can vary widely between individuals.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eincomplete penetrance\u003C/b\u003E\u003C/span\u003E is the false statement.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 245,
    "Name": "White Dot syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich of the following statements regarding punctate inner choroidopathy (PIC) is FALSE?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EPunctate inner choroidopathy is an inflammatory chorioretinal disorder that typically affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyoung myopic women\u003C/b\u003E\u003C/span\u003E. It presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emultiple small yellow-white lesions\u003C/b\u003E\u003C/span\u003E at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior pole\u003C/b\u003E\u003C/span\u003E, usually without significant anterior segment or vitreous inflammation.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EA key complication of PIC is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoroidal neovascularisation (CNV)\u003C/b\u003E\u003C/span\u003E, which develops in a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubstantial proportion of patients up to 30-40%\u003C/b\u003E\u003C/span\u003E in published series. CNV is a major cause of visual loss in PIC and often requires anti-VEGF therapy.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, the statement that CNV develops in only \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5%\u003C/b\u003E\u003C/span\u003E of patients is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efalse\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 246,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient presents with \u003C/span\u003Epigmentary retinopathy\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Eanosmia\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003Eataxia\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich dietary component is most likely responsible for this clinical picture?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis constellation of features is characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERefsum disease\u003C/b\u003E\u003C/span\u003E, a rare \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal recessive inborn error of metabolism\u003C/b\u003E\u003C/span\u003E caused by deficiency of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephytanic acid \u03B1-hydroxylase (PHYH)\u003C/b\u003E\u003C/span\u003E. The defect leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaccumulation of phytanic acid\u003C/b\u003E\u003C/span\u003E, a branched-chain fatty acid derived from the diet.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ETypical features include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPigmentary retinopathy\u003C/b\u003E\u003C/span\u003E (often presenting like retinitis pigmentosa)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPeripheral neuropathy and cerebellar ataxia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAnosmia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESensorineural deafness\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECardiomyopathy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIchthyosis\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EManagement includes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eplasmapheresis\u003C/b\u003E\u003C/span\u003E in acute settings and long-term adherence to a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephytanic-acid-restricted diet\u003C/b\u003E\u003C/span\u003E (avoiding dairy fat, ruminant meat, and certain fish).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBeta-lipoprotein deficiency\u003C/b\u003E\u003C/span\u003E \u2192 abetalipoproteinaemia (acanthocytosis, fat malabsorption)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECopper\u003C/b\u003E\u003C/span\u003E \u2192 Wilson disease (Kayser-Fleischer rings, hepatic and neurological disease)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EZinc\u003C/b\u003E\u003C/span\u003E \u2192 no such retinoneurological syndrome\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 247,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the pattern of inheritance of \u003Cspan class=\u0022s1\u0022\u003ELeber\u2019s congenital amaurosis (LCA)\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeber\u2019s congenital amaurosis\u003C/b\u003E\u003C/span\u003E is a group of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esevere, early-onset retinal dystrophies\u003C/b\u003E\u003C/span\u003E presenting in infancy with profound visual impairment, nystagmus, and markedly reduced or absent ERG responses. The condition is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost commonly inherited in an autosomal recessive pattern\u003C/b\u003E\u003C/span\u003E, with mutations identified in multiple genes (e.g. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERPE65, CEP290, GUCY2D\u003C/b\u003E\u003C/span\u003E).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is important not to confuse this with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeber hereditary optic neuropathy (LHON)\u003C/b\u003E\u003C/span\u003E, which affects young adults and is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emitochondrially inherited\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003ERemember:\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELCA \u2192 autosomal recessive retinal dystrophy (infancy)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELHON \u2192 mitochondrial optic neuropathy (young adults)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 248,
    "Name": "White Dot syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn \u003C/span\u003Ebirdshot chorioretinopathy\u003Cspan class=\u0022s1\u0022\u003E, which of the following \u003C/span\u003EERG findings is LEAST likely\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EERG abnormalities in \u003C/span\u003E\u003Cb\u003Ebirdshot chorioretinopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E closely \u003C/span\u003E\u003Cb\u003Ecorrelate with disease severity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and are central to both \u003C/span\u003E\u003Cb\u003Emonitoring progression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Eguiding immunosuppressive therapy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ETypical ERG features include:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EReduced b-wave amplitude\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EReduced oscillatory potentials\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EProlonged implicit time of 30-Hz flicker;\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u0026nbsp;the \u003C/span\u003E\u003Cb\u003Emost sensitive and earliest abnormality\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn \u003C/span\u003E\u003Cb\u003Eearly disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the ERG may be \u003C/span\u003E\u003Cb\u003Enormal or only subtly abnormal\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EHowever, in \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Esevere disease\u003C/b\u003E\u003C/span\u003E, the ERG is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eclearly abnormal\u003C/b\u003E\u003C/span\u003E, not equivocal.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ETherefore, an \u003Ci\u003Eequivocal ERG in severe disease\u003C/i\u003E is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eleast likely\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003ERemember:\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBirdshot = HLA-A29 \u002B ERG-driven management\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E30-Hz flicker implicit time delay is the earliest and most sensitive ERG change\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 249,
    "Name": "Birdshot Chorioretinopathy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich description best fits the fundus appearance of \u003Cspan class=\u0022s1\u0022\u003Ebirdshot chorioretinopathy\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EBirdshot chorioretinopathy is characterised by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emultiple, cream-coloured or hypopigmented choroidal lesions\u003C/b\u003E\u003C/span\u003E, classically described as \u003Ci\u003E\u201Cbirdshot from a shotgun.\u201D\u003C/i\u003E These lesions:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAre \u003C/span\u003E\u003Cb\u003Eoval and ill-defined\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAre distributed \u003C/span\u003E\u003Cb\u003Ebetween the equator and mid-periphery\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETypically \u003C/span\u003E\u003Cb\u003Espare the fovea early\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBecome more visible over time as inflammation evolves\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022https://img1.wsimg.com/isteam/ip/d4b6c44c-e4e5-4e6a-b1c1-812b3ccb5a4d/c7805637-42f3-403d-a1ef-44ff4102b0ae.jpg/:/cr=t:0%25,l:0%25,w:100%25,h:100%25/rs=w:400,cg:true\u0022\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFoveal atrophic spots\u003C/b\u003E\u003C/span\u003E suggest macular dystrophies or advanced inflammatory disease\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPigmented mid-peripheral lesions\u003C/b\u003E\u003C/span\u003E are more typical of healed chorioretinitis (e.g. toxoplasmosis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripapillary atrophy\u003C/b\u003E\u003C/span\u003E is non-specific and not diagnostic of birdshot\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003ERemember:\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBirdshot = cream-coloured hypopigmented lesions in the mid-peripheral fundus \u002B HLA-A29 \u002B ERG abnormalities.\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 250,
    "Name": "Lattice retinal degeneration",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 60-year-old moderate myope presents with a \u003Cspan class=\u0022s1\u0022\u003E1-week history of flashes and floaters\u003C/span\u003E. Examination reveals a \u003Cspan class=\u0022s1\u0022\u003Epartial posterior vitreous detachment\u003C/span\u003E. The retina is flat with \u003Cspan class=\u0022s1\u0022\u003Eno retinal breaks\u003C/span\u003E, but an area of \u003Cspan class=\u0022s1\u0022\u003Elattice degeneration\u003C/span\u003E is noted in the superotemporal periphery.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most appropriate management?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELattice degeneration\u003C/b\u003E\u003C/span\u003E is a recognised \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erisk factor\u003C/b\u003E\u003C/span\u003E for rhegmatogenous retinal detachment, particularly in myopic eyes. However, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ein the absence of an associated retinal tear or hole\u003C/b\u003E\u003C/span\u003E, prophylactic treatment is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot indicated\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey points:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMost patients with lattice degeneration \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enever develop retinal detachment\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEvidence does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot support prophylactic laser or cryotherapy\u003C/b\u003E\u003C/span\u003E for asymptomatic lattice without breaks.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUnnecessary treatment carries risks, including iatrogenic breaks and scarring.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAppropriate management is:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReassurance and education\u003C/b\u003E\u003C/span\u003E about warning symptoms (new flashes, floaters, curtain-like vision loss)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPrompt re-examination\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E if symptoms worsen\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThus, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eobservation alone\u003C/b\u003E\u003C/span\u003E is the correct approach.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 251,
    "Name": "Electrophysiology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich condition is most likely to produce an inverted (negative) ERG on electrophysiological testing?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA \u003C/span\u003E\u003Cb\u003Enegative (inverted) ERG\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is characterised by a \u003C/span\u003E\u003Cb\u003Erelatively preserved a-wave\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with a \u003C/span\u003E\u003Cb\u003Emarkedly reduced b-wave\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, indicating dysfunction \u003C/span\u003E\u003Cb\u003Epost-photoreceptor\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, most commonly at the \u003C/span\u003E\u003Cb\u003Ebipolar cell level\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThis pattern is classically seen in conditions that disrupt signal transmission between \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ephotoreceptors and bipolar cells\u003C/b\u003E\u003C/span\u003E, including:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECongenital stationary night blindness (CSNB)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EX-linked retinoschisis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECentral retinal artery or vein occlusion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (acute setting)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EMelanoma Associated Retinopathy\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EQuinine toxicity\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBirdshot Chorioretinopathy\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThe other options are less likely:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinitis pigmentosa\u003C/b\u003E\u003C/span\u003E \u2192 both a- and b-waves are reduced\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeber\u2019s congenital amaurosis\u003C/b\u003E\u003C/span\u003E \u2192 severely reduced or absent ERG overall\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBest disease\u003C/b\u003E\u003C/span\u003E \u2192 full-field ERG is typically normal (EOG is abnormal)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cimg src=\u0022/upload-2025-12-14-e059aed0-41ab-46da-8b81-ddb164577cf0.png\u0022\u003E\u003C/h3\u003E\u003Cdiv\u003E*Table from Oxford Handbook for Ophthalmology\u003C/div\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003Ch3\u003ERemember:\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENegative ERG = intact photoreceptors, impaired bipolar cell function [inner retina]\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 252,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient is found to have \u003C/span\u003Einferotemporal retinoschisis\u003Cspan class=\u0022s1\u0022\u003E with associated \u003C/span\u003Emacular pigmentary changes\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003Emode of inheritance\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E of this condition?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis clinical picture is characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked retinoschisis (XLRS)\u003C/b\u003E\u003C/span\u003E, caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERS1 gene\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey features supporting the diagnosis:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInferotemporal peripheral retinoschisis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (classical location)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMacular involvement\u003C/b\u003E\u003C/span\u003E with pigmentary change or spoke-wheel pattern\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPredominantly affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emales\u003C/b\u003E\u003C/span\u003E, with female carriers usually asymptomatic\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften associated with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enegative ERG\u003C/b\u003E\u003C/span\u003E (reduced b-wave)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EXLRS is therefore inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked recessive\u003C/b\u003E\u003C/span\u003E pattern.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-14-0c38da5a-cf8f-4a93-8400-e328c2699143.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: small; font-style: italic;\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: Montserrat, Arial, sans-serif; letter-spacing: normal;\u0022\u003ECXLRS remains a clinical diagnosis. Affected males typically have characteristic foveal schisis (\u003C/span\u003E\u003Ca class=\u0022figure-link\u0022 href=\u0022https://www.asrs.org/content/images/cms/congenital_x_linked_retinoschisis_fig_1.png\u0022 title=\u0022\nFigure 1.\n\u0022 style=\u0022border-style: initial; border-color: initial; border-image: initial; font-family: Montserrat, Arial, sans-serif; outline: 0px; vertical-align: baseline; color: rgba(0, 69, 170, 0.5); transition: 0.1s ease-in-out; letter-spacing: normal;\u0022\u003EFigure 1\u003C/a\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: Montserrat, Arial, sans-serif; letter-spacing: normal;\u0022\u003E). The peripheral retina also may be involved (\u003C/span\u003E\u003Ca class=\u0022figure-link\u0022 href=\u0022https://www.asrs.org/content/images/cms/congenital_x_linked_retinoschisis_fig_2.png\u0022 title=\u0022\nFigure 2.\n\u0022 style=\u0022border-style: initial; border-color: initial; border-image: initial; font-family: Montserrat, Arial, sans-serif; outline: 0px; vertical-align: baseline; color: rgba(0, 69, 170, 0.5); transition: 0.1s ease-in-out; letter-spacing: normal;\u0022\u003EFigure 2\u003C/a\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: Montserrat, Arial, sans-serif; letter-spacing: normal;\u0022\u003E), with splitting of the retinal layers resulting in a blister-like elevation of the lower part of the retina. In severe cases retinal detachment may occur. CXLRS typically affects both eyes, although often not to the same degree.\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EImage and comment source:\u0026nbsp;\u003Ca href=\u0022https://www.asrs.org/patients/retinal-diseases/14/congenital-x-linked-retinoschisis\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ECongenital X-Linked Retinoschisis\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
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    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 253,
    "Name": "Retinal Detachment",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn which situation is \u003C/span\u003Edegenerative retinoschisis\u003Cspan class=\u0022s1\u0022\u003E most likely to progress to a \u003C/span\u003Erhegmatogenous retinal detachment\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDegenerative retinoschisis is usually a \u003C/span\u003E\u003Cb\u003Ebenign and stable condition\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Progression to a true \u003C/span\u003E\u003Cb\u003Eretinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E occurs \u003C/span\u003E\u003Cb\u003Eonly when there is a pathway for vitreous fluid to access the subretinal space\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThis requires:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebreak in the inner leaf\u003C/b\u003E\u003C/span\u003E \u2192 allows vitreous to enter the schisis cavity\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebreak in the outer leaf\u003C/b\u003E\u003C/span\u003E \u2192 allows fluid to pass into the subretinal space\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EWhen \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eboth layers are breached\u003C/b\u003E\u003C/span\u003E, fluid can move from the vitreous cavity to the subretinal space, producing a \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Erhegmatogenous retinal detachment\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EIsolated inner- or outer-leaf breaks \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Ealone\u003C/b\u003E\u003C/span\u003E are insufficient to cause detachment.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-14-f460f1a2-87ae-48cd-aa6b-0c342f880908.jpg\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Ca href=\u0022https://www.vrsurgeryonline.com/13-rhegmatogenous-retinal-detachment-special-scenarios/03-retinoschisis-retinal-detachment/\u0022\u003EA Large Outer Retinal Hole Leading to a Detachment in an Underlying Retinoschisis\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-14-3ba5bae5-4df5-4058-a408-357d70e10c2c.jpeg\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Ca href=\u0022https://www.vrsurgeryonline.com/13-rhegmatogenous-retinal-detachment-special-scenarios/03-retinoschisis-retinal-detachment/\u0022\u003EAn OCT image of the Tear with Underlying Schisis\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003EImages source:\u0026nbsp;\u003Ca href=\u0022https://www.vrsurgeryonline.com/13-rhegmatogenous-retinal-detachment-special-scenarios/03-retinoschisis-retinal-detachment/\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EVitreoretinal Surgery Online\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003ERemember:\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinoschisis \u002B inner \u0026amp; outer leaf breaks = true retinal detachment risk.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEither break alone = usually stable, observe.\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 254,
    "Name": "Macular Hole",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following factors is \u003Cspan class=\u0022s1\u0022\u003ELEAST important\u003C/span\u003E for successful \u003Cspan class=\u0022s1\u0022\u003Emacular hole surgery\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe key determinants of macular hole closure are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esurgical\u003C/b\u003E\u003C/span\u003E, not positional:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitrectomy\u003C/b\u003E\u003C/span\u003E removes anteroposterior vitreomacular traction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EILM peeling\u003C/b\u003E\u003C/span\u003E eliminates tangential traction and reduces reopening rates.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGas tamponade\u003C/b\u003E\u003C/span\u003E provides a temporary scaffold promoting hole apposition and closure.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe role of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposturing\u003C/b\u003E\u003C/span\u003E (face-down positioning) is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emuch less critical\u003C/b\u003E\u003C/span\u003E. Multiple randomised trials and meta-analyses show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh closure rates even with limited or no posturing\u003C/b\u003E\u003C/span\u003E, particularly for small-to-medium full-thickness macular holes.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile some surgeons still recommend short-term posturing in selected cases (e.g. large holes), it is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethe least important factor\u003C/b\u003E\u003C/span\u003E among those listed.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EFurther reading:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Ca href=\u0022https://pmc.ncbi.nlm.nih.gov/articles/PMC7852599/\u0022\u003EFactors affecting anatomical and visual outcome after macular hole surgery: findings from a large prospective UK cohort\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ED H Steel 1,2,, P H J Donachie 3, G W Aylward 4, D A Laidlaw 5, T H Williamson 5, D Yorston 6; the BEAVRS Macular hole outcome group\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
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  },
  {
    "Id": 255,
    "Name": "Optic disc anomalies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003Epresents with \u003C/span\u003Egradual visual deterioration\u003Cspan class=\u0022s1\u0022\u003E in the right eye. On examination, Visual acuity is \u003C/span\u003ELogMAR 0.3 (right)\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003ELogMAR 0.0 (left)\u003Cspan class=\u0022s1\u0022\u003E. Fundus examination shows bilateral optic disc pits. OCT shows \u003C/span\u003Efoveal schisis with associated subretinal fluid\u003Cspan class=\u0022s1\u0022\u003E in the right eye, while the left eye is normal.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most appropriate initial treatment?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis presentation is typical of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic disc pit maculopathy\u003C/b\u003E\u003C/span\u003E, where fluid from the optic pit tracks into the inner retina, causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinoschisis and/or serous macular detachment\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInitial management\u003C/b\u003E\u003C/span\u003E is generally \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econservative or minimally invasive\u003C/b\u003E\u003C/span\u003E, particularly when visual acuity is relatively preserved. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELaser photocoagulation\u003C/b\u003E\u003C/span\u003E applied in one or more light rows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebetween the optic disc and the macular detachment\u003C/b\u003E\u003C/span\u003E aims to create a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echorioretinal adhesion\u003C/b\u003E\u003C/span\u003E, forming a barrier that limits further fluid migration from the pit into the macula.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EUnfortunately, Laser photocoagulation therapy has not had much success in most studies, patients treated did not notice improvement, in fact some reported more visual disturbance after the treatment\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold; text-decoration-line: underline;\u0022\u003EMore invasive options:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVitrectomy with gas tamponade\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (\u00B1 ILM peel) is reserved for \u003C/span\u003E\u003Cb\u003Epersistent or progressive cases\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EStudies have shown promising long-term results in both retinal re-attachments (50-95% of patients) and visual improvement(\u0026gt;50% of patients).\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px;\u0022\u003ESeveral studies have demonstrated high success rates using \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eintravitreal gas tamponade\u003C/span\u003E\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, with or without barrier laser applied to the temporal disc margin. These approaches achieved fluid resolution in approximately 50\u201375% of cases, with corresponding significant visual improvement. However, recurrence is common, and repeat gas injections are frequently required to maintain anatomical success\u003C/span\u003E\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EPDT\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E and \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Eintravitreal steroids\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E have \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Eno established role\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E in optic disc pit maculopathy.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EIn Summary:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003EGiven that this patient has optic disc pit-associated maculopathy with schisis and subretinal fluid, laser photocoagulation at the temporal disc edge remains the least invasive and most appropriate initial treatment, with escalation to vitrectomy or gas tamponade if needed.\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EPrognosis:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cul\u003E\u003Cli\u003EIf optic disc pit maculopathy develops, approximately 80% of patients progress to a visual acuity of LogMAR 1.00 or worse.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EIn the absence of treatment, visual decline typically occurs within six months.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EIn contrast, surgical intervention has been associated with favourable anatomical and functional outcomes, with recent studies reporting success rates of up to 87%.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ESource:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://eyewiki.org/Optic_Pits\u0022\u003EEyeWiki - Optic disc pits\u003C/a\u003E\u003C/div\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 256,
    "Name": "AMD",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following genes is associated with an \u003C/span\u003Eincreased risk of age related macular degeneration (AMD)\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EAge-related macular degeneration has a strong \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egenetic component\u003C/b\u003E\u003C/span\u003E, with many risk variants involving the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomplement pathway\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECFH (Complement Factor H) gene\u003C/b\u003E\u003C/span\u003E, particularly the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EY402H polymorphism\u003C/b\u003E\u003C/span\u003E, is one of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Estrongest and most consistently replicated genetic risk factors\u003C/b\u003E\u003C/span\u003E for AMD. CFH plays a regulatory role in the alternative complement pathway, and dysfunction leads to chronic inflammation at the level of the retinal pigment epithelium and Bruch\u2019s membrane.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; text-decoration-line: underline;\u0022\u003EOther important AMD-associated loci include:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EARMS2/HTRA1\u003C/b\u003E\u003C/span\u003E on chromosome 10\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC3, CFB, CFI\u003C/b\u003E\u003C/span\u003E (additional complement pathway genes)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cspan style=\u0022font-family: Arial; text-decoration-line: underline;\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022\u0022\u003EThe \u003C/span\u003E\u003Cb style=\u0022\u0022\u003EBCSC\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022\u0022\u003E identifies two key \u003C/span\u003E\u003Cb style=\u0022\u0022\u003Egenetic susceptibility loci\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022\u0022\u003E associated with the development of \u003C/span\u003E\u003Cb style=\u0022\u0022\u003Eage-related macular degeneration (AMD)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022\u0022\u003E:\u003C/span\u003E\u003C/span\u003E\u003Cspan style=\u0022font-family: Arial;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cbr\u003E\u003Cul\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003ECFH (chromosome 1q31)\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E encodes \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003Ecomplement factor H\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E, a regulator of the alternative complement pathway. The \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003EY402H variant\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E increases AMD risk by approximately \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003E4.6-fold in heterozygotes\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E and \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003E7.4-fold in homozygotes\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003EARMS2 (chromosome 10q26)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E, short for \u003Ci\u003EAge-Related Maculopathy Susceptibility 2\u003C/i\u003E, has a gene product with incompletely understood function. The \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003EA69S variant\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E is associated with a \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E2.7-fold increase in AMD risk in heterozygotes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E and an \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E8.2-fold increase in homozygotes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px; font-family: Arial; color: rgb(14, 14, 14);\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cp class=\u0022p2\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003EIndividuals who are \u003C/span\u003E\u003Cb style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003Ehomozygous for risk variants in both CFH and ARMS2\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003E have a \u003C/span\u003E\u003Cb style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003Emarkedly elevated risk\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003E, estimated to be \u003C/span\u003E\u003Cb style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(255, 0, 0);\u0022\u003Eup to 50-fold higher\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022font-family: Arial; letter-spacing: 0.14994px; color: rgb(14, 14, 14);\u0022\u003E than the general population.\u003C/span\u003E\u003Cbr\u003E\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal;\u0022\u003E\u003Cspan style=\u0022font-family: Arial;\u0022\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EThe other options are incorrect:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPAX6\u003C/b\u003E\u003C/span\u003E \u2192 ocular development (aniridia)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECHM\u003C/b\u003E\u003C/span\u003E \u2192 choroideremia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETIGR (MYOC)\u003C/b\u003E\u003C/span\u003E \u2192 primary open-angle glaucoma\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 257,
    "Name": "Macular Hole",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 74-year-old woman undergoes vitrectomy for a \u003Cspan class=\u0022s1\u0022\u003Emacular hole\u003C/span\u003E but is unable to maintain prolonged postoperative posturing due to \u003Cspan class=\u0022s1\u0022\u003Eosteoarthritis\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat concentration of C3F8 gas is most appropriate to use?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPerfluoropropane (C3F8)\u003C/b\u003E\u003C/span\u003E is a long-acting intraocular gas that expands to approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efour times its injected volume\u003C/b\u003E\u003C/span\u003E when used at 100% concentration and can persist in the eye for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eup to 8 weeks\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor vitrectomy, a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-expansile concentration\u003C/b\u003E\u003C/span\u003E is required to avoid excessive postoperative IOP rise. The accepted non-expansile range for C3F8 is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E12-16% mixed with air\u003C/b\u003E\u003C/span\u003E, making \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E14%\u003C/b\u003E\u003C/span\u003E the appropriate choice.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn patients who struggle with posturing, a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elonger-acting gas\u003C/b\u003E\u003C/span\u003E such as C3F8 is preferred over SF6, as it provides \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprolonged tamponade\u003C/b\u003E\u003C/span\u003E despite limited positioning.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor comparison:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESF6\u003C/b\u003E\u003C/span\u003E doubles its volume within ~2 days, lasts ~2 weeks, and has a non-expansile concentration of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E20-30%\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ERemember:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tMacular hole \u002B poor posturing \u2192 choose long-acting gas (C3F8 12-16%).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u2022\tC3F8 = long duration; SF6 = shorter duration.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 258,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhich investigation most reliably establishes the diagnosis of Best vitelliform macular dystrophy?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBest vitelliform macular dystrophy\u003C/b\u003E\u003C/span\u003E is most reliably diagnosed using \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eelectro-oculography (EOG)\u003C/b\u003E\u003C/span\u003E. The hallmark finding is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereduced light peak-to-dark trough ratio (Arden ratio)\u003C/b\u003E\u003C/span\u003E, reflecting dysfunction of the retinal pigment epithelium.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey points:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEOG is abnormal even when visual acuity and fundus appearance are relatively preserved\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially early in the disease.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFull-field ERG is typically normal\u003C/b\u003E\u003C/span\u003E, as photoreceptor function is largely intact.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDark adaptation\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVEP\u003C/b\u003E\u003C/span\u003E are not diagnostic for Best disease.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 259,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ERegarding \u003Cspan class=\u0022s1\u0022\u003Efamilial exudative vitreoretinopathy (FEVR)\u003C/span\u003E, which of the following statements is \u003Cspan class=\u0022s1\u0022\u003EFALSE\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFEVR is a \u003C/span\u003E\u003Cb\u003Egenetically heterogeneous retinal vascular disorder\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E characterised by \u003C/span\u003E\u003Cb\u003Eincomplete peripheral retinal vascularisation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, most commonly affecting the \u003C/span\u003E\u003Cb\u003Etemporal retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. Recognised clinical features include \u003C/span\u003E\u003Cb\u003Eperipheral avascular retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Eneovascularisation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Eexudation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Etractional retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Edisc dragging\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EInheritance patterns in FEVR include:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAutosomal dominant\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (most common)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EX-linked recessive\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAutosomal recessive\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (less common)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ETherefore, describing FEVR as \u003Ci\u003Etypically autosomal recessive\u003C/i\u003E is incorrect.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EAdvanced disease often requires \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Evitreoretinal surgery\u003C/b\u003E\u003C/span\u003E, but outcomes are frequently limited due to severe tractional changes and chronic pathology, supporting the truth of the other statements.\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
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    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 260,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 12-year-old boy presents to clinic with \u003C/span\u003Ebilateral RPE mottling at the maculae\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Emoderate reduction in visual acuity to 6/12\u003Cspan class=\u0022s1\u0022\u003E in both eyes. Fluorescein angiography is shown below\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2025-12-14-02af7953-6b65-4905-8319-c7cf19056e61.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStargardt disease\u003C/b\u003E\u003C/span\u003E (ABCA4-related macular dystrophy) classically presents in childhood or adolescence with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral central visual loss\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERPE mottling\u003C/b\u003E\u003C/span\u003E at the macula.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe hallmark fluorescein angiographic finding is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cdark choroid\u201D\u003C/b\u003E\u003C/span\u003E, caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexcess lipofuscin accumulation within the RPE\u003C/b\u003E\u003C/span\u003E, which \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eblocks background choroidal fluorescence\u003C/b\u003E\u003C/span\u003E from the choriocapillaris.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cimg src=\u0022https://www.researchgate.net/profile/Rehan-Hussain-2/publication/327148232/figure/fig2/AS:717320766894080@1548034006397/Fluorescein-angiography-demonstrates-classic-dark-or-silent-choroid-due-to-masking-of.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EFluorescein angiography demonstrates classic dark or \u0027silent\u0027 choroid due to masking of choroidal fluorescence, with staining of the pisciform flecks.\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EImage source:\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003Ca href=\u0022https://www.tandfonline.com/doi/full/10.1080/14712598.2018.1513486?utm_source=researchgate.net\u0026amp;utm_medium=article\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EStargardt macular dystrophy and evolving therapies\u003C/a\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EThe other options are less likely:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBest disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 subfoveal lipofuscin deposition, but \u003C/span\u003E\u003Cb\u003Eno generalised loss of choroidal fluorescence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on FFA\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EChoroideraemia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Egyrate atrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 show \u003C/span\u003E\u003Cb\u003Etrue chorioretinal and choriocapillaris atrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, usually with \u003C/span\u003E\u003Cb\u003Eobvious mid-peripheral fundus changes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on examination, not isolated macular involvement at presentation\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 261,
    "Name": "Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following features is \u003Cspan class=\u0022s1\u0022\u003ELEAST consistent\u003C/span\u003E with \u003Cspan class=\u0022s1\u0022\u003Eretinoschisis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDegenerative (senile) retinoschisis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E typically occurs in \u003C/span\u003E\u003Cb\u003Eolder, emmetropic or mildly hypermetropic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E individuals and is \u003C/span\u003E\u003Cb\u003Enot strongly associated with high myopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. High myopia is much more closely linked to \u003C/span\u003E\u003Cb\u003Erhegmatogenous retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not retinoschisis.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThe other features are characteristic of retinoschisis:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBeaten-metal appearance\u003C/b\u003E\u003C/span\u003E reflects splitting of the inner retinal layers.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELesions are often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral\u003C/b\u003E\u003C/span\u003E and classically occur in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einferotemporal quadrant\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EAbsolute field defect\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 262,
    "Name": "FFA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following statements about \u003C/span\u003Efundus fluorescein angiography (FFA)\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003ELEAST true\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFFA\u003C/b\u003E\u003C/span\u003E, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoroidal circulation fills first\u003C/b\u003E\u003C/span\u003E, followed shortly by the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal arterial phase\u003C/b\u003E\u003C/span\u003E. This occurs because the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoriocapillaris is fenestrated\u003C/b\u003E\u003C/span\u003E, allowing rapid dye leakage and producing the characteristic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echoroidal flush\u003C/b\u003E\u003C/span\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ERegarding the other options:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EClassic CNV\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E typically shows \u003C/span\u003E\u003Cb\u003Eearly, well-defined hyperfluorescence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with progressive leakage.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOccult CNV\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E generally demonstrates \u003C/span\u003E\u003Cb\u003Epoorly defined early fluorescence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003E\u003Cb\u003Elate leakage\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIndocyanine green (ICG)\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~98% protein-bound\u003C/b\u003E\u003C/span\u003E, far more than fluorescein (~80%), making statement \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ED true\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": true,
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  },
  {
    "Id": 263,
    "Name": "Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following conditions is associated with an \u003Cspan class=\u0022s1\u0022\u003Eabsolute peripheral visual field defect\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinoschisis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E causes a \u003C/span\u003E\u003Cb\u003Etrue splitting of the neurosensory retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, resulting in \u003C/span\u003E\u003Cb\u003Eloss of functioning retinal tissue\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in the affected area. This produces an \u003C/span\u003E\u003Cb\u003Eabsolute scotoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on peripheral visual field testing.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EIn contrast:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGiant retinal tear\u003C/b\u003E\u003C/span\u003E may cause a field defect, but this depends on whether a retinal detachment is present and its extent; it is not intrinsically associated with a fixed absolute defect.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPaving stone degeneration\u003C/b\u003E\u003C/span\u003E involves outer retinal and choriocapillaris atrophy but typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not produce visual field loss\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESnail track degeneration\u003C/b\u003E\u003C/span\u003E is a peripheral vitreoretinal degeneration associated with retinal breaks, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not itself cause an absolute field defect\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb\u003ERemember:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinoschisis \u2192 absolute scotoma\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinal detachment \u2192 relative scotoma (unless chronic and extensive)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 264,
    "Name": "Vitreous",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EPatients are most likely to be \u003Cspan class=\u0022s1\u0022\u003Esymptomatic from vitreous floaters\u003C/span\u003E under which of the following conditions?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFloaters are perceived when \u003C/span\u003E\u003Cb\u003Evitreous opacities cast shadows on the retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. The degree of symptomatology depends on both the \u003C/span\u003E\u003Cb\u003Edistance of the opacity from the retina\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and the \u003C/span\u003E\u003Cb\u003Eeffective pupil size\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECloser opacities\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E produce \u003C/span\u003E\u003Cb\u003Esharper, more distinct shadows\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, making them more noticeable.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmaller pupil\u003C/b\u003E\u003C/span\u003E increases depth of focus and reduces light scatter, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eenhancing the contrast\u003C/b\u003E\u003C/span\u003E of the shadow cast by the opacity.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p4\u0022\u003EIn contrast, opacities that are \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Efarther from the retina\u003C/b\u003E\u003C/span\u003E or viewed through a \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Elarger pupil\u003C/b\u003E\u003C/span\u003E cast blurrier, less distinct shadows and are therefore less symptomatic.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-size: 25.054px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-size: 25.054px;\u0022\u003ERemember:\u003C/span\u003E\u003C/b\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECloser floater \u002B smaller pupil = more symptomatic.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis explains why floaters are often more noticeable in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebright light\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 265,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich statement about \u003C/span\u003Efamilial exudative vitreoretinopathy (FEVR)\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003ELEAST true\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFEVR is a \u003C/span\u003E\u003Cb\u003Egenetically heterogeneous disorder\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of retinal vascular development. While \u003C/span\u003E\u003Cb\u003Eautosomal recessive inheritance can occur\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the \u003C/span\u003E\u003Cb\u003Emost common inheritance pattern is autosomal dominant\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ESupporting points for the other options:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFEVR is an important cause of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal detachment in children and infants\u003C/b\u003E\u003C/span\u003E, particularly tractional or exudative RD.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGenetic linkage has been described on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echromosome 11\u003C/b\u003E\u003C/span\u003E (e.g. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFZD4\u003C/b\u003E\u003C/span\u003E), among other loci involved in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWnt signalling pathway\u003C/b\u003E\u003C/span\u003E (LRP5, TSPAN12, NDP).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESubretinal exudation\u003C/b\u003E\u003C/span\u003E is a recognised feature due to peripheral retinal non-perfusion and neovascular leakage.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 266,
    "Name": "Uveal Effusion syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the most appropriate management for \u003C/span\u003Eidiopathic uveal effusion syndrome without nanophthalmos\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIdiopathic uveal effusion syndrome (UES) without nanophthalmos\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E differs fundamentally from nanophthalmic UES in both \u003C/span\u003E\u003Cb\u003Epathophysiology and management\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enanophthalmos\u003C/b\u003E\u003C/span\u003E, thickened sclera and impaired trans-scleral outflow are central \u2192 \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esclerectomy/sclerostomy\u003C/b\u003E\u003C/span\u003E is effective. [\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Enanophthalmos and the presence of clinically detectable thickened/rigid sclera are a good predictor both for histologically abnormal sclera and of a good response to surgery.]\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-nanophthalmic (idiopathic) UES\u003C/b\u003E\u003C/span\u003E, scleral thickness is normal, and scleral surgery is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eusually ineffective\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003ENote: Nanophthalmic eyes axial length: 16 mm or less\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EFor idiopathic UES:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPars plana vitrectomy\u003C/b\u003E\u003C/span\u003E is the preferred treatment, as it reduces vitreous traction and facilitates resolution of choroidal effusions and associated serous retinal detachment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcetazolamide\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Esystemic steroids\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may be tried but have \u003C/span\u003E\u003Cb\u003Eunreliable and often transient benefit\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFull-thickness sclerectomy\u003C/b\u003E\u003C/span\u003E is not indicated without scleral thickening.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 267,
    "Name": "Retinal tears",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn which of the following conditions is a \u003Cspan class=\u0022s1\u0022\u003Eposterior vitreous detachment (PVD)\u003C/span\u003E most typically present?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egiant retinal tear (GRT)\u003C/b\u003E\u003C/span\u003E is classically associated with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior vitreous detachment\u003C/b\u003E\u003C/span\u003E. The acute separation of the posterior hyaloid generates strong \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecircumferential vitreoretinal traction\u003C/b\u003E\u003C/span\u003E, predisposing to the formation of a large (\u0026gt;90\u00B0) full-thickness retinal tear.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options are less likely to be associated with PVD:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal dialysis\u003C/b\u003E\u003C/span\u003E \u2192 typically traumatic and occurs at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eora serrata\u003C/b\u003E\u003C/span\u003E, often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewithout PVD\u003C/b\u003E\u003C/span\u003E, especially in younger patients.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETraumatic macular hole\u003C/b\u003E\u003C/span\u003E \u2192 results from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanteroposterior compression\u003C/b\u003E\u003C/span\u003E of the globe rather than vitreous separation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAtrophic round hole retinal detachment\u003C/b\u003E\u003C/span\u003E \u2192 usually occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewithout PVD\u003C/b\u003E\u003C/span\u003E, particularly in young myopes, and is due to retinal thinning rather than traction.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 268,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost likely mechanism\u003Cspan class=\u0022s1\u0022\u003E underlying a \u003C/span\u003Eparadoxical pupil response\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eparadoxical pupil response\u003C/b\u003E\u003C/span\u003E refers to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupillary constriction in darkness\u003C/b\u003E\u003C/span\u003E or dilation in response to light offset, most classically described in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econe dysfunction syndromes\u003C/b\u003E\u003C/span\u003E (e.g. cone dystrophies, achromatopsia).\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe prevailing explanation is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erelative preservation of S-cone (blue cone) function\u003C/b\u003E\u003C/span\u003E, with loss of L- and M-cone input. This results in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunopposed S-cone signalling\u003C/b\u003E\u003C/span\u003E, which abnormally drives the pupillary light reflex pathway, producing a paradoxical response.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options are incorrect:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EConvergence in the dark\u003C/b\u003E\u003C/span\u003E does not account for a true paradoxical light response.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDenervation hypersensitivity\u003C/b\u003E\u003C/span\u003E explains tonic pupils, not paradoxical reactions.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe phenomenon is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclinically detectable\u003C/b\u003E\u003C/span\u003E and not restricted to laboratory testing.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 269,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA child presents with \u003C/span\u003Ereduced visual acuity (6/36)\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Ebull\u2019s-eye maculopathy\u003Cspan class=\u0022s1\u0022\u003E, a \u003C/span\u003Ereduced b-wave on ERG\u003Cspan class=\u0022s1\u0022\u003E, and a \u003C/span\u003Ereduced EOG\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBatten disease\u003C/b\u003E\u003C/span\u003E (juvenile neuronal ceroid lipofuscinosis) is characterised by early-onset \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogressive visual loss\u003C/b\u003E\u003C/span\u003E, often presenting with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebull\u2019s-eye maculopathy\u003C/b\u003E\u003C/span\u003E. Retinal electrophysiology typically shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReduced ERG b-wave\u003C/b\u003E\u003C/span\u003E \u2192 inner retinal dysfunction\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAbnormal EOG\u003C/b\u003E\u003C/span\u003E \u2192 retinal pigment epithelium involvement\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis combination reflects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewidespread retinal degeneration\u003C/b\u003E\u003C/span\u003E, which is typical of Batten disease.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003ERemember:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHomocystinuria\u003C/b\u003E\u003C/span\u003E \u2192 ectopia lentis (inferonasal), thromboembolic disease, intellectual disability; not a bull\u2019s-eye maculopathy with characteristic ERG/EOG findings.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EZellweger syndrome\u003C/b\u003E\u003C/span\u003E \u2192 severe neonatal presentation with hypotonia, craniofacial abnormalities, and early death; ocular findings are present but the clinical context here fits poorly.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 270,
    "Name": "Vitrectomy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich type of cataract is most commonly associated with a \u003Cspan class=\u0022s1\u0022\u003Egas-filled eye\u003C/span\u003E (e.g. after vitreoretinal surgery)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPosterior subcapsular cataract\u003C/b\u003E\u003C/span\u003E is the cataract type most commonly associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintraocular gas tamponade\u003C/b\u003E\u003C/span\u003E following vitrectomy.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EContributing mechanisms include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDirect contact\u003C/b\u003E\u003C/span\u003E between gas and the posterior lens capsule\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAltered lens metabolism and oxygen tension\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAccelerated epithelial cell migration beneath the posterior capsule\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EPSC formation is therefore frequent after vitreoretinal surgery, particularly in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephakic patients\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 271,
    "Name": "PCV",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the most appropriate management option for \u003Cspan class=\u0022s1\u0022\u003Epolypoidal choroidal vasculopathy (PCV)\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p2\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPCV is less responsive to anti-VEGF monotherapy\u003C/b\u003E\u003C/span\u003E than other forms of CNV.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEVEREST trials\u003C/b\u003E\u003C/span\u003E showed that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Everteporfin photodynamic therapy (PDT)\u003C/b\u003E\u003C/span\u003E, alone or combined with ranibizumab, achieves \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperior polyp regression\u003C/b\u003E\u003C/span\u003E compared with ranibizumab alone.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPLANET study\u003C/b\u003E\u003C/span\u003E demonstrated that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaflibercept monotherapy\u003C/b\u003E\u003C/span\u003E produced visual acuity gains \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomparable to aflibercept plus deferred PDT\u003C/b\u003E\u003C/span\u003E (\u224810.7 ETDRS letters), with most patients not requiring PDT.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EOverall, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPDT remains central for polyp closure\u003C/b\u003E\u003C/span\u003E, while anti-VEGF -particularly aflibercept- provides good functional outcomes.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/blockquote\u003E\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 272,
    "Name": "Argyrosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following conditions is associated with a \u003Cspan class=\u0022s1\u0022\u003Edark choroid\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular argyrosis\u003C/b\u003E\u003C/span\u003E results from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echronic silver deposition\u003C/b\u003E\u003C/span\u003E, typically after prolonged ingestion or exposure to colloidal silver. It is characterised by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediffuse brown-black granular deposits in Bruch\u2019s membrane\u003C/b\u003E\u003C/span\u003E, which block choroidal fluorescence on angiography and produce the classic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cdark choroid\u201D\u003C/b\u003E\u003C/span\u003E appearance.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EClinically, we can remember it as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Cdark sky with silver stars\u201D\u003C/b\u003E\u003C/span\u003E, reflecting:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGeneralised choroidal darkening\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELeopard-spotting or drusen-like changes\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe other options do \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E cause a dark choroid:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChalcosis\u003C/b\u003E\u003C/span\u003E \u2192 sunflower cataract, Kayser-Fleischer-like changes\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHydroxychloroquine\u003C/b\u003E\u003C/span\u003E \u2192 parafoveal/bull\u2019s-eye maculopathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETamoxifen\u003C/b\u003E\u003C/span\u003E \u2192 crystalline maculopathy\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 273,
    "Name": "Macular Hole",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following types of \u003Cspan class=\u0022s1\u0022\u003Emacular hole\u003C/span\u003E has the \u003Cspan class=\u0022s1\u0022\u003Ebest prognosis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGrade 3 macular hole with an operculum\u003C/b\u003E\u003C/span\u003E indicates that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanteroposterior vitreomacular traction has been released\u003C/b\u003E\u003C/span\u003E, as the operculum represents avulsed retinal tissue attached to the posterior hyaloid. This release of traction is associated with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EHigher rates of \u003C/span\u003E\u003Cb\u003Eanatomical closure\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBetter \u003C/span\u003E\u003Cb\u003Evisual prognosis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EReduced ongoing tractional forces\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efull-thickness macular hole with PVD\u003C/b\u003E\u003C/span\u003E (Grade 4) lacks the operculum and often represents a more advanced stage.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESurrounding subretinal fluid and intraretinal cystic changes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E reflect \u003C/span\u003E\u003Cb\u003Echronicity and retinal damage\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which are associated with poorer functional outcomes.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EGood Preoperative Prognostic Factors in Macular Hole Surgery\u003C/b\u003E\u003C/p\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIdiopathic macular holes\u003C/b\u003E\u003C/span\u003E have a better prognosis than \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etraumatic macular holes\u003C/b\u003E\u003C/span\u003E that have not resolved spontaneously and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopic macular holes\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EShorter duration of symptoms\u003C/b\u003E\u003C/span\u003E is associated with better outcomes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBetter preoperative visual acuity\u003C/b\u003E\u003C/span\u003E predicts improved postoperative vision.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEarlier stage macular holes\u003C/b\u003E\u003C/span\u003E have a more favourable prognosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESmaller macular hole size\u003C/b\u003E\u003C/span\u003E is associated with higher closure rates and better visual outcomes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOCT-based indices\u003C/b\u003E\u003C/span\u003E (e.g. hole size parameters and configuration metrics) can be used preoperatively to help predict prognosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 274,
    "Name": "Retinal Detachment",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient presents following \u003C/span\u003Eocular trauma\u003Cspan class=\u0022s1\u0022\u003E with an \u003C/span\u003Einferior rhegmatogenous retinal detachment\u003Cspan class=\u0022s1\u0022\u003E, associated with \u003C/span\u003Eflashes and floaters\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost appropriate next management step\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn \u003C/span\u003E\u003Cb\u003Etraumatic retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly when there are \u003C/span\u003E\u003Cb\u003Einferior breaks\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Emultiple small retinal breaks near the ora serrata\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, or \u003C/span\u003E\u003Cb\u003Edialyses\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, a \u003C/span\u003E\u003Cb\u003Escleral buckle\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a key component of management.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EKey principles:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInferior retinal breaks\u003C/b\u003E\u003C/span\u003E are less effectively supported by intraocular gas alone due to buoyancy limitations.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETraumatic RDs\u003C/b\u003E\u003C/span\u003E often involve \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral pathology\u003C/b\u003E\u003C/span\u003E (e.g. dialysis, multiple small tears) best addressed externally.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Escleral buckle provides permanent support\u003C/b\u003E\u003C/span\u003E to the vitreous base and inferior retina.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eoptimal approach is often a combined pars plana vitrectomy with scleral buckle.\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EWhy the other options are less suitable:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAir or gas alone\u003C/b\u003E\u003C/span\u003E \u2192 inadequate tamponade for inferior breaks\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESilicone oil\u003C/b\u003E\u003C/span\u003E \u2192 reserved for complex PVR, giant tears, or when posturing is not possible\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 275,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhat is the approximate risk of blindness at 5 years after new vessels at the disc (NVD) are detected in a patient with type 1 diabetes if left untreated?\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENVD = high-risk proliferative diabetic retinopathy (PDR)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EData from the \u003C/span\u003E\u003Cb\u003EDiabetic Retinopathy Study (DRS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E showed that \u003C/span\u003E\u003Cb\u003Euntreated high-risk PDR\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E carries a risk of \u003C/span\u003E\u003Cb\u003Esevere visual loss (\u22645/200)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of approximately:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E~25-30% at 2 years\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E~40-50% by 5 years\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003ERemember:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EType 1 diabetes\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigher risk of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPDR\u003C/b\u003E\u003C/span\u003E than type 2\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESevere NPDR\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E~\u003C/span\u003E\u003Cb\u003E50% risk of PDR within 1 year\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVery severe NPDR\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E~\u003C/span\u003E\u003Cb\u003E45% risk of high-risk PDR within 1 year\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMacular oedema\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMore common in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etype 2 diabetes\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPrevalence after ~15 years: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EType 1 \u2248 15%\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EType 2 \u2248 25%\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 276,
    "Name": "Macular Hole",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following conditions is \u003Cspan class=\u0022s1\u0022\u003ELEAST likely\u003C/span\u003E to cause a \u003Cspan class=\u0022s1\u0022\u003Emacular hole\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMacular holes typically result from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emechanical or tractional forces\u003C/b\u003E\u003C/span\u003E acting on the fovea.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular trauma\u003C/b\u003E\u003C/span\u003E \u2192 well-recognised cause due to sudden anteroposterior compression.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh myopia\u003C/b\u003E\u003C/span\u003E \u2192 predisposes to foveal thinning, traction, and myopic macular holes.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELong-standing retinal detachment\u003C/b\u003E\u003C/span\u003E \u2192 chronic retinal changes and traction may lead to macular hole formation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EIn contrast, \u003C/span\u003E\u003Cb\u003Econe dystrophy\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E is a \u003C/span\u003E\u003Cb\u003Eprimary photoreceptor degenerative disorder\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E and does \u003C/span\u003E\u003Cb\u003Enot cause structural foveal defects such as macular holes\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022 style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 277,
    "Name": "Retinal Dialysis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following retinal lesions \u003Cspan class=\u0022s1\u0022\u003Erequires treatment\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinal dialysis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a circumferential retinal break at the \u003C/span\u003E\u003Cb\u003Eora serrata\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, commonly traumatic, and carries a \u003C/span\u003E\u003Cb\u003Ehigh risk of progressive rhegmatogenous retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. \u003C/span\u003E\u003Cb\u003EProphylactic treatment (e.g., laser or cryotherapy)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is therefore indicated.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELattice degeneration with holes\u003C/b\u003E\u003C/span\u003E: prophylactic treatment is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot routinely indicated\u003C/b\u003E\u003C/span\u003E in asymptomatic patients without detachment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAtrophic round holes\u003C/b\u003E\u003C/span\u003E: usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebenign\u003C/b\u003E\u003C/span\u003E, often without vitreoretinal traction, and typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eobserved\u003C/b\u003E\u003C/span\u003E unless associated with subretinal fluid or symptoms.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 278,
    "Name": "Retinal dystrophies",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003Eend-stage retinitis pigmentosa\u003C/span\u003E, which electrophysiological finding is most likely to be found?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinitis pigmentosa (RP)\u003C/b\u003E\u003C/span\u003E, progressive degeneration of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephotoreceptors\u003C/b\u003E\u003C/span\u003E leads to marked reduction or extinction of both \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EERG a and b waves\u003C/b\u003E\u003C/span\u003E. As the disease advances, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal pigment epithelium (RPE) dysfunction\u003C/b\u003E\u003C/span\u003E also develops, resulting in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabnormal electro-oculogram (EOG)\u003C/b\u003E\u003C/span\u003E with a reduced Arden ratio.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn early RP, EOG may be relatively preserved, but in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eend-stage disease\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eboth ERG and EOG are abnormal\u003C/b\u003E\u003C/span\u003E, reflecting widespread photoreceptor and RPE involvement.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 279,
    "Name": "White Dot syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich \u003C/span\u003Ewhite dot syndrome\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003Emost likely to develop choroidal neovascularisation (CNV)\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPIC\u003C/b\u003E\u003C/span\u003E carries the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehighest risk of CNV\u003C/b\u003E\u003C/span\u003E among the white dot syndromes, with reported rates ranging from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~20% up to 70%\u003C/b\u003E\u003C/span\u003E in different series. CNV is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emajor cause of visual loss\u003C/b\u003E\u003C/span\u003E in PIC and often requires \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanti-VEGF therapy\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBirdshot chorioretinopathy\u003C/b\u003E\u003C/span\u003E \u2192 CNV is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Euncommon\u003C/b\u003E\u003C/span\u003E; vision loss is more often due to chronic inflammation and retinal dysfunction.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAPMPPE\u003C/b\u003E\u003C/span\u003E \u2192 CNV is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E, with most cases resolving without neovascular complications.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 280,
    "Name": "DVLA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAccording to \u003C/span\u003EDVLA Group 1 (car/motorcycle) guidance (2014)\u003Cspan class=\u0022s1\u0022\u003E, which of the following conditions \u003C/span\u003Emust be reported immediately to the DVLA\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBlepharospasm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E must be \u003C/span\u003E\u003Cb\u003Ereported to the DVLA\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, even if mild or treated. Driving may continue \u003C/span\u003E\u003Cb\u003Eonly if supported by satisfactory medical reports\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. If severe, \u003C/span\u003E\u003Cb\u003Edriving is not normally permitted\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, even with treatment.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETemporary visual impairment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E after surgery (e.g., patching) \u003C/span\u003E\u003Cb\u003Edoes not require notification\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E unless it \u003C/span\u003E\u003Cb\u003Epersists beyond 3 months\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGlaucoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E requires notification \u003C/span\u003E\u003Cb\u003Eonly if visual field defects are bilateral\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMonocularity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E must be reported \u003C/span\u003E\u003Cb\u003Eonly if one eye has no light perception (NPL)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. If there is \u003C/span\u003E\u003Cb\u003Eany light perception\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, notification is \u003C/span\u003E\u003Cb\u003Enot required\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth Part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 281,
    "Name": "Bacteriology Media",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWith regard to routine media used in bacteriology, which\nstatement is MOST likely to be correct?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003ECorrect Answer:\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E MacConkey\u2019s agar is an appropriate medium to culture gram-negative rods.\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cdiv\u003EMacConkey\u2019s agar is a selective and differential medium designed to isolate and differentiate gram-negative rods, particularly members of the Enterobacteriaceae family. It contains bile salts and crystal violet, which inhibit gram-positive organisms, and lactose with a pH indicator to differentiate lactose fermenters (pink colonies) from non-fermenters (colorless colonies). This makes it ideal for culturing gram-negative rods such as E. coli and Klebsiella.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EWhy Other Options Are Incorrect:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022\tChocolate agar: Used for fastidious organisms like Haemophilus influenzae and Neisseria species, not anaerobic rods.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tMeat broth: A nutrient-rich medium but not specific for acanthamoeba; acanthamoeba requires non-nutrient agar with an overlay of E. coli for growth.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022\tNutrient agar: A general-purpose medium that supports many non-fastidious organisms but does not specifically select for gram-negative cocci.\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 282,
    "Name": "Herpes Simplex Keratitis",
    "Body": "\u003Cspan style=\u0022font-size: 11pt; line-height: 115%;\u0022\u003E\u003Cspan style=\u0022font-family: Arial; font-weight: bold;\u0022\u003EWith regard to Herpes\nsimplex infections of the anterior segment of the eye, which of the following\nstatements is MOST likely to be correct?\u003Cbr\u003E\u003C/span\u003E\u003Cbr\u003E\n\u003C!--[endif]--\u003E\u003C/span\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003ELocalised debridement is recommended to remove viral load as a treatment option for dendritic ulcers.\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation\u003C/span\u003E:\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EHerpes simplex epithelial keratitis, typically presenting as a dendritic ulcer, is caused by active viral replication within corneal epithelial cells. The cornerstone of treatment is antiviral therapy, either topical (such as trifluridine or ganciclovir) or systemic (oral acyclovir or valacyclovir). Mechanical debridement of the ulcer is a recognized adjunctive measure that reduces viral load and promotes epithelial healing when combined with antiviral therapy. This approach is particularly useful in resource-limited settings or when rapid reduction of viral burden is desired.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003EWhy Other Options Are Incorrect:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EA dendritic ulcer does contain live virus within infected epithelial cells.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EDisciform keratitis represents an immune-mediated stromal reaction associated with underlying endotheliitis. It does not occur without endothelial involvement, making this statement false.\u003C/div\u003E\u003Cdiv\u003ERecurrent HSV keratitis typically leads to decreased corneal sensation due to trigeminal nerve involvement. Normal corneal sensitivity is not characteristic of recurrent disease.\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cimg src=\u0022/upload-2026-01-19-26ee9710-cca8-4088-a2ad-e3da89937b1a.jpg\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 283,
    "Name": "ETDRS and Number Needed to Treat",
    "Body": "\u003Cspan style=\u0022font-size: 11pt; line-height: 115%; font-family: Arial; font-weight: bold;\u0022\u003EIn the Early\nTreatment Diabetic Retinopathy Study (ETDRS) for laser treatment of diabetic\nmacular oedema, moderate visual loss occurred in 12% of treated eyes compared\nto 24% of untreated eyes in three years. Which of these is MOST likely to be\nthe approximate value of numbers needed to treat in this study?\u003C/span\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003E9\u0026nbsp;\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003ENumber Needed to Treat (NNT) is the number of patients (or eyes) that need to be treated to prevent one additional adverse outcome: NNT = 1 \u00F7 ARR. The number needed to treat (NNT) is calculated as the inverse of the absolute risk reduction (ARR)\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\nAbsolute Risk Reduction (ARR) is the difference in event rates between control and treatment groups: ARR = Control Event Rate \u2212 Treatment Event Rate.\u003C/div\u003E\u003Cdiv\u003EIn this study, the risk of moderate visual loss was 24% in untreated eyes and 12% in treated eyes.\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;ARR = 24% \u2212 12% = 12% (or 0.12).\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;NNT = 1 \u00F7 ARR = 1 \u00F7 0.12 \u2248 8.3, which rounds to approximately 9.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;This means that for every 9 eyes treated with laser, one case of moderate visual loss is prevented over three years.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe ETDRS study historically reported this benefit per eye, not per patient.\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 284,
    "Name": " MRI Sequence Identification",
    "Body": "\u003Cspan style=\u0022font-size:11.0pt;line-height:115%;\nfont-family:\u0026quot;Cambria\u0026quot;,serif;mso-ascii-theme-font:minor-latin;mso-fareast-font-family:\n\u0026quot;MS Mincho\u0026quot;;mso-fareast-theme-font:minor-fareast;mso-hansi-theme-font:minor-latin;\nmso-bidi-font-family:Arial;mso-bidi-theme-font:minor-bidi;mso-ansi-language:\nEN-US;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003EWhat is the MOST\nlikely type of MRI sequence seen in this image?\u003C/span\u003E\u003Cimg src=\u0022/upload-2026-01-19-c6678adf-0388-41a1-aa8b-354c2b0e17d0.png\u0022\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\u003C/span\u003E\u0026nbsp;\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;Fluid-attenuated inversion recovery (FLAIR)\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EThe MRI image shows a brain scan with high signal intensity in white matter and cerebrospinal fluid (CSF) appearing dark, which is characteristic of a FLAIR sequence. FLAIR is a modified T2-weighted sequence where the CSF signal is suppressed, making it particularly useful for detecting lesions adjacent to CSF spaces, such as periventricular plaques in multiple sclerosis or subarachnoid pathology.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EWhy Other Options Are Incorrect:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(DWI):\u003C/span\u003E Diffusion-weighted imaging highlights acute ischemia with bright restricted diffusion areas, but the overall appearance here is not typical for DWI.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(T1 with contrast):\u003C/span\u003E T1-weighted images show CSF as dark and gray matter lighter than white matter; contrast enhancement highlights lesions, which is not evident here.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003E(T2 with contrast):\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E T2-weighted images show CSF as bright, unlike this image where CSF is dark due to inversion recovery suppression.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-20-de334ce8-ef9f-489a-a467-431f4a0c7d17.jpg\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 285,
    "Name": "Thygeson\u0027s Keratitis",
    "Body": "\u003Cspan style=\u0022font-size:11.0pt;line-height:115%;\nfont-family:\u0026quot;Cambria\u0026quot;,serif;mso-ascii-theme-font:minor-latin;mso-fareast-font-family:\n\u0026quot;MS Mincho\u0026quot;;mso-fareast-theme-font:minor-fareast;mso-hansi-theme-font:minor-latin;\nmso-bidi-font-family:Arial;mso-bidi-theme-font:minor-bidi;mso-ansi-language:\nEN-US;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003EYou are asked to see\na woman aged between 25 and 30 years who gives a history of recurrent episodes\nof tearing, foreign body sensation, photophobia, and mild reduction in vision\naffecting both eyes. During an acute attack she has mild conjunctival hyperaemia\nand numerous small coarse corneal epithelial opacities, which are clustered in\nthe central cornea and stain with fluorescein. Which is the MOST likely\ndiagnosis?\u003Cbr\u003E\n\u003C!--[if !supportLineBreakNewLine]--\u003E\u003Cbr\u003E\n\u003C!--[endif]--\u003E\u003C/span\u003E",
    "Explanation": "\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003ECorrect Answer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003EThygeson\u0027s keratitis\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u0026nbsp;Explanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Thygeson\u0027s superficial punctate keratitis is a chronic, recurrent corneal condition that typically affects young adults. It is characterized by small, coarse, gray-white epithelial opacities clustered in the central cornea, which stain with fluorescein. Patients often present with tearing, photophobia, foreign body sensation, and mild visual disturbance during episodes. The conjunctival involvement is minimal, with only mild hyperaemia, and the condition follows a relapsing-remitting course over several years. The hallmark feature is the presence of discrete epithelial lesions without significant stromal involvement, distinguishing it from other conditions.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EWhy Other Options Are Incorrect:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E Adenovirus keratitis usually follows epidemic keratoconjunctivitis and presents with subepithelial infiltrates rather than discrete epithelial opacities. Keratoconjunctivitis sicca is associated with dry eye and diffuse punctate erosions, not clustered coarse lesions. Superior limbic keratitis primarily affects the superior bulbar conjunctiva and limbus, not the central cornea.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-20-ad489677-e742-44ab-92da-a0478709475d.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-20-761fd80c-8794-4c4a-8731-420dbc207b34.jpg\u0022\u003E\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003EThgryson\u0027s punctate keratitis\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 286,
    "Name": " Orbital Floor Fracture with Inferior Rectus Entrapment",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022mso-margin-top-alt:auto;mso-margin-bottom-alt:auto;\nline-height:normal\u0022\u003E\u003Cspan style=\u0022font-size:12.0pt;font-family:\u0026quot;Times New Roman\u0026quot;,serif;\nmso-fareast-font-family:\u0026quot;Times New Roman\u0026quot;\u0022\u003EA 4-year-old boy presents having\nfallen off his bicycle and having hit his face on the handlebar. Which of these\nis \u003Cb\u003ELEAST consistent\u003C/b\u003E with a fracture of the orbital floor with entrapment\nof the inferior rectus muscle on the injured side?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\n\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAfferent pupil defect.\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOrbital floor fractures with inferior rectus entrapment typically present with restricted ocular motility, especially in elevation and depression, due to mechanical tethering of the muscle. Associated features include nausea, vomiting, and bradycardia (oculocardiac reflex), particularly in children, and a white-eyed blowout fracture appearance with minimal external signs of trauma. The anterior segment usually remains quiet.\nAn afferent pupillary defect (APD), however, suggests optic nerve involvement or severe globe injury, which is not characteristic of isolated orbital floor fracture with muscle entrapment. Therefore, APD is the least consistent finding.\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 287,
    "Name": "Depth of Focus After Cataract Surgery",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022mso-margin-top-alt:auto;mso-margin-bottom-alt:auto;\nline-height:normal\u0022\u003E\u003Cspan style=\u0022font-size:12.0pt;font-family:\u0026quot;Times New Roman\u0026quot;,serif;\nmso-fareast-font-family:\u0026quot;Times New Roman\u0026quot;\u0022\u003EWhich of the following patients are\nMOST likely to have increased depth of focus following cataract surgery with a\nmonofocal lens?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cbr\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 288,
    "Name": "Sensitivity of ESR for Diagnosing GCA",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022mso-margin-top-alt:auto;mso-margin-bottom-alt:auto;\nline-height:normal\u0022\u003E\u003Cspan style=\u0022font-size:12.0pt;font-family:\u0026quot;Times New Roman\u0026quot;,serif;\nmso-fareast-font-family:\u0026quot;Times New Roman\u0026quot;\u0022\u003EData from a study of Anterior\nIschaemic Optic Neuropathy (AION) identifies that 20% of patients with AION\nhave Giant Cell Arteritis (GCA) confirmed by temporal artery biopsy (TAB).\nAssume \u003Cb\u003E80% of TAB-positive patients have a high ESR\u003C/b\u003E, and \u003Cb\u003E10% of\nTAB-negative patients have a high ESR\u003C/b\u003E. Using the data from this study, what\nis the approximate sensitivity of the ESR for diagnosing GCA?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\u003C/span\u003E\n\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;80%\u0026nbsp;\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Sensitivity measures the proportion of true positives correctly identified by the test:\u0026nbsp; \u0026nbsp; \u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0022Sensitivity\u0022= (True Positives / All Patients with Disease) \u00D7100\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EAssume 100 AION patients:\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; TAB positive = 20% \u2192 20 patients\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;High ESR among TAB positive = 80% \u2192 16 patients\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0022Sensitivity\u0022=16/20\u00D7100=80%\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Specificity measures the proportion of true negatives correctly identified.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EHere, 10% of TAB-negative patients have high ESR, which reduces specificity because of false positives.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003ESPIN \u0026amp; SNOUT Mnemonics:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;SPIN = Specificity Positive rules IN disease \u2192 A highly specific test, when positive, confirms disease.\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;SNOUT = Sensitivity Negative rules OUT disease \u2192 A highly sensitive test, when negative, excludes disease.\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 289,
    "Name": "B-scan Signs of Raised Intracranial Pressure",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022mso-margin-top-alt:auto;mso-margin-bottom-alt:auto;\nline-height:normal\u0022\u003E\u003Cspan style=\u0022font-size:12.0pt;font-family:\u0026quot;Times New Roman\u0026quot;,serif;\nmso-fareast-font-family:\u0026quot;Times New Roman\u0026quot;\u0022\u003EWhich one of the following signs on\nB scan ultrasound is MOST likely to suggest raised intracranial pressure?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ECorrect Answer:\n\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;Fusiform swelling of the optic nerve with low-to-medium, regular, internal reflectivity\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003EExplanation:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ERaised intracranial pressure often leads to papilledema, which can be detected on B-scan ultrasound as fusiform (spindle-shaped) swelling of the optic nerve. The swelling appears with low-to-medium internal reflectivity and a regular pattern because the nerve sheath is distended by cerebrospinal fluid. This finding correlates with optic nerve sheath diameter enlargement, a recognized indirect sign of increased intracranial pressure.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOther options are incorrect: An echolucent circle suggests optic nerve sheath fluid but is not the classic description for papilledema; medium-to-high, irregular reflectivity indicates optic nerve drusen rather than raised ICP; highly reflective areas also correspond to calcified drusen, not papilledema.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EClinical Pearls:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022\tOptic nerve sheath diameter \u0026gt;5 mm on B-scan is a strong indicator of raised ICP.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u2022\tB-scan is useful when fundus view is obscured (e.g., media opacity).\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u2022\tDifferentiate papilledema from optic nerve head drusen by reflectivity pattern: drusen = highly reflective, irregular; papilledema = low-to-medium, regular.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-22-b02bedb0-5686-4a6f-86bd-cad3f022d365.jpg\u0022 class=\u0022\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003Ean ocular US image shows papilledema\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-22-97db03ac-bc98-46a3-876e-c64a1cfad4bf.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003Ean ocular US image shows optic disc drusen\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 290,
    "Name": "Mitomycin C and Glaucoma Drainage surgery ",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EWith regard to Mitomycin C used in glaucoma\ndrainage surgery, which of these statements is MOST likely to be correct?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;It can cause limbal stem cell deficiency\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EMitomycin C is a potent antimetabolite commonly used during glaucoma drainage surgeries (like trabeculectomy) to reduce postoperative scarring by inhibiting fibroblast proliferation. Its mechanism targets DNA synthesis, making it more effective than 5-Fluorouracil (5FU) at equivalent concentrations. One significant side effect is cytotoxicity to the ocular surface, particularly the limbus, which harbors corneal epithelial stem cells. Damage to these stem cells can result in limbal stem cell deficiency, leading to poor epithelial healing, persistent epithelial defects, and vision-threatening surface complications.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOther options:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003EMitomycin C is, in fact, more potent than 5FU\u003C/div\u003E\u003Cdiv\u003Ethe typical concentration used is 0.2 mg/mL (which equals 0.02%, not 0.2%).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EMitomycin C broadly inhibits cell proliferation, not specifically mast cell migration.\u0026nbsp;\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 291,
    "Name": "Drug induced papilledema",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EDrug induced papilledema is MOST likely to be\ndue to which one of the following?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;Isotretinoin\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\nPapilledema refers to optic disc swelling secondary to raised intracranial pressure (ICP). Drug-induced papilledema typically results from medications that can cause idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri. Among the options listed, isotretinoin is the most established culprit for this condition.\n\nIsotretinoin, a retinoid used primarily for severe acne, is well-documented to cause raised intracranial pressure, particularly in young patients. The mechanism is thought to involve altered cerebrospinal fluid (CSF) dynamics and reduced CSF absorption.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E(Pamidronate): Bisphosphonates have been associated with orbital inflammation and uveitis but not typically papilledema.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E(Sildenafil): PDE5 inhibitors can cause non-arteritic anterior ischemic optic neuropathy (NAION) and transient visual disturbances, but not papilledema from raised ICP.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E(Tamoxifen): This selective estrogen receptor modulator can cause crystalline retinopathy and rarely optic neuropathy, but not papilledema.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 292,
    "Name": "Apraclonidine usage",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EWhich of the following statements is MOST\nlikely to be correct?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;Apraclonidine may cross the Blood brain barrier of children under one year of age, resulting in respiratory depression\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003E\u0026nbsp;Explanation:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Apraclonidine is an alpha-adrenergic agonist used pharmacologically to diagnose Horner\u0027s syndrome through the reversal of ptosis and miosis in the affected eye due to denervation supersensitivity. However, it carries important safety considerations, particularly in pediatric populations.\n\nIn children under one year of age, the blood-brain barrier is incompletely developed and more permeable. Apraclonidine can cross this immature barrier and exert central nervous system effects, including sedation, bradycardia, hypotension, and potentially life-threatening respiratory depression. For this reason, apraclonidine is contraindicated in infants and young children.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold; text-decoration-line: underline;\u0022\u003EWhy the other options are incorrect?\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EIn acute Horner\u0027s syndrome (especially within 48 hours of onset, such as from carotid dissection), denervation supersensitivity has not yet developed. Apraclonidine testing is unreliable in this timeframe and may yield false-negative results. The test is most reliable in chronic Horner\u0027s syndrome (typically after 2-3 days to weeks).\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EApraclonidine works primarily as a weak alpha-1 agonist and alpha-2 agonist. The diagnostic effect in Horner\u0027s syndrome relies on alpha-1 receptor denervation supersensitivity in the dilator pupillae muscle of the affected eye, not alpha-2 supersensitivity.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EBrimonidine is not used for diagnosing Horner\u0027s syndrome. It is a potent alpha-2 agonist used to lower intraocular pressure in glaucoma. Like apraclonidine, brimonidine can also cross the blood-brain barrier in children and cause severe CNS and respiratory depression, making it contraindicated in young children.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 293,
    "Name": "Blood supply of the optic nerve",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following statements is MOST\nlikely to be true with respect to the blood supply of the optic nerve?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003EAnswer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;The retrolaminar optic nerve is supplied by branches of the pia vessels and central retinal artery\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\nThe optic nerve has a complex, segmental blood supply that is clinically important for understanding various optic neuropathies. The nerve is anatomically divided into four portions: intraocular (optic nerve head), intraorbital, intracanalicular, and intracranial segments, each with distinct vascular supply.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EThe retrolaminar optic nerve (the portion immediately posterior to the lamina cribrosa within the scleral canal and extending approximately 1-2 mm behind the globe) receives dual blood supply from both pial vessels (derived from the ophthalmic artery and its branches) and centrifugal branches of the central retinal artery. This dual supply creates a watershed zone that is particularly vulnerable to ischemia.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOption A is incorrect: The ophthalmic artery is a branch of the internal carotid artery, not the external carotid artery. It typically arises from the internal carotid just after it exits the cavernous sinus.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOption B is incorrect: The lamina cribrosa is primarily supplied by branches of the short posterior ciliary arteries (SPCAs), specifically the Para optic branches, and the circle of Zinn-Haller (an anastomotic circle formed by SPCAs). While short ciliary arteries do contribute, they are not the sole or primary supply; the more accurate terminology emphasizes posterior ciliary circulation.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EOption C is incorrect: The optic disc (optic nerve head) is predominantly supplied by the short posterior ciliary arteries via the circle of Zinn-Haller and paraoptic branches. The central retinal artery supplies primarily the nerve fiber layer on the disc surface, not the bulk of the optic disc tissue. A cilioretinal artery (present in 15-30% of individuals) supplies part of the retina, not the optic disc itself.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003ETo Sum Up:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u2022 The ophthalmic artery arises from the internal carotid artery (medial to the anterior clinoid process).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022 The optic nerve head has segmental blood supply: prelaminar (SPCAs), laminar (circle of Zinn-Haller from SPCAs), retrolaminar (pial vessels \u002B CRA branches).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022 Non-arteritic anterior ischemic optic neuropathy (NAION) affects the optic nerve head supplied by posterior ciliary arteries.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022 Posterior ischemic optic neuropathy affects the retrolaminar and orbital portions supplied by pial vessels.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u2022 The watershed zone between different vascular territories makes certain optic nerve regions vulnerable to ischemic damage.\u0026nbsp;\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 294,
    "Name": "ROP",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAccording to the 2008 RCOphth guidelines, when should a baby born at 26 weeks gestational age be screened for ROP?\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EROP screening in infants born \u0026lt;27 weeks GA should start at 30\u201331 weeks postmenstrual age, regardless of postnatal age.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENotes:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EROP screening \u2013 timing of first examination\u003C/b\u003E\u003C/h3\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EInfants born \u0026lt;31\u002B0 weeks\u2019 gestation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u2192 First ROP screen at \u003C/span\u003E\u003Cb\u003E31\u201332 weeks postmenstrual age\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOR\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E at \u003C/span\u003E\u003Cb\u003E4 weeks postnatal age\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u2192 \u003C/span\u003EUse whichever is\u003Cb\u003E later\u003C/b\u003E\u003C/p\u003E\u003C/blockquote\u003E\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EInfants born \u226531\u002B0 weeks\u2019 gestation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u2192 First ROP screen at \u003C/span\u003E\u003Cb\u003E36\u201337 weeks postmenstrual age\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOR\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E at \u003C/span\u003E\u003Cb\u003E4 weeks postnatal age\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u2192 \u003C/span\u003EUse whichever is \u003Cb\u003Esooner\u003C/b\u003E\u003C/p\u003E\u003C/blockquote\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EThe full guidelines:\u0026nbsp;\u003C/span\u003E\u003Ca href=\u0022https://www.rcpch.ac.uk/sites/default/files/2024-10/rop-screening-guideline-full-2022_updated-2024.pdf\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EUK screening of retinopathy of prematurity guideline - 2024\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 295,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 53-year-old woman with \u003Cspan class=\u0022s1\u0022\u003Etype 1 diabetes\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003Eprimary open angle glaucoma\u003C/span\u003E presents with progressive visual loss in her \u003Cspan class=\u0022s1\u0022\u003Eright eye\u003C/span\u003E. Her visual acuity is \u003Cspan class=\u0022s1\u0022\u003E6/18\u003C/span\u003E, and OCT reveals \u003Cspan class=\u0022s1\u0022\u003Ecentral macular thickness of 500\u202F\u00B5m\u003C/span\u003E. Fundus fluorescein angiography shows a \u003Cspan class=\u0022s1\u0022\u003Emixed ischaemic-exudative pattern\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most appropriate management?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EKey considerations for this patient:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003EOCT shows central macular thickening \u2265500 \u03BCm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u2192 qualifies for anti-VEGF under \u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003ENICE guidelines\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFFA shows mixed ischaemic and exudative maculopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnti-VEGF is still appropriate, even if macula is ischaemic.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EResponse may be reduced, but treatment is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot contraindicated\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECoexisting glaucoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteroids (e.g., triamcinolone)\u003C/b\u003E\u003C/span\u003E risk raising IOP - not ideal here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEvidence from key studies:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDRCR.net Protocol I\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003ERESTORE\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E trial:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\uD83D\uDC49 \u003Ci\u003ERanibizumab is superior to laser monotherapy.\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\uD83D\uDC49 \u003Ci\u003EIn patients with good glycaemic control, anti-VEGF leads to better functional outcomes.\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ol\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Col start=\u00221\u0022\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 296,
    "Name": "OHT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 72-year-old woman is referred by her optometrist with an intraocular pressure (IOP) of \u003Cspan class=\u0022s1\u0022\u003E23 mmHg\u003C/span\u003E. Gonioscopy confirms \u003Cspan class=\u0022s1\u0022\u003Eopen angles\u003C/span\u003E, and her \u003Cspan class=\u0022s1\u0022\u003Ecentral corneal thickness (CCT) is 535 \u00B5m\u003C/span\u003E. Optic discs are healthy and visual fields are full.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EAccording to the \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E2022 NICE NG81 guidelines\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, what is the most appropriate management for this patient?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAccording to the \u003C/span\u003E\u003Cb\u003E2022 NICE NG81 guidelines\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the decision to \u003C/span\u003E\u003Cb\u003Etreat or monitor ocular hypertension (OHT)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E depends on:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIOP level\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAge\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECentral corneal thickness (CCT)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPresence of optic nerve damage or visual field defects\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EIn this patient:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIOP = 23 mmHg\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003EBelow treatment threshold\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECCT = 535 \u00B5m\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003ENormal\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo disc or field changes\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAge = 72 years\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003EFor patients \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eaged 60\u002B\u003C/b\u003E\u003C/span\u003E with:\u003C/blockquote\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003EIOP between 22\u201325 mmHg\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/blockquote\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003ENormal CCT\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/blockquote\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cb\u003ENo glaucomatous damage\u003C/b\u003E\u003C/blockquote\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14); min-height: 19.4px;\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; color: rgb(14, 14, 14);\u0022\u003E\u003Cspan style=\u0022font-family: Arial; font-size: large;\u0022\u003E\u2705 NICE 2022 \u003Cspan class=\u0022s3\u0022 style=\u0022\u0022\u003E\u003Cb\u003Erecommends discharge from care\u003C/b\u003E\u003C/span\u003E, with advice to attend regular sight tests.\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-24-014e7828-b4c2-48d7-a856-edd8168b1d7d.png\u0022\u003E\u003C/p\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cbr\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUnder the 2022 NICE guidelines, patients over 60 with IOP \u0026lt;26 mmHg, normal CCT, and no disc or field changes can be safely discharged.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 297,
    "Name": "OHT",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 58-year-old man is referred by his optician with \u003C/span\u003Ebilateral raised intraocular pressure (IOP)\u003Cspan class=\u0022s1\u0022\u003E. Goldmann tonometry confirms \u003C/span\u003EIOP of 26 mmHg in both eyes\u003Cspan class=\u0022s1\u0022\u003E, with \u003C/span\u003Ecentral corneal thickness (CCT) of 567 \u00B5m\u003Cspan class=\u0022s1\u0022\u003E. There is \u003C/span\u003Eno evidence of glaucomatous optic neuropathy or visual field loss\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EAccording to the \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E2022 NICE Glaucoma Guideline (NG81)\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, what is the most appropriate management?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2022 NICE NG81\u003C/b\u003E\u003C/span\u003E guideline reflects updated evidence, including data from the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELiGHT Trial\u003C/b\u003E\u003C/span\u003E, which demonstrated that \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESLT is at least as effective as topical medications\u003C/b\u003E\u003C/span\u003E in lowering IOP and delaying disease progression in ocular hypertension (OHT) and early primary open-angle glaucoma (POAG).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003E\uD83D\uDD0D This patient:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP = 26 mmHg\u003C/b\u003E\u003C/span\u003E \u2192 exceeds the treatment threshold\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECCT = 567 \u03BCm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 not thin, but does \u003C/span\u003E\u003Cb\u003Enot alter decision to treat\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E at this IOP\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAge = 58 years\u003C/b\u003E\u003C/span\u003E \u2192 not suitable for discharge\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo glaucoma yet \u2192 diagnosis = ocular hypertension\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 1.75rem; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022letter-spacing: 0.14994px; font-size: large;\u0022\u003ENICE NG81 (2022) Recommendation:\u003C/b\u003E\u003C/h3\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u201C\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOffer SLT as first-line treatment\u003C/b\u003E\u003C/span\u003E to people with ocular hypertension or chronic open-angle glaucoma if they are suitable for treatment.\u201D\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cblockquote style=\u0022margin-bottom: 0px; margin-left: 15px; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-size-adjust: none; font-language-override: normal; font-kerning: auto; font-optical-sizing: auto; font-feature-settings: normal; font-variation-settings: normal; font-variant-position: normal; font-variant-emoji: normal; font-stretch: normal; line-height: normal; font-family: \u0026quot;Helvetica Neue\u0026quot;; color: rgb(14, 14, 14);\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u2013 If SLT is \u003C/span\u003E\u003Cb\u003Enot suitable\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, offer a \u003C/span\u003E\u003Cb\u003Egeneric prostaglandin analogue\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/blockquote\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003ETherefore, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESLT is the preferred first-line intervention\u003C/b\u003E\u003C/span\u003E in eligible patients, as in this case.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium;\u0022\u003EOther options are incorrect:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: medium;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB. Beta-blocker\u003C/b\u003E\u003C/span\u003E\u0026nbsp;: Used if prostaglandins and SLT are not suitable or tolerated\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC. Discharge:\u003C/b\u003E\u003C/span\u003E\u0026nbsp;Not appropriate with IOP \u226526 mmHg\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ED. Prostaglandin analogue:\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E\u0026nbsp;Acceptable \u003C/span\u003E\u003Cb\u003Eif SLT is not suitable\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but not the first-line per NG81\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p6\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p6\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p6\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p6\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-24-5d1374eb-5b97-4da9-89ff-90c979d27837.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 298,
    "Name": "ROP",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAccording to the \u003C/span\u003Emost recent Royal College of Ophthalmologists guidelines\u003Cspan class=\u0022s1\u0022\u003E for the treatment of \u003C/span\u003Eretinopathy of prematurity (ROP)\u003Cspan class=\u0022s1\u0022\u003E, which of the following clinical scenarios \u003C/span\u003Emeets the treatment threshold\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecurrent RCOphth guidance\u003C/b\u003E\u003C/span\u003E for ROP treatment thresholds aligns with the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EETROP (Early Treatment for ROP) study\u003C/b\u003E\u003C/span\u003E and international consensus. Treatment is recommended for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EType 1 ROP\u003C/b\u003E\u003C/span\u003E, defined as:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EZone I\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, any stage \u003C/span\u003E\u003Cb\u003Ewith plus disease\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EZone I\u003C/b\u003E\u003C/span\u003E, Stage 3 (even \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewithout\u003C/b\u003E\u003C/span\u003E plus disease)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EZone II\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, Stage 2 or 3 \u003C/span\u003E\u003Cb\u003Ewith plus disease\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EZone II Stage 2 with plus disease \u003C/span\u003E\u003Cb\u003Eclearly meets the threshold for treatment\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EWhy the other options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EA. Zone III, Stage 3 with plus\u003C/b\u003E\u003C/span\u003E \u2192 Treatment is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot indicated\u003C/b\u003E\u003C/span\u003E; zone III is peripheral, and stage 3 alone doesn\u2019t meet criteria\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB. Zone I, Stage 1 with plus\u003C/b\u003E\u003C/span\u003E \u2192 Stage 1 in Zone I even with plus is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot sufficient\u003C/b\u003E\u003C/span\u003E unless progression is evident\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ED. Zone II, Stage 3 without plus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003EPlus disease is essential\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E for treatment indication in Zone II\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EAccess the full guidelines:\u0026nbsp;\u003C/b\u003E\u003Ca href=\u0022https://www.rcophth.ac.uk/wp-content/uploads/2022/03/Treating-Retinopathy-of-Prematurity-in-the-UK.pdf\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ETreating ROP - 2025 RCOphth guidelines\u003C/a\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-24-907ec723-bada-4672-b0ed-4138d2297d2e.png\u0022\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 299,
    "Name": "MRI",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is a \u003Cspan class=\u0022s1\u0022\u003Econtraindication to MRI\u003C/span\u003E scanning?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECochlear implants\u003C/b\u003E\u003C/span\u003E are generally considered a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econtraindication to MRI\u003C/b\u003E\u003C/span\u003E, particularly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eolder models\u003C/b\u003E\u003C/span\u003E that are not MRI-compatible. Some modern cochlear implants may be conditionally safe at specific field strengths, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emany still pose risks\u003C/b\u003E\u003C/span\u003E of heating, movement, or malfunction due to the magnetic field.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large; text-decoration-line: underline;\u0022\u003EOther options:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAllergy to gadolinium\u003C/b\u003E\u003C/span\u003E \u2192 Not a contraindication to MRI itself; only to contrast-enhanced studies. Non-contrast MRI can still be performed safely.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFirst trimester pregnancy\u003C/b\u003E\u003C/span\u003E \u2192 MRI is not absolutely contraindicated. Although caution is advised due to theoretical risks, it may still be justified if essential and without contrast.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETitanium ocular implant\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Titanium is \u003C/span\u003E\u003Cb\u003Enon-ferromagnetic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and MRI-safe.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 300,
    "Name": "Pellucid marginal degeneration",
    "Body": "\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-24-c06c471f-7bf9-417a-8399-0f3c4e12bff2.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EBased on the corneal topography image provided, which of the following is the \u003Cspan class=\u0022s1\u0022\u003Emost likely diagnosis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe image shows \u003C/span\u003E\u003Cb\u003Eclassic features of Pellucid Marginal Degeneration (PMD)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInferior peripheral corneal steepening\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u201CCrab claw\u201D or kissing dove appearance\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E on the topographic map\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe area of steepening is \u003C/span\u003E\u003Cb\u003Ebelow the visual axis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, with \u003C/span\u003E\u003Cb\u003Ecentral corneal thinning absent\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe central cornea remains relatively flat, and astigmatism is typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eagainst-the-rule\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EWhy other options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMooren\u2019s ulcer\u003C/b\u003E\u003C/span\u003E \u2192 Presents as a peripheral, crescent-shaped stromal ulcer with overhanging edges, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot associated with this topographic pattern\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EKeratoconus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Typically shows \u003C/span\u003E\u003Cb\u003Ecentral or paracentral steepening\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and thinning, not the \u003C/span\u003E\u003Cb\u003Einferior band pattern\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPost-LASIK ectasia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 Would show \u003C/span\u003E\u003Cb\u003Ecentral or paracentral irregularity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and often \u003C/span\u003E\u003Cb\u003Ecentral thinning\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not peripheral steepening\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 301,
    "Name": "Thryoid Investigations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following \u003Cspan class=\u0022s1\u0022\u003Eimaging modalities\u003C/span\u003E is most useful in assessing \u003Cspan class=\u0022s1\u0022\u003Edisease activity\u003C/span\u003E in a patient with thyroid eye disease?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESTIR sequence in MRI\u003C/b\u003E\u003C/span\u003E is the most helpful imaging modality for evaluating \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eactive orbital inflammation\u003C/b\u003E\u003C/span\u003E in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethyroid eye disease (TED)\u003C/b\u003E\u003C/span\u003E. STIR is a fat-suppressed sequence that enhances the visibility of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esoft tissue oedema\u003C/b\u003E\u003C/span\u003E, including within the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eextraocular muscles\u003C/b\u003E\u003C/span\u003E, and correlates well with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EClinical activity score (CAS)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDisease activity phase\u003C/b\u003E\u003C/span\u003E (active vs quiescent)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EResponse to immunosuppression\u003C/b\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis makes it superior to standard MRI sequences or CT for evaluating \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edisease activity\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EContrast-enhanced CT scan\u003C/b\u003E\u003C/span\u003E \u2192 Useful for anatomy and surgical planning, but not for assessing inflammatory activity\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFLAIR MRI\u003C/b\u003E\u003C/span\u003E \u2192 Used for neuroimaging (e.g., demyelination); not optimal for orbit\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ET1-weighted MRI\u003C/b\u003E\u003C/span\u003E \u2192 Good for structural definition, but not sensitive to inflammation or oedema\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 302,
    "Name": "Diabetes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAccording to the \u003C/span\u003Emost recent WHO diagnostic criteria\u003Cspan class=\u0022s1\u0022\u003E, which of the following findings \u003C/span\u003Emeets the threshold for a diagnosis of diabetes mellitus\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Elatest WHO criteria\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (2019 and reaffirmed in 2022) state that \u003C/span\u003E\u003Cb\u003Ediabetes mellitus can be diagnosed\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in any of the following situations \u003C/span\u003E\u003Cb\u003E(confirmed on repeat testing unless symptoms are present):\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFasting plasma glucose \u2265 7.0 mmol/L\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E2-hour plasma glucose \u2265 11.1 mmol/L\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E during an OGTT\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERandom plasma glucose \u2265 11.1 mmol/L\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in a patient with symptoms\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHbA1c \u2265 6.5% (48 mmol/mol)\u003C/b\u003E\u003C/span\u003E using a standardised method\u003C/p\u003E\n\u003C/li\u003E\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHbA1c \u0026gt; 6.0%\u003C/b\u003E\u003C/span\u003E \u2192 Below diagnostic threshold (must be \u2265 6.5%)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFasting plasma glucose \u0026gt; 6.5 mmol/L\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2192 \u003C/span\u003E\u003Cb\u003Ediagnostic threshold is \u2265 7.0 mmol/L\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ED. Glucosuria\u003C/b\u003E\u003C/span\u003E \u2192 Non-specific; not diagnostic without blood glucose confirmation\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 303,
    "Name": "Consent",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAn 84-year-old woman with dense bilateral cataracts and \u003Cspan class=\u0022s1\u0022\u003Eadvanced dementia\u003C/span\u003E attends clinic. She is \u003Cspan class=\u0022s1\u0022\u003Eunable to understand, retain, or weigh medical information\u003C/span\u003E, and therefore \u003Cspan class=\u0022s1\u0022\u003Elacks capacity\u003C/span\u003E to consent for surgery. Which of the following statements is \u003Cspan class=\u0022s1\u0022\u003Ecorrect\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EUnder the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMental Capacity Act (2005)\u003C/b\u003E\u003C/span\u003E, if an adult lacks capacity:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehealth and welfare LPA\u003C/b\u003E\u003C/span\u003E, registered and in effect, has legal authority to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emake decisions\u003C/b\u003E\u003C/span\u003E regarding medical treatment, including consent to or refusal of surgery.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsence\u003C/b\u003E\u003C/span\u003E of such an LPA, healthcare professionals must act in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epatient\u2019s best interests\u003C/b\u003E\u003C/span\u003E, following a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebest interest meeting\u003C/b\u003E\u003C/span\u003E process involving the care team and family.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENext of kin alone has no legal standing\u003C/b\u003E\u003C/span\u003E to consent unless they are the registered LPA.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn most cases, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecapacity assessments are clinical\u003C/b\u003E\u003C/span\u003E and do \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot require a psychiatrist\u003C/b\u003E\u003C/span\u003E, unless the case is complex or contested.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EOnly a registered health and welfare LPA can legally provide consent for a patient who lacks capacity; next of kin cannot.\u003C/b\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 304,
    "Name": "DVLA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient attends a cataract pre\u2011assessment clinic. His \u003C/span\u003Ebinocular visual acuity is 6/15\u003Cspan class=\u0022s1\u0022\u003E, but he is able to \u003C/span\u003Eread a vehicle number plate at 20\u202Fmetres in good daylight\u003Cspan class=\u0022s1\u0022\u003E. Slit\u2011lamp examination reveals \u003C/span\u003Ebilateral cortical cataracts\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat advice regarding \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003Edriving\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E should be given to this patient?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EAccording to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDVLA Group 1 (car and motorcycle) visual standards\u003C/b\u003E\u003C/span\u003E, a patient must meet \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eboth\u003C/b\u003E\u003C/span\u003E of the following criteria to drive legally:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00221\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENumber plate test\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAbility to read a vehicle registration plate at \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E20 metres\u003C/b\u003E\u003C/span\u003E in good daylight (post\u2011September 2001 plates)\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ol\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EAND\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Col start=\u00222\u0022\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVisual acuity requirement\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBinocular best\u2011corrected visual acuity of at least 6/12 (Snellen 0.5)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOr 6/12 in the only eye if monocular\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ol\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBecause \u003C/span\u003E\u003Cb\u003Eboth criteria must be satisfied\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, this patient \u003C/span\u003E\u003Cb\u003Edoes not meet the DVLA legal standard for driving\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, regardless of lighting conditions.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThere is \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eno provision\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E in DVLA guidance allowing patients to drive only in good light, and clinicians should not give conditional advice that contradicts DVLA rules.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Col start=\u00222\u0022\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ol\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 305,
    "Name": "Drug induced Optic neuropathy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following medications is \u003C/span\u003Emost likely to cause an optic neuropathy\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmiodarone\u003C/b\u003E\u003C/span\u003E is a well-established cause of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edrug-induced optic neuropathy\u003C/b\u003E\u003C/span\u003E, typically presenting as:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPainless, bilateral or asymmetric vision loss\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESwollen or pale optic discs\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESlowly progressive course\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften seen in patients on long-term therapy\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: large;\u0022\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: large;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETamoxifen\u003C/b\u003E\u003C/span\u003E \u2192 Causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecrystalline maculopathy\u003C/b\u003E\u003C/span\u003E and retinal pigment epithelial changes, not optic neuropathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGold\u003C/b\u003E\u003C/span\u003E \u2192 Known to cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eocular chrysiasis\u003C/b\u003E\u003C/span\u003E (corneal and conjunctival gold deposits), but not optic neuropathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECidofovir\u003C/b\u003E\u003C/span\u003E \u2192 Associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior uveitis\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehypotony\u003C/b\u003E\u003C/span\u003E, not optic nerve damage\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EAmiodarone is one of several drugs known to cause optic neuropathy, alongside ethambutol, isoniazid, vigabatrin, and chloramphenicol.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 306,
    "Name": "Retinoschisis",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EWhich of the following is least consistent\nwith the diagnosis of retinoschisis?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EHigh myopia\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700; font-style: italic; text-decoration-line: underline;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u0026nbsp;Explanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ERetinoschisis is a splitting of the neurosensory retina into two layers, typically at the outer plexiform layer (between the outer nuclear layer and inner nuclear layer). It is most commonly degenerative (acquired) in nature and must be distinguished from rhegmatogenous retinal detachment.\u003C/div\u003E\u003Cdiv\u003EUnderstanding the clinical features helps differentiate these conditions and guide appropriate management.\n\nHigh myopia is actually a risk factor for retinal detachment, not retinoschisis. Degenerative retinoschisis typically occurs in hyperopic or emmetropic eyes, affecting 7% of the population over 40 years. The association with myopia is weak, making this the least consistent feature with retinoschisis diagnosis. In contrast, high myopia is strongly associated with posterior vitreous detachment and tractional retinal breaks leading to rhegmatogenous retinal detachment.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EThe remaining options are characteristic features of retinoschisis: The beaten metal or \u0022frosted\u0022 appearance on the inner retinal surface is a pathognomonic sign of retinoschisis. This results from the splitting of retinal layers creating a shimmering, reflective quality on the inner leaf of the schisis cavity. This appearance is highly specific for retinoschisis and helps distinguish it from retinal detachment.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EDegenerative retinoschisis has a characteristic bilateral distribution, most commonly affecting the inferotemporal quadrant (60-70% of cases), followed by the superotemporal quadrant. This bilateral, symmetric presentation in the inferotemporal location is a classic feature. In contrast, rhegmatogenous retinal detachments are typically unilateral and more commonly occur in the superior quadrants due to gravity-dependent subretinal fluid accumulation.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EWhen laser photocoagulation is applied to retinoschisis, there is typically no visible reaction or whitening because the inner leaf of the split retina lacks normal metabolic activity and the photoreceptors are separated from the RPE by the outer leaf. This absence of laser uptake is a key distinguishing feature. A visible laser reaction would suggest an intact retina, as seen in retinal detachment where the sensory retina remains as one layer (though detached from RPE). The question asks for \u0022least consistent,\u0022 so the presence of a visible reaction would actually argue against retinoschisis.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u0026nbsp;Mnemonic:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E \u0022Retinoschisis - SPLIT\u0022\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\nS = Symmetric and bilateral\u003C/div\u003E\u003Cdiv\u003EP = Progresses slowly\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EL = Lower (inferotemporal) location most common\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EI = Inner leaf has beaten metal appearance\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003ET = Thin, immobile, no holes typically seen\u0026nbsp;\u003C/div\u003E\u003C/div\u003E",
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    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 307,
    "Name": "IOL Refractive Surprise - Hyperopic Shift",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EA patient undergoes routine cataract surgery\nwith a planned refractive outcome of -0.5DS. The axial length was 23.0 mm. When\nrefracted four weeks postoperatively they are found to be \u002B2.50DS. Of the\nfollowing, which is the MOST likely cause of this refractive surprise?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EThe correct answer is\u003C/span\u003E: \u003Cspan style=\u0022font-weight: bold;\u0022\u003EThe A constant used in the biometry calculation was too low for the implanted IOL.\u003C/span\u003E\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;The key to this question lies in understanding the relationship between IOL power and refractive outcome.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003EP = A \u2212 0.9K \u2212 2.5AL\u003C/div\u003E\u003Cdiv\u003EWhen an A constant is too low, the biometry formula systematically predicts a lower intraocular lens power than is optically required for that particular eye. Since a weaker IOL produces a hyperopic (positive) refractive shift, this mechanism directly explains the observed outcome: the patient targeted \u22120.5 DS but achieved \u002B2.50 DS, representing approximately a \u002B3.0 dioptre hyperopic surprise.\u003C/div\u003E\u003Cdiv\u003EThe axial length of 23.0 mm is normal, making formula selection differences between Hoffer Q and SRK/T irrelevant\u2014both would be concordant at this length.\u003C/div\u003E\u003Cdiv\u003ESulcus placement without power adjustment would position the IOL more anteriorly, making it effectively stronger and causing a myopic shift in the opposite direction from what was observed.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EReversed implantation of an anteriorly angulated posterior-biconvex IOL typically produces a myopic shift of up to 0.9 dioptre, not the substantial hyperopic surprise documented here.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ETherefore, a systematic biometry error caused by an insufficiently low A constant represents the most parsimonious explanation for this refractive outcome in an otherwise normal-length eye.\u003C/span\u003E\u003C/div\u003E",
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    "CategoryId": 1,
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  },
  {
    "Id": 308,
    "Name": "Fundus Fluorescein Angiography - Protein Binding",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EWhich of the following statements regarding\nFundus Fluorescein Angiography (FFA) is LEAST likely to be true?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThe dye used in FFA is more protein bound in the blood compared with ICG (Indocyanine Green)\u003C/span\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EProtein Binding Facts:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;- Fluorescein (used in Fundus Fluorescein Angiography):\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E70-85% protein-bound to serum albumin\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E- Indocyanine Green: \u0026gt;98% protein-bound to albumin, alpha-1 lipoproteins, and globulins\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-style: italic; text-decoration-line: underline;\u0022\u003E\u0026nbsp;Analysis of Other Options (Why They Are TRUE):\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-style: italic; text-decoration-line: underline;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EClassic choroidal neovascularization shows a characteristic Fundus Fluorescein Angiography pattern. In the early phase (first 1-2 minutes), the choroidal neovascularization membrane appears hypo-fluorescent (dark) because the newly formed vessels have not yet filled with dye. As the angiogram progresses, classic choroidal neovascularization demonstrates progressive hyperfluorescence with well-demarcated lacy borders in a wheel-spoke pattern, followed by late leakage (5-10 minutes) that obscures the boundaries. This early hypo-fluorescence transitioning to hyperfluorescence is a defining characteristic of classic choroidal neovascularization according to the Macular Photocoagulation Study criteria.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EOccult choroidal neovascularization includes two subtypes: fibrovascular pigment epithelial detachment and late leakage of undetermined source. Both subtypes demonstrate early hypo-fluorescence before late-phase changes become apparent. Fibrovascular pigment epithelial detachment shows irregular retinal pigment epithelium elevation with early hypo-fluorescence or stippled fluorescence, followed by late persistent fluorescence. Late leakage of undetermined source shows no hyperfluorescence in the early phase (remaining hypo-fluorescent), with speckled hyperfluorescence appearing only in the late phase (after 2-5 minutes). The key distinguishing feature from classic choroidal neovascularization is that occult lesions show late leakage without early well-demarcated hyperfluorescence.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhile the choroid receives 85-90% of ocular blood flow and blood reaches both circulations nearly simultaneously (around 10-15 seconds), clinically we visualize distinct retinal arterial filling at 10-12 seconds as clearly defined vascular structures, while the choroidal flush appears at 10-15 seconds as diffuse background fluorescence. The retinal vessels are the first clearly identifiable vascular structures that \u0022light up\u0022 individually during Fundus Fluorescein Angiography. The choroid fills as a diffuse \u0022flush\u0022 rather than as distinct individual vessels. From a clinical Fundus Fluorescein Angiography interpretation perspective, we identify and describe retinal arterial filling as a distinct phase, making this statement true in clinical practice.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E",
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    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 309,
    "Name": "Ocular Myasthenia Gravis - Clinical Signs",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EWhich of the following clinical signs is LEAST\nlikely to be of help in making the diagnosis of ocular myasthenia gravis?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E \u003Cspan style=\u0022font-weight: bold;\u0022\u003EBilateral symmetrical ptosis\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EExplanation:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Ocular myasthenia gravis is an autoimmune disorder caused by antibodies against acetylcholine receptors at the neuromuscular junction. This leads to fatigable muscle weakness that worsens with sustained activity and improves with rest. The hallmark clinical feature is the development of asymmetric ocular muscle weakness that demonstrates clear fatigability.\u003C/div\u003E\u003Cdiv\u003EBilateral symmetrical ptosis is LEAST helpful because bilateral symmetrical ptosis is atypical for myasthenia gravis. The condition characteristically produces asymmetric or unilateral ptosis that may fluctuate throughout the day. When ptosis is bilateral in myasthenia, one eyelid is almost always more affected than the other, creating noticeable asymmetry. Finding perfectly symmetrical bilateral ptosis should prompt consideration of alternative diagnoses such as bilateral third nerve palsy, chronic progressive external ophthalmoplegia, mitochondrial myopathy, or oculopharyngeal muscular dystrophy. This sign would actually suggest against myasthenia gravis rather than support the diagnosis.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ESustained closure of the eye lids giving rise to scleral show is helpful as it describes the orbicularis oculi fatigue phenomenon. When patients forcefully close their eyelids for a sustained period, the orbicularis muscles fatigue. Upon opening the eyes, there is incomplete relaxation and persistent contraction causing lid retraction, which reveals white sclera below the inferior limbus (scleral show). This fatigability of the orbicularis muscle is characteristic of myasthenia gravis and represents a useful bedside test.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ESustained upgaze producing bilateral ptosis is very helpful as sustained upgaze is one of the most valuable clinical tests for ocular myasthenia. Asking the patient to maintain upgaze for 30-60 seconds places sustained demand on the levator palpebrae superioris. In myasthenia gravis, progressive ptosis develops as the muscle fatigues, often becoming apparent within 30 seconds. The degree of ptosis typically worsens the longer upgaze is maintained and improves dramatically after a brief period of rest with eyes closed. This fatigue test has high sensitivity and specificity for ocular myasthenia.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EUpper lid twitching on return to primary position after prolonged downgaze is specifc to MG and it is called\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ECogan\u0027s Lid Twitch Sign.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 310,
    "Name": "Cyclophosphamide Side Effects in Granulomatosis Polyangiitis",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EA 55 year old man with granulomatosis\npolyangiitis is being treated with cyclophosphamide. Which of these drug side\neffects is he MOST likely to experience?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EMarrow suppression\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline; font-style: italic;\u0022\u003EExplanation:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;Cyclophosphamide is an alkylating agent commonly used to treat severe systemic vasculitis including granulomatosis polyangiitis (formerly Wegener\u0027s granulomatosis). While it has multiple potential side effects, bone marrow suppression (myelosuppression) is the most frequently encountered adverse effect, affecting nearly all patients to some degree.\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ECyclophosphamide causes dose-dependent bone marrow toxicity that primarily affects rapidly dividing white blood cells (leukopenia/neutropenia), followed by platelets (thrombocytopenia), and less commonly red blood cells (anemia). The nadir of white blood cell count typically occurs 7-14 days after each dose. Regular monitoring with complete blood counts is essential, and doses must be reduced or delayed if white cell counts fall below safe thresholds (typically WCC \u0026lt; 4.0 x 10\u2079/L or neutrophils \u0026lt; 1.5 x 10\u2079/L). Severe myelosuppression increases infection risk and can be life-threatening, making this the most clinically significant side effect requiring constant vigilance.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ECyclophosphamide commonly causes - alopecia (hair loss) not Hirsutism. Hirsutism is more characteristic of corticosteroid therapy or medications with androgenic effects.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhile hemorrhagic cystitis is indeed a serious and potentially life-threatening complication of cyclophosphamide therapy, it occurs less frequently than bone marrow suppression. Hemorrhagic cystitis develops in approximately 10-40% of patients (depending on cumulative dose and duration), whereas myelosuppression affects virtually all patients to some degree. The toxic metabolite acrolein causes direct bladder damage, and risk is reduced through adequate hydration, frequent voiding, and administration of mesna (which binds and neutralizes acrolein). However, in terms of frequency, marrow suppression remains more common.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EOsteoporosis is NOT a direct side effect of cyclophosphamide.\u003C/span\u003E\u003C/div\u003E",
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    "CategoryId": 5,
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  },
  {
    "Id": 311,
    "Name": "Basilar artery syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA man wakes from a coma with \u003C/span\u003Ebilateral complete ophthalmoplegia\u003Cspan class=\u0022s1\u0022\u003E, including \u003C/span\u003Epupil involvement\u003Cspan class=\u0022s1\u0022\u003E, and reports \u003C/span\u003Evisual disturbance\u003Cspan class=\u0022s1\u0022\u003E. Examination reveals \u003C/span\u003Enormal motor function in all limbs\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich vessel is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely site of embolic occlusion\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis clinical picture is characteristic of \u003C/span\u003E\u003Cb\u003E\u201Ctop of the basilar syndrome\u201D\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, caused by an \u003C/span\u003E\u003Cb\u003Eembolic occlusion at the distal end of the basilar artery\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. This territory includes:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERostral brainstem\u003C/b\u003E\u003C/span\u003E (midbrain and upper pons)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThalami\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOccipital lobes\u003C/b\u003E\u003C/span\u003E (via posterior cerebral arteries)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EKey features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBilateral ophthalmoplegia\u003C/b\u003E\u003C/span\u003E (often involving all cranial nerves controlling eye movement)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPupil involvement\u003C/b\u003E\u003C/span\u003E due to oculomotor nerve and midbrain damage\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVisual hallucinations or cortical blindness\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPreserved motor function in limbs\u003C/b\u003E\u003C/span\u003E, since corticospinal tracts are often spared\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInternal carotid artery\u003C/b\u003E\u003C/span\u003E \u2192 Would likely affect anterior circulation (e.g. MCA/ACA territory), often with unilateral motor/sensory deficits\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPICA\u003C/b\u003E\u003C/span\u003E \u2192 Classically causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elateral medullary syndrome\u003C/b\u003E\u003C/span\u003E (Wallenberg), which includes vertigo, ataxia, and sensory deficits;\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot complete ophthalmoplegia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPCOM\u003C/b\u003E\u003C/span\u003E \u2192 Can compress the third nerve causing \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eisolated CN III palsy\u003C/b\u003E\u003C/span\u003E, but not bilateral ophthalmoplegia with visual cortex signs\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBilateral ophthalmoplegia with pupil involvement and visual disturbance, but preserved motor function, strongly suggests top of the basilar artery syndrome.\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-26-7750b5a2-1914-48e2-902c-8865687df9ef.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 312,
    "Name": "Facial nerve palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA lesion in which of the following anatomical locations is most likely to cause \u003Cspan class=\u0022s1\u0022\u003Einability to fully close the eyelid\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eorbicularis oculi muscle\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, responsible for \u003C/span\u003E\u003Cb\u003Eeyelid closure\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, is innervated by the \u003C/span\u003E\u003Cb\u003Etemporal and zygomatic branches of the facial nerve (CN VII)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. A lesion affecting the \u003C/span\u003E\u003Cb\u003Efacial nerve\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E therefore impairs eyelid closure.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EThe \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ecerebellopontine angle (CPA)\u003C/b\u003E\u003C/span\u003E is the most common site for lesions (e.g. acoustic neuroma/vestibular schwannoma, meningioma) that involve multiple cranial nerves\u2014especially:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECN V (trigeminal)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECN VI (abducens)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECN VII (facial)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECN VIII (vestibulocochlear)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EA CPA lesion affecting \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003ECN VII\u003C/b\u003E\u003C/span\u003E results in \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eipsilateral facial palsy\u003C/b\u003E\u003C/span\u003E, including \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eincomplete eyelid closure\u003C/b\u003E\u003C/span\u003E (lagophthalmos).\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECavernous sinus\u003C/b\u003E\u003C/span\u003E \u2192 Affects CN III, IV, V1/V2, and VI\u2014but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot CN VII\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVentral midbrain\u003C/b\u003E\u003C/span\u003E \u2192 Typically involves ocular motor pathways (CN III, vertical gaze), not eyelid closure\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELateral medulla\u003C/b\u003E\u003C/span\u003E \u2192 Causes lateral medullary syndrome (e.g. dysphagia, vertigo, Horner\u2019s), but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot CN VII dysfunction\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 313,
    "Name": "Cerebellopontine angle tumour",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following conditions is \u003C/span\u003Emost likely\u003Cspan class=\u0022s1\u0022\u003E to present with \u003C/span\u003Efacial paralysis\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Eipsilateral loss of corneal sensation\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecerebellopontine angle tumour\u003C/b\u003E\u003C/span\u003E (e.g. vestibular schwannoma) typically affects cranial nerves:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECN V\u003C/b\u003E\u003C/span\u003E \u2013 sensory loss in the face and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ereduced corneal sensation\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECN VI\u003C/b\u003E\u003C/span\u003E \u2013 abduction weakness\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECN VII\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2013 \u003C/span\u003E\u003Cb\u003Efacial weakness/paralysis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECN VIII\u003C/b\u003E\u003C/span\u003E \u2013 sensorineural hearing loss and tinnitus\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThis makes it the \u003C/span\u003E\u003Cb\u003Eclassic lesion causing both facial nerve palsy and ipsilateral reduced corneal reflex\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, due to simultaneous involvement of \u003C/span\u003E\u003Cb\u003ECN V and CN VII\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMillard-Gubler syndrome\u003C/b\u003E\u003C/span\u003E \u2192 Lesion in the pons affecting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECN VI and VII\u003C/b\u003E\u003C/span\u003E, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot CN V\u003C/b\u003E\u003C/span\u003E, so corneal sensation is preserved\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECavernous sinus meningioma\u003C/b\u003E\u003C/span\u003E \u2192 Affects CN III, IV, V1/V2, VI, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot CN VII\u003C/b\u003E\u003C/span\u003E (facial motor)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGradenigo\u2019s syndrome\u003C/b\u003E\u003C/span\u003E \u2192 Affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECN V and VI\u003C/b\u003E\u003C/span\u003E, due to petrous apicitis; facial paralysis is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E a feature\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 314,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 26-year-old woman presents with \u003Cspan class=\u0022s1\u0022\u003Eanisocoria\u003C/span\u003E, first noted 3 days ago. Examination reveals a \u003Cspan class=\u0022s1\u0022\u003Edilated, non-reactive left pupil\u003C/span\u003E, while the right pupil shows normal direct and consensual light reflexes.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EPharmacologic testing of the left pupil shows:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECocaine 4%\u003C/span\u003E \u2192 no change\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EHydroxyamphetamine 1%\u003Cspan class=\u0022s1\u0022\u003E \u2192 no change\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAdrenaline 1:1000\u003Cspan class=\u0022s1\u0022\u003E \u2192 no change\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EPilocarpine 1%\u003Cspan class=\u0022s1\u0022\u003E \u2192 no change\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis is a classic presentation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epharmacologic mydriasis\u003C/b\u003E\u003C/span\u003E, where the pupil is dilated due to exposure to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emydriatic agents\u003C/b\u003E\u003C/span\u003E (e.g. anticholinergics such as atropine or sympathomimetics).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EKey diagnostic clue:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Edilated pupil does not constrict with pilocarpine 1%\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which is a \u003C/span\u003E\u003Cb\u003Edirect muscarinic agonist\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEven Holmes-Adie or third nerve palsy pupils would constrict with pilocarpine 1%\u003C/b\u003E\u003C/span\u003E (due to denervation hypersensitivity or intact parasympathetic efferent pathway).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epharmacologically blocked iris sphincter\u003C/b\u003E\u003C/span\u003E will not respond to pilocarpine because receptors are blocked (e.g. atropine, tropicamide).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EAdditionally:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHorner\u2019s syndrome presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emiosis\u003C/b\u003E\u003C/span\u003E, not mydriasis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThird nerve palsy may cause mydriasis, but the pupil typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eresponds to pilocarpine\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHolmes-Adie pupil is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etonic\u003C/b\u003E\u003C/span\u003E and also \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eresponds to dilute pilocarpine (0.1%)\u003C/b\u003E\u003C/span\u003E due to cholinergic supersensitivity\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 315,
    "Name": "Midbrain syndromes",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA lesion results in \u003Cspan class=\u0022s1\u0022\u003Eipsilateral ophthalmoplegia\u003C/span\u003E (including ptosis and pupil involvement) and \u003Cspan class=\u0022s1\u0022\u003Econtralateral hemiplegia\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhere is the lesion most likely located?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis clinical picture is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWeber\u2019s syndrome\u003C/b\u003E\u003C/span\u003E, which is caused by a lesion in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eventromedial midbrain\u003C/b\u003E\u003C/span\u003E, typically due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eischaemia\u003C/b\u003E\u003C/span\u003E (e.g. from occlusion of penetrating branches of the posterior cerebral artery).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EKey findings in Weber\u2019s syndrome:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIpsilateral third nerve palsy\u003C/b\u003E\u003C/span\u003E: ptosis, ophthalmoplegia, mydriasis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EContralateral hemiparesis or hemiplegia\u003C/b\u003E\u003C/span\u003E: due to involvement of corticospinal tract in the cerebral peduncle\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDorsal midbrain\u003C/b\u003E\u003C/span\u003E \u2192 Associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EParinaud\u2019s syndrome\u003C/b\u003E\u003C/span\u003E (upgaze palsy, light-near dissociation), not hemiplegia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDorsal pons\u003C/b\u003E\u003C/span\u003E \u2192 May affect horizontal gaze centres and facial nerve (e.g. Foville\u2019s syndrome)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVentral pons\u003C/b\u003E\u003C/span\u003E \u2192 Classically associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMillard-Gubler\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elocked-in syndrome\u003C/b\u003E\u003C/span\u003E, typically involving CN VI/VII and corticospinal tract, but not CN III\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 316,
    "Name": "Parietal lobe lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient presents with a \u003C/span\u003Ecomplete left homonymous hemianopia\u003Cspan class=\u0022s1\u0022\u003E. On \u003C/span\u003Eoptokinetic nystagmus (OKN) testing\u003Cspan class=\u0022s1\u0022\u003E, they are \u003C/span\u003Eunable to follow the drum when rotated to the right\u003Cspan class=\u0022s1\u0022\u003E, but \u003C/span\u003Ecan follow it when rotated to the left\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhere is the most likely site of the lesion?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis is a classic description of a \u003C/span\u003E\u003Cb\u003Eright parietal lobe lesion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E affecting \u003C/span\u003E\u003Cb\u003Esmooth pursuit pathways\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. The \u003C/span\u003E\u003Cb\u003Eparietal lobe\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is responsible for \u003C/span\u003E\u003Cb\u003Eipsilateral visual attention and pursuit\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially for OKN in the \u003C/span\u003E\u003Cb\u003Esame direction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EIn this case:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eleft homonymous hemianopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E suggests a lesion \u003C/span\u003E\u003Cb\u003Eposterior to the optic chiasm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, most likely in the \u003C/span\u003E\u003Cb\u003Eright hemisphere\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Easymmetric OKN\u003C/b\u003E\u003C/span\u003E, where the patient fails to follow rightward motion, is characteristic of a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright parietal lesion\u003C/b\u003E\u003C/span\u003E, which impairs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eipsilateral pursuit\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EOccipital lobe lesions\u003C/b\u003E\u003C/span\u003E, even if they cause homonymous hemianopia, do \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Enot impair OKN responses\u003C/b\u003E\u003C/span\u003E, since pursuit pathways are intact.\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h4\u003E\u003Ch4\u003E\u003Cb\u003EOther options are incorrect:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERight frontal lobe\u003C/b\u003E\u003C/span\u003E \u2192 Affects saccades, not pursuit\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeft occipital lobe\u003C/b\u003E\u003C/span\u003E \u2192 Would cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright hemianopia\u003C/b\u003E\u003C/span\u003E, inconsistent with findings\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERight occipital lobe\u003C/b\u003E\u003C/span\u003E \u2192 Could cause left hemianopia, but would \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot impair OKN\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELeft parietal lobe\u003C/b\u003E\u003C/span\u003E \u2192 Would affect leftward OKN and right visual field\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/h3\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 317,
    "Name": "Pupil",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents with \u003Cspan class=\u0022s1\u0022\u003Eright-sided miosis and mild ptosis\u003C/span\u003E. Pharmacological testing of the \u003Cspan class=\u0022s1\u0022\u003Eright pupil\u003C/span\u003E shows:\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ECocaine 4%\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; --\u0026gt;\u0026nbsp;\u003C/span\u003ENo dilatation\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EHydroxyamphetamine 1%\u003Cspan class=\u0022Apple-tab-span\u0022\u003E\u0026nbsp;--\u0026gt;\u0026nbsp;\u003C/span\u003ENo dilatation\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhere is the lesion MOST likely located?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe clinical features and pharmacological test results are \u003C/span\u003E\u003Cb\u003Ediagnostic of a post-ganglionic (third-order) Horner\u2019s syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECocaine 4%\u003C/b\u003E\u003C/span\u003E blocks norepinephrine reuptake and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efails to dilate\u003C/b\u003E\u003C/span\u003E in Horner\u2019s (but does not localise the lesion).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHydroxyamphetamine 1%\u003C/b\u003E\u003C/span\u003E stimulates norepinephrine release from the post-ganglionic neuron.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo dilation with hydroxyamphetamine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E = \u003C/span\u003E\u003Cb\u003Epost-ganglionic lesion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003ELesions affecting the \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Einternal carotid artery\u003C/b\u003E\u003C/span\u003E (e.g. \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Ecarotid dissection\u003C/b\u003E\u003C/span\u003E, aneurysm, or cavernous sinus pathology) disrupt \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Ethird-order sympathetic fibres\u003C/b\u003E\u003C/span\u003E, which run with the artery into the skull.\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 318,
    "Name": "Non-Arteritic Anterior Ischaemic Optic Neuropathy (NAION)",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 70 year old hypertensive woman wakes with\npainless loss of vision in the right eye. She has a visual acuity of 6/18 in\nthe right eye and 6/6 in the left eye. Her right visual field shows an\naltitudinal defect. Her right optic disc is swollen. She has a CRP of 5 mg/L\nand a blood sugar of 13.5 mmol/L. Which of the following is the MOST likely\ndiagnosis?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003ENon-arteritic anterior ischaemic optic neuropathy\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline;\u0022\u003E\u0026nbsp;Explanation:\u003C/span\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThis presentation is most consistent with \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Enon-arteritic anterior ischaemic optic neuropathy (NAION);\u0026nbsp;\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Ethe most common acute optic neuropathy in individuals over 50. It is characterised by \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Epainless, sudden vision loss\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, often with an \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Ealtitudinal visual field defect\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Eoptic disc oedema\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, and \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Evascular risk factors\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E (e.g. diabetes, hypertension), in the absence of features suggestive of \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Egiant cell arteritis (GCA)\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/div\u003E\n\n\n\n\n\n\n\n\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis patient\u2019s \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECRP is 5 mg/L\u003C/b\u003E\u003C/span\u003E, within normal range (\u0026lt;10 mg/L), effectively \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexcluding GCA\u003C/b\u003E\u003C/span\u003E, which typically shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emarkedly elevated inflammatory markers\u003C/b\u003E\u003C/span\u003E (CRP \u0026gt;50 mg/L, ESR \u0026gt;70 mm/hr). In contrast, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Earteritic AION\u003C/b\u003E\u003C/span\u003E (AAION) also presents with more profound vision loss and systemic symptoms such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eheadache, jaw claudication, or scalp tenderness\u003C/b\u003E\u003C/span\u003E, which are absent here.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe presence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediabetes (glucose 13.5 mmol/L)\u003C/b\u003E\u003C/span\u003E supports NAION, as microvascular compromise of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eshort posterior ciliary arteries\u003C/b\u003E\u003C/span\u003E is the likely mechanism. The presence of a \u201Cdisc at risk\u201D (small cup-to-disc ratio) further predisposes to ischaemia.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiabetic papillopathy\u003C/b\u003E\u003C/span\u003E, although seen in diabetics, tends to occur in younger patients (\u0026lt;50), is often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral\u003C/b\u003E\u003C/span\u003E, causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emild vision loss\u003C/b\u003E\u003C/span\u003E, and features \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edifferent visual field defects\u003C/b\u003E\u003C/span\u003E (e.g. enlarged blind spot), making it unlikely in this 70-year-old patient with a unilateral altitudinal defect.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptic neuritis\u003C/b\u003E\u003C/span\u003E is also improbable; it typically affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyounger adults (20\u201340 years)\u003C/b\u003E\u003C/span\u003E, presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epain on eye movement\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecentral scotomas\u003C/b\u003E\u003C/span\u003E, and more pronounced \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecolor vision deficits\u003C/b\u003E\u003C/span\u003E. This patient\u2019s \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eage\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsence of pain\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epattern of vision loss\u003C/b\u003E\u003C/span\u003E all argue against optic neuritis.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 319,
    "Name": "Painful red eye",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan lang=\u0022EN\u0022\u003EA low myope 36 year old was recently started\non a new drug for epilepsy. She presents with visual disturbance and a painful\nred eye. The pupil is not reacting to light, fixed and dilated.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following treatment options would\nbe the LEAST likely treatment of choice in the initial management plan?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cbr\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute angle-closure glaucoma (AACG)\u003C/b\u003E\u003C/span\u003E likely triggered by medication-induced \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupillary block\u003C/b\u003E\u003C/span\u003E (a recognised adverse effect of some antiepileptics with anticholinergic properties).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFirst-line treatment\u003C/b\u003E\u003C/span\u003E focuses on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erapid intraocular pressure (IOP) reduction\u003C/b\u003E\u003C/span\u003E to preserve optic nerve function and relieve symptoms.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcetazolamide\u003C/b\u003E\u003C/span\u003E (IV or PO, 500\u202Fmg) is the standard first-line agent, reducing aqueous humour production by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecarbonic anhydrase inhibition\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIV mannitol\u003C/b\u003E\u003C/span\u003E is indicated when IOP is critically high (\u0026gt;50\u202FmmHg) or if corneal oedema limits other interventions.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPilocarpine\u003C/b\u003E\u003C/span\u003E is avoided initially when the IOP is very high, as the ischaemic iris may not respond, and it can paradoxically worsen pupillary block.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELaser peripheral iridotomy (LPI)\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edefinitive treatment\u003C/b\u003E\u003C/span\u003E but should only be performed once IOP is controlled and the cornea is clear.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECyclodiode\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot appropriate\u003C/b\u003E\u003C/span\u003E here --\u0026gt; it is a cyclodestructive procedure reserved for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erefractory glaucoma\u003C/b\u003E\u003C/span\u003E, not acute AACG.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 320,
    "Name": "Paediatric Strabismus Diagnosis",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAn\n18-month-old child is referred with a history from the parent of seeing the\neyes \u201Cnot move correctly.\u201D This is worse when tired or daydreaming. Examination\nis difficult as the child is tired and fractious. The vision is recorded as 6/9\nwith Kay\u2019s pictures with both eyes open, but it is not possible to record\nmonocular acuities. Orthoptic assessment has shown that the eyes are aligned\nfor near fixation but there is a deviation measuring 20 prism dioptres base in,\nat distance fixation. What is the MOST likely diagnosis?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cbr\u003E\u003Cdiv\u003E\u25CF\tIntermittent exotropia is the most likely diagnosis in a young child who presents with a history of periodic eye misalignment, especially when tired or inattentive, and who demonstrates a larger exodeviation at distance than near.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF\tIn intermittent exotropia, parents often notice the eyes \u201Cgoing out\u201D when the child is daydreaming, tired, or not concentrating. The deviation is typically more apparent at distance fixation, as described here (20 prism dioptres base in at distance, aligned at near), which is characteristic of this type of strabismus.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF\tAtypical Duane\u2019s syndrome would usually present with abnormal abduction/adduction movements and possible globe retraction, not typical distance-related exodeviation.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF\tInfantile exotropia (congenital exotropia) is rare and usually presents in the first few months of life, not as an intermittent phenomenon at 18 months.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF\tNormal eyes are very unlikely due to the clear evidence of distance exodeviation and parental concern.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 321,
    "Name": "24-hour Intraocular Pressure (IOP) Measurement",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:6.0pt;margin-right:0in;margin-bottom:6.0pt;\nmargin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ERegarding\n24-hour intraocular pressure (IOP) measurement, which of the following\nstatements is most likely to be CORRECT?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cbr\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThe Triggerfish contact lens sensor\u003C/b\u003E\u003C/span\u003E is a device that monitors \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erelative changes\u003C/b\u003E\u003C/span\u003E in ocular volume or corneoscleral strain over 24 hours. It provides \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ea pattern of IOP-related fluctuations\u003C/b\u003E\u003C/span\u003E rather than absolute pressure values in mmHg. This makes it useful in identifying nocturnal peaks and circadian rhythms, which are increasingly recognised as risk factors in glaucoma progression.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProstaglandin analogues\u003C/b\u003E\u003C/span\u003E (e.g., latanoprost) are superior to beta-blockers in maintaining IOP control during the night, as beta-blockers have \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediminished nocturnal efficacy\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGAT\u003C/b\u003E\u003C/span\u003E, though the gold standard for IOP measurement, is unsuitable for overnight monitoring due to its reliance on upright positioning, corneal anaesthesia, and patient cooperation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP increases in the supine position\u003C/b\u003E\u003C/span\u003E during sleep due to elevated episcleral venous pressure and changes in aqueous outflow, not in the upright position.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 322,
    "Name": "Light-Near Dissociation\u2014Pupillary Reflex Pathways",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is LEAST likely to give rise to a phenomenon where the pupils do not respond to light, but where miosis on stimulating the near reflex is preserved?\u003C/span\u003E",
    "Explanation": "\u003Cbr\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\u25CF Light-near dissociation describes pupils that constrict with accommodation (near response) but not to direct light. This points to a disruption in the light reflex pathway, with the near reflex arc remaining intact.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF Common causes include:\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;1-Ciliary ganglion lesion (e.g., Adie\u2019s tonic pupil): Light response typically lost or diminished, but the near response is relatively preserved.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;2- Pineal tumour (dorsal midbrain syndrome/Parinaud\u2019s): The lesion interrupts the fibers that mediate the light reflex in the pretectal area, while the near response pathway, which may bypass this region, is spared.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;3-Treponemal (syphilitic) infection: Argyll Robertson pupil is small, irregular, reacts to accommodation but not to light.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF Lesion in the longitudinal fasciculus (i.e., medial longitudinal fasciculus/MLF): This structure coordinates horizontal eye movements (e.g., internuclear ophthalmoplegia) and is not part of the direct or indirect pupillary reflex pathways. It therefore does NOT cause light-near dissociation, making it the correct answer to the question.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 323,
    "Name": "Mitochondrial Inheritance in Ophthalmic Diseases",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich ONE of the following exhibits mitochondrial inheritance?\u003C/span\u003E",
    "Explanation": "\u003Cbr\u003E\u003Cdiv\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF Mitochondrial inheritance refers to the \u003Cspan style=\u0022font-weight: bold;\u0022\u003Eexclusive\u003C/span\u003E maternal transmission of genetic material contained within mitochondrial DNA (mtDNA).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003EChronic progressive external ophthalmoplegia (CPEO) is a cardinal example of a disorder with mitochondrial inheritance.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EClassical presentation is bilateral ptosis progressing to symmetric, painless, slowly progressive ophthalmoplegia, often accompanied by myopathy and, in syndromic cases, retinopathy, cardiac conduction defects, or other systemic features.\u0026nbsp;\u003C/li\u003E\u003Cli\u003EMuscle biopsy may show ragged-red fibers and demonstrate cytochrome c oxidase (COX)-negative fibers, supporting mitochondrial etiology.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003EOther options:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF Myotonic dystrophy: Autosomal dominant trinucleotide (CTG) repeat expansion in DMPK gene; shows multisystem involvement but not mitochondrial inheritance.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF Refsum disease: Autosomal recessive peroxisomal disorder caused by mutations in the PHYH or PEX7 genes, leading to phytanic acid accumulation with retinal degeneration and neuropathy.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF Vitamin D resistant rickets (X-linked hypophosphatemia): Caused by PHEX gene mutations (X-linked dominant); primarily affects phosphate handling in the kidney and does not involve mitochondrial genetics.\u0026nbsp;\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 324,
    "Name": "Management\u2014Persistent Epithelial Defect After Severe Chemical Burn",
    "Body": "The patient shown in the photograph below is recovering from a severe chemical burn and is exhibiting a large non-healing persistent corneal epithelial defect that has not changed over the course of 10 days. The eye is red, inflamed, with hazy corneal stroma but no corneal thinning. What would be the MOST appropriate next stage of management of this case?\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-26-576d3ce9-460f-4a22-86c0-9d49fd60484b.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003Cbr\u003E\u003Cdiv\u003E\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CF\tPersistent epithelial defects after severe chemical burns reflect stromal inflammation, limbal stem cell dysfunction, and impaired corneal healing due to chronic surface toxicity and inflammation. With a large epithelial defect persisting 10 days post-injury and no corneal thinning or perforation, the primary goal is to promote re-epithelialization, protect the ocular surface, suppress inflammation, and prevent secondary complications.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold; text-decoration-line: underline;\u0022\u003E\u25CF\tMost appropriate next step:\u003C/span\u003E\u003C/div\u003E\u003Cblockquote style=\u0022margin: 0 0 0 40px; border: none; padding: 0px;\u0022\u003E\u003Cdiv\u003E1- Amniotic membrane graft provides a biological scaffold, anti-inflammatory, and anti-fibrotic effects conducive to epithelial healing.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E2-Autologous serum eye drops are rich in growth factors, vitamins, and anti-inflammatory mediators, mimicking natural tears and facilitating epithelialization.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E3-Tarsorrhaphy (partial or temporary) reduces exposure, encourages healing, and protects the defect from further desiccation and trauma.\u0026nbsp;\u003C/div\u003E\u003C/blockquote\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tDefinitive stem cell transplantation is reserved for chronic or refractory cases where limbal stem cell deficiency is confirmed, and initial medical/surgical surface stabilization has failed; attempting such invasive grafts during acute inflammation raises the risk of graft failure.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF\tBotulinum toxin induced ptosis can be considered for exposure keratopathy but is less targeted than direct surface reconstruction and is generally reserved for cases where surgical closure is contraindicated.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tTopical therapy alone (lubrication, steroids, antibiotics, potassium ascorbate) is foundational but insufficient when large epithelial defects fail to heal after 7-10 days despite appropriate conservative measures.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 325,
    "Name": "Paediatric Vitreoretinal Disease\u2014Syndromic Associations",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 12-month-old developmentally delayed boy with hearing impairment is referred. Examination findings include hand movements vision and bilateral white retrolental masses. The child\u0027s skin is normal. Which of these is the MOST likely diagnosis?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENorrie disease\u003C/b\u003E\u003C/span\u003E is a rare \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked recessive disorder\u003C/b\u003E\u003C/span\u003E caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENDP gene\u003C/b\u003E\u003C/span\u003E, affecting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal angiogenesis\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einner ear\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebrain development\u003C/b\u003E\u003C/span\u003E. The condition typically presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral congenital blindness\u003C/b\u003E\u003C/span\u003E due to a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epseudoglioma;\u0026nbsp;\u003C/b\u003E\u003C/span\u003Ea white, fibrovascular mass behind the lens. Over time, this mass may calcify, mimicking retinoblastoma radiographically. However, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esyndromic features\u003C/b\u003E\u003C/span\u003E such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esensorineural hearing loss\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintellectual disability\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edevelopmental delay\u003C/b\u003E\u003C/span\u003E point strongly toward Norrie disease.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital rubella\u003C/b\u003E\u003C/span\u003E: May cause cataracts and deafness, but the full triad (cardiac, ocular, auditory) is not described here, and pseudoglioma is not a classic feature.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIncontinentia pigmenti\u003C/b\u003E\u003C/span\u003E: X-linked dominant, usually fatal in males; survivors often show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecutaneous findings\u003C/b\u003E\u003C/span\u003E (vesicular, verrucous, hyperpigmented stages), which are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsent here\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERetinoblastoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Bilateral cases do exist, and leukocoria is common, but it is \u003C/span\u003E\u003Cb\u003Enot associated with hearing loss or neurodevelopmental delay\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 326,
    "Name": "GCA",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Egiant cell arteritis (GCA)\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003Eincorrect\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhile \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EESR\u003C/b\u003E\u003C/span\u003E has historically been used to assess inflammation in GCA, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC-reactive protein (CRP)\u003C/b\u003E\u003C/span\u003E has been shown to be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore sensitive and specific\u003C/b\u003E\u003C/span\u003E, and less influenced by age, gender, and haematological variations. CRP rises earlier than ESR in most inflammatory states and is now regarded as the superior acute-phase marker in suspected GCA.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGCA is indeed more common in females\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etongue claudication\u003C/b\u003E\u003C/span\u003E is a well-recognised but less common symptom due to ischaemia of the lingual artery.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003EOn \u003C/span\u003E\u003Cb\u003Etemporal artery biopsy\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E, the characteristic finding includes \u003C/span\u003E\u003Cb\u003Efragmentation, reduplication, or disruption of the internal elastic lamina\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E, with a \u003C/span\u003E\u003Cb\u003Etransmural infiltrate of lymphocytes and macrophages\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E, often forming \u003C/span\u003E\u003Cb\u003Emultinucleated giant cells\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 327,
    "Name": "Chiasmal lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient with a chiasmal lesion undergoes Goldmann perimetry, which reveals a \u003Cspan class=\u0022s1\u0022\u003Eleft eye only \u201Cpie in the sky\u201D (superotemporal) field defect\u003C/span\u003E. Which of the following best describes the most likely lesion location?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis visual field defect pattern is classic for a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ejunctional scotoma\u003C/b\u003E\u003C/span\u003E, caused by a lesion at the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ejunction of the optic nerve and chiasm\u003C/b\u003E\u003C/span\u003E. Specifically, it affects:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIpsilateral optic nerve fibers\u003C/b\u003E\u003C/span\u003E, leading to a central scotoma in that eye (not always reported by patients)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECrossed inferonasal fibers\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E from the \u003C/span\u003E\u003Cb\u003Econtralateral eye\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (via \u003C/span\u003E\u003Cb\u003EWilbrand\u2019s knee\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E), causing a \u003C/span\u003E\u003Cb\u003Esuperotemporal defect\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in the opposite eye\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn this case, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleft eye has a superotemporal (\u201Cpie in the sky\u201D) defect\u003C/b\u003E\u003C/span\u003E, indicating that the lesion is affecting:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eright inferonasal retinal fibers\u003C/b\u003E\u003C/span\u003E (which cross at the chiasm)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThus, the lesion is located at the \u003C/span\u003E\u003Cb\u003Eanterior junction of the right optic nerve and chiasm\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis explains why the defect appears \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilaterally\u003C/b\u003E\u003C/span\u003E, and why the field loss is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperotemporal\u003C/b\u003E\u003C/span\u003E in one eye.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://eyewiki-images.s3.us-east-va.perf.cloud.ovh.us/5/50/Junctional_Scotoma300.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-size: 12.3704px; letter-spacing: normal; background-color: rgb(248, 249, 250);\u0022\u003EJunctional Scotoma\u0026nbsp;Humphrey visual 30-2 showing central depression in the left eye and superotemporal loss of field in the right eye.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 328,
    "Name": "Hydrocephalus",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is the most frequent cause of \u003Cspan class=\u0022s1\u0022\u003Ecommunicating hydrocephalus\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECommunicating hydrocephalus\u003C/b\u003E\u003C/span\u003E arises when cerebrospinal fluid (CSF) \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecirculates freely through the ventricular system\u003C/b\u003E\u003C/span\u003E but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot properly reabsorbed\u003C/b\u003E\u003C/span\u003E into the venous system via the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Earachnoid granulations\u003C/b\u003E\u003C/span\u003E. The most common cause of this condition is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubarachnoid haemorrhage (SAH)\u003C/b\u003E\u003C/span\u003E. The blood products from SAH obstruct or damage the arachnoid villi, impairing CSF absorption.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther known causes include \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emeningitis\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econgenital absence or dysfunction of arachnoid granulations\u003C/b\u003E\u003C/span\u003E, but SAH remains the most common acquired cause in clinical practice.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EColloid cysts\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EArnold\u2013Chiari malformations\u003C/b\u003E\u003C/span\u003E typically cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-communicating (obstructive) hydrocephalus\u003C/b\u003E\u003C/span\u003E due to physical obstruction within the ventricular system (e.g. at the foramen of Monro or fourth ventricle outflow tracts).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 329,
    "Name": "Medullary lesions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents with sudden-onset vertigo. On examination, there is hoarseness of voice, dysmetria and dysdiadochokinesia on the right, loss of pin-prick and temperature sensation on the left side of the body, and similar sensory loss on the right side of the face. Where is the most likely site of the lesion?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis clinical picture is characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elateral medullary syndrome\u003C/b\u003E\u003C/span\u003E (Wallenberg syndrome), typically caused by occlusion of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior inferior cerebellar artery (PICA)\u003C/b\u003E\u003C/span\u003E. The key features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVertigo and nystagmus\u003C/b\u003E\u003C/span\u003E: from involvement of the vestibular nuclei\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIpsilateral cerebellar signs\u003C/b\u003E\u003C/span\u003E (dysmetria, dysdiadochokinesia): due to inferior cerebellar peduncle involvement\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EContralateral loss of pain and temperature on the body\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: from damage to the \u003C/span\u003E\u003Cb\u003Elateral spinothalamic tract\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIpsilateral facial sensory loss\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (pain and temperature): due to \u003C/span\u003E\u003Cb\u003Espinal trigeminal nucleus/tract\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E involvement\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHoarseness and dysphagia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: from involvement of the \u003C/span\u003E\u003Cb\u003Enucleus ambiguus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (CN IX, X)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIpsilateral Horner\u2019s syndrome\u003C/b\u003E\u003C/span\u003E (not mentioned here, but commonly seen)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options are less consistent:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC1-C2 spinal cord lesion\u003C/b\u003E\u003C/span\u003E would not produce crossed sensory findings or bulbar signs\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECerebellar vermis\u003C/b\u003E\u003C/span\u003E lesions primarily cause truncal ataxia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPontine lesions\u003C/b\u003E\u003C/span\u003E typically involve facial weakness and horizontal gaze abnormalities\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj53U_WM8ZYdjYmdHqpEQlnvwMFcKJ_-8BgPzgj7EpMBM2_cDQaES2GLZWShx-EctUPE5D75sB8WvLO6MFZ8pK6To-8K1udqT9hiRW1isNEqZs7dEjLKA3VwLrMDn1fmhhZzWeiIG1omw/s640/pica\u002Bcopy.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 330,
    "Name": "Myasthenia Gravis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements is \u003Cspan class=\u0022s1\u0022\u003Etrue\u003C/span\u003E regarding the treatment of myasthenia gravis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAzathioprine\u003C/b\u003E\u003C/span\u003E is an immunosuppressant commonly used for long-term control of myasthenia gravis. It helps reduce the need for corticosteroids and maintains disease remission.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPlasmapheresis\u003C/b\u003E\u003C/span\u003E (plasma exchange) is effective for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eshort-term improvement\u003C/b\u003E\u003C/span\u003E and is particularly used in acute exacerbations or pre-operatively, but it is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot suitable\u003C/b\u003E\u003C/span\u003E for chronic long-term control due to logistical burden and risks.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThymectomy\u003C/b\u003E\u003C/span\u003E is most effective in antibody-positive (especially \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacetylcholine receptor antibody-positive\u003C/b\u003E\u003C/span\u003E) patients, not in seronegative cases. It is most beneficial in younger patients with generalized MG and a hyperplastic thymus.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorticosteroids\u003C/b\u003E\u003C/span\u003E are actually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erecommended\u003C/b\u003E\u003C/span\u003E in myasthenic crisis, but they should be used cautiously due to potential for transient worsening at initiation. They are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot contraindicated\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 331,
    "Name": "Fetal alcohol syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following ocular abnormalities is \u003Cspan class=\u0022s1\u0022\u003Emost commonly\u003C/span\u003E associated with fetal alcohol syndrome?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EOptic nerve hypoplasia is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost frequently reported ocular anomaly\u003C/b\u003E\u003C/span\u003E in fetal alcohol syndrome, seen in up to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E50%\u003C/b\u003E\u003C/span\u003E of cases. It reflects the broader impact of alcohol on neurodevelopment during gestation. Other commonly associated ocular signs include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETortuous retinal vessels\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShort palpebral fissures\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEpicanthal folds, ptosis, and telecanthus\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMicrophthalmos\u003C/b\u003E\u003C/span\u003E (less frequent than ON hypoplasia)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPersistent fetal vasculature\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Erarely, cataract or coloboma\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile microphthalmos, cataract, and coloboma can occur in FAS, they are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless consistent\u003C/b\u003E\u003C/span\u003E findings compared to optic nerve hypoplasia.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://www.aafp.org/content/dam/brand/aafp/pubs/afp/issues/2005/0715/p279-f1.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan style=\u0022color: rgb(40, 40, 40); font-family: \u0026quot;Museo Sans\u0026quot;, Tahoma, sans-serif; letter-spacing: normal;\u0022\u003ECharacteristic facial features in a child with fetal alcohol spectrum disorders. Findings may include a smooth philtrum, thin upper lip, upturned nose, flat nasal bridge and midface, epicanthal folds, small palpebral fissures, and small head circumference.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 332,
    "Name": "Optic disc swelling",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient with poorly controlled diabetes presents with \u003C/span\u003Ebilateral optic disc swelling\u003Cspan class=\u0022s1\u0022\u003E. A \u003C/span\u003ECT scan of the head is reported as normal\u003Cspan class=\u0022s1\u0022\u003E. What is the \u003C/span\u003Emost appropriate next investigation\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIn the setting of \u003C/span\u003E\u003Cb\u003Ebilateral optic disc swelling\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with a \u003C/span\u003E\u003Cb\u003Enormal CT scan\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the key concern is to rule out \u003C/span\u003E\u003Cb\u003Eraised intracranial pressure\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Esecondary causes of papilloedema or optic neuropathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, such as:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntracranial mass lesions\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOptic nerve sheath meningioma or glioma\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInflammatory/infective causes (e.g., optic neuritis, sarcoidosis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIdiopathic intracranial hypertension (IIH)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EAn \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EMRI with gadolinium\u003C/b\u003E\u003C/span\u003E offers superior soft tissue detail and is the preferred next step to assess:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Eoptic nerves and chiasm\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital pathology\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVenous sinus thrombosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (especially with MRV)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESigns of raised ICP\u003C/b\u003E\u003C/span\u003E, such as flattening of the posterior globe or empty sella\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELumbar puncture (LP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E should only be performed \u003C/span\u003E\u003Cb\u003Eafter serious structural pathology has been excluded\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E by MRI, due to the risk of brain herniation.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EFFA\u003C/b\u003E\u003C/span\u003E may demonstrate leakage in true papilloedema but does not elucidate the underlying cause.\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EOcular ultrasound\u003C/b\u003E\u003C/span\u003E is useful in cases of buried disc drusen but is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Enot the first-line\u003C/b\u003E\u003C/span\u003E test in this context.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 333,
    "Name": "Squamous cell carcinoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following \u003Cspan class=\u0022s1\u0022\u003Ehistopathological findings\u003C/span\u003E is most consistent with a diagnosis of \u003Cspan class=\u0022s1\u0022\u003Esquamous cell carcinoma\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESquamous cell carcinoma (SCC)\u003C/b\u003E\u003C/span\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emalignant tumour of keratinocytes\u003C/b\u003E\u003C/span\u003E, arising from the squamous layer of the epidermis. Key histological hallmarks include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPleomorphic epithelial cells\u003C/b\u003E\u003C/span\u003E with hyperchromatic, prominent nuclei\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAbundant eosinophilic cytoplasm\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratin pearls\u003C/b\u003E\u003C/span\u003E: concentric whorls of keratinized cells \u2014 a hallmark of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewell-differentiated SCC\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIntercellular bridges\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may also be visible\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options represent different tumours:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E(vascular channel proliferation): typical of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eangiosarcoma\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E(palisading basal cells): classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebasal cell carcinoma (BCC)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E(foamy cytoplasm \u002B Oil Red O stain): characteristic of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esebaceous gland carcinoma\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://upload.wikimedia.org/wikipedia/commons/c/ca/Histopathology_of_squamous-cell_carcinoma.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
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  },
  {
    "Id": 334,
    "Name": "Rhabdomyosarcoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA B-scan ultrasound is performed for a patient presenting with \u003C/span\u003Eunilateral proptosis\u003Cspan class=\u0022s1\u0022\u003E. It reveals a \u003C/span\u003Eheterogeneous, well-defined intra-conal mass\u003Cspan class=\u0022s1\u0022\u003E with \u003C/span\u003Eirregular borders\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Elow internal reflectivity\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe B-scan features are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehighly characteristic of orbital rhabdomyosarcoma\u003C/b\u003E\u003C/span\u003E, the most common primary orbital malignancy in children:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHeterogeneous\u003C/b\u003E\u003C/span\u003E internal structure\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIrregular margins\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELow internal reflectivity\u003C/b\u003E\u003C/span\u003E on ultrasound due to its cellular, poorly organized architecture\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERapid onset of proptosis\u003C/b\u003E\u003C/span\u003E, often with inflammatory signs\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESchwannoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a benign, encapsulated nerve sheath tumour, \u003C/span\u003E\u003Cb\u003Elow reflectivity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but \u003C/span\u003E\u003Cb\u003Ewell-circumscribed and homogeneous\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECavernous haemangioma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (most common benign orbital tumour in adults): \u003C/span\u003E\u003Cb\u003Emoderate to high reflectivity\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Esmooth borders\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eslow-growing\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECapillary haemangioma\u003C/b\u003E\u003C/span\u003E (seen in infants): \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehyperechoic\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompressible\u003C/b\u003E\u003C/span\u003E, and often associated with skin discoloration\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://www.researchgate.net/profile/Luis-Gorospe/publication/10595168/figure/fig7/AS:337314590019603@1457433473958/a-c-Orbital-rhabdomyosarcoma-a-Ultrasound-scan-shows-a-solid-well-defined-hypoechoic.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Ch1 class=\u0022nova-legacy-e-text nova-legacy-e-text--size-m nova-legacy-e-text--family-display nova-legacy-e-text--spacing-none nova-legacy-e-text--color-inherit\u0022 itemprop=\u0022caption\u0022 style=\u0022color: rgb(17, 17, 17); font-weight: 400; font-family: Roboto, Arial, sans-serif; font-size: 0.875rem; line-height: 1.3; margin-bottom: 0px; letter-spacing: normal;\u0022\u003Ea\u2013c Orbital rhabdomyosarcoma. a Ultrasound scan shows a solid, well-defined hypoechoic mass (arrows). b Axial T1-weight- ed and c coronal T1-weighted contrast-enhanced MR images show how the lesion (asterisk) displaces the muscular conus inferomedially (arrowheads). Note moderate and uniform contrast uptake by the tumor\u0026nbsp;\u0026nbsp;\u003C/h1\u003E",
    "Choices": [],
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  },
  {
    "Id": 335,
    "Name": "Rhabdomyosarcoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Erhabdomyosarcoma\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003Etrue\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ERhabdomyosarcoma is the \u003C/span\u003E\u003Cb\u003Emost frequent primary malignant orbital tumour in the paediatric population\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, typically presenting around the \u003C/span\u003E\u003Cb\u003Eage of 8\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E years and showing a \u003C/span\u003E\u003Cb\u003Eslight male predominance\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It accounts for approximately \u003C/span\u003E\u003Cb\u003E4% of all childhood cancers\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EKey clinical features:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERapidly progressive \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral non-axial proptosis\u003C/b\u003E\u003C/span\u003E (not axial)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOften associated with \u003C/span\u003E\u003Cb\u003Einflammatory signs and ptosis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMay \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emimic orbital cellulitis\u003C/b\u003E\u003C/span\u003E, leading to diagnostic challenges\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EAnatomical origin:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E37% \u003C/span\u003E\u003Cb\u003Eextraconal\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E17% \u003C/span\u003E\u003Cb\u003Eintraconal\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E47% \u003C/span\u003E\u003Cb\u003Emixed\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFrequently arises in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperonasal quadrant\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 336,
    "Name": "Rhabdomyosarcoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 7-year-old girl presents with a 2-week history of \u003C/span\u003Esudden-onset painful unilateral axial proptosis\u003Cspan class=\u0022s1\u0022\u003E and overlying lid erythema. She is apyrexial. A \u003C/span\u003ECT scan shows a non-enhancing, poorly defined mass of homogenous tissue density\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ERhabdomyosarcoma, though rare, is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common primary malignant orbital tumour in children\u003C/b\u003E\u003C/span\u003E, typically presenting between ages \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E7-8 years\u003C/b\u003E\u003C/span\u003E. It often manifests as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erapidly progressive, painful, unilateral proptosis\u003C/b\u003E\u003C/span\u003E with inflammatory signs, mimicking \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorbital cellulitis\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EImaging features on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECT\u003C/b\u003E\u003C/span\u003E include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPoorly defined, \u003C/span\u003E\u003Cb\u003Ehomogeneous soft tissue mass\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENon-enhancing\u003C/b\u003E\u003C/span\u003E or mildly enhancing\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMay show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebone erosion\u003C/b\u003E\u003C/span\u003E in advanced cases\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther differential diagnoses:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECapillary haemangioma\u003C/b\u003E\u003C/span\u003E: common in infants \u0026lt;1 year, usually painless, and slow-growing\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELymphangioma\u003C/b\u003E\u003C/span\u003E: also presents earlier; may cause acute proptosis if haemorrhage occurs within the lesion\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOrbital varices\u003C/b\u003E\u003C/span\u003E: cause intermittent proptosis, worsened by Valsalva, not constant or painful\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 337,
    "Name": "Carotid Cavenrous Fistula",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient presents with \u003C/span\u003Eunilateral proptosis\u003Cspan class=\u0022s1\u0022\u003E that has been \u003C/span\u003Eslowly progressing over several months\u003Cspan class=\u0022s1\u0022\u003E. He reports \u003C/span\u003Ereduced visual acuity\u003Cspan class=\u0022s1\u0022\u003E, particularly with \u003C/span\u003Eeye movement\u003Cspan class=\u0022s1\u0022\u003E. On examination, there is \u003C/span\u003Eengorgement of the conjunctiva\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Eexaggerated ocular pulsation\u003Cspan class=\u0022s1\u0022\u003E noted on tonometry.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe constellation of \u003C/span\u003E\u003Cb\u003Eprogressive unilateral proptosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Edilated conjunctival vessels\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eocular pulsation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is characteristic of a \u003C/span\u003E\u003Cb\u003Ecarotid-cavernous fistula\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (CCF). In this case, the \u003C/span\u003E\u003Cb\u003Egradual onset\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Emild to moderate symptoms\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E suggest a \u003C/span\u003E\u003Cb\u003Elow-flow (indirect)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E CCF.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIndirect CCFs\u003C/b\u003E\u003C/span\u003E often arise \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espontaneously\u003C/b\u003E\u003C/span\u003E, particularly in elderly hypertensive women. They cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egradual symptoms\u003C/b\u003E\u003C/span\u003E, often with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edilated episcleral veins\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epulsatile IOP\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediplopia\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evisual loss\u003C/b\u003E\u003C/span\u003E from venous congestion or optic neuropathy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn contrast, a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edirect CCF\u003C/b\u003E\u003C/span\u003E is typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh-flow\u003C/b\u003E\u003C/span\u003E, usually following \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etrauma\u003C/b\u003E\u003C/span\u003E, and presents \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacutely\u003C/b\u003E\u003C/span\u003E with severe chemosis, bruit, and more dramatic proptosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003E- Orbital varices\u003C/b\u003E\u003C/span\u003E can cause intermittent proptosis exacerbated by Valsalva, not persistent pulsation.\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003E- Cavernous haemangiomas\u003C/b\u003E\u003C/span\u003E are benign, slow-growing masses and do not cause pulsation or conjunctival congestion.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENotes on CCF:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cul\u003E\u003Cli\u003E80% of patients with CCF develop ocular hypertension\u0026nbsp;\u003C/li\u003E\u003Cli\u003E25% develop optic disc cupping\u0026nbsp;\u003C/li\u003E\u003Cli\u003E20% visual field defects.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u0026nbsp;This is due to raised episcleral venous pressure causing a secondary open-angle glaucoma.\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022https://www.researchgate.net/publication/382769087/figure/fig1/AS:11431281264391645@1722558729763/Anatomical-Illustration-of-the-Carotid-Cavernous-Fistula-CCF-ICA-Internal-carotid.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Ch1 class=\u0022nova-legacy-e-text nova-legacy-e-text--size-m nova-legacy-e-text--family-display nova-legacy-e-text--spacing-none nova-legacy-e-text--color-inherit\u0022 itemprop=\u0022caption\u0022 style=\u0022color: rgb(17, 17, 17); font-weight: 400; font-family: Roboto, Arial, sans-serif; font-size: 0.875rem; line-height: 1.3; margin-bottom: 0px; letter-spacing: normal;\u0022\u003EAnatomical Illustration of the Carotid Cavernous Fistula (CCF). ICA: Internal carotid artery Image Credit: Sura H. Talib\u003C/h1\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-01-27-609ed8a7-7acf-45da-a8fc-7df5c0100659.png\u0022\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 338,
    "Name": "Hyperostosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following is \u003C/span\u003Emost likely to cause orbital hyperostosis\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital hyperostosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E refers to \u003C/span\u003E\u003Cb\u003Ebony thickening of the orbital walls\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, typically due to \u003C/span\u003E\u003Cb\u003Ereactive bone formation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It is \u003C/span\u003E\u003Cb\u003Emost classically associated with orbital meningioma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly \u003C/span\u003E\u003Cb\u003Eoptic nerve sheath meningiomas\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, where the tumour induces \u003C/span\u003E\u003Cb\u003Ereactive sclerosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Ehyperostosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of adjacent bone.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMeningioma\u003C/b\u003E\u003C/span\u003E is the most common tumour associated with this feature, often presenting with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogressive visual loss\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eproptosis\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic canal narrowing\u003C/b\u003E\u003C/span\u003E due to bone overgrowth.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFibrous dysplasia\u003C/b\u003E\u003C/span\u003E can cause orbital bone expansion and bony deformity, but it usually involves broader craniofacial changes and is not specific to the orbit or associated with hyperostosis in the same pattern.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERhabdomyosarcoma\u003C/b\u003E\u003C/span\u003E is a soft tissue malignancy with no association with bone sclerosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVarices\u003C/b\u003E\u003C/span\u003E are venous malformations and do not affect orbital bone.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022https://www.researchgate.net/publication/332197503/figure/fig5/AS:963434137022476@1606712006238/Sphenoid-wing-meningioma-with-hyperostotic-lateral-orbital-bone-white-arrow-tumour.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Ch1 class=\u0022nova-legacy-e-text nova-legacy-e-text--size-m nova-legacy-e-text--family-display nova-legacy-e-text--spacing-none nova-legacy-e-text--color-inherit\u0022 itemprop=\u0022caption\u0022 style=\u0022color: rgb(17, 17, 17); font-weight: 400; font-family: Roboto, Arial, sans-serif; font-size: 0.875rem; line-height: 1.3; margin-bottom: 0px; letter-spacing: normal;\u0022\u003ESphenoid wing meningioma with hyperostotic lateral orbital bone (white arrow), tumour within sphenoid sinus (red arrow) with compression of the optic nerve\u003C/h1\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 339,
    "Name": "Entropion",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 77-year-old woman presents with \u003C/span\u003Esenile lower lid entropion\u003Cspan class=\u0022s1\u0022\u003E. Examination reveals \u003C/span\u003Egeneralised horizontal lower lid laxity\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich of the following procedures is \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost appropriate\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis is a classic presentation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einvolutional (senile) entropion\u003C/b\u003E\u003C/span\u003E, where the pathophysiology typically involves:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHorizontal lid laxity\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDehiscence or attenuation of lower lid retractors\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOverriding of preseptal over pretarsal orbicularis oculi\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEnophthalmos or poor orbital support\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in elderly patients\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EQuickert procedure\u003C/b\u003E\u003C/span\u003E is designed to correct all of the above by:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EShortening the lower eyelid\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (horizontal tightening)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPlacing everting sutures\u003C/b\u003E\u003C/span\u003E via a lid-splitting approach\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESometimes includes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretractor plication\u003C/b\u003E\u003C/span\u003E if needed\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003EWhy other options less appropriate:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EJones procedure\u003C/b\u003E\u003C/span\u003E: Primarily targets retractor disinsertion (used for entropion without significant horizontal laxity).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWies procedure\u003C/b\u003E\u003C/span\u003E: Combines everting sutures and lid-splitting but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not address lid laxity\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETarsal fracture\u003C/b\u003E\u003C/span\u003E: Mainly used for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecicatricial entropion\u003C/b\u003E\u003C/span\u003E, not the involutional type.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 340,
    "Name": "Facial nerve palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAn 81-year-old woman presents to the emergency department with a \u003Cspan class=\u0022s1\u0022\u003E2-day history of left hemiplegia\u003C/span\u003E, consistent with a stroke. Examination reveals a \u003Cspan class=\u0022s1\u0022\u003Eleft upper motor neuron 7th nerve palsy\u003C/span\u003E and a \u003Cspan class=\u0022s1\u0022\u003Epoor Bell\u2019s phenomenon\u003C/span\u003E.\u0026nbsp;\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EFrom an \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eophthalmic management\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E perspective, what is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost appropriate initial approach\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis patient has an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacute upper motor neuron facial palsy\u003C/b\u003E\u003C/span\u003E with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor Bell\u2019s reflex\u003C/b\u003E\u003C/span\u003E, increasing the risk of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexposure keratopathy\u003C/b\u003E\u003C/span\u003E. While UMN facial palsy typically spares the forehead, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eincomplete blink and orbicularis weakness\u003C/b\u003E\u003C/span\u003E may still result in lagophthalmos and corneal drying, especially if Bell\u2019s phenomenon is impaired.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe most appropriate \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einitial conservative management\u003C/b\u003E\u003C/span\u003E includes:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntensive lubrication\u003C/b\u003E\u003C/span\u003E during the day (e.g., preservative-free drops hourly)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELubricating ointment and eye patch overnight\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EClose \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emonitoring for exposure signs\u003C/b\u003E\u003C/span\u003E (e.g., punctate keratopathy, epithelial defects)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis approach is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-invasive\u003C/b\u003E\u003C/span\u003E, suitable for the acute phase, and allows time for potential \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneurological recovery\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch4\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003C/h4\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChloramphenicol ointment\u003C/b\u003E\u003C/span\u003E: Not first-line unless there are signs of infection.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELevator recession\u003C/b\u003E\u003C/span\u003E: Reserved for chronic cases of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elagophthalmos or exposure\u003C/b\u003E\u003C/span\u003E due to upper lid retraction or poor closure, not indicated acutely.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELower lid traction suture\u003C/b\u003E\u003C/span\u003E: Used in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elower lid ectropion\u003C/b\u003E\u003C/span\u003E, not typically required in early UMN palsy with intact lid tone.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 341,
    "Name": "Mode of Action\u2014Propranolol in Lid Haemangiomas",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003EWhich\nof these is the LEAST likely mode of action of propranolol in the management of\nlid haemangiomas?\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u25CF\tPropranolol is a non-selective \u03B2-adrenergic antagonist and is the current standard of care for problematic infantile periocular haemangiomas. Its mechanisms include: \u03B2-receptor blockade promotes apoptosis and inhibits proliferation in endothelial cells of the haemangioma.\u0026nbsp;\u003Cdiv\u003E\u25CF\tVasoconstriction is mediated by inhibition of \u03B22-receptors, resulting in early blanching and regression.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u25CFPropranolol downregulates vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), thereby inhibiting new vessel formation during the active growth phase.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF\tBradycardia is a systemic side effect of propranolol, not a therapeutic mechanism for the tumour. The local efficacy is independent of changes in systemic blood flow; reduction in haemangioma size is not due to cardiac effects but direct action on the lesion\u2019s endothelium.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 342,
    "Name": "Post-Traumatic Secondary Glaucoma\u2014Anterior Segment Anatomy",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 35-year-old woman presents after being punched in her right eye. On examination her visual acuity is 6/18 right and 6/6 left. The right eye has a deep anterior chamber with dispersed red blood cells and fundus examination is normal. She is given no treatment. Six months later, the intraocular pressure is found to be 32 mmHg. Her right visual acuity is 6/9 with no refractive error and there is no anterior chamber activity. Which of the following is the MOST likely diagnosis?\u003C/span\u003E",
    "Explanation": "*Angle recession is the most likely diagnosis in this patient who developed delayed elevated intraocular pressure months after blunt trauma with initial findings of deep anterior chamber and microhyphaema.\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E* The pathophysiology involves a tear between the longitudinal and circular fibers of the ciliary muscle. Over time, this leads to trabecular meshwork dysfunction and increased IOP. Gonioscopic examination is essential- look for sectoral widening of the ciliary body band.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E* Other listed diagnoses are less likely in this scenario:\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u25CF\tAqueous misdirection (malignant glaucoma) typically presents with a shallow anterior chamber, often postoperatively.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u25CF\tGhost cell glaucoma occurs soon after vitreous haemorrhage migrates into the anterior chamber, rarely delayed for months after minor anterior hemorrhage.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u25CF\tLens dislocation (phacotopic/phacolytic glaucoma) usually causes refractive change, lens instability, or a shallow chamber.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 343,
    "Name": "Contraindications for Corneal Collagen Cross-Linking (CXL)",
    "Body": "\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003EWhich of the following conditions would be LEAST likely to be considered as a contra-indication for collagen cross linking?\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\u25CF\tCorneal collagen cross-linking (CXL) is indicated for progressive keratoconus and other corneal ectasias. The main safety concern is adequate corneal thickness, as UV-A exposure can damage the endothelium if the stromal bed is too thin.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tCorneal thickness of 450 \u00B5m is not a contraindication and safely allows standard (epi-off) CXL. The accepted threshold is generally \u2265400 \u00B5m after epithelial removal.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF\tOther options as contraindications:\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E1-\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ESystemic lupus erythematosus: Increases risk of severe postoperative complications (melting, poor healing).\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E2- History of herpes simplex: Associated with risk of viral reactivation post-CXL.\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E3- Recurrent erosion syndrome: Indicates abnormal epithelial healing, increasing risk of persistent defect after CXL.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u25CF\tAbsolute contraindications include even thinner corneas, active infection, and some cases of severe ocular surface disease\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 344,
    "Name": "Investigation\u2014Unilateral Optic Disc Swelling with Arcuate Visual Field Defect",
    "Body": "\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:\n115%;font-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:\nRoboto;mso-ansi-language:EN;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003EAn\nasymptomatic 65-year-old woman is referred by her optometrist with a unilateral\nswollen optic disc and an arcuate field defect. Which of these is the MOST\nappropriate initial investigation?\u003C/span\u003E\u003Cdiv\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:\n115%;font-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:\nRoboto;mso-ansi-language:EN;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-27-9a3b8e00-2304-4e40-af5e-5bc83186ec6d.png\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "In a 65-year-old with new unilateral optic disc swelling and a corresponding field defect, NAION is likely, but it is important that any optic neuropathy that cannot be confidently diagnosed clinically should be investigated with MRI of the orbits/brain with contrast as the first-line test.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003E*MRI excludes compressive, infiltrative, inflammatory, or demyelinating causes that can mimic NAION and may be sight- or life-threatening.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E*Fluorescein angiography can support a diagnosis of NAION (disc hypoperfusion and late leakage) but does not rule out retrobulbar or orbital pathology, so it is not the most appropriate initial investigation in this setting.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E*B scan ultrasound will only show elevated disc in the scan, which will not rule out intra-cranial lesions.\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 345,
    "Name": "Peripheral visual field defects and peripheral retinal pathology",
    "Body": "\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size: 12pt; line-height: 115%; font-family: Roboto; font-weight: bold;\u0022\u003EWhich\nof these is the MOST likely retinal pathology in a patient who presents with an\nabsolute peripheral field defect?\u003C/span\u003E",
    "Explanation": "\u25CF\tAn absolute peripheral field defect means complete loss of sensitivity in that area of the field, corresponding to full functional loss of the involved retina.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E*Degenerative peripheral retinoschisis causes splitting of the neurosensory retina, with the inner retinal layer functionally disconnected from the photoreceptors, producing a well-demarcated, stable, absolute scotoma on perimetry.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tPeripheral lattice, snail track and pavingstone degenerations are usually asymptomatic and rarely produce a discrete absolute peripheral defect on their own, while giant retinal tears typically present with symptoms of acute rhegmatogenous retinal detachment (flashes, floaters, progressive \u201Ccurtain\u201D of field loss) rather than an isolated, localized absolute scotoma.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 346,
    "Name": "Vitreous floaters\u2014optics and symptomatology",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich\nof the following statements about symptoms of floaters caused by vitreous\nopacities is MOST likely to be correct?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u25CF\tVitreous opacities cast shadows on the retina. The closer an opacity lies to the retina, the sharper and more distinct that shadow becomes on the photoreceptor layer, so the floater is perceived more clearly and is more symptomatic.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003E\u25CF\tWith a larger pupil, a wider cone of light enters the eye and a greater proportion of rays are intercepted by the opacity, producing a more extensive and noticeable disturbance in the retinal image. In contrast, a small pupil restricts the light bundle, so fewer rays interact with a given opacity and the symptoms can be less prominent. Therefore, the combination that maximizes symptoms is: opacities close to the retina with a large pupil.\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 347,
    "Name": "Pre\u2011operative allergy assessment for cataract surgery",
    "Body": "\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:\n115%;font-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:\nRoboto;mso-ansi-language:EN;mso-fareast-language:EN-US;mso-bidi-language:AR-SA\u0022\u003EA\n54\u2011year\u2011old patient is coming for cataract surgery. She is atopic and gives a\nhistory of allergy to chestnuts and kiwi fruit. Which of the following options\nwould you specifically ask about?\u003C/span\u003E",
    "Explanation": "\u25CF\tAllergy to chestnut and kiwi is strongly associated with the \u201Clatex\u2013fruit syndrome,\u201D in which IgE antibodies raised against natural rubber latex cross\u2011react with structurally similar proteins in certain fruits (classically banana, avocado, chestnut, and kiwi). In a patient with these food allergies, there is therefore a significantly increased risk of true latex hypersensitivity.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tBefore cataract surgery, it is essential to specifically ask about and document any history of latex allergy, as perioperative exposure (gloves, tubing, syringe plungers, etc.) can provoke severe, even life\u2011threatening anaphylaxis.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E*While chlorhexidine, fluorescein, and povidone\u2013iodine can all cause reactions, they are not specifically linked to chestnut/kiwi allergy; the key association here is with latex.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 348,
    "Name": "Sympathetic ophthalmia\u2014clinical features and management",
    "Body": "\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size: 12pt; line-height: 115%; font-family: Roboto; font-weight: bold;\u0022\u003EWhich\nof the following statements regarding established sympathetic ophthalmia is\nLEAST likely to be correct?\u003C/span\u003E",
    "Explanation": "\u25CF\tSympathetic ophthalmia is a bilateral granulomatous panuveitis following penetrating trauma or intraocular surgery to one eye (the \u201Cexciting\u201D eye). Posterior segment findings commonly include multifocal choroiditis, Dalen-Fuchs nodules and serous/exudative retinal detachments.\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tFundus fluorescein angiography typically demonstrates multiple pinpoint hyperfluorescent leaks in the early phases with progressive pooling and staining under the serous detachments.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tGranulomatous anterior uveitis with mutton\u2011fat keratic precipitates and nodules (granulomata) on the iris of one or both eyes is also a recognised feature.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tOnce sympathetic ophthalmia is established, treatment is based on high\u2011dose systemic corticosteroids and often additional systemic immunosuppressive therapy to control bilateral inflammation and preserve vision. Enucleation of the exciting eye is mainly a preventive measure if performed within about 10-14 days of the inciting injury and before the onset of disease; after sympathetic ophthalmia has developed, removing the traumatized eye rarely alters the course and is not considered primary treatment.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 349,
    "Name": "Evidence-based medicine\u2014ARR and NNT",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn\nthe ETDRS study for laser treatment of diabetic macular oedema, moderate visual\nloss occurred in 12% of treated eyes compared to 24% of untreated eyes in 3\nyears. What is the value of NNT (numbers needed to treat) in this study\napproximately?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u25CF\tNNT is calculated as the inverse of the absolute risk reduction (ARR).\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E* Here, the event rate is 24% in untreated eyes and 12% in treated eyes.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;ARR = 24% \u2212 12% = 12%\u003C/span\u003E (0.12 as a proportion).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003ETherefore,\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u25CF\tNNT=1/0.12\u22488.3\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u0026nbsp;\u003Cspan style=\u0022font-style: italic;\u0022\u003E\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; which is conventionally rounded up to 9 for NNT reporting\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tInterpreting this clinically: approximately 9 eyes require ETDRS-style laser treatment over 3 years to prevent one additional case of moderate visual loss compared with no treatment.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 350,
    "Name": "Diagnostic tests in aqueous\u2011deficient dry eye (ADDE)",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich\nof the following test results would be MOST likely to support a diagnosis of\naqueous\u2011deficient dry eye disease?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u25CF\tADDE is defined by reduced lacrimal secretion leading to tear film hyperosmolarity, which is a core mechanism of dry eye disease.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tSchirmer 15 mm/5 min: near\u2011normal; does not support significant aqueous deficiency.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tTBUT 11 s: essentially normal; reduced TBUT (\u0026lt;10 s) is more typical of evaporative DED (e.g. MGD).\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tOxford score 1: minimal staining; reflects mild surface damage and does not specifically indicate ADDE.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tTear hyperosmolarity is the best single marker for dry eye pathophysiology and is particularly elevated in moderate\u2013severe ADDE, so among the options it most strongly supports the diagnosis.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 351,
    "Name": "Refractive surprise after uncomplicated cataract surgery",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size: 12pt; line-height: 115%; font-family: \u0026quot;Nova Mono\u0026quot;; font-weight: bold;\u0022\u003EA 63\u2011year\u2011old woman undergoes uncomplicated cataract surgery\naiming for emmetropia. On returning to the post\u2011operative clinic her vision is\n6/60 unaided and 6/18 with -3.5 DS. Which is the MOST likely diagnosis?\u003C/span\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;font-family:Roboto;mso-fareast-font-family:\nRoboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u25CF\tShe was targeted for emmetropia but is now approximately -3.50 D myopic with good BCVA \u2192 this is a pure refractive (axial/ELP) issue, not primarily macular or corneal.\u0026nbsp;\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tCapsular bag distension syndrome (CBDS): fluid trapped behind the IOL pushes it anteriorly, increasing its effective power and causing an unexpected myopic shift with otherwise good, corrected acuity.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tCorneal oedema or CME would reduce BCVA and cause blur/distortion, with more hyperopic refraction.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u25CF\tIOL dislocation/tilt tends to cause decentration, irregular astigmatism, glare, not an isolated neat myopic shift.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 352,
    "Name": "Systemic drugs and diabetic macular oedema (DME)",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin-top:12.0pt;margin-right:0in;margin-bottom:\n6.0pt;margin-left:0in\u0022\u003E\u003Cspan lang=\u0022EN\u0022 style=\u0022font-size:12.0pt;line-height:115%;\nfont-family:Roboto;mso-fareast-font-family:Roboto;mso-bidi-font-family:Roboto\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich\nof the following systemic drugs is LEAST likely to be helpful in the treatment\nof diabetic macular oedema?\u003C/span\u003E\u003Co:p\u003E\u003C/o:p\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E*Pioglitazone (a thiazolidinedione) is the drug among the options that is least likely to be helpful; in fact, it is known to cause or exacerbate diabetic macular oedema (DMO) due to systemic fluid retention. It is associated with an increased risk of DMO development compared to other diabetes medications.\u003C/span\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;The other drugs listed have shown potential benefits in the management of diabetic retinopathy and DMO:\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u25CF Dapagliflozin (an SGLT2 inhibitor) has growing evidence suggesting it may have a beneficial effect on DMO by reducing retinal thickness and inflammation, and ongoing clinical trials are exploring its use as an adjunct therapy.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u25CF Fenofibrate (a fibric acid derivative) significantly slows the progression of diabetic retinopathy and reduces the need for laser treatment for maculopathy and proliferative retinopathy, including the development of macular oedema.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp; \u25CF Rosuvastatin (a statin) has been shown in some studies to reduce DMO progression and improve the resolution of existing DMO, possibly due to its anti-inflammatory effects and ability to reduce lipid exudation.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022white-space-collapse: preserve; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 353,
    "Name": " Treatment of intermediate uveitis with reduced vision",
    "Body": "\u003Cspan id=\u0022docs-internal-guid-c8d04b7c-7fff-607d-d570-42065bafd502\u0022\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022font-size: 12pt; font-family: Roboto, sans-serif; color: rgb(0, 0, 0); background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-variant-position: normal; font-variant-emoji: normal; vertical-align: baseline; white-space-collapse: preserve; font-weight: bold;\u0022\u003EA 33\u2011year\u2011old woman presents with a 2\u2011year history of poor vision in her left eye. Eight years earlier she had been diagnosed with intermediate uveitis. On examination her vision is 6/12 in the left eye. What is the MOST appropriate treatment?\u003C/span\u003E\u003C/p\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: 12pt; font-family: Roboto, sans-serif; color: rgb(0, 0, 0); background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-variant-position: normal; font-variant-emoji: normal; vertical-align: baseline; white-space-collapse: preserve;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003C/span\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cspan id=\u0022docs-internal-guid-7b0c394d-7fff-ba2a-aea0-b2920c4b2a09\u0022\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022font-size: 12pt; font-family: Roboto, sans-serif; color: rgb(0, 0, 0); background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-variant-position: normal; font-variant-emoji: normal; vertical-align: baseline; white-space-collapse: preserve;\u0022\u003EA young patient with known intermediate uveitis and chronic, unilateral reduced vision (6/12) is most likely to have uveitic cystoid macular oedema (CME) in that eye. For unilateral or clearly asymmetric intermediate uveitis with CME, the most appropriate first\u2011line therapy is a regional periocular corticosteroid injection (e.g. posterior sub\u2011Tenon/orbital floor triamcinolone), which delivers high drug levels to the macula with minimal systemic exposure.\u003C/span\u003E\u003C/p\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003E*Systemic steroid will work but exposes the whole body to steroid. It is p\u003C/span\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003Ereferred when disease is bilateral, severe, or associated with systemic inflammatory disease, or when periocular therapy fails/relapses quickly.\u003C/span\u003E\u003C/p\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003E*A systemic steroid\u2011sparing immunosuppressant like oral Cyclosporin for long\u2011term control, not the first step for isolated unilateral CME.\u003C/span\u003E\u003C/p\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003E*Topical steroids have poor penetration to the vitreous and macula; adequate for anterior uveitis but not for intermediate uveitis with CME.\u003C/span\u003E\u003C/p\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp dir=\u0022ltr\u0022 style=\u0022line-height:1.38;margin-top:12pt;margin-bottom:6pt;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan style=\u0022white-space-collapse: preserve;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C!--EndFragment--\u003E\u0026nbsp;\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022background-color: transparent; font-size: 12pt; white-space-collapse: preserve; color: rgb(0, 0, 0); font-family: Roboto, sans-serif; letter-spacing: 0.14994px;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/span\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
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  },
  {
    "Id": 354,
    "Name": "Unilateral Proptosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 43-year-old woman who smokes and is taking \u003Cspan class=\u0022s1\u0022\u003Etamoxifen\u003C/span\u003E presents with \u003Cspan class=\u0022s1\u0022\u003Egradual onset of unilateral proptosis\u003C/span\u003E. What is the \u003Cspan class=\u0022s1\u0022\u003Emost likely underlying cause\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThyroid eye disease (TED)\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common cause of both unilateral and bilateral proptosis\u003C/b\u003E\u003C/span\u003E in adults. It classically affects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emiddle-aged women\u003C/b\u003E\u003C/span\u003E, especially those who \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmoke\u003C/b\u003E\u003C/span\u003E, which is a well-established risk factor for both \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eonset and severity\u003C/b\u003E\u003C/span\u003E of TED. While TED is more commonly bilateral, it can be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral in up to 10-20%\u003C/b\u003E\u003C/span\u003E of cases, particularly in early or asymmetric disease.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlthough \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etamoxifen use\u003C/b\u003E\u003C/span\u003E raises the possibility of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emetastatic breast cancer\u003C/b\u003E\u003C/span\u003E, orbital metastases are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efar less common\u003C/b\u003E\u003C/span\u003E than TED and typically present with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epain, diplopia, rapid progression\u003C/b\u003E\u003C/span\u003E, or signs of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einfiltrative disease\u003C/b\u003E\u003C/span\u003E, which are not described here.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECavernous haemangiomas\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E are typically \u003C/span\u003E\u003Cb\u003Eslow-growing, benign intraconal tumours\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E presenting in middle age, but they are less common than TED and usually do \u003C/span\u003E\u003Cb\u003Enot occur in smokers with systemic autoimmune risk factors\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOrbital varices\u003C/b\u003E\u003C/span\u003E often cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintermittent proptosis\u003C/b\u003E\u003C/span\u003E triggered by valsalva manoeuvres, not gradual persistent proptosis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 355,
    "Name": "Basal cell carcinoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost common route of spread\u003Cspan class=\u0022s1\u0022\u003E for \u003C/span\u003Ebasal cell carcinoma\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBasal cell carcinoma (BCC)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is the \u003C/span\u003E\u003Cb\u003Emost common malignant eyelid tumour\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, but it has \u003C/span\u003E\u003Cb\u003Every low metastatic potential\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. The hallmark of BCC is \u003C/span\u003E\u003Cb\u003Eprogressive local tissue invasion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often with \u003C/span\u003E\u003Cb\u003Edestruction of adjacent structures\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly if neglected or in high-risk locations (e.g. medial canthus, orbit).\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELymphatic\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Ehaematogenous\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E spread are \u003C/span\u003E\u003Cb\u003Eextremely rare\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in BCC.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECSF spread\u003C/b\u003E\u003C/span\u003E is irrelevant in this context as BCC does not involve the central nervous system.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESquamous cell carcinoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, in contrast, has a \u003C/span\u003E\u003Cb\u003Ehigher risk of lymphatic spread\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and potential for metastasis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ETherefore, \u003C/span\u003E\u003Cb\u003Elocal invasion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E remains the \u003C/span\u003E\u003Cb\u003Eprimary and most clinically significant mode of spread\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E for BCC.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
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    "CategoryId": 9,
    "Category": null,
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  },
  {
    "Id": 356,
    "Name": "Orbit Anatomy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following combinations of bones form the \u003Cspan class=\u0022s1\u0022\u003Emedial wall of the orbit\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emedial wall of the orbit\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethinnest\u003C/b\u003E\u003C/span\u003E and most \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efragile\u003C/b\u003E\u003C/span\u003E orbital wall and comprises four bones:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMaxilla\u003C/b\u003E\u003C/span\u003E (specifically the frontal process)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELacrimal bone\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEthmoid bone\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (particularly the thin \u003C/span\u003E\u003Cb\u003Elamina papyracea\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBody of sphenoid\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis wall separates the orbit from the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eethmoid sinus\u003C/b\u003E\u003C/span\u003E, and trauma here may result in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorbital emphysema\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emedial wall blowout fractures\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022https://prod-images-static.radiopaedia.org/images/19311340/a2db73fd3be3c04a515e8998f1e6c5_big_gallery.jpeg\u0022\u003E\u003C/p\u003E\u003Cp style=\u0022margin-bottom: calc(1.16667em); color: rgb(61, 61, 61); font-family: \u0026quot;Open Sans\u0026quot;, sans-serif; letter-spacing: normal; background-color: rgb(238, 238, 238);\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003ESkull and facial bone diagrams.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp style=\u0022margin-bottom: 0px; color: rgb(61, 61, 61); font-family: \u0026quot;Open Sans\u0026quot;, sans-serif; letter-spacing: normal; background-color: rgb(238, 238, 238);\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003ELicense: All image files licensed under Creative Commons BY 3.0 OpenStax College, cnx.org\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EOther orbital walls include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERoof\u003C/b\u003E\u003C/span\u003E: frontal bone and lesser wing of sphenoid\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELateral wall\u003C/b\u003E\u003C/span\u003E: zygomatic bone and greater wing of sphenoid\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFloor\u003C/b\u003E\u003C/span\u003E: maxilla, zygomatic bone, and small part of palatine bone\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 357,
    "Name": "Orbital inflammation [IgG4 related]",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following ocular features is \u003Cspan class=\u0022s1\u0022\u003Emost commonly associated\u003C/span\u003E with IgG4-related ophthalmic disease?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIgG4-related ophthalmic disease (IgG4-ROD)\u003C/b\u003E\u003C/span\u003E is a systemic fibroinflammatory condition driven by IgG4-positive plasma cells. It \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecommonly affects the orbit\u003C/b\u003E\u003C/span\u003E, and less frequently intraocular tissues. The hallmark features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELacrimal gland enlargement\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (dacryoadenitis)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital mass lesions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (often bilateral)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInfraorbital nerve enlargement\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EExtraocular muscle involvement\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESclerosing inflammation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E leading to fibrosis\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EUveitis is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare\u003C/b\u003E\u003C/span\u003E in IgG4-related disease and not a typical manifestation of IgG4-ROD.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EHistopathology usually shows:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDense lymphoplasmacytic infiltrate\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EStoriform fibrosis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EObliterative phlebitis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EElevated serum IgG4 levels may support the diagnosis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EImaging (CT/MRI) typically shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ediffuse, homogenous enlargement\u003C/b\u003E\u003C/span\u003E of orbital structures with well-defined margins.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 358,
    "Name": "Thyroid Eye disease",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 42-year-old woman with known Graves\u2019 disease presents with \u003C/span\u003Emild lid retraction (\u0026lt;2 mm)\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Emild periorbital swelling\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Eno diplopia\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003Eintermittent foreign body sensation relieved by lubricants\u003Cspan class=\u0022s1\u0022\u003E. Examination confirms \u003C/span\u003Eexophthalmos \u0026lt;3 mm above normal\u003Cspan class=\u0022s1\u0022\u003E for her age and race.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EThere is \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eno evidence of optic neuropathy or corneal breakdown\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost appropriate next step in management\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emild thyroid eye disease (TED)\u003C/b\u003E\u003C/span\u003E, the emphasis is on \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econservative, supportive care\u003C/b\u003E\u003C/span\u003E and controlling modifiable risk factors:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESmoking cessation\u003C/b\u003E\u003C/span\u003E is critical, as smoking worsens TED and reduces treatment efficacy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESelenium supplementation (100 mcg twice daily)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E has been shown to \u003C/span\u003E\u003Cb\u003Ereduce disease progression and improve quality of life\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in patients with mild TED (as demonstrated in the EUGOGO study).\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther measures include artificial tears, sunglasses, lifestyle advice, and achieving \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eeuthyroid status\u003C/b\u003E\u003C/span\u003E, but selenium and smoking cessation are considered \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecore interventions\u003C/b\u003E\u003C/span\u003E for mild active disease.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECarbimazole\u003C/b\u003E\u003C/span\u003E may be used to manage hyperthyroidism but is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot a direct treatment\u003C/b\u003E\u003C/span\u003E for eye disease unless required for systemic control.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESteroids\u003C/b\u003E\u003C/span\u003E are reserved for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emoderate-to-severe active TED\u003C/b\u003E\u003C/span\u003E, not for mild cases.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-28-b51521c7-d5e4-4a03-afd8-5df8106cc156.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 359,
    "Name": "Sarcoidosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA young girl presents with a \u003C/span\u003Egeneralised rash\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Ejoint pain\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003Ebilateral lymphadenopathy\u003Cspan class=\u0022s1\u0022\u003E. Ocular examination reveals \u003C/span\u003Eband keratopathy\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Eanterior uveitis\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003Eretinal vasculitis\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely diagnosis\u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis multisystem presentation involving \u003C/span\u003E\u003Cb\u003Erash, arthralgia, and lymphadenopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, along with \u003C/span\u003E\u003Cb\u003Eocular findings of anterior uveitis, band keratopathy, and retinal vasculitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, is \u003C/span\u003E\u003Cb\u003Emost characteristic of sarcoidosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EOcular sarcoidosis may present with:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnterior uveitis\u003C/b\u003E\u003C/span\u003E, often granulomatous\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBand keratopathy\u003C/b\u003E\u003C/span\u003E, from chronic inflammation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal periphlebitis\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evasculitis\u003C/b\u003E\u003C/span\u003E, classically with \u201Ccandle-wax drippings\u201D\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESystemic signs such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elymphadenopathy\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erash\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Earthropathy\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhile \u003C/span\u003E\u003Cb\u003EJIA\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a common cause of uveitis in young girls, it \u003C/span\u003E\u003Cb\u003Etypically causes chronic, non-granulomatous anterior uveitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Edoes not cause retinal vasculitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E or generalized lymphadenopathy.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EUlcerative colitis\u003C/b\u003E\u003C/span\u003E may rarely have uveitis, but retinal vasculitis is not typical, and lymphadenopathy would be unusual.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 360,
    "Name": "Functional visual loss",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 13-year-old girl presents with a \u003Cspan class=\u0022s1\u0022\u003E2-day history of sudden vision loss\u003C/span\u003E in her right eye. Visual acuity is \u003Cspan class=\u0022s1\u0022\u003Ehand movements\u003C/span\u003E in the right eye and \u003Cspan class=\u0022s1\u0022\u003E6/6\u003C/span\u003E in the left. \u003Cspan class=\u0022s1\u0022\u003EPupil responses are normal\u003C/span\u003E and there is \u003Cspan class=\u0022s1\u0022\u003Eno RAPD\u003C/span\u003E. \u003Cspan class=\u0022s1\u0022\u003ESlit-lamp, fundus, OCT, and FFA\u003C/span\u003E findings are all normal bilaterally.\u0026nbsp;\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely response\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E when a \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E20-dioptre base-out prism\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E is placed in front of the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eright eye\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis presentation is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efunctional visual loss (FVL)\u003C/b\u003E\u003C/span\u003E in a child, particularly in the context of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enormal ocular examination and imaging\u003C/b\u003E\u003C/span\u003E, no RAPD, and a disproportionate visual acuity reduction.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003EThe \u003C/span\u003E\u003Cb\u003E20-dioptre base-out prism test\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E is useful for detecting \u003C/span\u003E\u003Cb\u003Enon-organic visual loss\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E. When a base-out prism is placed in front of one eye, both eyes should \u003C/span\u003E\u003Cb\u003Emove toward the apex of the prism\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E (in this case, to the \u003C/span\u003E\u003Cb\u003Eleft\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E) and then the \u003C/span\u003E\u003Cb\u003Efellow eye makes a corrective movement to restore fixation\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn true monocular visual loss, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno corrective movement occurs\u003C/b\u003E\u003C/span\u003E, because the brain does not detect displacement in the eye with no vision.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efunctional (non-organic) loss\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eboth eyes respond normally\u003C/b\u003E\u003C/span\u003E, as seen in this case: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eboth eyes move to the left\u003C/b\u003E\u003C/span\u003E, and the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eleft eye corrects fixation\u003C/b\u003E\u003C/span\u003E with adduction\u2014indicating that vision in the \u201Caffected\u201D eye is likely intact.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 361,
    "Name": "Cycloplegic refraction",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost appropriate drop combination\u003Cspan class=\u0022s1\u0022\u003E for \u003C/span\u003Ecycloplegic refraction\u003Cspan class=\u0022s1\u0022\u003E in a \u003C/span\u003E6-month-old infant\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFor \u003C/span\u003E\u003Cb\u003Ecycloplegic refraction in infants under 12 months\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, the recommended agents are \u003C/span\u003E\u003Cb\u003Elow-dose cyclopentolate (0.5% or 0.25%)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Elow-dose phenylephrine (1% or 2.5%)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. This combination provides adequate cycloplegia and mydriasis while \u003C/span\u003E\u003Cb\u003Eminimizing systemic side effects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly anticholinergic toxicity.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E1% cyclopentolate\u003C/b\u003E\u003C/span\u003E may be too strong and can cause systemic toxicity in young infants.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAtropine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is avoided in this age group due to its \u003C/span\u003E\u003Cb\u003Elong duration of action\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Ehigher risk of systemic effects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E10% phenylephrine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is \u003C/span\u003E\u003Cb\u003Econtraindicated in infants\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E due to the risk of \u003C/span\u003E\u003Cb\u003Ehypertensive crises and cardiovascular complications\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 362,
    "Name": "Blepharitis - corneal vascularisation",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 5-year-old boy is \u003C/span\u003Easymptomatic\u003Cspan class=\u0022s1\u0022\u003E but noted to have \u003C/span\u003Ebilateral superficial inferior corneal vascularisation\u003Cspan class=\u0022s1\u0022\u003E. What is the \u003C/span\u003Emost likely underlying cause\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn children, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echronic blepharokeratoconjunctivitis (BKC)\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common cause\u003C/b\u003E\u003C/span\u003E of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral inferior superficial corneal vascularisation\u003C/b\u003E\u003C/span\u003E, often without significant symptoms. It may be subtle and under-recognized but can lead to long-term complications like corneal scarring and amblyopia if untreated.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAllergic eye disease\u003C/b\u003E\u003C/span\u003E, such as vernal keratoconjunctivitis, typically affects the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperior\u003C/b\u003E\u003C/span\u003E cornea and is associated with intense itching and photophobia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAdenoviral keratitis\u003C/b\u003E\u003C/span\u003E causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubepithelial infiltrates\u003C/b\u003E\u003C/span\u003E and is more central/paracentral in distribution.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERosacea\u003C/b\u003E\u003C/span\u003E is rare in young children and more common in older children/adults.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 363,
    "Name": "Shaken baby syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EThe retinal findings seen in \u003Cspan class=\u0022s1\u0022\u003Eshaken-baby syndrome\u003C/span\u003E are \u003Cspan class=\u0022s1\u0022\u003Eleast similar\u003C/span\u003E to which of the following conditions?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EShaken-baby syndrome (SBS) typically causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eextensive, multilayered retinal haemorrhages -\u0026nbsp;\u003C/b\u003E\u003C/span\u003Eincluding \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epreretinal\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintraretinal\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubretinal-\u003C/b\u003E\u003C/span\u003E\u0026nbsp;often extending to the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral retina\u003C/b\u003E\u003C/span\u003E, and frequently too numerous to count. This pattern is most closely mimicked by other \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehaemorrhagic retinopathies\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETerson\u2019s syndrome\u003C/b\u003E\u003C/span\u003E: intraocular haemorrhage due to raised intracranial pressure (e.g., subarachnoid haemorrhage).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPurtscher\u2019s retinopathy\u003C/b\u003E\u003C/span\u003E: associated with trauma or acute pancreatitis; presents with cotton-wool spots, retinal whitening, and retinal haemorrhages.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECRVO\u003C/b\u003E\u003C/span\u003E: causes widespread intraretinal haemorrhages in all quadrants.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cp class=\u0022p1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EIn contrast,\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003Ecommotio retinae\u003C/span\u003E\u003C/span\u003E\u0026nbsp;presents with\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003Etransient retinal whitening\u003C/span\u003E\u003C/span\u003E\u0026nbsp;(particularly at the posterior pole), due to photoreceptor outer segment disruption after blunt trauma.\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EIt typically lacks haemorrhages\u003C/span\u003E\u003C/span\u003E, making it least like SBS.\u003C/p\u003E\u003Cp class=\u0022p3\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022https://media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12886-020-01666-9/MediaObjects/12886_2020_1666_Fig1_HTML.png?as=webp\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Ea\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E,\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Eb\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E\u0026nbsp;Fundus photography showing bilateral intraretinal and preretinal hemorrhages, with a boat-shaped premacular hematoma, which is in the right eye larger in size and surrounded with an elevated ring-shaped white retinal fold (arrowheads).\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Ec\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E\u0026nbsp;SS OCT scan through the macula of the right eye showing a dome-shaped highly reflective band corresponding to a detached internal limiting membrane (ILM) (orange arrow) with associated posterior shadowing from dense sub-ILM hemorrhage. Note the presence of retinal traction at the upper edge of the detached ILM corresponding to the perimacular elevated retinal fold seen clinically (asterix). Note also the fainter reflecting posterior hyaloid overlying the detached ILM superiorly (red arrows).\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Ed\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E\u0026nbsp;SS OCT scan through nasal retina showing diffuse inner retinal hyperreflectivity (arrows) and multifocal serous retinal detachment.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Ee\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E,\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022box-sizing: inherit; font-weight: bolder; color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003Ef\u003C/span\u003E\u003Cspan style=\u0022color: rgb(34, 34, 34); font-family: Merriweather, serif; letter-spacing: normal;\u0022\u003E\u0026nbsp;SS OCT scans of the left eye showing hyperreflective vitreous dots, a sub-ILM hemorrhage (arrow), wave-shaped retinal layers deformation, diffuse inner retinal hyperreflectivity, ellipsoid zone disruption, intraretinal hyperreflective dots, and serous retinal detachment\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003ESource of image:\u0026nbsp;\u003C/b\u003E\u003Ca href=\u0022https://link.springer.com/article/10.1186/s12886-020-01666-9\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ESwept-source OCT findings in shaken baby syndrome: case report\u003C/a\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 364,
    "Name": "Visual acuity testing in children",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost appropriate method\u003Cspan class=\u0022s1\u0022\u003E to assess \u003C/span\u003Evisual acuity\u003Cspan class=\u0022s1\u0022\u003E in an \u003C/span\u003E18-month-old child\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EFor very young children, particularly under \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2 years of age\u003C/b\u003E\u003C/span\u003E, conventional visual acuity testing methods (such as optotype or letter matching) are inappropriate due to limited cognitive and language development.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECardiff Cards\u003C/b\u003E\u003C/span\u003E use the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epreferential looking technique\u003C/b\u003E\u003C/span\u003E with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evanishing optotypes\u003C/b\u003E\u003C/span\u003E, and are specifically designed for infants and toddlers aged \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E6 months to 2 years\u003C/b\u003E\u003C/span\u003E. They require no verbal response and are based on the child\u2019s instinctive tendency to look at patterns over blank spaces.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKay pictures\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESonksen\u003C/b\u003E\u003C/span\u003E charts (crowded optotypes) are more suitable for children aged \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2 to 3\u002B years\u003C/b\u003E\u003C/span\u003E, once picture matching and sustained attention are possible.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESheridan-Gardiner\u003C/b\u003E\u003C/span\u003E is a letter matching test suited to children \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eover 3 years\u003C/b\u003E\u003C/span\u003E, who can reliably match letters using a key card.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022/upload-2026-01-28-d29e8601-8d7b-4089-9e75-a08d034bd14c.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 365,
    "Name": "X-linked Retinoschisis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 5-year-old boy is referred by his optician due to difficulty with reading at school. Slit lamp biomicroscopy reveals \u003Cspan class=\u0022s1\u0022\u003Efoveal microcysts.\u0026nbsp;\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely diagnosis\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EX-linked retinoschisis (XLRS) is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost likely diagnosis\u003C/b\u003E\u003C/span\u003E in a young boy presenting with reduced central vision and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efoveal microcystic changes\u003C/b\u003E\u003C/span\u003E. It typically presents \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebetween 3 and 6 years of age\u003C/b\u003E\u003C/span\u003E and is characterized by:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFoveal schisis\u003C/b\u003E\u003C/span\u003E: Seen as cystic-appearing spaces or spoke-wheel striae confined to the macula\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBilateral maculopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Often symmetrical\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripheral schisis\u003C/b\u003E\u003C/span\u003E: Found in ~50% of cases, most commonly inferotemporal\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinoschisin gene mutation\u003C/b\u003E\u003C/span\u003E on the X chromosome (RS1 gene)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EElectroretinogram (ERG)\u003C/b\u003E\u003C/span\u003E: May be normal in isolated foveal disease, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einverted waveform\u003C/b\u003E\u003C/span\u003E (reduced b-wave with preserved a-wave) is typical in peripheral schisis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EIncorrect options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERod monochromatism\u003C/b\u003E\u003C/span\u003E: Presents with nystagmus, photophobia, and reduced acuity from infancy; foveal cysts are not typical\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital stationary night blindness (CSNB)\u003C/b\u003E\u003C/span\u003E: Presents with nyctalopia and sometimes high myopia; not usually associated with foveal microcysts\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlue cone monochromatism\u003C/b\u003E\u003C/span\u003E: A rare cone dystrophy presenting with poor central vision and photophobia; fundus changes are less specific and usually show generalized cone dysfunction rather than foveal schisis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Feye.2017.281/MediaObjects/41433_2018_Article_BFeye2017281_Fig1_HTML.jpg?as=webp\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cdiv class=\u0022c-article-section__figure-content\u0022 style=\u0022box-sizing: inherit; margin-bottom: 16px; color: rgb(34, 34, 34); font-family: -apple-system, \u0026quot;system-ui\u0026quot;, \u0026quot;Segoe UI\u0026quot;, Roboto, Oxygen-Sans, Ubuntu, Cantarell, \u0026quot;Helvetica Neue\u0026quot;, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cdiv class=\u0022c-article-section__figure-description\u0022 data-test=\u0022bottom-caption\u0022 id=\u0022figure-1-desc\u0022 style=\u0022box-sizing: inherit;\u0022\u003E\u003Cp style=\u0022overflow-wrap: break-word; word-break: break-word; box-sizing: inherit; margin-bottom: 24px;\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003E(a\u2013e) The images correspond to a 13-year-old male patient (case No. 2) with XLRS. (a) Fundus color photography of the OD showing hyporeflective cystic spaces in the foveal and parafoveal regions. (b) SS-OCT of the OD revealing schisis (thick blue arrows) at the level of the INL (thin blue arrow). These images also show a small defect at the ELM, the EPIS ellipsoid zone, and COST (yellow rectangle). The upper/left (retinal) and lower/right (choroidal) areas show the topographic map with nine subfields as defined by the ETDRS-style grid. (c, d) A 6 \u00D7 6\u2009mm OCT-A showing superficial and deep vascular plexus (more prominent) with irregularities due to schisis at INL. OCT angiograms showed petaloid non-reflective area located predominantly inside of the deep vascular plexus. (e) An en-face OCT image at the level of the INL showing a spoke-like pattern in the foveal region and a reticular pattern in the parafoveal region.\u003C/span\u003E\u003C/p\u003E\u003Cp style=\u0022overflow-wrap: break-word; word-break: break-word; box-sizing: inherit; margin-bottom: 24px;\u0022\u003E\u003Cspan style=\u0022font-size: x-small;\u0022\u003EImage source:\u0026nbsp;\u003C/span\u003E\u003Ca href=\u0022https://www.nature.com/articles/eye2017281\u0022 target=\u0022_blank\u0022\u003ESwept-source and optical coherence tomography angiography in patients with X-linked retinoschisis\u003C/a\u003E\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 366,
    "Name": "Orbital cellulitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements is \u003Cspan class=\u0022s1\u0022\u003EFALSE\u003C/span\u003E regarding \u003Cspan class=\u0022s1\u0022\u003Echildhood orbital cellulitis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOrbital cellulitis in children\u003C/b\u003E\u003C/span\u003E is most commonly due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eextension of ethmoid sinusitis\u003C/b\u003E\u003C/span\u003E, not maxillary sinusitis. The \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elamina papyracea -\u0026nbsp;\u003C/b\u003E\u003C/span\u003Ea thin bony wall between the ethmoid sinus and the orbit- makes ethmoiditis the most frequent source of orbital spread.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore common over the age of 5\u003C/b\u003E\u003C/span\u003E, with an average age of presentation around \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E7 years\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECT scanning\u003C/b\u003E\u003C/span\u003E with contrast is the initial imaging modality of choice due to its rapid acquisition and ability to delineate orbital abscesses, sinus disease, and subperiosteal collections. MRI is reserved for suspected intracranial spread or complications.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntravenous antibiotics\u003C/b\u003E\u003C/span\u003E are the first-line treatment, and surgery (e.g., drainage of an abscess) is considered if there\u2019s no improvement or if there\u2019s a confirmed collection.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 367,
    "Name": "Rod monochromatism",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAn 18-month-old hyperopic boy presents with nystagmus, photophobia, and difficulty seeing in bright light. Visual acuity using Cardiff cards is logMAR 1.0. What is the \u003Cspan class=\u0022s1\u0022\u003Emost likely diagnosis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis clinical picture is classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erod monochromatism\u003C/b\u003E\u003C/span\u003E (complete achromatopsia), a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erare autosomal recessive disorder\u003C/b\u003E\u003C/span\u003E resulting from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomplete absence of cone function\u003C/b\u003E\u003C/span\u003E. It presents \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ein infancy\u003C/b\u003E\u003C/span\u003E with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENystagmus\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPhotophobia and hemeralopia\u003C/b\u003E\u003C/span\u003E (daylight visual impairment)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReduced visual acuity\u003C/b\u003E\u003C/span\u003E (logMAR 1.0 \u2248 Snellen 6/60)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHypermetropia\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese children often appear uncomfortable in daylight and demonstrate \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor navigation under bright conditions\u003C/b\u003E\u003C/span\u003E due to reliance on rods, which are oversaturated in photopic conditions.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EDifferential diagnoses:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlue cone monochromatism\u003C/b\u003E\u003C/span\u003E is milder and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EX-linked\u003C/b\u003E\u003C/span\u003E, with partial cone function (S-cones retained); \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopia\u003C/b\u003E\u003C/span\u003E is common, not hyperopia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EEnhanced S-cone syndrome (Goldmann-Favre)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E presents with \u003C/span\u003E\u003Cb\u003Enyctalopia (not photophobia)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and retinal degeneration, not evident here.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDeuteranopia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is an isolated red-green colour vision defect, \u003C/span\u003E\u003Cb\u003Enot associated with poor acuity or photophobia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 368,
    "Name": "Rhabdomyosarcoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA 7-year-old girl presents with a \u003C/span\u003E2-week history\u003Cspan class=\u0022s1\u0022\u003E of \u003C/span\u003Epainful, unilateral axial proptosis\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Elid erythema\u003Cspan class=\u0022s1\u0022\u003E. She is \u003C/span\u003Eapyrexial\u003Cspan class=\u0022s1\u0022\u003E. CT imaging reveals a \u003C/span\u003Ehomogeneous, poorly defined, non-enhancing orbital mass\u003Cspan class=\u0022s1\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich diagnosis is \u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERhabdomyosarcoma\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common primary orbital malignancy in children\u003C/b\u003E\u003C/span\u003E, typically presenting between ages \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E7-8 years\u003C/b\u003E\u003C/span\u003E. It characteristically causes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESudden-onset\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, progressive \u003C/span\u003E\u003Cb\u003Epainful proptosis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAxial displacement\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EErythematous lids\u003C/b\u003E\u003C/span\u003E, mimicking inflammation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECT scan\u003C/b\u003E\u003C/span\u003E: poorly defined, non-enhancing soft tissue mass\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey imaging clue: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehomogeneous mass with no enhancement\u003C/b\u003E\u003C/span\u003E, often with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebone erosion\u003C/b\u003E\u003C/span\u003E in advanced stages.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELymphangioma\u003C/b\u003E\u003C/span\u003E: Usually younger children (\u0026lt;4 years), \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-painful\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-axial\u003C/b\u003E\u003C/span\u003E; may present acutely \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eif hemorrhage\u003C/b\u003E\u003C/span\u003E occurs.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECapillary haemangioma\u003C/b\u003E\u003C/span\u003E: Common in infants (\u0026lt;1 year), usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperior orbit\u003C/b\u003E\u003C/span\u003E, painless and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eslow-growing\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital varices\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Present with \u003C/span\u003E\u003Cb\u003Eintermittent proptosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, worsened by Valsalva; \u003C/span\u003E\u003Cb\u003Enot painful\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and imaging shows \u003C/span\u003E\u003Cb\u003Edistensible venous channels\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 369,
    "Name": "Fourth Nerve Palsy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 30-year-old man presents with \u003Cspan class=\u0022s1\u0022\u003Etorsional diplopia\u003C/span\u003E following a \u003Cspan class=\u0022s1\u0022\u003Eclosed head injury\u003C/span\u003E sustained in a motorcycle accident \u003Cspan class=\u0022s1\u0022\u003E6 months ago\u003C/span\u003E. On examination, there is \u003Cspan class=\u0022s1\u0022\u003E12\u00B0 of excyclotorsion\u003C/span\u003E.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhich is the most appropriate surgical intervention?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe patient has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral fourth nerve palsy\u003C/b\u003E\u003C/span\u003E, the most common cranial nerve injury following \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclosed head trauma\u003C/b\u003E\u003C/span\u003E, particularly when \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexcyclotorsion \u0026gt;10\u00B0\u003C/b\u003E\u003C/span\u003E is present. Other supportive signs include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMinimal vertical deviation in primary gaze\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETorsional diplopia as primary complaint\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChin-down posture\u003C/b\u003E\u003C/span\u003E, V-pattern esotropia\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAlternating hypertropia on head tilt\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHarada-Ito surgery\u003C/b\u003E\u003C/span\u003E selectively tightens the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior fibers of the superior oblique\u003C/b\u003E\u003C/span\u003E, which are responsible for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintorsion\u003C/b\u003E\u003C/span\u003E. This corrects \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexcyclotorsion\u003C/b\u003E\u003C/span\u003E while minimally affecting vertical movement; making it the procedure of choice for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etorsional diplopia\u003C/b\u003E\u003C/span\u003E in bilateral fourth nerve palsy.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EObservation\u003C/b\u003E\u003C/span\u003E is inappropriate given persistent, symptomatic torsional diplopia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESuperior oblique resection\u003C/b\u003E\u003C/span\u003E risks worsening vertical misalignment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInferior oblique myectomy\u003C/b\u003E\u003C/span\u003E would increase excyclotorsion; contraindicated here.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://childrenseye.org/wiki/lib/exe/fetch.php?w=512\u0026amp;tok=e3d9bb\u0026amp;media=harada-ito.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Ch1 class=\u0022sectionedit1 page-header pb-3 mb-4 mt-5\u0022 id=\u0022harada-ito_procedure\u0022 style=\u0022font-size: 36px; font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-weight: 500; line-height: 1.1; color: rgb(45, 45, 45); border-bottom-width: 1px; border-bottom-color: rgb(238, 238, 238); letter-spacing: normal; margin-top: 3rem !important; margin-bottom: 1.5rem !important; padding-bottom: 1rem !important;\u0022\u003EHarada-Ito Procedure\u003Ca class=\u0022anchorjs-link \u0022 href=\u0022https://childrenseye.org/wiki/doku.php?id=harada_ito#harada-ito_procedure\u0022 aria-label=\u0022Anchor link for: harada ito_procedure\u0022 data-anchorjs-icon=\u0022\uE9CB\u0022 style=\u0022background-color: transparent; color: rgb(51, 153, 243); opacity: 0; font-family: anchorjs-icons; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-variant-position: normal; font-variant-emoji: normal; font-weight: normal; line-height: 1; padding-left: 0.375em;\u0022\u003E\u003C/a\u003E\u003C/h1\u003E\u003Cdiv class=\u0022level1\u0022 style=\u0022color: rgb(102, 102, 102); font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003C/div\u003E\u003Ch2 class=\u0022sectionedit2 page-header pb-3 mb-4 mt-5\u0022 id=\u0022purpose\u0022 style=\u0022font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-weight: 500; line-height: 1.1; color: rgb(45, 45, 45); border-bottom-width: 1px; border-bottom-color: rgb(238, 238, 238); letter-spacing: normal; margin-top: 3rem !important; margin-bottom: 1.5rem !important; padding-bottom: 1rem !important;\u0022\u003E\u003Cspan style=\u0022font-size: large;\u0022\u003EPurpose\u003Cspan style=\u0022line-height: 1; padding-left: 0.375em;\u0022\u003E\u003Ca class=\u0022anchorjs-link \u0022 href=\u0022https://childrenseye.org/wiki/doku.php?id=harada_ito#purpose\u0022 aria-label=\u0022Anchor link for: purpose\u0022 data-anchorjs-icon=\u0022\uE9CB\u0022 style=\u0022background-color: transparent; color: rgb(51, 153, 243); opacity: 0; font-family: anchorjs-icons; font-variant-numeric: normal; font-variant-east-asian: normal; font-variant-alternates: normal; font-variant-position: normal; font-variant-emoji: normal; font-weight: normal; line-height: 1; padding-left: 0.375em;\u0022\u003E\u003C/a\u003E\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\u003Cdiv class=\u0022level2\u0022 style=\u0022color: rgb(102, 102, 102); font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cul class=\u0022 fix-media-list-overlap\u0022 style=\u0022margin-bottom: 10px; overflow: hidden;\u0022\u003E\u003Cli class=\u0022level1\u0022\u003E\u003Cdiv class=\u0022li\u0022\u003EStrengthen Incylotorsion effect of the Superior Oblique without affecting vertical alignment\u003C/div\u003E\u003C/li\u003E\u003Cli class=\u0022level1\u0022\u003E\u003Cdiv class=\u0022li\u0022\u003EMost useful with a functioning superior oblique and excyclotorsion present\u003C/div\u003E\u003C/li\u003E\u003Cli class=\u0022level1\u0022\u003E\u003Cdiv class=\u0022li\u0022\u003ECan create 10-15 degrees of incyclotorsion\u003C/div\u003E\u003C/li\u003E\u003Cli class=\u0022level1\u0022\u003E\u003Cdiv class=\u0022li\u0022\u003EThe effect may wain 20-30% with time\u003C/div\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Ch2 class=\u0022sectionedit3 page-header pb-3 mb-4 mt-5\u0022 id=\u0022description\u0022 style=\u0022font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-weight: 500; line-height: 1.1; color: rgb(45, 45, 45); border-bottom-width: 1px; border-bottom-color: rgb(238, 238, 238); letter-spacing: normal; margin-top: 3rem !important; margin-bottom: 1.5rem !important; padding-bottom: 1rem !important;\u0022\u003E\u003Cspan style=\u0022font-size: large;\u0022\u003EDescription\u003C/span\u003E\u003C/h2\u003E\u003Ch2 class=\u0022sectionedit3 page-header pb-3 mb-4 mt-5\u0022 id=\u0022description\u0022 style=\u0022font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-weight: 500; line-height: 1.1; color: rgb(45, 45, 45); border-bottom-width: 1px; border-bottom-color: rgb(238, 238, 238); letter-spacing: normal; margin-top: 3rem !important; margin-bottom: 1.5rem !important; padding-bottom: 1rem !important;\u0022\u003E\u003Cspan style=\u0022color: rgb(102, 102, 102); font-size: 14px; font-weight: 400;\u0022\u003ETranspose the anterior 1/3 to 1/2 of the superior oblique tendon fibers to the superior border of the lateral rectus muscle. Fixate the tendon 8 mm posterior to and 2 mm superior to the superior border of the lateral rectus muscle. Tightening only the radially oriented fibers will avoid a significant change in vertical deviation but there may be an exoshift in down-gaze.\u003C/span\u003E\u003C/h2\u003E\u003Cdiv class=\u0022level2\u0022 style=\u0022color: rgb(102, 102, 102); font-family: \u0026quot;Open Sans\u0026quot;, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cp style=\u0022margin-bottom: 10px;\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp style=\u0022margin-bottom: 10px;\u0022\u003ESource:\u0026nbsp;\u003Ca href=\u0022https://childrenseye.org/wiki/doku.php?id=harada_ito\u0022 target=\u0022_blank\u0022\u003EHarada Ito\u003C/a\u003E\u003C/p\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 370,
    "Name": "Intermittent exotropia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost common form of exotropia\u003Cspan class=\u0022s1\u0022\u003E seen in \u003C/span\u003Echildhood\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntermittent exotropia\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost frequent type of exotropia in children\u003C/b\u003E\u003C/span\u003E, typically presenting between \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2 and 5 years of age\u003C/b\u003E\u003C/span\u003E. It is often noticed by parents when the child is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edaydreaming, tired, or fixating at distance\u003C/b\u003E\u003C/span\u003E. The deviation is not constant and may be well-controlled for near tasks in early stages.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOver time, intermittent exotropia may \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprogress to constant exotropia\u003C/b\u003E\u003C/span\u003E if untreated. Management depends on the frequency and severity of the deviation and may include \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eobservation, orthoptic exercises, or surgery\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EConsecutive exotropia\u003C/b\u003E\u003C/span\u003E occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epostoperatively\u003C/b\u003E\u003C/span\u003E after overcorrection of esotropia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInfantile exotropia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is rare and often associated with \u003C/span\u003E\u003Cb\u003Eneurological or syndromic disorders\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESecondary exotropia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E refers to exotropia from \u003C/span\u003E\u003Cb\u003Evision loss or disruption of fusion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 371,
    "Name": "Consecutive exotropia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements is \u003Cspan class=\u0022s1\u0022\u003ETRUE\u003C/span\u003E regarding \u003Cspan class=\u0022s1\u0022\u003Econsecutive exotropia\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConsecutive exotropia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E refers to an \u003C/span\u003E\u003Cb\u003Eexodeviation that develops following surgical correction of esotropia\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. It is \u003C/span\u003E\u003Cb\u003Emore common in hyperopic children\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially if a reduction in hyperopic correction decreases the accommodative-convergence drive.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EIncreasing \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Emyopic correction\u003C/b\u003E\u003C/span\u003E (or reducing hyperopic correction) can enhance accommodative effort and \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Estimulate convergence\u003C/b\u003E\u003C/span\u003E, thereby \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ereducing the angle of exotropia\u003C/b\u003E\u003C/span\u003E. This approach can help manage small-angle deviations nonsurgically.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003EKey facts:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOccurs after esotropia surgery\u003C/b\u003E\u003C/span\u003E, not exotropia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAdduction is usually preserved\u003C/b\u003E\u003C/span\u003E, unless there\u2019s muscle slippage or scarring.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore common in hyperopes\u003C/b\u003E\u003C/span\u003E, not myopes.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 372,
    "Name": "Brown Syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAn 8-year-old girl is noted on routine examination to have limited elevation in adduction of the right eye. Elevation in abduction is full. There is overaction of the left superior rectus, with otherwise normal ocular motility. Bielschowsky head tilt test is negative.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBrown\u2019s syndrome\u003C/b\u003E\u003C/span\u003E is caused by a restriction of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperior oblique tendon\u003C/b\u003E\u003C/span\u003E (typically at the trochlea), leading to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elimited elevation in adduction\u003C/b\u003E\u003C/span\u003E. Key features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENormal elevation in abduction\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo muscle sequelae\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, apart from possible \u003C/span\u003E\u003Cb\u003Econtralateral superior rectus overaction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (as seen here)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENegative Bielschowsky head tilt test\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo superior oblique overaction (which would suggest an IO palsy)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Emost important differential\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E is \u003C/span\u003E\u003Cb\u003Einferior oblique palsy\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E, but this would typically:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EShow \u003C/span\u003E\u003Cb\u003Epositive head tilt test\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EDemonstrate \u003C/span\u003E\u003Cb\u003Esuperior oblique overaction\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EShow \u003C/span\u003E\u003Cb\u003Efull muscle sequelae\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options ruled out:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDuane\u2019s syndrome\u003C/b\u003E\u003C/span\u003E (typically involves limited abduction/adduction and globe retraction, not vertical restriction)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESuperior rectus restriction\u003C/b\u003E\u003C/span\u003E would not spare elevation in abduction\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EClick on the link below to see a video of Brown syndrome:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Ca href=\u0022https://youtu.be/EIFdiWftzsI?si=9AqrTolzQ9lBQ6Xk\u0022 target=\u0022_blank\u0022\u003EBrown Syndrome video\u003C/a\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 373,
    "Name": "Side effects of Immunosuppressive agent",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient is started on an immunosuppressive agent for retinal vasculitis. The patient develops gum hyperplasia. Which of the following drugs is MOST likely to cause this complication?\u003C/div\u003E",
    "Explanation": "The correct answer is Ciclosporin.\u003Cdiv\u003E\u003Cbr\u003E\u003Cdiv\u003EGingival hyperplasia is a well\u2011recognised adverse effect of ciclosporin therapy, caused by increased fibroblast proliferation and excessive extracellular matrix deposition within gingival tissues. This complication is classically associated with ciclosporin and is significantly less common with tacrolimus, despite both being calcineurin inhibitors.\u0026nbsp;\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EMycophenolate mofetil does not cause gingival overgrowth; instead, it commonly produces gastrointestinal upset and bone\u2011marrow suppression.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EPrednisolone is also not associated with gum hyperplasia and typically causes Cushingoid features, hyperglycaemia, and osteoporosis.\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 374,
    "Name": "Interpretation of an anterior\u2011surface corneal topography map",
    "Body": "A patient undergoes corneal topography as part of the evaluation for reduced best\u2011corrected visual acuity. Based on the topography map shown, what is the most likely diagnosis?\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-02-02-be6736f0-8497-44dd-ae4c-59b7d5863b05.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe most likely diagnosis is postoperative LASIK.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe topography shows a large central flattened zone (blue) surrounded by a relatively normal or steeper mid\u2011periphery (green\u2013yellow\u2013red). This pattern reflects the typical myopic ablation profile seen after LASIK, where central corneal tissue is removed, producing central flattening rather than steepening. In contrast, keratoconus shows inferior steepening, not central flattening, with a pronounced warm\u2011coloured cone; this is clearly absent here.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPellucid marginal degeneration presents a characteristic \u201Ccrab\u2011claw\u201D or \u201Cbutterfly\u201D pattern with inferior band\u2011like thinning and peripheral steepening, which is also not present.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ECentral corneal scarring would yield irregular, non\u2011symmetric distortions rather than a smooth, symmetric ablation\u2011type flattening pattern.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe simulated keratometry values in the mid\u201130s further support a post\u2011ablation cornea, as keratoconus typically shows increased K values ( \u0026gt;47 D ) from steepening, not reduced ones. Taken together, the round central blue zone, surrounding steeper periphery, low K values, and regular symmetric appearance strongly indicate a post\u2011LASIK corneal surface rather than ectasia or scarring.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 375,
    "Name": "Most suitable mydriatic regimen for a 4\u2011month\u2011old baby",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the MOST suitable mydriatic regime for dilating the pupils of a baby aged four months?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe correct answer is \u003Cstrong\u003Ephenylephrine 2.5% plus cyclopentolate 0.5%\u003C/strong\u003E.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a 4\u2011month\u2011old, the key exam principle is to achieve reliable dilation while minimising systemic toxicity: infants are particularly susceptible to anticholinergic CNS and cardiopulmonary adverse effects from cyclopentolate, so \u003Cstrong\u003E0.5% is the preferred infant strength\u003C/strong\u003E rather than 1% (which increases the risk of agitation, feeding intolerance, tachycardia, and other systemic effects).\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPhenylephrine is added to improve mydriasis by stimulating the dilator muscle, and \u003Cstrong\u003E2.5% is the standard paediatric concentration\u003C/strong\u003E used in infant examination protocols; higher concentrations increase the likelihood of systemic hypertension/tachycardia and are generally avoided when a lower strength is adequate.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhen dilating babies, an important practical safety point that examiners like is to reduce systemic absorption by nasolacrimal occlusion and wiping excess drops, which is specifically recommended in neonatal/infant guidance.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 376,
    "Name": "Familial Exudative Vitreoretinopathy (FEVR) \u2014 least likely to be true",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following statements regarding Familial Exudative Vitreoretinopathy (FEVR) is LEAST likely to be true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe correct answer \u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eis \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EFEVR is most commonly inherited in an autosomal recessive pattern\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EMost individuals with FEVR have an \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eautosomal dominant\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E form, especially in association with \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EFZD4\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E or \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003ELRP5\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, so autosomal recessive inheritance is not the predominant pattern.\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\n\u003Cstrong\u003ELinkage to chromosome 11\u003C/strong\u003E is well established, as several major FEVR\u2011related genes\u2014including \u003Cstrong\u003EFZD4\u003C/strong\u003E and \u003Cstrong\u003ELRP5\u003C/strong\u003E\u2014are located on this chromosome. \u003Cbr\u003E\n\u003Cstrong\u003ESubretinal exudates\u003C/strong\u003E are compatible with the disease, since abnormal peripheral vascularisation leads to leakage and exudation.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u0026nbsp; \u003Cbr\u003EFEVR also contributes to \u003Cstrong\u003Eretinal detachments in infants and children\u003C/strong\u003E, as incomplete vascularisation and secondary traction can lead to detachment early in life.\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 377,
    "Name": "headaches, disc swelling, retinal haemorrhages and cotton\u2011wool spots",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 24\u2011year\u2011old man has been feeling slightly unwell for two weeks and complains of constant headaches. His visual acuity is 0.00 LogMAR each eye. His optic discs appear swollen. There are scattered retinal haemorrhages and cotton wool spots in both eyes. Which one of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EThe most likely diagnosis is \u003Cstrong\u003Emalignant hypertension\u003C/strong\u003E. The combination of bilateral disc swelling, cotton\u2011wool spots, and widespread retinal haemorrhages strongly aligns with the retinal picture described in acute severe hypertension. Malignant hypertension produces end\u2011organ retinal damage with cotton\u2011wool spots, intraretinal haemorrhages, hard exudates, and papilloedema in severe cases, as documented in clinical series and reviews of hypertensive retinopathy.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EDiabetic retinopathy generally develops after years of hyperglycaemia and rarely presents acutely with disc oedema in an otherwise well young adult. Idiopathic intracranial hypertension can cause papilloedema but does not produce bilateral cotton\u2011wool spots and haemorrhages of this pattern. Optic nerve drusen causes pseudopapilloedema rather than true swelling and does not cause widespread ischaemic retinal signs. The acute retinal findings here\u2014cotton\u2011wool spots, haemorrhages, and swollen discs\u2014form the classic appearance of hypertensive crisis affecting the retina.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 378,
    "Name": "82\u2011year\u2011old with IOP 23\u202FmmHg",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these treatments is MOST likely to be appropriate for an 82\u2011year\u2011old with an intraocular pressure of 23\u202FmmHg and a cup\u2011to\u2011disc ratio of 0.7 with full visual fields and no family history of glaucoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe most appropriate option is \u003Cstrong\u003Ereview in six months\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn intraocular pressure of 23\u202FmmHg in an elderly patient, combined with a cup\u2013disc ratio of 0.7 but \u003Cstrong\u003Enormal visual fields\u003C/strong\u003E and \u003Cstrong\u003Eno family history\u003C/strong\u003E, is highly consistent with \u003Cstrong\u003Ephysiological cupping\u003C/strong\u003E rather than established glaucoma. Optic disc size increases with age, and larger discs can naturally display larger cups without corresponding neuroretinal rim loss.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn this situation, initiating treatment with a beta\u2011blocker or a prostaglandin analogue is unnecessary without evidence of progressive structural or functional change.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDischarging the patient is also premature because the optic nerve appearance still warrants cautious observation. A planned re\u2011evaluation in six months allows monitoring for any early structural or pressure\u2011related progression while avoiding overtreatment.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 379,
    "Name": "cataract surgery with new bradycardia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EYou are about to start cataract surgery on a 78\u2011year\u2011old woman when you notice that the pulse oximeter is recording a pulse of 40\u202FBPM. At pre\u2011assessment her pulse rate was 65\u202FBPM. She is a type 2 diabetic on metformin and has glaucoma treated with timolol drops. She has no chest pain, breathlessness or palpitations. Which management is MOST appropriate?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe most appropriate management is \u003Cstrong\u003Eto defer surgery and undertake medical assessment\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA new bradycardia of 40\u202FBPM in an elderly patient represents a significant perioperative risk, even in the absence of symptoms. Topical timolol can cause systemic beta\u2011blockade with clinically relevant bradycardia, and older adults are particularly susceptible. Proceeding with surgery under local anaesthesia still carries cardiovascular risk if the cause of the bradycardia has not been evaluated.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EContinuing with the operation or simply informing the GP fails to address a potentially unstable underlying cardiac issue, while immediate referral for assessment ensures safe optimisation and consideration of modifying or withholding timolol if needed.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 380,
    "Name": "Blepharoplasty with IOP 40\u202FmmHg",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn elderly woman presents to A\u0026amp;E three hours after bilateral lower lid blepharoplasties. She reports pain and sudden loss of vision in her right eye. The casualty officer measures an intraocular pressure of 40\u202FmmHg. Which of the following is MOST likely to be an appropriate part of your IMMEDIATE management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EThe most appropriate immediate step is \u003C/span\u003E\u003Cstrong style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Edisinsertion of the lids from the lateral canthus\u003C/strong\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003Cbr\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003ESudden vision loss, severe periocular pain, and a marked rise in intraocular pressure shortly after eyelid surgery strongly indicate an \u003C/span\u003E\u003Cstrong style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Eorbital compartment syndrome\u003C/strong\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E caused by postoperative retrobulbar haemorrhage.\u003C/span\u003E\u003Cbr\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EVision depends on immediate decompression to restore perfusion to the optic nerve and retina. The most effective and time\u2011critical intervention is \u003C/span\u003E\u003Cstrong style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Eurgent lateral canthotomy and inferior cantholysis\u003C/strong\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E, which rapidly relieves orbital pressure.\u003C/span\u003E\u003Cbr\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EMedical therapy such as intravenous acetazolamide or corticosteroids may be used as adjuncts but \u003C/span\u003E\u003Cstrong style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003Emust not delay decompression\u003C/strong\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003Cbr\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003Cspan style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EOpening the surgical wound alone is insufficient to decompress the orbit effectively.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 381,
    "Name": "Thyroid eye disease \u2013 muscle involvement sequence",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn thyroid eye disease, the MOST likely sequence of muscle involvement is:\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe correct sequence is \u003Cstrong\u003Einferior rectus \u2192 medial rectus \u2192 superior rectus \u2192 lateral rectus\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThyroid eye disease classically follows the \u201CI\u2011M\u2011S\u2011L\u201D pattern, with the inferior rectus being the most commonly and most severely affected muscle due to its high glycosaminoglycan deposition and tight fascial constraints, leading to early restriction in upgaze. The medial rectus is generally involved next, producing esotropia and limited abduction. Superior rectus involvement follows, and the lateral rectus is typically the last muscle affected. This well\u2011recognised progression reflects the anatomical susceptibility and compartmental characteristics of each extraocular muscle within the orbit.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 382,
    "Name": "FAP\u2011associated retinal finding",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFamilial adenomatous polyposis is MOST likely to be associated with which of the following?\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe correct association is \u003Cstrong\u003Emultiple atypical CHRPE\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn familial adenomatous polyposis, the retinal lesions are typically numerous, bilateral, and characteristically irregular in shape with scalloped or depigmented margins. They differ from solitary CHRPE and from grouped bear\u2011track pigmentation, both of which are benign, unrelated findings.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EMultiple atypical lesions are highly specific and may appear years before gastrointestinal manifestations, making them a valuable ocular marker in affected families.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 383,
    "Name": "GCA second\u2011line therapy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich second\u2011line agent is NOT recommended for Giant Cell Arteritis according to the British Society of Rheumatology Guidelines (2020)?\u003C/span\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EThe correct answer is Tumour Necrosis Factor inhibitor.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E The 2020 BSR guideline emphasises glucocorticoids with steroid\u2011sparing evidence only for \u003Cstrong\u003Etocilizumab\u003C/strong\u003E and, to a lesser extent, \u003Cstrong\u003Emethotrexate\u003C/strong\u003E, and it \u003Cstrong\u003Edoes not recommend anti\u2011TNF therapy\u003C/strong\u003E for GCA.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAzathioprine or ciclosporin\u003C/span\u003E may be considered only in selected cases with limited evidence, whereas \u003Cspan style=\u0022font-weight: bold;\u0022\u003Edapsone \u003C/span\u003Eis not a recommended therapy but the guideline\u2019s explicit \u201Cdo not use\u201D stance applies to anti\u2011TNF agents- hence this is the best \u201CNOT recommended\u201D choice.\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
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  },
  {
    "Id": 384,
    "Name": "Orthoptic tests",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following tests \u003Cspan class=\u0022s1\u0022\u003Edoes not require the use of glasses\u003C/span\u003E for completion?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFrisby Test\u003C/b\u003E\u003C/span\u003E evaluates stereoacuity using real depth cues created by varying the thickness of transparent plates, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erequiring no glasses\u003C/b\u003E\u003C/span\u003E. It\u2019s ideal for children and patients unable to tolerate or understand glasses-based tests.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn contrast:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETitmus Fly\u003C/b\u003E\u003C/span\u003E test uses \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPolaroid glasses\u003C/b\u003E\u003C/span\u003E to present separate images to each eye for stereoacuity assessment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETNO Test\u003C/b\u003E\u003C/span\u003E uses \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ered-green anaglyph glasses\u003C/b\u003E\u003C/span\u003E for stereopsis testing with random dot patterns.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWorth 4-Dot Test\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E requires \u003C/span\u003E\u003Cb\u003Ered-green glasses\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E to assess \u003C/span\u003E\u003Cb\u003Ebinocular vision, suppression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eretinal correspondence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-03-a082ae16-a58c-445c-b12e-0c29eb2a93bb.png\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 385,
    "Name": "Alphabet Patterns",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following surgical approaches is \u003Cspan class=\u0022s1\u0022\u003Emost appropriate\u003C/span\u003E for correcting an \u003Cspan class=\u0022s1\u0022\u003EA\u2011pattern strabismus\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EAn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EA\u2011pattern deviation\u003C/b\u003E\u003C/span\u003E is characterized by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egreater esodeviation in upgaze\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egreater exodeviation in downgaze\u003C/b\u003E\u003C/span\u003E. Surgical correction aims to weaken the pattern by altering the vertical position of the horizontal rectus muscles.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe useful mnemonic is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMALE\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMedial recti \u2192 Apex\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of the pattern\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELateral recti \u2192 Ends\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of the pattern\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EFor an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EA\u2011pattern\u003C/b\u003E\u003C/span\u003E, the apex is in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eupgaze\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Emedial recti are transposed superiorly\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Elateral recti are transposed inferiorly\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis repositions the muscles to reduce the vertical incomitance responsible for the pattern.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 386,
    "Name": "Chemical injury",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents with a chemical (alkali) injury to the left eye. Which of the following clinical signs is the \u003Cspan class=\u0022s1\u0022\u003Emost concerning\u003C/span\u003E indicator of severe ocular damage?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERoper-Hall classification\u003C/b\u003E\u003C/span\u003E is used to assess severity and prognosis in ocular chemical injuries. Among the features listed:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStromal haze obscuring the iris\u003C/b\u003E\u003C/span\u003E suggests \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGrade IV injury\u003C/b\u003E\u003C/span\u003E, associated with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor visual prognosis\u003C/b\u003E\u003C/span\u003E due to deep stromal damage and risk of limbal stem cell failure.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELimbal ischaemia of 30%\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E falls within \u003C/span\u003E\u003Cb\u003EGrade II\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, with a relatively \u003C/span\u003E\u003Cb\u003Efavourable prognosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELoss of epithelium\u003C/b\u003E\u003C/span\u003E is expected in chemical injuries and alone does not indicate poor prognosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAC flare\u003C/b\u003E\u003C/span\u003E reflects intraocular inflammation but is not a primary prognostic marker compared to corneal and limbal findings.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe degree of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal transparency loss\u003C/b\u003E\u003C/span\u003E (as seen with stromal haze obscuring iris details) is a critical indicator of structural compromise and correlates with long-term visual outcomes.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022https://eyewiki-images.s3.us-east-va.perf.cloud.ovh.us/1/1b/Burnlegend2.JPG\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 387,
    "Name": "Persistent epithelial defects",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents 10 days after a chemical injury to the right eye with a \u003Cspan class=\u0022s1\u0022\u003Epersistent, non-healing corneal epithelial defect\u003C/span\u003E measuring 6\u00D74\u202Fmm. There is \u003Cspan class=\u0022s1\u0022\u003Eno stromal scarring\u003C/span\u003E. What is the most appropriate next step in management?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn the subacute phase of a chemical injury, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epersistent epithelial defects\u003C/b\u003E\u003C/span\u003E that fail to heal by day 10 despite conservative therapy (e.g. lubrication, vitamin C, antibiotics) may benefit from \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eamniotic membrane grafting (AMT)\u003C/b\u003E\u003C/span\u003E. AMT promotes epithelialization, reduces inflammation, and provides a biological scaffold for healing.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopical steroids\u003C/b\u003E\u003C/span\u003E should be avoided at this stage as they \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eimpair epithelial healing\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELimbal stem cell transplantation\u003C/b\u003E\u003C/span\u003E is inappropriate in the presence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eongoing inflammation\u003C/b\u003E\u003C/span\u003E and should be delayed until the ocular surface is stabilized.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPreservative-free lubricants\u003C/b\u003E\u003C/span\u003E are essential but alone insufficient for large, persistent epithelial defects.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-03-102b039c-d565-4e8d-a71c-9c82934348a9.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 388,
    "Name": "Soft CL wear \u0026 microbial keratitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is MOST likely to be true with respect to soft contact lens wear and microbial keratitis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E \u003Cstrong\u003EThe correct answer is Removal of the contact lens is advised if the eye becomes red, even if the eye is comfortable.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nStandard patient\u2011safety advice is to \u003Cstrong\u003Eremove lenses immediately and seek eye care if redness, pain, photophobia or blurred vision occur\u003C/strong\u003E, because these can herald microbial keratitis.  Sleeping in lenses \u003Cstrong\u003Edoes increase infection risk\u003C/strong\u003E, including with modern extended\u2011wear and silicone hydrogel designs.  Swimming \u003Cstrong\u003Eis not made safe by chlorination\u003C/strong\u003E; water exposure (pools, hot tubs, showers) is a recognised risk for \u003Cstrong\u003EAcanthamoeba\u003C/strong\u003E and other pathogens in contact lens wearers\u2014lenses should be removed before water activities.  Routine \u201Cweekly\u201D protein removal is \u003Cstrong\u003Enot a universal recommendation\u003C/strong\u003E with today\u2019s care systems; current guidance emphasises daily \u003Cstrong\u003Erub\u2011and\u2011rinse\u003C/strong\u003E and appropriate disinfection with multipurpose or peroxide systems rather than fixed weekly enzymatic cleaning for all users.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 389,
    "Name": "Iridodialysis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents one month after blunt ocular trauma from a golf ball to the right eye. At the time of injury, there was a 30% hyphaema and \u003Cspan class=\u0022s1\u0022\u003Evitreous prolapse into the anterior chamber\u003C/span\u003E. Current intraocular pressure is \u003Cspan class=\u0022s1\u0022\u003E30\u202FmmHg\u003C/span\u003E.\u0026nbsp;\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Emost likely cause\u003C/span\u003E\u003Cspan class=\u0022s2\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhile \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eangle recession\u003C/b\u003E\u003C/span\u003E is a common long-term cause of raised IOP following blunt trauma, this scenario includes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreous prolapse into the anterior chamber\u003C/b\u003E\u003C/span\u003E, which is an important clue suggesting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eiridodialysis\u003C/b\u003E\u003C/span\u003E with zonular dehiscence. Iridodialysis refers to the disinsertion of the iris root from the ciliary body, and if extensive enough, it may allow \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evitreous to prolapse through a peripheral defect\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey findings pointing to iridodialysis:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHyphaema\u003C/b\u003E\u003C/span\u003E: Occurs due to tearing at the iris root (common in iridodialysis).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVitreous in anterior chamber\u003C/b\u003E\u003C/span\u003E: Suggests a structural defect at the iris root or angle, especially when associated with zonular dehiscence.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP elevation\u003C/b\u003E\u003C/span\u003E: Can occur if the prolapsed vitreous blocks the trabecular meshwork or due to associated trabecular trauma.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EBy contrast:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAngle recession\u003C/b\u003E\u003C/span\u003E is associated with IOP elevation and can occur alongside these signs, but does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot explain\u003C/b\u003E\u003C/span\u003E anteriorly displaced vitreous unless zonular or iris root trauma coexists.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECyclodialysis cleft\u003C/b\u003E\u003C/span\u003E typically causes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehypotony\u003C/b\u003E\u003C/span\u003E, not hypertension.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAqueous misdirection\u003C/b\u003E\u003C/span\u003E usually arises post-surgery and is rare post-trauma.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESummary\u003C/b\u003E\u003C/span\u003E: While both angle recession and iridodialysis are possible post-trauma, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eiridodialysis better explains all clinical features here\u003C/b\u003E\u003C/span\u003E, including hyphaema, vitreous prolapse, and raised IOP.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb style=\u0022text-decoration-line: underline;\u0022\u003EFurther Reading:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cspan style=\u0022font-weight: bold; font-style: italic;\u0022\u003EAngle-recession glaucoma: long-term clinical outcomes over a 10-year period in traumatic microhyphema.\u003C/span\u003E\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003ENg DS, Ching RH, Chan CW.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u2022\t62 out of 97 patients had microhyphema and 35 had gross hyphema.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u0026nbsp;\u2022\tAmong the traumatic microhyphema patients, 47 (75.8 %) had angle recession and 4 (6.5 %) had glaucoma with mean follow-up of 49 months (range 6-98 months).\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u0026nbsp;\u2022\tA statistically significant association was found between angle recession greater than 180\u00B0 and the occurrence of glaucoma (p \u0026lt; 0.01).\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u0026nbsp;\u2022\tNo statistically significant differences were found between groups of patients with microhyphema or gross hyphema regarding the incidence of angle recession and glaucoma.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u0026nbsp;\u2022\tThe complications of angle recession and glaucoma in patients after traumatic microhyphema appear similar to those found in patients after gross hyphema.\u0026nbsp;\u0026nbsp;\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 390,
    "Name": "Ciliary body melanoma sign",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60\u2011year\u2011old woman presents with a pigmented lesion in the periphery of her left iris. Which of these characteristics would make you MOST suspicious of a ciliary body melanoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EProminent episcleral vessel in the same quadrant.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nA dilated, tortuous \u003Cstrong\u003Eepiscleral \u201Csentinel\u201D vessel\u003C/strong\u003E overlying the quadrant of a pigmented peripheral iris lesion is a classic warning sign of an underlying ciliary body melanoma because the tumour recruits deep scleral/episcleral blood supply. Conjunctival vessels are more superficial and less specific; an \u003Cstrong\u003Eirregular pupil\u003C/strong\u003E is nonspecific (can occur with benign iris lesions, synechiae or previous inflammation); and a \u003Cstrong\u003E\u201Csatellite\u201D lesion\u003C/strong\u003E implies conjunctival melanoma spread rather than a hidden ciliary body mass. In suspected cases, confirm with gonioscopy and anterior\u2011segment imaging (UBM/AS\u2011OCT), and look for secondary signs such as sectoral cataract or raised IOP.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 391,
    "Name": "Ocular myasthenia \u2014 first\u2011line test",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA patient presents with right\u2011sided ptosis and intermittent binocular diplopia. They feel otherwise well and deny breathing or swallowing problems. Examination reveals normal eye movements and pupils, but the ptosis becomes worse following sustained up\u2011gaze. You also notice the right upper eyelid twitch when the patient takes up fixation after looking down.\u003Cbr\u003EWhat is the best first\u2011line investigation to confirm the diagnosis?\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAcetylcholine receptor antibodies\u003C/strong\u003E are the best first\u2011line investigation. The history of fatigable ptosis and intermittent diplopia with \u003Cstrong\u003ECogan\u2019s lid twitch\u003C/strong\u003E after downgaze is typical of ocular myasthenia. A serologic test is non\u2011invasive, widely available, and sufficiently specific to confirm the diagnosis when positive, even though sensitivity is lower in purely ocular disease.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003ESingle\u2011fibre electromyography\u003C/strong\u003E is the most sensitive test but is resource\u2011intensive and not usually the first step.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003ETensilon (edrophonium) testing\u003C/strong\u003E has largely fallen out of favour due to safety and availability issues.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003E\u003Cbr\u003E\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EMRI head\u003C/strong\u003E is not needed first when the clinical picture strongly suggests neuromuscular junction disease without localising neurological signs; imaging is reserved for atypical features or to exclude alternative pathology.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 392,
    "Name": "Orbital radiotherapy in thyroid eye disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following statements relating to the administration of external beam orbital radiotherapy for thyroid\u2011associated ophthalmopathy is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EIt is effective in patients with ocular motility problems\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EExternal beam orbital radiotherapy is particularly useful for active, moderate disease with restrictive myopathy, reducing EOM inflammation and improving diplopia (typical regimen ~20\u202FGy in 10 fractions).\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIt is \u003Cstrong\u003Enot\u003C/strong\u003E usually repeatable because of cumulative orbital dose constraints, whereas iodine\u2011131 therapy for thyroid disease can be repeated.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EDiabetic retinopathy\u003C/strong\u003E is a relative contraindication due to risk of radiation retinopathy, so radiotherapy is not the treatment of choice in such patients.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EEfficacy is \u003Cstrong\u003Eenhanced when combined with systemic corticosteroids\u003C/strong\u003E, not with iodine\u2011131, which may actually exacerbate thyroid eye disease unless steroid\u2011covered.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 393,
    "Name": "Nyctalopia after bariatric surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 54\u2011year\u2011old female underwent bariatric surgery two years previously to try and control her weight. She is now complaining of nyctalopia. Which of these vitamins is the MOST likely therapy the patient requires?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EVitamin A.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nBariatric (especially malabsorptive) procedures can lead to deficiency of fat\u2011soluble vitamins; vitamin A deficiency is a well\u2011documented cause of \u003Cstrong\u003Enyctalopia\u003C/strong\u003E due to impaired rhodopsin regeneration in rod photoreceptors, and vision typically improves with vitamin A repletion.  Thiamine, vitamin C, and vitamin D deficiencies have other systemic manifestations but are not primary causes of night blindness.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 394,
    "Name": "Aponeurotic ptosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 76\u2011year\u2011old pseudophakic Caucasian woman is referred to the general clinic with insidious onset ptosis. Examination reveals palpebral fissure measurements of 7\u202Fmm, an upper reflex distance of 2\u202Fmm, lid skin crease of 12\u202Fmm and good levator function in both lids. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAponeurotic ptosis\u003C/strong\u003E is most likely. The picture is classic for involutional/aponeurotic dehiscence: elderly patient with gradual onset, \u003Cstrong\u003Egood levator function\u003C/strong\u003E but \u003Cstrong\u003Ehigh lid crease (12\u202Fmm)\u003C/strong\u003E and reduced MRD1 (2\u202Fmm). Pseudophakia further supports a levator aponeurosis disinsertion after cataract surgery. \u003Cspan style=\u0022font-weight: bold;\u0022\u003EBlepharochalasis\u003C/span\u003E typically affects younger patients with recurrent eyelid edema and atrophic skin rather than isolated ptosis. \u003Cspan style=\u0022font-weight: bold;\u0022\u003EMyasthenia gravis\u003C/span\u003E would suggest variability, fatigability, and other neuromuscular signs. \u003Cspan style=\u0022font-weight: bold;\u0022\u003EMyotonic dystrophy\u003C/span\u003E causes bilateral ptosis with \u003Cstrong\u003Epoor\u003C/strong\u003E levator function and systemic myotonia, which are not present here.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
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  },
  {
    "Id": 395,
    "Name": "Adie (tonic) pupil",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these statements regarding idiopathic tonic pupil (Adie syndrome/pupil) is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EThe affected pupil becomes progressively more miotic with time.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EAn Adie pupil typically starts enlarged with light\u2013near dissociation and segmental sphincter palsy; over years it often evolves into a smaller \u201Clittle old Adie,\u201D reflecting chronic denervation and aberrant re\u2011innervation.  Confirmation is by \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Esupersensitivity to dilute pilocarpine\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E (commonly 0.125% or even 0.0625%), not phenylephrine; constriction of the tonic pupil with these weak muscarinic concentrations supports the diagnosis.  Adie pupil is \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eusually unilateral at presentation\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E and more common in women, though it may become bilateral over time.  There is \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eno typical association with myopia\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E; instead, patients may have near blur from accommodative paresis.\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 396,
    "Name": "Cyclodialysis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the \u003Cspan class=\u0022s1\u0022\u003Emost common setting\u003C/span\u003E in which a cyclodialysis cleft occurs?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecyclodialysis cleft\u003C/b\u003E\u003C/span\u003E results from the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edisinsertion of the ciliary body from the scleral spur\u003C/b\u003E\u003C/span\u003E, creating an abnormal pathway for aqueous humour to flow into the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuprachoroidal space\u003C/b\u003E\u003C/span\u003E, bypassing conventional outflow pathways. This typically leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eocular hypotony\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlunt trauma\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common cause\u003C/b\u003E\u003C/span\u003E, often due to rapid anterior-posterior compression of the globe.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIatrogenic causes\u003C/b\u003E\u003C/span\u003E (e.g. intraocular surgery, particularly glaucoma or anterior segment procedures) are also known but less frequent.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongenital clefts\u003C/b\u003E\u003C/span\u003E are exceedingly rare.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehypotony\u003C/b\u003E\u003C/span\u003E is typical, secondary \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eelevated IOP\u003C/b\u003E\u003C/span\u003E can occur transiently if the cleft is partially blocked by inflammatory debris or blood, but this is not characteristic.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 397,
    "Name": "Suspected GCA work\u2011up",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 74\u2011year\u2011old woman presents with generalised fatigue and a history of transient horizontal diplopia. Ocular examination is normal except for an isolated cotton wool spot in the left fundus. Which ONE of the following tests would you be MOST likely to recommend to help establish the diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003ETemporal artery biopsy\u003C/strong\u003E is the best next test. The age, systemic fatigue and \u003Cstrong\u003Etransient diplopia\u003C/strong\u003E point toward giant cell arteritis, in which diplopia is a recognised neuro\u2011ophthalmic manifestation and correlates with biopsy\u2011proven disease in a subset of patients.  The \u003Cstrong\u003Ecotton\u2011wool spot\u003C/strong\u003E adds weight by indicating retinal ischemia, which is reported among the ocular signs of GCA.  Current guidance recommends a \u003Cstrong\u003Econfirmatory test\u003C/strong\u003E when GCA is suspected, with \u003Cstrong\u003Etemporal artery biopsy\u003C/strong\u003E (or vascular ultrasound where available) used to establish the diagnosis.  An ice\u2011pack test targets myasthenia gravis, a brain MRI is not first\u2011line for this presentation, and a skeletal muscle biopsy would not help confirm a cranial large\u2011vessel vasculitis.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 398,
    "Name": "Mitochondrial replacement \u0026 who benefits least",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn vitro fertilisation has variations which include pro\u2011nuclear transfer and maternal spindle transfer. From a theoretical viewpoint, which of the following diseases would be LEAST likely to benefit from such techniques?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003ELeber congenital amaurosis\u003C/strong\u003E is least likely to benefit. Pro\u2011nuclear transfer and maternal spindle transfer are \u003Cstrong\u003Emitochondrial replacement therapy\u003C/strong\u003E techniques designed to prevent transmission of \u003Cem\u003Ematernally inherited mitochondrial DNA (mtDNA) mutations\u003C/em\u003E by moving the parents\u2019 nuclear DNA into a donor oocyte with healthy mitochondria; they target mtDNA disease, not disorders caused by \u003Cstrong\u003Enuclear\u003C/strong\u003E gene defects.\u003C/p\u003E\u003Cp\u003EMost forms of Leber congenital amaurosis arise from \u003Cstrong\u003Enuclear\u2011encoded retinal genes\u003C/strong\u003E (e.g., \u003Cem\u003ERPE65\u003C/em\u003E, \u003Cem\u003ECEP290\u003C/em\u003E, and \u0026gt;20 others), so avoiding maternal mtDNA does not address the underlying genetics.  In contrast, \u003Cstrong\u003EKearns\u2011Sayre syndrome\u003C/strong\u003E (mtDNA deletion), \u003Cstrong\u003ELeber hereditary optic neuropathy\u003C/strong\u003E (mtDNA point mutations in complex I genes), and \u003Cstrong\u003Emyoclonic epilepsy with ragged red fibres\u003C/strong\u003E (classically the mtDNA \u003Cem\u003EMT\u2011TK\u003C/em\u003E mutation) are \u003Cstrong\u003EmtDNA disorders\u003C/strong\u003E, which\u2014at least theoretically\u2014are the intended targets for mitochondrial replacement to reduce transmission risk.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 399,
    "Name": "ERG pattern \u2014 abnormal a\u2011wave \u0026 reduced b\u2011wave",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following conditions is MOST likely to result in a abnormal A wave and reduced B Wave on ERG ?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cp style=\u0022font-weight: 400;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ECancer\u2011associated retinopathy.\u003C/strong\u003E\u003C/p\u003E\u003Cp style=\u0022\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nAutoimmune attack against photoreceptor proteins (classically anti\u2011recoverin) in cancer\u2011associated retinopathy causes \u003Cstrong style=\u0022font-weight: 400;\u0022\u003Eprimary photoreceptor dysfunction\u003C/strong\u003E, so the full\u2011field ERG typically shows \u003Cstrong style=\u0022font-weight: 400;\u0022\u003Eabnormal (reduced) a\u2011waves with secondary reduction of b\u2011waves\u003C/strong\u003E under both scotopic and photopic conditions.\u0026nbsp;\u003C/p\u003E\n\u003Cp style=\u0022font-weight: 400;\u0022\u003EBy contrast, \u003Cstrong\u003Emelanoma\u2011associated retinopathy\u003C/strong\u003E and \u003Cstrong\u003Econgenital stationary night blindness\u003C/strong\u003E characteristically produce an \u003Cstrong\u003Eelectronegative ERG\u003C/strong\u003E (relatively preserved a\u2011wave with a disproportionately reduced b\u2011wave) reflecting ON\u2011bipolar pathway dysfunction. \u003Cstrong\u003EQuinine toxicity\u003C/strong\u003E can yield a negative ERG as well, but early changes often emphasize inner\u2011retinal/bipolar dysfunction and can be variable; this is less specific than the photoreceptor\u2011targeted pattern seen in cancer\u2011associated retinopathy.\u003C/p\u003E\n\u003Cp style=\u0022\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 400,
    "Name": "NHS shingles vaccination",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these statements is MOST accurate with regard to the NHS Shingles vaccination service?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EThe most accurate statement is that \u003Cstrong\u003Evaccination is still beneficial even if a person has had shingles within the last two years\u003C/strong\u003E. People can develop shingles more than once, so UK advice is to vaccinate once the acute episode has resolved; there is no special waiting period beyond recovery.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EOther statements don\u2019t hold up to current guidance. Protection is not described as lifelong, and the \u003Cstrong\u003Eneed for any future boosters has not yet been determined\u003C/strong\u003E, so promising permanent immunity is inaccurate.  A previous \u003Cstrong\u003Echickenpox (varicella) vaccination is not a contraindication\u003C/strong\u003E; eligible adults should still receive Shingrix when they reach the qualifying age or risk group.  Finally, the programme is \u003Cstrong\u003Enot a blanket offer to everyone over 70\u003C/strong\u003E. In England it is offered to defined age cohorts (with a phased roll\u2011out starting at 65 and ongoing eligibility for 70\u201379 up to the 80th birthday) and to adults with severe immunosuppression, rather than to all comers above a single age cut\u2011off.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 401,
    "Name": "Systemic steroids with new metamorphopsia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 24\u2011year\u2011old man who is taking systemic steroids for pulmonary sarcoidosis reports slight distortion of vision in his right eye for two weeks. His visual acuity in this eye is reduced to 6/9. Which one of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EThe correct answer is Central serous chorioretinopathy (CSCR).\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E In a young male with recent\u2011onset metamorphopsia and mild reduction in acuity, concurrent \u003Cstrong\u003Esystemic corticosteroid use\u003C/strong\u003E is a hallmark risk factor that strongly points to CSCR, which typically presents in men in their 20s\u201350s with acute or subacute central distortion and a serous neurosensory detachment.  By contrast, \u003Cstrong\u003Ecystoid macular oedema\u003C/strong\u003E more often follows intraocular surgery, uveitis, or vascular disease,\u0026nbsp;making it less compatible with this vignette. \u003Cstrong\u003EJuxtafoveal (macular) telangiectasia type 2\u003C/strong\u003E is usually a \u003Cstrong\u003Ebilateral, middle\u2011aged\u003C/strong\u003E presentation with slow progression and temporal foveal telangiectasia/thinning on multimodal imaging, not an abrupt unilateral event in a 24\u2011year\u2011old.  Finally, an isolated \u003Cstrong\u003Epigment epithelial detachment\u003C/strong\u003E as a primary diagnosis is far more typical of \u003Cstrong\u003Eage\u2011related macular degeneration\u003C/strong\u003E in older adults; while small PEDs can accompany CSCR, they do not best explain this acute steroid\u2011related presentation.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E(A similar question appeared in a previous FRCOphth part 2 written exam)\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 402,
    "Name": "Ruptured globe repair",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents following an assault with a glass bottle. On examination of the left eye, vision is perception of light. There is a full-thickness corneal laceration extending across the limbus into the posterior sclera with vitreous prolapse and a total hyphaema. Anterior segment views are poor.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most appropriate surgical management?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis case describes an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eopen globe injury\u003C/b\u003E\u003C/span\u003E with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFull-thickness corneoscleral laceration\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVitreous prolapse\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENo view of posterior segment due to total hyphaema\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EVision reduced to perception of light\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn such cases:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPrimary repair\u003C/b\u003E\u003C/span\u003E is essential to restore globe integrity.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPars plana vitrectomy (PPV)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may be warranted \u003C/span\u003E\u003Cb\u003Eat the time of primary repair\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E when:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThere is \u003C/span\u003E\u003Cb\u003Evitreous loss through the wound\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThere is a high risk of \u003C/span\u003E\u003Cb\u003Etractional complications\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, such as \u003C/span\u003E\u003Cb\u003Eretinal detachment\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThere is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor posterior view\u003C/b\u003E\u003C/span\u003E that prevents assessment, and immediate intervention is feasible in a specialist vitreoretinal setting\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEnucleation or evisceration\u003C/b\u003E\u003C/span\u003E at this stage is not appropriate, even in eyes with poor vision, unless there is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eno visual potential and high risk of sympathetic ophthalmia\u003C/b\u003E\u003C/span\u003E (which should be assessed later, not acutely).\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 403,
    "Name": "Lyme disease",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents with intermediate and posterior uveitis. He reports a history of trekking in the United States and recalls developing a circinate rash on his leg during the trip.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely causative organism?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003Ehe clinical scenario is consistent with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELyme disease\u003C/b\u003E\u003C/span\u003E, caused by \u003Ci\u003EBorrelia burgdorferi\u003C/i\u003E, a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Espirochaete\u003C/b\u003E\u003C/span\u003E transmitted by the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIxodes tick\u003C/b\u003E\u003C/span\u003E, which is endemic in parts of the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENortheast and upper Midwest USA\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey clues include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETrekking exposure\u003C/b\u003E\u003C/span\u003E (risk of tick bite)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EErythema migrans\u003C/b\u003E\u003C/span\u003E: classically a circinate or \u201Cbull\u2019s-eye\u201D rash\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular involvement\u003C/b\u003E\u003C/span\u003E (posterior/intermediate uveitis, retinal vasculitis) during late stages of systemic infection\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular Lyme disease\u003C/b\u003E\u003C/span\u003E can occur in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStage II or III\u003C/b\u003E\u003C/span\u003E of infection and may present with:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntermediate/posterior uveitis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENeuro-ophthalmic signs (cranial neuropathies, optic neuritis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinitis or vasculitis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EBartonella henselae\u003C/i\u003E: Cat-scratch disease; typically causes neuroretinitis, not associated with trekking or rash\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ETreponema pallidum\u003C/i\u003E: Syphilis can mimic anything but rash and travel history more typical of Lyme\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EHistoplasma capsulatum\u003C/i\u003E: Linked with Presumed Ocular Histoplasmosis Syndrome (POHS), but not associated with rash or recent travel to tick-endemic areas\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 404,
    "Name": "Schistosomiasis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the intermediate host involved in the life cycle of schistosomiasis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchistosomiasis\u003C/b\u003E\u003C/span\u003E, also known as bilharzia, is caused by parasitic flatworms called \u003Ci\u003Eschistosomes\u003C/i\u003E. It is transmitted through contact with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efreshwater contaminated by larval forms (cercariae)\u003C/b\u003E\u003C/span\u003E released by specific \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efreshwater snails\u003C/b\u003E\u003C/span\u003E, which act as the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintermediate host\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHumans\u003C/b\u003E\u003C/span\u003E serve as the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edefinitive host\u003C/b\u003E\u003C/span\u003E, where the adult worms reside in the venous system and lay eggs.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eeggs\u003C/b\u003E\u003C/span\u003E are passed in urine or feces into water, where they hatch into miracidia, which then \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einfect freshwater snails\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWithin the snail, the parasite undergoes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Easexual multiplication\u003C/b\u003E\u003C/span\u003E before emerging as cercariae that infect humans through the skin.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis snail-host stage is crucial in the transmission cycle and is a major target for public health control efforts.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 405,
    "Name": "SLE investigations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich is the most commonly found autoantibody in systemic lupus erythematosus (SLE)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ESystemic lupus erythematosus (SLE) is an autoimmune disease with a broad range of autoantibodies. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAntinuclear antibodies (ANA)\u003C/b\u003E\u003C/span\u003E are present in over 95% of SLE cases and serve as a screening test. Among the ANA subtypes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnti-dsDNA\u003C/b\u003E\u003C/span\u003E is the most \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Especific\u003C/b\u003E\u003C/span\u003E for SLE and also the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost commonly found\u003C/b\u003E\u003C/span\u003E subtype in these patients; present in ~70% of cases.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIts presence correlates with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edisease activity\u003C/b\u003E\u003C/span\u003E, particularly lupus nephritis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnti-Ro (SSA)\u003C/b\u003E\u003C/span\u003E can also occur in SLE, but it is more commonly associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubacute cutaneous lupus\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneonatal lupus\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ec-ANCA\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ep-ANCA\u003C/b\u003E\u003C/span\u003E are associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evasculitides\u003C/b\u003E\u003C/span\u003E, such as granulomatosis with polyangiitis and microscopic polyangiitis, respectively, not SLE.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 406,
    "Name": "Granulomatosis with polyangiitis (Wegener\u2019s)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient with a prior episode of peripheral ulcerative keratitis presents with new-onset right-sided proptosis due to an orbital mass. The history includes left elbow arthritis, and a recent chest X-ray reveals a pulmonary nodule.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EWhat is the most likely underlying diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe combination of:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPeripheral ulcerative keratitis (PUK)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EArthritis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPulmonary nodule\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOrbital mass with proptosis\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u2026is highly characteristic of \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EGranulomatosis with polyangiitis (GPA, formerly Wegener\u2019s granulomatosis)\u003C/b\u003E\u003C/span\u003E. GPA is a necrotizing granulomatous vasculitis affecting small to medium vessels, commonly involving the \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eupper and lower respiratory tracts, kidneys, joints, and eyes\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EKey distinguishing features:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOrbital mass\u003C/b\u003E\u003C/span\u003E is a well-recognised ophthalmic manifestation of GPA.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPUK\u003C/b\u003E\u003C/span\u003E is a classical ocular complication due to vasculitis of episcleral vessels.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPulmonary nodules\u003C/b\u003E\u003C/span\u003E (especially cavitating) are typical.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EArthritis\u003C/b\u003E\u003C/span\u003E is common.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EOther Options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChurg-Strauss (EGPA)\u003C/b\u003E\u003C/span\u003E: Typically associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Easthma\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eeosinophilia\u003C/b\u003E\u003C/span\u003E. PUK and orbital masses are less frequent.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESLE\u003C/b\u003E\u003C/span\u003E: Rarely causes orbital masses; PUK can occur but less commonly.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESarcoidosis\u003C/b\u003E\u003C/span\u003E: Can affect the orbit, but does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot cause PUK\u003C/b\u003E\u003C/span\u003E. Lung involvement usually presents as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehilar lymphadenopathy or interstitial disease\u003C/b\u003E\u003C/span\u003E, not nodules.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 407,
    "Name": "Hypoglycaemia in Diabetic patients",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA hospitalised patient with brittle type 1 diabetes mellitus collapses and is found to be unconscious due to hypoglycaemia. What is the most appropriate immediate treatment?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunconscious hypoglycaemic patient\u003C/b\u003E\u003C/span\u003E who cannot safely tolerate oral carbohydrates, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eintravenous glucose\u003C/b\u003E\u003C/span\u003E is the treatment of choice. The most effective option is:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E50% dextrose IV\u003C/b\u003E\u003C/span\u003E, given as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebolus (commonly 50 mL = 25 g glucose)\u003C/b\u003E\u003C/span\u003E, provides rapid correction of hypoglycaemia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlternatives depend on context:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGlucagon 1 mg IM/SC\u003C/b\u003E\u003C/span\u003E is used if IV access is not immediately available.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E10% or 20% dextrose\u003C/b\u003E\u003C/span\u003E may be used for continuous infusion or maintenance after initial correction but are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot first-line for acute correction\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5% dextrose\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etoo dilute\u003C/b\u003E\u003C/span\u003E for rapid reversal of severe hypoglycaemia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ERapid correction is essential to prevent \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneurological damage\u003C/b\u003E\u003C/span\u003E in unconscious hypoglycaemia.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 408,
    "Name": "Parinaud\u2019s oculoglandular syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient presents with unilateral granulomatous conjunctivitis and ipsilateral preauricular lymphadenopathy. What is the most likely causative organism?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EParinaud\u2019s oculoglandular syndrome\u003C/b\u003E\u003C/span\u003E is a rare ocular manifestation of systemic infection, typically presenting with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUnilateral granulomatous conjunctivitis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIpsilateral preauricular (or submandibular) lymphadenopathy\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common cause\u003C/b\u003E\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecat-scratch disease\u003C/b\u003E\u003C/span\u003E, which is due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBartonella henselae\u003C/b\u003E\u003C/span\u003E, a gram-negative bacillus. It is transmitted via scratches, bites, or contact with infected cat saliva.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther rare infectious causes include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ETularemia\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ETuberculosis\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003ESyphilis\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EHerpes simplex\u003C/i\u003E\u003Ci\u003E\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EChlamydia trachomatis\u003C/i\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EHowever, \u003Ci\u003EBartonella\u003C/i\u003E remains the most frequent and exam-relevant answer.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 409,
    "Name": "Mucous membrane pemphigoid (MMP)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about mucous membrane pemphigoid (MMP) is TRUE?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMucous membrane pemphigoid (MMP)\u003C/b\u003E\u003C/span\u003E is a chronic autoimmune subepithelial blistering disease that primarily affects mucous membranes. The key features are:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHistopathology\u003C/b\u003E\u003C/span\u003E: The hallmark finding is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elinear deposition of IgG\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EC3\u003C/b\u003E\u003C/span\u003E, and sometimes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIgA\u003C/b\u003E\u003C/span\u003E along the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebasement membrane zone\u003C/b\u003E\u003C/span\u003E (BMZ) on direct immunofluorescence.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpidemiology\u003C/b\u003E\u003C/span\u003E: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFemales are more commonly affected\u003C/b\u003E\u003C/span\u003E than males, typically at a ratio of around 2:1.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOral mucosa\u003C/b\u003E\u003C/span\u003E is the most commonly involved site;\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epresent in ~80%\u003C/b\u003E\u003C/span\u003E of cases.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESkin involvement\u003C/b\u003E\u003C/span\u003E occurs in only \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E~20-30%\u003C/b\u003E\u003C/span\u003E of cases, not 80%.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cimg src=\u0022https://images-provider.frontiersin.org/api/ipx/w=370\u0026amp;f=webp/https://www.frontiersin.org/files/Articles/437108/fimmu-10-00034-HTML-r1/image_m/fimmu-10-00034-g001.jpg\u0022\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; letter-spacing: normal; font-size: small;\u0022\u003EDiagnostic strategy for MMP. The diagnosis of MMP is confirmed by clinical features and positive DIF results. In DIF-negative or DIF-unavailable cases, at least one serological or histological finding is needed.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan style=\u0022color: rgb(0, 0, 0); font-family: ThinSpaceFallback, InftyFallback, MuseoSans, Helvetica, Arial, sans-serif; letter-spacing: normal; font-size: small;\u0022\u003EDIF, direct immunofluorescence; IIF, indirect immunofluorescence; ELISA, enzyme-linked immunosorbent assay; H\u0026amp;E, hematoxylin and eosin staining.\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 410,
    "Name": "ESR levels",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is a recognised cause of a \u003Ci\u003Elow\u003C/i\u003E erythrocyte sedimentation rate (ESR)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EESR (erythrocyte sedimentation rate)\u003C/b\u003E\u003C/span\u003E is a nonspecific marker of inflammation that can be influenced by several physiological and pathological conditions. It is affected by plasma proteins (e.g., fibrinogen), red cell mass, and the properties of red cells (e.g., size, shape, and concentration).\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPolycythaemia\u003C/b\u003E\u003C/span\u003E leads to a low ESR because the increased red cell mass reduces the fall rate of erythrocytes due to increased blood viscosity and decreased plasma fibrinogen relative to red cells. Other causes include: Sickle cell disease, hypogammaglobulinemia, and hyperviscosity state.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPregnancy\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efemale sex\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eolder age\u003C/b\u003E\u003C/span\u003E are all associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eincreased\u003C/b\u003E\u003C/span\u003E ESR values, due to higher fibrinogen levels and alterations in plasma composition. Other causes include: malignancy, inflammation, and infection.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EEstimated Normal values [rough estimate]:\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cul\u003E\u003Cli\u003EMen: Age (in years) / 2\u003C/li\u003E\u003Cli\u003EWomen: ( [age in years]\u002B 10) / 2\u003C/li\u003E\u003C/ul\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 411,
    "Name": "Sarcoidosis Histology",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following histological features is most characteristic of \u003Cspan class=\u0022s1\u0022\u003Esarcoidosis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESarcoidosis\u003C/b\u003E\u003C/span\u003E is a granulomatous inflammatory disease most commonly associated with:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENon-caseating granulomas\u003C/b\u003E\u003C/span\u003E (i.e., lacking central necrosis, unlike tuberculosis)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA core of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eepithelioid histiocytes\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELanghans-type multinucleated giant cells\u003C/b\u003E\u003C/span\u003E (not to be confused with Langerhans cells of the skin/immune system)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESurrounding \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECD4\u002B helper T lymphocytes\u003C/b\u003E\u003C/span\u003E, not cytotoxic T cells\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EIncorrect Options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECaseating granulomas\u003C/b\u003E\u003C/span\u003E: Suggestive of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etuberculosis\u003C/b\u003E\u003C/span\u003E or fungal infections.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELangerhans cells\u003C/b\u003E\u003C/span\u003E: Antigen-presenting dendritic cells seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELangerhans cell histiocytosis\u003C/b\u003E\u003C/span\u003E, not sarcoidosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPeripheral rim of killer T cells\u003C/b\u003E\u003C/span\u003E: Inconsistent with typical sarcoid granuloma, which is CD4\u002B dominant.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 412,
    "Name": "Tubulointerstitial nephritis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 12-year-old boy presents with bilateral non-granulomatous anterior uveitis. Which renal condition is \u003Cspan class=\u0022s1\u0022\u003Emost likely\u003C/span\u003E to be associated?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe constellation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral non-granulomatous anterior uveitis\u003C/b\u003E\u003C/span\u003E in a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echild or adolescent\u003C/b\u003E\u003C/span\u003E, especially if idiopathic, should raise strong suspicion for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETINU syndrome\u003C/b\u003E\u003C/span\u003E (Tubulointerstitial Nephritis and Uveitis). Key points:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMore common in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echildren and adolescents\u003C/b\u003E\u003C/span\u003E, average age ~15\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUveitis often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprecedes or follows\u003C/b\u003E\u003C/span\u003E renal symptoms by weeks\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERenal impairment may be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emild and subclinical\u003C/b\u003E\u003C/span\u003E, requiring urinalysis for detection\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUveitis is typically \u003C/span\u003E\u003Cb\u003Ebilateral, non-granulomatous anterior\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EIncorrect options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIgA nephropathy\u003C/b\u003E\u003C/span\u003E: Common in children but not associated with uveitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFanconi syndrome\u003C/b\u003E\u003C/span\u003E: Involves proximal tubular dysfunction, rarely linked to uveitis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGoodpasture\u2019s syndrome\u003C/b\u003E\u003C/span\u003E: Characterised by anti-GBM antibodies causing pulmonary-renal syndrome; not uveitis.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 413,
    "Name": "Endogenous endophthalmitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhat is the \u003C/span\u003Emost common causative organism\u003Cspan class=\u0022s1\u0022\u003E of \u003Ci\u003Eendogenous endophthalmitis\u003C/i\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEndogenous endophthalmitis\u003C/b\u003E\u003C/span\u003E results from hematogenous spread of organisms to the eye from a distant infectious focus. Unlike post-surgical or trauma-related (exogenous) cases, endogenous endophthalmitis is more often caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efungal pathogens\u003C/b\u003E\u003C/span\u003E, particularly in immunocompromised or hospitalised patients with indwelling catheters or IV drug use.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Ci\u003ECandida albicans\u003C/i\u003E\u003C/b\u003E\u003C/span\u003E is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common\u003C/b\u003E\u003C/span\u003E cause overall, particularly in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWestern world\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Ci\u003EAspergillus fumigatus\u003C/i\u003E\u003C/b\u003E\u003C/span\u003E can cause endophthalmitis but is less frequent and more associated with immunosuppressed states.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBacterial causes such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Ci\u003EStaphylococcus aureus\u003C/i\u003E\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Ci\u003EStreptococcus pneumoniae\u003C/i\u003E\u003C/b\u003E\u003C/span\u003E do occur, but less commonly than \u003Ci\u003ECandida\u003C/i\u003E, especially in high-risk patients.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERegional variation exists\u003C/b\u003E\u003C/span\u003E: Gram-negative organisms (e.g., \u003Ci\u003EKlebsiella\u003C/i\u003E) dominate in parts of Asia.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 414,
    "Name": "Ciliary body melanoma",
    "Body": "\u003Cp class=\u0022MsoNormal\u0022 style=\u0022margin: 0cm; font-size: 12pt; font-family: Calibri, sans-serif; color: rgb(0, 0, 0); letter-spacing: normal;\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich peripheral iris nodule feature is \u003Cspan class=\u0022s1\u0022\u003Emost suggestive of ciliary body melanoma\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDilated sentinel episcleral vessels\u003C/b\u003E\u003C/span\u003E are a hallmark sign of underlying posterior segment pathology such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eciliary body melanoma\u003C/b\u003E\u003C/span\u003E. These vessels reflect increased vascular supply to a growing intraocular mass and are often the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efirst external clue\u003C/b\u003E\u003C/span\u003E to a deeply seated tumor.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther key features suggestive of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eciliary body melanoma\u003C/b\u003E\u003C/span\u003E include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETumor extension anteriorly into the iris or posteriorly through the sclera\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELocal iris displacement or sectoral cataract formation\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInvolvement of trabecular meshwork causing secondary glaucoma\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERing melanomas that encircle the ciliary body\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELow intraocular pressure due to ciliary body shutdown\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile features like an irregular pupil or pigmented iris lesions may occur in other iris pathologies, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eepiscleral hyperaemia with sentinel vessels\u003C/b\u003E\u003C/span\u003E is more specific for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior uveal melanoma\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 415,
    "Name": "Infectious scleritis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich ocular procedure carries the highest risk of \u003Cspan class=\u0022s1\u0022\u003Epost-operative infectious scleritis\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInfectious scleritis\u003C/b\u003E\u003C/span\u003E is a rare but serious complication that accounts for approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5-10%\u003C/b\u003E\u003C/span\u003E of all scleritis cases. Unlike immune-mediated scleritis, it does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E respond to steroids and may be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eexacerbated\u003C/b\u003E\u003C/span\u003E by them. Clinical differentiation is crucial, as timely antimicrobial therapy is essential.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAmong ophthalmic surgeries, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epterygium excision -\u003C/b\u003E\u003C/span\u003Eespecially when combined with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eadjuvants like mitomycin C or beta irradiation-\u003C/b\u003E\u003C/span\u003Eis the most frequently implicated procedure in post-operative infectious scleritis. These adjuvants impair wound healing and compromise scleral integrity, making it more susceptible to pathogens such as \u003Ci\u003EPseudomonas aeruginosa\u003C/i\u003E or fungal organisms.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther procedures (e.g., cataract, glaucoma, or strabismus surgeries) carry a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emuch lower\u003C/b\u003E\u003C/span\u003E risk in comparison.\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 416,
    "Name": "Presumed ocular histoplasmosis syndrome (POHS)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich of the following findings is \u003C/span\u003Emost consistent\u003Cspan class=\u0022s1\u0022\u003E with a diagnosis of \u003C/span\u003Epresumed ocular histoplasmosis syndrome (POHS)?\u003C/span\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPresumed ocular histoplasmosis syndrome (POHS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is classically defined by the \u003C/span\u003E\u003Cb\u003Etriad\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPeripapillary atrophy\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201CHisto spots\u201D\u003C/b\u003E\u003C/span\u003E: punched-out chorioretinal scars in the mid-periphery and posterior pole\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMaculopathy due to CNVM\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ECritically, \u003C/span\u003E\u003Cb\u003Eintraocular inflammation is absent\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Evitritis or anterior uveitis (e.g., iris nodules)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E would argue against the diagnosis.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003EPOHS has an epidemiological link to areas endemic for \u003Ci\u003EHistoplasma capsulatum\u003C/i\u003E, particularly in the Mississippi\u2013Ohio River Valley. There is \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003Eno association with HLA-DQ2\u003C/b\u003E\u003C/span\u003E, but increased prevalence has been reported for \u003Cspan class=\u0022s3\u0022\u003E\u003Cb\u003EHLA-B7 and HLA-DR2\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 417,
    "Name": "Steroid eye drops",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA steroid molecule bound to which of the following compounds is \u003Cspan class=\u0022s1\u0022\u003Emost likely\u003C/span\u003E to penetrate the cornea effectively and reach the anterior chamber?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EFor effective \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal penetration\u003C/b\u003E\u003C/span\u003E, a drug must exhibit \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eboth lipophilic and hydrophilic properties\u003C/b\u003E\u003C/span\u003E to cross the epithelium and stroma. Steroid formulations are modified to enhance these properties:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcetate esters\u003C/b\u003E\u003C/span\u003E (e.g. prednisolone acetate) are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elipophilic\u003C/b\u003E\u003C/span\u003E, penetrate the cornea \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Every effectively\u003C/b\u003E\u003C/span\u003E, and reach therapeutic levels in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior chamber\u003C/b\u003E\u003C/span\u003E. These are typically formulated as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuspensions\u003C/b\u003E\u003C/span\u003E, so \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eshaking the bottle\u003C/b\u003E\u003C/span\u003E is necessary to ensure correct dosing.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAlcohol formulations\u003C/b\u003E\u003C/span\u003E also have good penetration but are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless effective\u003C/b\u003E\u003C/span\u003E than acetate esters.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPhosphate esters\u003C/b\u003E\u003C/span\u003E are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehydrophilic\u003C/b\u003E\u003C/span\u003E, making them less effective for corneal penetration, though they are more stable and usually available as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esolutions\u003C/b\u003E\u003C/span\u003E, which are easier to use.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESulphate-bound steroids\u003C/b\u003E\u003C/span\u003E are uncommon in ophthalmic formulations and are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epoor penetrants\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 418,
    "Name": "Herpes Simplex Keratitis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the \u003Cspan class=\u0022s1\u0022\u003Eprophylactic oral dose\u003C/span\u003E of acyclovir in patients with recurrent \u003Cspan class=\u0022s1\u0022\u003Eherpes simplex eye disease\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003EHerpetic Eye Disease Study (HEDS)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E demonstrated that \u003C/span\u003E\u003Cb\u003Eoral acyclovir 400\u202Fmg BD\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E significantly reduces the recurrence of \u003C/span\u003E\u003Cb\u003Eherpes simplex keratitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly \u003C/span\u003E\u003Cb\u003Estromal disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProphylaxis\u003C/b\u003E\u003C/span\u003E is typically considered in cases with recurrent disease, post-keratoplasty, or during topical steroid use.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E400\u202Fmg five times per day\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is used in \u003C/span\u003E\u003Cb\u003Eactive epithelial disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not prophylaxis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELower doses\u003C/b\u003E\u003C/span\u003E like 200\u202Fmg BD are insufficient for prophylaxis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E800\u202Fmg five times daily\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is reserved for \u003C/span\u003E\u003Cb\u003Eherpes zoster ophthalmicus\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not HSV.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 419,
    "Name": " Ciclosporin A",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EA patient develops \u003C/span\u003Ehalitosis\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003Egingival hypertrophy around the molar region\u003Cspan class=\u0022s1\u0022\u003E. Which of the following medications is the \u003C/span\u003Emost likely cause\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGingival hyperplasia\u003C/b\u003E\u003C/span\u003E (or gingival overgrowth) is a known adverse effect of several drugs. Among the options listed:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECiclosporin A\u003C/b\u003E\u003C/span\u003E is most strongly associated with gingival hypertrophy, particularly in the molar regions. It stimulates fibroblast proliferation and extracellular matrix production.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECalcium channel blockers\u003C/b\u003E\u003C/span\u003E (especially nifedipine) and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephenytoin\u003C/b\u003E\u003C/span\u003E (an anti-convulsant) are also classic causes, but not listed here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAzathioprine\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Emethotrexate\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003E\u003Cb\u003Eanti-TNF agents\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may cause oral ulcers or mucositis, but they do \u003C/span\u003E\u003Cb\u003Enot typically cause gingival overgrowth\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 420,
    "Name": "Rituximab",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following best describes the \u003Cspan class=\u0022s1\u0022\u003Emechanism of action\u003C/span\u003E of \u003Cspan class=\u0022s1\u0022\u003Erituximab\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERituximab\u003C/b\u003E\u003C/span\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echimeric monoclonal antibody\u003C/b\u003E\u003C/span\u003E that targets the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECD20 antigen\u003C/b\u003E\u003C/span\u003E, which is found on the surface of pre-B and mature B lymphocytes. Binding to CD20 leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EB-cell depletion\u003C/b\u003E\u003C/span\u003E via multiple mechanisms including antibody-dependent cytotoxicity, complement-mediated lysis, and apoptosis.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is used in conditions where pathogenic B cells play a role, such as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evasculitis\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-Hodgkin\u2019s lymphoma\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erheumatoid arthritis\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eorbital inflammatory disease\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not inhibit IL-2 or TNF-\u03B1\u003C/b\u003E\u003C/span\u003E, and it is not an interferon agonist.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 421,
    "Name": "Iatrogenic Pigmentary retinopathy - Thioridazine",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient with a history of psychiatric illness develops signs of \u003Cspan class=\u0022s1\u0022\u003Epigmentary retinopathy\u003C/span\u003E. Which of the following medications is the \u003Cspan class=\u0022s1\u0022\u003Emost likely cause\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThioridazine\u003C/b\u003E\u003C/span\u003E, a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephenothiazine antipsychotic\u003C/b\u003E\u003C/span\u003E, is well known for causing a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edose-dependent pigmentary retinopathy\u003C/b\u003E\u003C/span\u003E, particularly at doses exceeding 800\u202Fmg/day.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003EKey features of \u003C/span\u003E\u003Cb\u003Ethioridazine-induced retinopathy\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEarly: Non-specific macular pigment changes\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdvanced: Salt-and-pepper fundus, nyctalopia, decreased vision, optic atrophy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPathophysiology: Damage to \u003C/span\u003E\u003Cb\u003Eretinal pigment epithelium\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Echoriocapillaris\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIrreversible in many cases if not recognised early\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options:\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELithium\u003C/b\u003E\u003C/span\u003E: Causes oculogyric crises and nystagmus, not pigmentary changes\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOlanzapine\u003C/b\u003E\u003C/span\u003E: May cause blurred vision or dry eye but not retinopathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECarbamazepine\u003C/b\u003E\u003C/span\u003E: Can cause diplopia and nystagmus, but no retinal toxicity\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Chr\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 422,
    "Name": "Vigabatrin",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhich \u003C/span\u003Emedication\u003Cspan class=\u0022s1\u0022\u003E is most likely to cause \u003C/span\u003Ebinasal visual field defects\u003Cspan class=\u0022s1\u0022\u003E?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVigabatrin\u003C/b\u003E\u003C/span\u003E, an antiepileptic that inhibits GABA transaminase, is associated with a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Echaracteristic visual field defect\u003C/b\u003E\u003C/span\u003E:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EConcentric peripheral constriction\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often with \u003C/span\u003E\u003Cb\u003Etemporal and macular sparing\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EManifests as \u003C/span\u003E\u003Cb\u003Ebinasal field defects\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIrreversible\u003C/b\u003E\u003C/span\u003E optic neuropathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ESigns: \u003C/span\u003E\u003Cb\u003EOptic disc pallor\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, RNFL atrophy, but \u003C/span\u003E\u003Cb\u003Epreserved central acuity\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EOther options:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHydroxychloroquine\u003C/b\u003E\u003C/span\u003E: Central/paracentral visual loss due to maculopathy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmiodarone\u003C/b\u003E\u003C/span\u003E: May cause vortex keratopathy and optic neuropathy, but not binasal field loss\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETamoxifen\u003C/b\u003E\u003C/span\u003E: Crystalline maculopathy and retinal deposits, not associated with nasal field loss\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOphthalmic monitoring of patients on vigabatrin includes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EBaseline and follow-up \u003C/span\u003E\u003Cb\u003Evisual fields (e.g., Humphrey 120)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EFundus and \u003C/span\u003E\u003Cb\u003ERNFL imaging\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EMonitoring \u003C/span\u003E\u003Cb\u003Eevery 6 months for 5 years\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, then annually\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022text-decoration-line: underline;\u0022\u003EFurther reading:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://pmc.ncbi.nlm.nih.gov/articles/PMC10947413/\u0022 target=\u0022_blank\u0022\u003EOcular examinations, findings, and toxicity in children taking vigabatrin\u003C/a\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://curriculum.rcophth.ac.uk/wp-content/uploads/2015/01/2008-SCI-020-The-Ocular-Side-Effects-of-Vigabatrin-Sabril.pdf\u0022 target=\u0022_blank\u0022\u003EThe Ocular Side-Effects of Vigabatrin (Sabril)\u003C/a\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://curriculum.rcophth.ac.uk/wp-content/uploads/2015/01/2008-SCI-020-The-Ocular-Side-Effects-of-Vigabatrin-Sabril.pdf\u0022 target=\u0022_blank\u0022\u003E\u0026nbsp;\u003C/a\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 423,
    "Name": "Cyclophosphamide",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is the \u003Cspan class=\u0022s1\u0022\u003Emost common complication\u003C/span\u003E associated with \u003Cspan class=\u0022s1\u0022\u003Ecyclophosphamide\u003C/span\u003E therapy?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECyclophosphamide\u003C/b\u003E\u003C/span\u003E is a cytotoxic alkylating agent used in the management of severe inflammatory diseases (e.g., vasculitis) and some malignancies. Its \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edose-limiting and most frequent adverse effect\u003C/b\u003E\u003C/span\u003E is:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBone marrow suppression\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly affecting \u003C/span\u003E\u003Cb\u003Eneutrophils and lymphocytes\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMonitoring with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efull blood count\u003C/b\u003E\u003C/span\u003E is mandatory during treatment\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EOther notable adverse effects:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHaemorrhagic cystitis\u003C/b\u003E\u003C/span\u003E: Caused by the toxic metabolite \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eacrolein\u003C/b\u003E\u003C/span\u003E; reduced by ensuring adequate hydration or using \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emesna\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBladder carcinoma\u003C/b\u003E\u003C/span\u003E: A \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elong-term risk\u003C/b\u003E\u003C/span\u003E, more likely with cumulative exposure\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHepatitis\u003C/b\u003E\u003C/span\u003E: Rare but possible\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGonadal toxicity\u003C/b\u003E\u003C/span\u003E: Can cause infertility, particularly in higher doses\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 424,
    "Name": "Tamoxifen retinopathy",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Etamoxifen\u003C/span\u003E is \u003Cspan class=\u0022s1\u0022\u003Etrue\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETamoxifen\u003C/b\u003E\u003C/span\u003E is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eselective oestrogen receptor modulator (SERM)\u003C/b\u003E\u003C/span\u003E, not an anti-progesterone agent. It is primarily used in hormone receptor-positive breast cancer.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOcular toxicity is dose-related\u003C/b\u003E\u003C/span\u003E, not idiosyncratic. Risk increases with cumulative doses \u0026gt;100\u202Fg.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETamoxifen retinopathy\u003C/b\u003E\u003C/span\u003E is characterised by:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERefractile crystalline deposits\u003C/b\u003E\u003C/span\u003E in the inner retina (typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewhite\u003C/b\u003E\u003C/span\u003E, not black)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECystoid macular oedema (CMO)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which may lead to \u003C/span\u003E\u003Cb\u003Evisual impairment\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERarely, optic neuritis or pseudocystic foveal cavitation\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ERoutine OCT monitoring may detect early subclinical changes.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 425,
    "Name": "MEK inhibitors",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is \u003Cspan class=\u0022s1\u0022\u003Eleast likely\u003C/span\u003E to occur as a side effect of MEK inhibitor therapy?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMEK inhibitors\u003C/b\u003E\u003C/span\u003E, used in oncology (notably for metastatic melanoma), are known to cause a wide range of ophthalmic adverse effects (OAEs), often grouped under \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMEK-associated retinopathy (MEKAR)\u003C/b\u003E\u003C/span\u003E. These include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESerous retinal detachments\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVisual disturbances\u003C/b\u003E\u003C/span\u003E and transient VA reduction\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUveitis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPunctate epithelial erosions (PEE)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECentral retinal vein occlusion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (rare but reported)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003E\u003Cspan class=\u0022s3\u0022\u003EHowever, \u003C/span\u003E\u003Cb\u003Eraised intraocular pressure (IOP)\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E is \u003C/span\u003E\u003Cb\u003Enot a recognised or common adverse effect\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E of MEK inhibitors, making it the \u003C/span\u003E\u003Cb\u003Eleast likely\u003C/b\u003E\u003Cspan class=\u0022s3\u0022\u003E of the options listed.\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 426,
    "Name": "Methotrexate",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is the \u003Cspan class=\u0022s1\u0022\u003Emost commonly occurring\u003C/span\u003E side effect of methotrexate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMethotrexate is an anti-metabolite and folate antagonist widely used in inflammatory diseases and oncology. Its adverse effect profile includes:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMost common side effects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGastrointestinal upset\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EElevated liver enzymes and hepatotoxicity\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMucocutaneous effects (e.g., stomatitis, ulcers)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELess common but serious side effects\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EInterstitial pneumonitis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBone marrow suppression\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENephrotoxicity (rare)\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn clinical studies, \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ehepatotoxicity\u003C/b\u003E\u003C/span\u003E (elevated transaminases) has consistently been one of the \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Emost frequently observed adverse effects\u003C/b\u003E\u003C/span\u003E, occurring in up to \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003E18%\u003C/b\u003E\u003C/span\u003E of patients. While bone marrow suppression and pneumonitis are serious, they occur \u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eless frequently\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/p\u003E\u003Cp class=\u0022p4\u0022\u003E\u003Cb\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/b\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 427,
    "Name": "LASIK",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements best reflects LASIK outcomes?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA major LASIK meta-analysis, synthesising outcomes across thousands of patients and multiple platforms, demonstrated the following key findings:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPatient satisfaction\u003C/b\u003E\u003C/span\u003E was extremely high: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E92%-98%\u003C/b\u003E\u003C/span\u003E, with an average of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E96.3%\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E96%\u003C/b\u003E\u003C/span\u003E of patients achieved a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epostoperative spherical equivalent within \u00B11.00 D\u003C/b\u003E\u003C/span\u003E, a benchmark of refractive precision.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDry eye symptoms\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehalos/glare\u003C/b\u003E\u003C/span\u003E tend to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eresolve or improve\u003C/b\u003E\u003C/span\u003E over time, not persist.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EWhile \u003C/span\u003E\u003Cb\u003ELASIK initially reduces corneal sensation\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, re-innervation does occur.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 428,
    "Name": "Neovascular glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following conditions is associated with the development of neovascular glaucoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENeovascular glaucoma (NVG)\u003C/b\u003E\u003C/span\u003E is a severe secondary glaucoma caused by retinal ischemia leading to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erelease of VEGF\u003C/b\u003E\u003C/span\u003E, which stimulates neovascularisation of the iris and angle.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUGH syndrome\u003C/b\u003E\u003C/span\u003E: Caused by mechanical trauma from IOL malposition. It leads to anterior segment inflammation, hyphema, and IOP elevation; but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot retinal ischemia\u003C/b\u003E\u003C/span\u003E, so \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot typically associated with NVG\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EICE syndrome\u003C/b\u003E\u003C/span\u003E: Characterised by endothelial cell proliferation and membrane formation over the angle, leading to peripheral anterior synechiae and secondary angle-closure. \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENeovascularisation is not a feature\u003C/b\u003E\u003C/span\u003E, hence \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot a usual cause of NVG\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOcular Ischaemic Syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: Results from \u003C/span\u003E\u003Cb\u003Esevere carotid artery stenosis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E. The resultant \u003C/span\u003E\u003Cb\u003Echronic retinal hypoperfusion\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is a classic cause of \u003C/span\u003E\u003Cb\u003Eneovascularisation of the iris (rubeosis iridis)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003ENVG\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially in late stages.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 429,
    "Name": "Retinal Astrocytoma",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the most likely diagnosis for the fundus finding shown below?\u003C/span\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-02-05-126b3913-bc97-410e-8030-a0bb0e5caadc.webp\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003Cp style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; border-radius: 0px !important;\u0022\u003ERetinal astrocytic hamartomas (sometimes called retinal astrocytoma) are benign glial cell tumors. They are often encountered as an asymptomatic lesion in screening of patients with tuberous sclerosis complex, but may be sporadic. Diagnosis is largely clinical and may be supported by ancillary tests. In tuberous sclerosis, retinal findings are significantly associated with concurrent neurological and renal disease. Growth or complications of RAH requiring treatment are rare.\u003C/p\u003E\u003Cdiv\u003ESource:\u0026nbsp;\u003Ca href=\u0022https://eyewiki.org/Retinal_Astrocytic_Hamartoma\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ERetinal Astrocytoma\u003C/a\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-02-05-2f7ce6fd-6fc8-4ffa-8b94-4c0f2d2f9461.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 430,
    "Name": "Microspherophakia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about microspherophakia is \u003Cspan class=\u0022s1\u0022\u003Etrue\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMicrospherophakia is a congenital condition in which the crystalline lens is abnormally small and spherical. This increases the lens curvature and refractive power, resulting in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh lenticular myopia\u003C/b\u003E\u003C/span\u003E, lens instability, and a significant risk of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epupillary block glaucoma\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EPupillary block in this condition is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eworsened by miotics\u003C/b\u003E\u003C/span\u003E, as these increase contact between the lens and iris. Instead, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecycloplegic agents\u003C/b\u003E\u003C/span\u003E are used to move the lens posteriorly and relieve the block.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EMicrospherophakia is classically associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWeill\u2013Marchesani syndrome\u003C/b\u003E\u003C/span\u003E, which follows an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal recessive inheritance pattern\u003C/b\u003E\u003C/span\u003E and is characterised by short stature, brachydactyly, and reduced joint mobility. It can also be seen in other systemic conditions such as Marfan syndrome, Alport syndrome, congenital rubella, and hyperlysinaemia.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ECardiac involvement in associated syndromes is typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emitral valve prolapse\u003C/b\u003E\u003C/span\u003E (as seen in Marfan syndrome), not mitral stenosis.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 431,
    "Name": "Cataract in Systemic conditions",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following systemic conditions is correctly matched with its associated cataract morphology?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ESystemic conditions often present with characteristic cataract morphologies:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDown syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: commonly associated with \u003C/span\u003E\u003Cb\u003Ebilateral lamellar cataracts\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMyotonic dystrophy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: classically presents with \u003C/span\u003E\u003Cb\u003EChristmas tree (polychromatic)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E cataracts.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWilson\u2019s disease\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: shows \u003C/span\u003E\u003Cb\u003Esunflower cataracts\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E due to copper deposition.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAmiodarone\u003C/b\u003E\u003C/span\u003E is linked to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal verticillata\u003C/b\u003E\u003C/span\u003E, not anterior capsular cataracts.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 432,
    "Name": "Cataract surgery - Corneal guttata",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn a patient with corneal guttata being assessed for cataract surgery, which statement best reflects current understanding of preoperative risk assessment?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ESpecular microscopy is the most reliable method for evaluating \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eendothelial cell count and morphology\u003C/b\u003E\u003C/span\u003E, making it the best tool for predicting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal decompensation risk\u003C/b\u003E\u003C/span\u003E after cataract surgery in patients with guttata. A low endothelial cell count (especially \u0026lt;1000 cells/mm\u00B2), polymegathism, or pleomorphism on specular microscopy are all red flags.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EWhile central corneal thickness (CCT) via pachymetry may provide indirect evidence of endothelial health, it remains \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eless sensitive\u003C/b\u003E\u003C/span\u003E, as significant endothelial damage can be present even with normal thickness; especially early in the disease course. Also, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ea normal morning pachymetry doesn\u2019t rule out endothelial compromise\u003C/b\u003E\u003C/span\u003E, as corneal hydration may normalize overnight.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ERoutine combined phaco \u002B endothelial keratoplasty is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot indicated\u003C/b\u003E\u003C/span\u003E for every patient with guttat; only those with advanced Fuchs\u2019 dystrophy or clear signs of decompensation.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 433,
    "Name": "Blepharochalasis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements is most accurate regarding blepharochalasis syndrome?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EBlepharochalasis is a rare condition typically affecting children and adolescents, often young females around puberty. It presents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erecurrent, painless, transient eyelid oedema\u003C/b\u003E\u003C/span\u003E, usually affecting the upper lids. Although early episodes resolve completely, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eeach attack tends to last about 2 days\u003C/b\u003E\u003C/span\u003E, and with repeated inflammation, patients may develop \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eptosis, atrophic and wrinkled skin, and prolapse of orbital fat or lacrimal gland\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIt is \u003C/span\u003E\u003Cb\u003Enot limited to people over 50;\u0026nbsp;\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003Equite the opposite.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epresence of ptosis does not exclude\u003C/b\u003E\u003C/span\u003E the diagnosis; in fact, it\u2019s often part of the clinical picture.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEpisodes are typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-tender\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eresolve within 48 hours\u003C/b\u003E\u003C/span\u003E on average.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 434,
    "Name": "Internuclear ophthalmoplegia (INO)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich statement most accurately describes internuclear ophthalmoplegia (INO)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe defining feature of INO is impaired adduction of the affected eye with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eslowed saccadic velocity\u003C/b\u003E\u003C/span\u003E, and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabducting nystagmus\u003C/b\u003E\u003C/span\u003E in the contralateral eye. This results from damage to the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emedial longitudinal fasciculus (MLF)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIschaemic INO\u003C/b\u003E\u003C/span\u003E often recovers well, similar to other ischaemic cranial nerve palsies.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EConvergence may be spared or impaired\u003C/b\u003E\u003C/span\u003E, especially in bilateral INO, and is not a reliable discriminator.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUnilateral INO\u003C/b\u003E\u003C/span\u003E is more commonly associated with infarction than with multiple sclerosis, while \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral INO\u003C/b\u003E\u003C/span\u003E is more characteristic of MS.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 435,
    "Name": "Progressive supranuclear palsy (PSP)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 65-year-old woman presents with new-onset difficulty initiating eye opening after voluntary or involuntary lid closure, particularly associated with impaired vertical saccades. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis presentation\u2014\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edifficulty opening the eyes (apraxia of lid opening)\u003C/b\u003E\u003C/span\u003E with impaired \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evertical saccades,\u0026nbsp;\u003C/b\u003E\u003C/span\u003Eis classic for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EProgressive Supranuclear Palsy (PSP)\u003C/b\u003E\u003C/span\u003E, a neurodegenerative tauopathy that affects the brainstem and basal ganglia.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey clinical pointers include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EImpaired \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evoluntary vertical eye movements\u003C/b\u003E\u003C/span\u003E (especially downgaze early on)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EApraxia of lid opening\u003C/b\u003E\u003C/span\u003E, often mistaken for ptosis or blepharospasm\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFrontalis overaction on attempted eye opening\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMidbrain atrophy (\u201Chummingbird sign\u201D on MRI)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPineal tumours\u003C/b\u003E\u003C/span\u003E may affect vertical gaze (via dorsal midbrain syndrome) but are rare in elderly adults.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWilson disease\u003C/b\u003E\u003C/span\u003E is more typical in younger patients.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHydrocephalus\u003C/b\u003E\u003C/span\u003E is unlikely to present with isolated vertical saccade impairment or lid apraxia.\u003C/p\u003E",
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    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 436,
    "Name": "anterior ischaemic optic neuropathy (AION)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements about \u003Cspan class=\u0022s1\u0022\u003Eanterior ischaemic optic neuropathy (AION)\u003C/span\u003E is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon-arteritic AION (NAION)\u003C/b\u003E\u003C/span\u003E, approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E40% of patients\u003C/b\u003E\u003C/span\u003E experience some degree of spontaneous visual improvement, particularly if initial acuity was moderately affected. This is in contrast to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Earteritic AION (AAION)\u003C/b\u003E\u003C/span\u003E, where profound and permanent vision loss is more common.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EA \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esmall, crowded disc\u003C/b\u003E\u003C/span\u003E (a \u201Cdisc at risk\u201D) is the anatomical risk factor; not a large cup-to-disc ratio.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENAION typically presents \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epainlessly\u003C/b\u003E\u003C/span\u003E, unlike AAION which may involve periocular pain.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFellow eye involvement in NAION is about \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E15% over 5 years\u003C/b\u003E\u003C/span\u003E, not 50%.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EIn AAION, involvement of fellow eye occurs in 25% of patients in 6 days (and in 95% of untreated patients).\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EIn NAION, 50% achieve 6/9 or better, while in AAION, 40% are associated with permanent visual loss.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 437,
    "Name": "Cluster Headache",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 40-year-old hypertensive man reports a 12-month history of severe, strictly left-sided periorbital pain occurring once or twice daily in clusters lasting weeks at a time. The attacks consistently begin in the late morning, last 15-60 minutes, and are associated with ipsilateral red eye, lacrimation, ptosis, and nasal congestion. Occasional episodes have occurred on the right side. Which of the following statements is most likely true about this condition?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe clinical description fits \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecluster headache\u003C/b\u003E\u003C/span\u003E, a subtype of trigeminal autonomic cephalalgia. Key features include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStrictly unilateral\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Eexcruciating periorbital pain\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAutonomic signs\u003C/b\u003E\u003C/span\u003E on the affected side (conjunctival injection, lacrimation, ptosis, nasal congestion)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAttacks occur in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclusters\u003C/b\u003E\u003C/span\u003E (over weeks), often with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecircadian patterning\u003C/b\u003E\u003C/span\u003E (suggesting hypothalamic involvement)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFunctional imaging (e.g. fMRI, PET)\u003C/b\u003E\u003C/span\u003E in patients during cluster attacks has shown \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eipsilateral posterior hypothalamic activation\u003C/b\u003E\u003C/span\u003E, a characteristic feature of the condition.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGamma knife radiosurgery\u003C/b\u003E\u003C/span\u003E is not a standard treatment for cluster headache; it is used in trigeminal neuralgia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDihydroergotamine\u003C/b\u003E\u003C/span\u003E is less effective than \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etriptans\u003C/b\u003E\u003C/span\u003E or \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigh-flow oxygen\u003C/b\u003E\u003C/span\u003E, and timing is critical.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERemissions\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E can vary, but in \u003C/span\u003E\u003Cb\u003Echronic cluster headache\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, remission may be absent or brief;\u0026nbsp;\u003C/span\u003E\u003Cb style=\u0022letter-spacing: 0.14994px;\u0022\u003Eless than six months\u003C/b\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-02-05-2fc457db-4f05-4523-ab14-c083a4d846d9.png\u0022\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 438,
    "Name": "Trachoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn the context of endemic regions, what is the first-line surgical procedure for managing trachomatous trichiasis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilamellar tarsal rotation (BLTR)\u003C/b\u003E\u003C/span\u003E procedure is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erecommended first-line treatment\u003C/b\u003E\u003C/span\u003E for trachomatous trichiasis in endemic regions. It is a straightforward, effective technique that can be performed by ophthalmologists or trained ophthalmic assistants in community settings.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe choice of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eabsorbable vs non-absorbable sutures\u003C/b\u003E\u003C/span\u003E (e.g., silk, vicryl) \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not significantly alter surgical outcomes\u003C/b\u003E\u003C/span\u003E. Both are considered acceptable by WHO and community eye health programs, making the use of either type of suture appropriate in first-line management.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdvanced procedures like \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emucous membrane grafting\u003C/b\u003E\u003C/span\u003E are reserved for complex or recurrent cases and not recommended as initial treatment in endemic settings.\u003C/p\u003E",
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    "CategoryId": 6,
    "Category": null,
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  },
  {
    "Id": 439,
    "Name": "Senile involutional ptosis",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich statement is most accurate regarding senile involutional ptosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003ESenile involutional ptosis, or aponeurotic ptosis, results from disinsertion or attenuation of the levator aponeurosis. In these patients:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELevator function is typically normal\u003C/b\u003E\u003C/span\u003E (usually \u226512 mm), distinguishing it from myogenic or neurogenic ptosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EM\u00FCller muscle-conjunctival resection is effective\u003C/b\u003E\u003C/span\u003E for mild ptosis (1-2 mm) in patients with good levator function and a positive phenylephrine test;\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot contraindicated\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cb\u003Enormal MRD1 is approximately 4 mm\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, not 3 mm.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESevere ptosis (\u0026gt;4 mm)\u003C/b\u003E\u003C/span\u003E has a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehigher risk of surgical undercorrection\u003C/b\u003E\u003C/span\u003E, as greater amounts of lifting are required and levator adjustment becomes technically more challenging.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
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  },
  {
    "Id": 440,
    "Name": "Orbital Lymphoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich statement is most accurate regarding orbital lymphoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EOrbital lymphoma, particularly extranodal marginal zone B-cell lymphoma (ENMZL), is the most common type of primary orbital lymphoma. It:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften presents as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epainless proptosis or mass effect\u003C/b\u003E\u003C/span\u003E, typically without inflammatory signs.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot treated by excision\u003C/b\u003E\u003C/span\u003E; instead, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebiopsy followed by radiotherapy\u003C/b\u003E\u003C/span\u003E (even in bilateral cases) is the mainstay.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EENMZL is indolent\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, whereas \u003C/span\u003E\u003Cb\u003Emantle cell lymphoma is more aggressive\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often systemic and with poorer prognosis.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHas been reported with increased incidence in patients with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elongstanding thyroid eye disease\u003C/b\u003E\u003C/span\u003E, possibly due to chronic orbital inflammation providing a pro-lymphomatous environment.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 441,
    "Name": "Choroidal Melanoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the most common site of metastasis from choroidal melanoma?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EChoroidal melanoma is the most common primary intraocular malignancy in adults. Despite effective local control through radiotherapy or enucleation, metastatic spread can occur; often \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eyears or even decades later\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EThe liver is by far the most frequent site of metastasis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, involved in up to 90% of metastatic cases.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther less common sites include the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elungs, bones, and brain\u003C/b\u003E\u003C/span\u003E, but these typically follow hepatic spread.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe Collaborative Ocular Melanoma Study (COMS) reports 5- and 10-year metastasis rates of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E25% and 34%\u003C/b\u003E\u003C/span\u003E, respectively, even after successful local therapy.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 442,
    "Name": "Melanocytoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following statements regarding melanocytoma is MOST likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EMelanocytoma is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebenign, pigmented tumour\u003C/b\u003E\u003C/span\u003E that most frequently arises on the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoptic disc\u003C/b\u003E\u003C/span\u003E, though it may also involve adjacent \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretina, choroid, or sclera;\u0026nbsp;\u003C/b\u003E\u003C/span\u003Eso it is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot exclusive to the uvea\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EDespite often being asymptomatic, up to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E90% of patients\u003C/b\u003E\u003C/span\u003E may show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Evisual field defects\u003C/b\u003E\u003C/span\u003E, including blind spot enlargement or arcuate defects due to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecompression of optic nerve fibres\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERAPD may be present\u003C/b\u003E\u003C/span\u003E even when visual acuity is preserved, indicating subtle optic nerve dysfunction.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003EAlthough \u003C/span\u003E\u003Cb\u003Eoptic disc melanocytomas can grow\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E slowly over time, \u003C/span\u003E\u003Cb\u003Emalignant transformation is rare\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E, estimated at \u003C/span\u003E\u003Cb\u003E1-2%\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E, making the \u003C/span\u003E\u003Cb\u003Elow risk of conversion to melanoma\u003C/b\u003E\u003Cspan class=\u0022s2\u0022\u003E the most accurate and relevant statement here.\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-05-8f8c18fd-d988-439d-b1ee-9e71133d1cca.png\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 443,
    "Name": "Charles Bonnet Syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn patients with low vision, which statement best describes visual release hallucinations (Charles Bonnet syndrome)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVisual release hallucinations\u003C/b\u003E\u003C/span\u003E, also known as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECharles Bonnet syndrome\u003C/b\u003E\u003C/span\u003E, are complex visual hallucinations experienced by individuals with significant visual impairment, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost often in the elderly\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThese hallucinations occur \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewith the eyes open\u003C/b\u003E\u003C/span\u003E, unlike those in sleep disorders or psychosis.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThey are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot psychiatric\u003C/b\u003E\u003C/span\u003E in origin and are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot influenced by psychological illness;\u0026nbsp;\u003C/b\u003E\u003C/span\u003Epatients are fully aware the images are not real.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EARMD is a common underlying cause\u003C/b\u003E\u003C/span\u003E, but the syndrome does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot affect 90%\u003C/b\u003E\u003C/span\u003E of ARMD patients; the estimated prevalence in ARMD is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E10-40%\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efrequency varies\u003C/b\u003E\u003C/span\u003E significantly; some report multiple daily episodes, others have them less frequently. It is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot characteristically 1-2 times per day\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, the most consistently accurate and defining feature is that the hallucinations occur \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ewhile the eyes are open\u003C/b\u003E\u003C/span\u003E, reflecting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edeafferentation of visual cortex\u003C/b\u003E\u003C/span\u003E due to visual loss.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 444,
    "Name": "Primary Open angle glaucoma",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn relation to intraocular pressure (IOP) measurement, which statement is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiurnal variation in IOP\u003C/b\u003E\u003C/span\u003E is a key consideration in glaucoma management, especially in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprimary open-angle glaucoma (POAG)\u003C/b\u003E\u003C/span\u003E. These patients often show \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elarger fluctuations\u003C/b\u003E\u003C/span\u003E, sometimes up to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E10\u202FmmHg\u003C/b\u003E\u003C/span\u003E in a 24-hour period.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EIOP is actually higher when lying down\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E compared to standing, due to elevated \u003C/span\u003E\u003Cb\u003Eepiscleral venous pressure (EVP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E in the supine position.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECentral corneal thickness (CCT)\u003C/b\u003E\u003C/span\u003E does affect IOP readings, especially with Goldmann applanation tonometry. However, the effect is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot linear;\u0026nbsp;\u003C/b\u003E\u003C/span\u003Ea 100\u202F\u03BCm increase does \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot always equal a 1\u202FmmHg rise\u003C/b\u003E\u003C/span\u003E, and correction formulas are only \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erough approximations\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP does not typically reduce\u003C/b\u003E\u003C/span\u003E with age in healthy individuals, though \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eolder age increases glaucoma risk\u003C/b\u003E\u003C/span\u003E and may be associated with IOP elevation in some cases.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
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    "HighYield": false,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 445,
    "Name": "Acanthamoeba",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich statement about \u003Cspan class=\u0022s1\u0022\u003EAcanthamoeba\u003C/span\u003E is most accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EAcanthamoeba castellanii\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003EA. polyphaga\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E are the two most common species causing human infections, particularly \u003C/span\u003E\u003Cb\u003Ekeratitis\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Egranulomatous amoebic encephalitis (GAE)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlthough \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Econtact lens wear\u003C/b\u003E\u003C/span\u003E is the major risk factor, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba\u003C/b\u003E\u003C/span\u003E is \u003Ci\u003Enot\u003C/i\u003E the most common cause of lens-related infections;\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebacterial keratitis\u003C/b\u003E\u003C/span\u003E (e.g., \u003Ci\u003EPseudomonas\u003C/i\u003E) is more frequent.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThe trophozoite form\u003C/b\u003E\u003C/span\u003E is the \u003Ci\u003Epathogenic\u003C/i\u003E and \u003Ci\u003Eactive\u003C/i\u003E feeding stage, while the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecystic form\u003C/b\u003E\u003C/span\u003E is the \u003Ci\u003Eresistant\u003C/i\u003E, dormant stage that contributes to treatment challenges.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba\u003C/b\u003E\u003C/span\u003E is found in many body sites and environments, and can cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esystemic disease\u003C/b\u003E\u003C/span\u003E (e.g., encephalitis), not just ocular infections.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EOver 80% of Acanthamoeba keratitis appears in contact lens wearers\u003C/span\u003E.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003EIn one study, 75% of the patients were contact lens wearers; 40% wore daily soft lenses, 22% wore rigid gas permeable lenses, and 38% wore extended wear or other lenses. \u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u2022\u003Cspan class=\u0022Apple-tab-span\u0022\u003E\t\u003C/span\u003EAcanthamoeba exist in two forms: trophozoites and cysts.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003EThe trophozoites are mobile and consume bacteria (which allows for the diagnosis on E. coli plates).\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003EThe trophozoites form double walled cysts which are incredibly resistant to methods of eradication (including freezing, heating, and irradiation).\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u2022\u003Cspan class=\u0022Apple-tab-span\u0022\u003E\t\u003C/span\u003EAcanthamoeba trophozoites and cysts can also be identified with the help of Gram, Giemsa-Wright, hematoxylin and eosin, periodic acid-Schiff, calcoflour white, or other stains. Confocal microscopy has also been used to diagnose Acanthamoeba cysts with some success.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u2022\u003Cspan class=\u0022Apple-tab-span\u0022\u003E\t\u003C/span\u003EAcanthamoeba is ubiquitous.\u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp; \u003C/span\u003ECorneal trauma, followed by exposure to the parasite (often through a water supply or contact lens solution) in a patient with low tear levels of anti-Acanthamoeba IgA leads to infection. \u003Cspan class=\u0022Apple-converted-space\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 446,
    "Name": "Myopia",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich statement regarding \u003Cspan class=\u0022s1\u0022\u003Emyopia\u003C/span\u003E is most likely to be true?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMyopia is significantly \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore prevalent in Asia\u003C/b\u003E\u003C/span\u003E, particularly East and Southeast Asia, compared to Western countries. In places like Taiwan and Singapore, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eup to 84%\u003C/b\u003E\u003C/span\u003E of high school students are myopic.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGlobal prevalence is much higher than 10%; projections suggest \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehalf the world\u2019s population\u003C/b\u003E\u003C/span\u003E may be myopic by 2050.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIncidence rates in Asia are \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efar higher than 2%\u003C/b\u003E\u003C/span\u003E, particularly in children and adolescents.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlthough \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emyopia is a risk factor for glaucoma\u003C/b\u003E\u003C/span\u003E, especially normal tension glaucoma, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eassociation is not firmly established\u003C/b\u003E\u003C/span\u003E through large-scale population studies to the extent that it would be considered a proven clinical link.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EA meta-analysis showed that more time spent on outdoor activities was associated with lower odds of myopia. The odds of myopia decreased by 2% for every additional hour of time spent outdoors per week\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\n\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u2022\u003Cspan class=\u0022Apple-tab-span\u0022\u003E\t\u003C/span\u003EThere may be a threshold of 10 to 14 hours spent outdoors per week to prevent myopia onset\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 447,
    "Name": "Traumatic Hyphema",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhat is the risk of developing glaucoma in a patient who presents with total hyphaema following trauma?\u003C/span\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb style=\u0022font-size: medium; text-decoration-line: underline;\u0022\u003E\uD83D\uDD34 Traumatic Hyphema \u2013 Key Facts\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EEpidemiology:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E75% male predominance\u003C/b\u003E\u003C/span\u003E, male:female ratio 3:1\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E77% of cases occur in patients \u0026lt;30 years\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, especially ages 10\u201320\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EAetiology:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMost common site of bleeding: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanterior ciliary body tear\u003C/b\u003E\u003C/span\u003E (\u224871%)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003ENatural History:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EUncomplicated duration\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: 5\u20136 days\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMean duration of elevated IOP\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: ~6 days\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERebleeding\u003C/b\u003E\u003C/span\u003E increases risk of raised IOP:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo rebleed: ~5% develop high IOP\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EWith rebleed: ~52%\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EIntraocular Pressure:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E50% overall incidence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E of raised IOP\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIOP \u0026gt;22 mmHg\u003C/b\u003E\u003C/span\u003E seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E32%\u003C/b\u003E\u003C/span\u003E at some point\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigher risk in patients with sickle cell hemoglobinopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, particularly African descent \u2192 risk of \u003C/span\u003E\u003Cb\u003Ecentral retinal artery occlusion\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EClinical Grading of Hyphema:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGrade 1\u003C/b\u003E\u003C/span\u003E: \u0026lt;\u2153 of anterior chamber\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EGrade 2\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: \u2153\u2013\u00BD\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGrade 3\u003C/b\u003E\u003C/span\u003E: \u0026gt;\u00BD but not total\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGrade 4\u003C/b\u003E\u003C/span\u003E: total (\u201C8-ball\u201D or \u201Cblackball\u201D hyphema)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EGlaucoma Risk:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EOverall relative risk\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E after hyphema: \u003C/span\u003E\u003Cb\u003E6.9\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EIf \u003C/span\u003E\u003Cb\u003E360\u00B0 angle recession\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E: risk \u2191 to \u003C/span\u003E\u003Cb\u003E7.5\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERisk stratified by blood level:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u0026lt; 1/2 chamber: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E13.5%\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: 700;\u0022\u003E1/2\u003C/span\u003E\u003Cspan style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E chamber: \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022color: rgb(14, 14, 14); font-family: \u0026quot;.AppleSystemUIFont\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003E27%\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETotal: \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E52%\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 448,
    "Name": "Peripheral ulcerative keratitis (PUK)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn peripheral ulcerative keratitis (PUK), which oral medication helps prevent corneal melting and complications?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EPUK is driven by immune\u2011mediated collagenolysis and stromal melt due to upregulated matrix metalloproteinases (collagenases). Tetracyclines (e.g., doxycycline 100\u202Fmg BD or tetracycline 250\u202Fmg QID) have a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enon\u2011antibiotic anti\u2011collagenase effect\u003C/b\u003E\u003C/span\u003E by inhibiting matrix metalloproteinases and neutrophil activity. This slows stromal degradation and reduces the risk of perforation.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdjuncts commonly used for the same purpose include:\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOral vitamin C\u003C/b\u003E\u003C/span\u003E (500\u202Fmg QID) to support collagen synthesis\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ETopical N\u2011acetylcysteine 20%\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E (collagenase inhibitor)\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopical medroxyprogesterone 1%\u003C/b\u003E\u003C/span\u003E (reduces collagenase production)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ECephalosporins and fluoroquinolones treat infection but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edo not inhibit collagenase activity\u003C/b\u003E\u003C/span\u003E, so they do not prevent corneal melt in immune\u2011mediated PUK.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 449,
    "Name": "Iatrogenic macular hole - Post PPV",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 63-year-old male, two weeks after vitrectomy with ERM and ILM peeling for an epiretinal membrane, presents with mildly reduced visual acuity. His preoperative BCVA was \u003Cspan class=\u0022s1\u0022\u003E0.4 LogMAR (20/50)\u003C/span\u003E and is now \u003Cspan class=\u0022s1\u0022\u003E0.48 LogMAR (20/60)\u003C/span\u003E in the left eye. Imaging shows an eccentric full-thickness hole in the temporal macular area. What is the most appropriate next step in management?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Ci\u003EEccentric full-thickness macular hole (FTMH):\u0026nbsp;\u003C/i\u003Ea rare complication seen in about 2% of eyes after ERM and ILM peeling. Proposed mechanisms include trauma to M\u00FCller cells, de-roofing of intraretinal cysts, ILM contraction, ILM-staining dye toxicity, or direct surgical injury.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EObservation is appropriate. These eccentric FTMHs typically do not affect central visual function unless they involve the fovea or papillomacular bundle. In this case, the hole is located \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etemporally\u003C/b\u003E\u003C/span\u003E, so not central. It poses minimal visual threat and rarely leads to subretinal fluid or retinal detachment, except in highly myopic eyes.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe current visual acuity of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.48 LogMAR (20/60)\u003C/b\u003E\u003C/span\u003E is acceptable and expected at this early postoperative stage. There is no need for re-intervention, especially since both ERM and ILM have been adequately peeled centrally.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EOcriplasmin is ineffective because the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eposterior hyaloid has already been detached\u003C/b\u003E\u003C/span\u003E, as evidenced by imaging.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 450,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich retinal sign most strongly indicates a high risk of progression from severe non-proliferative diabetic retinopathy (NPDR) to proliferative diabetic retinopathy (PDR)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EAccording to the ETDRS, cotton-wool spots are poor predictors of progression to proliferative disease. In contrast, IRMA and venous beading are strong indicators of progression. The presence of IRMA in just one quadrant is sufficient to classify retinopathy as severe NPDR under the \u201C4:2:1 rule.\u201D This rule underpins much of the grading system used in diabetic eye screening and risk stratification.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EData from large-scale studies (ETDRS, WESDR) show that when IRMA is present in severe NPDR, the eye has a 17% risk of progressing to high-risk PDR within 1 year and around 40% within 3 years.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 451,
    "Name": "Retinitis Pigmentosa",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is \u003Ci\u003Eincorrect\u003C/i\u003E regarding retinitis pigmentosa (RP)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EBone spicules are a classic but not universal feature of retinitis pigmentosa. Some patients present without this hallmark finding, a variant referred to as \u003Ci style=\u0022font-weight: bold;\u0022\u003Eretinitis pigmentosa sine pigmento\u003C/i\u003E.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EThese patients still exhibit other characteristic signs of RP, such as optic disc pallor and narrowed retinal arterioles.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EBone spicules form due to dispersion of pigment from the retinal pigment epithelium (RPE), accumulating in perivascular areas. However, their absence does not exclude the diagnosis.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EMoreover, similar pigmentation patterns may appear in other retinal pathologies like post-traumatic scarring or infectious retinopathies (e.g., syphilis, diffuse unilateral subacute neuroretinitis).\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 452,
    "Name": "Tay-Sachs disease",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following best explains the child\u2019s condition, with this finding in the fundus examination and neurodevelopmental regression?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-05-025d9d94-c702-4a1f-90b7-3664af4245b9.png\u0022\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThe clinical presentation and fundus photograph showing a cherry red spot are characteristic of \u003Cspan style=\u0022font-weight: bold;\u0022\u003ETay-Sachs disease.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003EThis neurodegenerative lysosomal storage disorder is caused by a deficiency of the enzyme hexosaminidase A, leading to the accumulation of GM2 ganglioside within neuronal lysosomes.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003ERetinal involvement manifests as a cherry-red spot at the macula; due to a pale surrounding retina from ganglion cell accumulation, contrasting with the fovea, which is devoid of these cells.\u0026nbsp;\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003ENeurological signs like seizures, hypotonia, increased startle reflex, and developmental regression support the diagnosis.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn contrast, Batten disease involves ceroid lipofuscin accumulation, Gaucher\u2019s disease is caused by glucocerebroside deposition, and amniotic fluid embolism is an acute maternal condition unrelated to the scenario.\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-05-35c2126e-8a7e-44a8-bc54-9e680abcc69a.png\u0022\u003E\u003C/p\u003E\u003Ch1 class=\u0022nova-legacy-e-text nova-legacy-e-text--size-m nova-legacy-e-text--family-display nova-legacy-e-text--spacing-none nova-legacy-e-text--color-inherit\u0022 itemprop=\u0022caption\u0022 style=\u0022color: rgb(17, 17, 17); font-family: Roboto, Arial, sans-serif; font-size: 0.875rem; line-height: 1.3; margin-bottom: 0px; letter-spacing: normal;\u0022\u003E\u003Cspan style=\u0022font-weight: normal;\u0022\u003ECherry-red spot in Tay-Sachs disease. The right frame shows normal retina. The circle surrounds the macula, lateral to the optic nerve. The left frame shows the macula of a child with Tay-Sachs disease. The cherry-red center is the normal retina of the fovea at the center of the macula.\u003C/span\u003E\u003C/h1\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: normal;\u0022\u003EImage source:\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(85, 85, 85); font-family: Roboto, Arial, sans-serif; letter-spacing: normal;\u0022\u003EDOI:\u003C/span\u003E\u003Ca class=\u0022nova-legacy-e-link nova-legacy-e-link--color-inherit nova-legacy-e-link--theme-decorated\u0022 rel=\u0022noopener\u0022 target=\u0022_blank\u0022 href=\u0022https://doi.org/10.1016/j.ejmhg.2011.07.007?urlappend=%3Futm_source%3Dresearchgate.net%26utm_medium%3Darticle\u0022 style=\u0022text-decoration-line: underline; outline: none; font-family: Roboto, Arial, sans-serif; border-style: initial; border-color: initial; border-image: initial; background-image: none; background-position: initial; background-size: initial; background-repeat: initial; background-attachment: initial; background-origin: initial; background-clip: initial; cursor: pointer; display: inline; letter-spacing: normal;\u0022\u003E10.1016/j.ejmhg.2011.07.007\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 453,
    "Name": "Cat-scratch disease",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 17-year-old male presents with two weeks of rapidly reduced vision in the left eye, which progressed over several days. Examination reveals left best-corrected visual acuity of 20/200 (LogMAR 1.0), a relative afferent pupillary defect, and impaired colour vision. Visual field testing shows global depression. Fundus photo shows left optic disc swelling with a macular star pattern. When an underlying cause is identified, what is the most likely aetiology of this presentation?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EThis patient has clinical features consistent with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneuroretinitis\u003C/b\u003E\u003C/span\u003E, a condition marked by optic disc swelling and characteristic macular star formation. Though many cases are idiopathic, when an infectious etiology is found, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common culprit is Bartonella henselae -\u003C/b\u003E\u003C/span\u003Ea \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Egram-negative rod-\u0026nbsp;\u003C/b\u003E\u003C/span\u003Eassociated with cat-scratch disease.\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003ENeuroretinitis may also be caused by other infectious agents (e.g., syphilis, Lyme, EBV, toxoplasmosis), but \u003Ci\u003EBartonella\u003C/i\u003E remains the most frequent identifiable cause.\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe condition is often self-limiting in immunocompetent individuals, but treatment with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoxycycline \u00B1 rifampin\u003C/b\u003E\u003C/span\u003E is sometimes used, especially in confirmed Bartonella cases. Interestingly, many affected patients \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edo not recall a cat scratch or bite\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 454,
    "Name": "Vitreomacular traction (VMT)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 53-year-old man presents with reduced vision in the right eye for several months. The OCT shows tenting of the retina consistent with vitreomacular traction (VMT). Which statement about this condition is accurate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-05-d3d1e8aa-6796-4208-a9cd-e568d036312a.png\u0022\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\n\n\n\n\n\n\n\n\u003Cp\u003E\u003C/p\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe OCT shows vitreomacular traction (VMT) with characteristic tenting of the retina caused by incomplete separation of the posterior vitreous from the macula.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis traction may lead to:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECystoid macular edema\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EShallow retinal detachment\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDecreased and distorted central vision\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETypical examination findings:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAbnormal vitreous opacity over the macula\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMacular traction extending to the optic nerve\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EFluorescein angiography may demonstrate dye leakage from macular retinal vessels and the optic disc\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathophysiology:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EVMT is considered a subset of epiretinal membrane pathology\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGlial cells are the predominant cell type involved\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESurgical management:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPars plana vitrectomy for VMT has demonstrated visual improvement of \u22652 lines in 75% of eyes (McDonald et al., Ophthalmology 1994; 101:1397\u2013402)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPharmacologic management:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOcriplasmin is a recombinant protease that targets fibronectin and laminin at the vitreoretinal interface\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is administered via intravitreal injection\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDay 28 resolution rates:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E26% in ocriplasmin-treated eyes\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E10% in placebo-treated eyes\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003ESource:\u0026nbsp;\u003Ca href=\u0022https://iovs.arvojournals.org/article.aspx?articleid=2353949\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe Phase III MIVI-TRUST Clinical Trial Data: Subgroup Responder Analysis of a Single Intravitreal Injection of Ocriplasmin in patients with Vitreomacular Traction\u003C/a\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 455,
    "Name": "Stickler Syndrome",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 40-year-old male\u003Cspan class=\u0022s1\u0022\u003E presents with \u003C/span\u003Ebilateral macula-off retinal detachments\u003Cspan class=\u0022s1\u0022\u003E. History reveals a \u003C/span\u003Edominant family inheritance\u003Cspan class=\u0022s1\u0022\u003E pattern (\u201Cfamily curse\u201D), \u003C/span\u003Ejoint hypermobility\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Emidfacial hypoplasia\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003Emicrognathia\u003Cspan class=\u0022s1\u0022\u003E, and \u003C/span\u003Ehearing difficulty\u003Cspan class=\u0022s1\u0022\u003E. What is the most likely diagnosis?\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EStickler syndrome\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is the \u003C/span\u003E\u003Cb\u003Emost common hereditary vitreoretinopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with systemic manifestations.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIt is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecollagen type II disorder\u003C/b\u003E\u003C/span\u003E, inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E pattern, typically due to mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECOL2A1 gene\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EPart of the group of \u003C/span\u003E\u003Cb\u003Ehereditary hyaloideoretinopathies with optically empty vitreous\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which are divided into:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThose with only ocular signs: e.g., Jansen and Wagner diseases.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThose with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esystemic signs\u003C/b\u003E\u003C/span\u003E: e.g., Stickler syndrome, Weill\u2013Marchesani, and dwarfism-related variants.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb\u003EOcular Features:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EUp to \u003C/span\u003E\u003Cb\u003E60% develop retinal detachment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, often \u003C/span\u003E\u003Cb\u003Ebilateral and macula-off\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERetinal breaks\u003C/b\u003E\u003C/span\u003E in \u0026gt;90% due to:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPremature vitreous liquefaction\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigh myopia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERadial perivascular lattice degeneration\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003ESlit lamp shows \u003C/span\u003E\u003Cb\u003Eoptically empty\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and \u003C/span\u003E\u003Cb\u003Eliquefied vitreous\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESubcapsular cataracts\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may also be present.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb\u003ESystemic Features:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ECraniofacial abnormalities\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPierre-Robin sequence\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Ecleft palate\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Emidface flattening\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Emicrognathia\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EJoint hypermobility\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, \u003C/span\u003E\u003Cb\u003Eosteoarthritis\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ESensorineural hearing loss\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EJoint pain\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is common\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Ch3\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cb\u003EManagement:\u003C/b\u003E\u003C/h3\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EConsider \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprophylactic laser retinopexy\u003C/b\u003E\u003C/span\u003E for lattice degeneration, particularly in:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigh-risk patients\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPatients with prior RD in the fellow eye\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 456,
    "Name": "DR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 45-year-old woman with poorly-controlled diabetes undergoes a routine dilated fundus exam. She is asymptomatic with visual acuity of LogMAR 0.10 in both eyes. On slit-lamp examination, there is contiguous neovascularisation of the pupil and iris, but not the angle. Fundoscopy shows four-quadrant intraretinal haemorrhages without retinal or vitreous neovascularisation. Macular contact lens examination reveals no thickening. Fluorescein angiography shows multiple hyperfluorescent foveal spots with one slow-leaking point. What is the most appropriate management for this patient?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis patient has \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eneovascularization of the iris (NVI)\u003C/b\u003E\u003C/span\u003E, seen as contiguous neovascularization of the pupil and iris, without angle involvement.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAccording to \u003C/span\u003E\u003Cb\u003EETDRS (Early Treatment Diabetic Retinopathy Study)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, this finding signifies \u003C/span\u003E\u003Cb\u003Eproliferative diabetic retinopathy (PDR)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E and requires prompt \u003C/span\u003E\u003Cb\u003Epanretinal photocoagulation (PRP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EAlthough \u003C/span\u003E\u003Cb\u003Efluorescein angiography (FA)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E shows macular leakage, there is \u003C/span\u003E\u003Cb\u003Eno retinal thickening on slit-lamp contact lens exam\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, which means the patient does \u003C/span\u003E\u003Cb\u003Enot\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E meet the definition of \u003C/span\u003E\u003Cb\u003Eclinically significant macular edema (CSME)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECSME is a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebiomicroscopic diagnosis\u003C/b\u003E\u003C/span\u003E, not made based solely on FA or OCT findings.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe vision is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELogMAR 0.1\u003C/b\u003E\u003C/span\u003E, confirming that her central visual function is well-preserved, supporting the decision \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E to initiate focal laser at this time.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnti-VEGF may be considered \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ein addition to\u003C/b\u003E\u003C/span\u003E PRP, especially in eyes with significant iris neovascularization, but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPRP remains the standard of care\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EOCT-based \u003C/span\u003E\u003Cb\u003Ecentral subfield thickness\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E may guide macular edema management, but \u003C/span\u003E\u003Cb\u003Eleakage alone on FA is not an indication for treatment\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1424,
    "Name": "Central Serous Chorioretinopathy CSCR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 26-year-old asymptomatic male presents for routine eye examination. His visual acuity is 0.0 LogMAR (20/20) in both eyes without correction. Fundus examination shows RPE mottling in the macula bilaterally. His fluorescein angiography (FA) is shown below. What is the most appropriate management for this patient?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-06-62874d20-5a57-47e2-b897-89dce11bb0f7.jpg\u0022\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Ca id=\u0022sp0020\u0022 style=\u0022background-image: none; background-position: 0px 0px; background-size: initial; background-repeat: repeat; background-attachment: scroll; background-origin: initial; background-clip: initial; border-style: none; border-color: initial; border-image: initial; outline: none 0px; vertical-align: baseline; font-family: Arial, Helvetica, sans-serif; letter-spacing: normal; text-align: justify; font-size: small; color: rgb(14, 13, 13);\u0022\u003EFluorescein angiogram shows leakage with an ink blot appearance. The hyperfluorescence starts as a pinpoint and then enlarges concentrically similar to the appearance of dropping ink onto a piece of paper.\u003C/a\u003E\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe clinical picture and FA findings are consistent with \u003Ci\u003Ecentral serous chorioretinopathy (CSCR)\u003C/i\u003E, a condition typically affecting young to middle-aged males and often discovered incidentally in asymptomatic patients.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECSCR involves idiopathic serous detachment of the subfoveal neurosensory retina, often associated with RPE changes and pigment epithelial detachment (PED). FA typically shows an expansile dot pattern of hyperfluorescence, as seen here.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAnti-VEGF therapy\u003C/b\u003E\u003C/span\u003E: Not indicated here. It is ineffective in CSCR unless a secondary choroidal neovascular membrane is present. The underlying mechanism of CSCR is related to choroidal hyperpermeability and congestion, not VEGF-driven neovascularisation.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPhotodynamic therapy\u003C/b\u003E\u003C/span\u003E: Effective in chronic symptomatic cases where subretinal fluid persists \u0026gt;3-4 months and involves the central macula. This patient is asymptomatic with no central involvement, so PDT is inappropriate.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFocal laser\u003C/b\u003E\u003C/span\u003E: Reserved for persistent subretinal fluid \u0026gt;3-4 months, especially if leakage is within 500 microns of the central macula. In this case, there is no vision reduction or central leakage; so laser is not justified.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EObservation\u003C/b\u003E\u003C/span\u003E: The most appropriate first-line approach. In asymptomatic CSCR with 0.0 LogMAR vision, spontaneous resolution occurs in ~90% of cases within 3-4 months. Observation is also suitable in mildly symptomatic patients as long as central vision is preserved and the duration is \u0026lt;4 months.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003Ca href=\u0022https://entokey.com/central-serous-chorioretinopathy-2/\u0022 target=\u0022_blank\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003ECentral Serous Chorioretinopathy\u003C/a\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://entokey.com/wp-content/uploads/2017/03/B9781455707379000722_f072-004-9781455707379.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca id=\u0022sp0025\u0022 style=\u0022color: rgb(74, 197, 167); background-image: none; background-position: 0px 0px; background-size: initial; background-repeat: repeat; background-attachment: scroll; background-origin: initial; background-clip: initial; border-style: none; border-color: initial; border-image: initial; font-size: 11.7px; outline: none 0px; vertical-align: baseline; font-family: Arial, Helvetica, sans-serif; letter-spacing: normal; text-align: justify;\u0022\u003EFluorescein angiogram shows leakage with a smoke stack appearance. The hyperfluorescence starts as a pinpoint and then migrates upward and subsequently diffuses laterally, leading to a mushroom cloud or umbrella-like appearance.\u003C/a\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1425,
    "Name": "Rhegmatogenous retinal detachment (RRD)",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 69-year-old African American phakic male with a known history of sickle cell disease presents with a macula-off rhegmatogenous retinal detachment (RRD), with multiple retinal breaks located both superiorly and inferiorly. What is the most appropriate surgical management option?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPars plana vitrectomy (PPV) is preferred in this patient due to:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMultiple breaks in both inferior and superior quadrants.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe macula being detached (macula-off status).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAvoiding the risks associated with scleral buckle in sickle cell disease.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EScleral buckling is contraindicated in patients with sickle cell disease due to increased risk of anterior segment ischemia.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAnterior segment ischemia in these patients can result from:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDetachment of extraocular muscles.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUse of local anaesthetic with epinephrine.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOverzealous photocoagulation or cryopexy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInadequate hydration or oxygenation.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EObservation is not appropriate as this is a surgical emergency requiring prompt intervention.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cbr\u003E\u003C/p\u003E\n\u003Cp class=\u0022p3\u0022\u003E\u003Cb\u003EReference:\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003Cp class=\u0022p4\u0022\u003ECartwright MJ, Blair CJ, Combs JL, Stratford TP. \u003Ci\u003EAnterior segment ischemia: a complication of retinal detachment repair in a patient with sickle cell trait.\u003C/i\u003E Ann Ophthalmol. 1990;22:333-4.\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1426,
    "Name": "Ocular toxoplasmosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40\u2011year\u2011old man presents with floaters and reduced vision in one eye. On examination he has vitritis and a pale lesion adjacent to the optic disc. Which of these is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EToxoplasmosis.\u003C/strong\u003E\u003Cbr\u003E\nThe combination of \u003Cstrong\u003Eunilateral floaters/reduced vision\u003C/strong\u003E, \u003Cstrong\u003Edense vitritis\u003C/strong\u003E, and a \u003Cstrong\u003Esolitary pale focus by the disc\u003C/strong\u003E is classic for ocular toxoplasmosis retinochoroiditis\u2014typically a \u003Cstrong\u003Efluffy white, focal necrotizing retinitis with overlying vitreous haze\u003C/strong\u003E (\u201Cheadlight in the fog\u201D), often \u003Cstrong\u003Eadjacent to an old chorioretinal scar\u003C/strong\u003E and sometimes juxtapapillary.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn contrast, \u003Cstrong\u003Eacute posterior multifocal placoid pigment epitheliopathy\u003C/strong\u003E presents with \u003Cstrong\u003Ebilateral multiple creamy placoid RPE\u2011level lesions\u003C/strong\u003E and usually \u003Cstrong\u003Elittle vitritis\u003C/strong\u003E, not a single vitritis\u2011obscured focus. \u003Cstrong\u003EAcute retinal necrosis\u003C/strong\u003E characteristically shows \u003Cstrong\u003Erapidly progressive, peripheral confluent necrotizing retinitis with occlusive arteriolar vasculitis and prominent intraocular inflammation\u003C/strong\u003E, rather than an isolated juxtapapillary lesion. \u003Cstrong\u003EBirdshot chorioretinopathy\u003C/strong\u003E is a \u003Cstrong\u003Ebilateral, HLA\u2011A29\u2013associated\u003C/strong\u003E posterior uveitis with \u003Cstrong\u003Enumerous cream choroidal spots\u003C/strong\u003E in middle\u2011aged patients; vitritis may occur but the pattern is diffuse, not a single focal retinitis.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1427,
    "Name": "Estimating squint size from corneal light reflex",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen assessing corneal reflexes in a squinting child, displacement of the corneal light reflex to the pupil margin (2\u202Fmm) suggests a squint of what size?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003E30 prism dioptres.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nOn the Hirschberg (corneal light\u2011reflex) estimate, a practical clinical rule is that \u003Cstrong\u003Eeach 1\u202Fmm of reflex decentration corresponds to ~15 prism dioptres\u003C/strong\u003E of deviation; when the reflex lies at the \u003Cstrong\u003Epupillary margin (\u22482\u202Fmm from the centre)\u003C/strong\u003E, the implied angle is therefore \u003Cstrong\u003Eabout 2\u202F\u00D7\u202F15\u202F=\u202F30\u202F\u2206\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1428,
    "Name": "Gene target for voretigene neparvovec (NICE)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ENICE has recommended voretigene neparvovec to treat inherited retinal disorders with which gene mutation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; line-height: 20px;\u0022\u003E\u003Cp style=\u0022font-style: normal; font-weight: 400;\u0022\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; line-height: 20px;\u0022\u003E\u003Cp style=\u0022font-style: normal; font-weight: 400;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ERPE65.\u003C/strong\u003E\u003Cbr\u003E\nNICE Highly Specialised Technologies guidance \u003Cstrong\u003EHST11\u003C/strong\u003E recommends voretigene neparvovec (Luxturna) for \u003Cstrong\u003ERPE65\u2011mediated inherited retinal dystrophies\u003C/strong\u003E in patients with \u003Cstrong\u003Ebiallelic RPE65 mutations\u003C/strong\u003E and sufficient viable retinal cells.\u003C/p\u003E\n\u003Cp style=\u0022font-style: normal; font-weight: 400;\u0022\u003E\u003Cstrong\u003EAssociated diseases for each gene in the options (for quick recall):\u003C/strong\u003E\u003C/p\u003E\n\u003Cul style=\u0022font-style: normal; font-weight: 400;\u0022\u003E\n\u003Cli\u003E\u003Cstrong\u003EUSH2A\u003C/strong\u003E \u2192 \u003Cstrong\u003EUsher syndrome type IIA\u003C/strong\u003E (hearing loss with retinitis pigmentosa) \u003Cstrong\u003Eand\u003C/strong\u003E \u003Cstrong\u003Eautosomal\u2011recessive nonsyndromic retinitis pigmentosa\u003C/strong\u003E.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ERPE65\u003C/strong\u003E \u2192 \u003Cstrong\u003ELeber congenital amaurosis / early\u2011onset severe retinal dystrophy.\u003C/strong\u003E\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EABCA4\u003C/strong\u003E \u2192 \u003Cstrong\u003EStargardt disease (STGD1/ABCA4 retinopathy)\u003C/strong\u003E; ABCA4 variants can also cause \u003Cstrong\u003Econe\u2011rod dystrophy\u003C/strong\u003E.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECNGA1\u003C/strong\u003E \u2192 \u003Cstrong\u003EAutosomal\u2011recessive retinitis pigmentosa\u003C/strong\u003E (rod CNG\u2011channel\u2013related RP).\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp style=\u0022\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1429,
    "Name": "Bitemporal field loss",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 27\u2011year\u2011old patient was found to have a bitemporal field loss on perimetry. Which of the following is LEAST likely to be the cause?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EParietal meningioma.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nTrue bitemporal hemianopia localizes to the \u003Cstrong\u003Eoptic chiasm\u003C/strong\u003E, most classically from \u003Cstrong\u003Epituitary adenomas\u003C/strong\u003E and occasionally from \u003Cstrong\u003Eintracranial aneurysms\u003C/strong\u003E (e.g., anterior communicating/internal carotid territory) compressing the chiasm. \u003Cstrong\u003ETilted optic discs\u003C/strong\u003E can also produce a \u003Cstrong\u003Ebitemporal hemianopia\u2011like (pseudo) defect\u003C/strong\u003E that may cross the vertical meridian, mimicking chiasmal disease.  By contrast, \u003Cstrong\u003Eparietal lobe lesions\u003C/strong\u003E (including parietal meningioma or parietal involvement by other tumours) affect the \u003Cstrong\u003Edorsal optic radiations\u003C/strong\u003E and typically cause a \u003Cstrong\u003Econtralateral inferior homonymous quadrantanopia/hemianopia\u003C/strong\u003E, not a heteronymous bitemporal defect\u2014hence this is the least likely cause in this scenario.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1430,
    "Name": "Seasonal allergic conjunctivitis in children",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ERegarding seasonal allergic conjunctivitis in children which of the following statements is MOST likely to be true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EThe allergic response is predominantly mediated by Th2\u2011lymphocytes.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nSeasonal allergic conjunctivitis is a classic \u003Cstrong\u003EIgE\u2011mediated type\u2011I hypersensitivity\u003C/strong\u003E in which \u003Cstrong\u003ETh2\u2011polarized immunity\u003C/strong\u003E (notably IL\u20114/IL\u20115/IL\u201113) drives mast\u2011cell sensitization/degranulation and eosinophilic inflammation; blocking Th2 signaling reduces conjunctival inflammation, underscoring this mechanism.  Although many children are affected\u2014population syntheses estimate \u003Cstrong\u003E\u22656\u201330%\u003C/strong\u003E for allergic conjunctivitis overall, often higher in pediatric cohorts\u2014diagnostic \u003Cstrong\u003Especific IgE is not positive in \u201Calmost all\u201D cases\u003C/strong\u003E and test performance varies; thus that claim is overstated.  The \u003Cstrong\u003Eearly (immediate) phase\u003C/strong\u003E of ocular allergy peaks at \u003Cstrong\u003E~20\u201330 minutes and typically subsides within about an hour\u003C/strong\u003E, with a separate late phase several hours later\u2014so an early phase \u201Clasting up to 2 hours\u201D is not the usual pattern.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1431,
    "Name": "Granulomatosis with polyangiitis (Wegener\u2019s)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 51\u2011year\u2011old man presents with proptosis associated with a destructive orbital mass. Six months previously he had a peripheral ulcerative keratitis. Which of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EGranulomatosis with polyangiitis.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nA prior \u003Cstrong\u003Eperipheral ulcerative keratitis (PUK)\u003C/strong\u003E strongly points to an underlying systemic vasculitis; PUK is classically associated with \u003Cstrong\u003EANCA\u2011associated disease, including GPA\u003C/strong\u003E, and can even be a presenting feature.  The current finding of \u003Cstrong\u003Eproptosis from a destructive orbital mass\u003C/strong\u003E fits orbital GPA, which frequently causes \u003Cstrong\u003Econtiguous sinonasal\u2013orbital granulomatous inflammation with paranasal bone erosion\u003C/strong\u003E on imaging; orbital involvement is common and may be the initial manifestation.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EBy contrast, \u003Cstrong\u003Emucormycosis\u003C/strong\u003E usually occurs in \u003Cstrong\u003Eimmunocompromised or acidotic diabetics\u003C/strong\u003E, presents acutely with necrosis/\u201Cblack eschar,\u201D and is an aggressive \u003Cstrong\u003Erhino\u2011orbital\u2013cerebral\u003C/strong\u003E infection rather than a subacute granulomatous mass.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EOrbital aspergillosis\u003C/strong\u003E is another invasive fungal sinus\u2011origin disease\u2014often in the immunocompromised\u2014and would not explain the antecedent PUK.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003ENecrobiotic xanthogranuloma\u003C/strong\u003E typically produces \u003Cstrong\u003Eyellow\u2011orange periorbital plaques\u003C/strong\u003E with a strong paraproteinaemia association, not a destructive orbital mass with prior vasculitic keratitis.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1432,
    "Name": "Neuromyelitis optica spectrum disorder",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is LEAST likely to be a core clinical characteristic described in the diagnostic criteria for Neuromyelitis Optica Spectrum Disorder?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EMononeuritis multiplex.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nModern NMOSD criteria (IPND 2015) define six \u003Cstrong\u003Ecore clinical characteristics\u003C/strong\u003E:\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Col\u003E\u003Cli\u003E\u003Cstrong\u003EOptic neuritis \u003C/strong\u003E(Acute inflammation of the optic nerve causing painful vision loss; in NMOSD it is often \u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Esevere\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, may be \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ebilateral\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E or involve long segments/chiasm, and is one of the most common core presentations)\u003C/span\u003E\u003C!--EndFragment--\u003E\u003C/li\u003E\u003Cli\u003E\u0026nbsp;\u003Cstrong\u003EAcute myelitis\u003C/strong\u003E (\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EAn inflammatory spinal cord attack that in NMOSD typically presents as \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Elongitudinally extensive transverse myelitis (LETM)\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E: an intramedullary lesion spanning \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u22653 vertebral segments\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, causing acute paraparesis/quadriparesis, a sensory level, and sphincter dysfunction),\u003C/span\u003E\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003EArea postrema syndrome\u003C/strong\u003E (\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ERecurrent, otherwise unexplained \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eintractable hiccups, nausea, and vomiting\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E due to involvement of the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Edorsal medulla/area postrema\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E; MRI often shows a lesion in this region\u003C/span\u003E).\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA\u003C/span\u003E\u003Cstrong\u003Ecute brainstem syndrome\u003C/strong\u003E,\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003ESymptomatic diencephalic syndrome\u003C/strong\u003E (e.g., narcolepsy) with typical MRI, and\u0026nbsp;\u003C/li\u003E\u003Cli\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003ESymptomatic cerebral syndrome\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E with NMOSD\u2011typical lesions; these features underpin diagnosis in both AQP4\u2011IgG\u2013positive and seronegative patients.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003C/ol\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EMononeuritis multiplex\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E is a \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eperipheral nerve vasculitic neuropathy\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E pattern (asymmetric, painful, multifocal nerve deficits) and is \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Enot part of the NMOSD core criteria\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, making it the least likely option here.\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1433,
    "Name": "Acute profound monocular vision loss in an 82\u2011year\u2011old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 82\u2011year\u2011old man presents with profound loss of vision in his right eye this morning (to PL). He has no previous ophthalmic history, no headache and denies jaw claudication and proximal myalgia. Apart from a dense right RAPD, ocular examination is normal. Which of these is the MOST appropriate immediate action?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EPrescribe high\u2011dose prednisolone once daily and arrange a temporal artery biopsy.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003E\u003Cbr\u003E\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EIn an 82\u2011year\u2011old with sudden, profound, painless monocular vision loss, a dense RAPD, and a normal fundus, the most likely emergency is \u003Cstrong\u003Earteritic posterior ischemic optic neuropathy from giant cell arteritis (GCA)\u003C/strong\u003E; PION is characteristically retrobulbar with an initially normal disc, and in older adults GCA is a key cause that can rapidly involve the fellow eye.  Because prevention of further visual loss is time\u2011critical, \u003Cstrong\u003Ehigh\u2011dose glucocorticoids must be started immediately\u003C/strong\u003E and \u003Cstrong\u003Etemporal artery biopsy arranged urgently\u003C/strong\u003E, rather than delaying treatment for investigations; biopsy remains diagnostic if performed within the first 1\u20132 weeks after steroids are started.  Typical initial regimens are oral prednisone 40\u201360\u202Fmg/day (up to 60\u201380\u202Fmg/day in visual involvement) or intravenous methylprednisolone in those with acute visual symptoms, with the aim of protecting the fellow eye even though vision already lost is unlikely to recover.  By contrast, prioritizing carotid imaging and aspirin aligns more with \u003Cstrong\u003Ecentral retinal artery occlusion\u003C/strong\u003E pathways and does not address the immediate GCA threat in this presentation.  Likewise, urgent CT or MRI of the optic pathway is not the initial priority when GCA is suspected; neuroimaging can follow, but steroid therapy should not be delayed while arranging it.\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1434,
    "Name": "Uveal Effusion Syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with idiopathic uveal effusion syndrome without nanophthalmos which of the following is the MOST appropriate management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EFull\u2011thickness sclerectomy (scleral windows).\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nIdiopathic uveal effusion syndrome in a non\u2011nanophthalmic eye is still most often approached as a problem of impaired uveoscleral/trans\u2011scleral outflow related to scleral factors and/or vortex\u2011vein congestion, so the management that most directly addresses the mechanism is \u003Cstrong\u003Escleral decompression with scleral windows/sclerectomy\u003C/strong\u003E. Surgical series and reviews describe medical therapy (including systemic steroids) as historically disappointing in true uveal effusion syndrome, while scleral surgery (sclerectomies and/or vortex\u2011vein decompression) can lead to resolution of the choroidal and serous retinal detachments.  Oral acetazolamide does not treat the underlying scleral resistance problem, and pars plana vitrectomy is not a mechanism\u2011based treatment for idiopathic uveal effusion.  (Although there are modern reports showing that some patients can improve with corticosteroids and avoid surgery, that benefit is variable and does not replace scleral windows as the classic \u201Cbest answer\u201D for idiopathic non\u2011nanophthalmic UES.)\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1435,
    "Name": "Biometry Pitfall After Refractive Surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to pre\u2011cataract surgery biometry, which of these statements is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EPrevious myopic excimer laser refractive surgery is likely to cause under\u2011estimation of the IOL power required if routine biometry is used without any correction factor.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EAfter myopic LASIK/PRK the anterior corneal curvature is flattened but the posterior surface is relatively unchanged, so standard keratometers (and many biometers) applying a fixed keratometric index and assumptions about anterior\u2013posterior curvature relationships tend to \u003Cstrong\u003Eoverestimate true corneal power\u003C/strong\u003E; when this inflated corneal power is fed into routine IOL formulas, the calculated IOL power is often \u003Cstrong\u003Etoo low\u003C/strong\u003E, \u2014which is exactly the same as saying routine biometry \u003Cstrong\u003Eunderestimates the IOL power required\u003C/strong\u003E unless a post\u2011refractive correction method is used.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe other statements are less likely as written. Keratometry error generally translates roughly \u003Cstrong\u003E1:1\u003C/strong\u003E into postoperative refractive surprise at the spectacle plane, so a 0.75 D K error would be expected to cause about a 0.75 D refractive error rather than 1.25 D.  Optical biometry (partial coherence interferometry) in silicone\u2011oil\u2013filled eyes is not intrinsically \u201Clow reliability\u201D; published work shows \u003Cstrong\u003Eacceptable accuracy/signal quality\u003C/strong\u003E, sometimes with device settings or adjustments, rather than being broadly unreliable.  Finally, short eyes remain difficult and some studies show systematic shifts depending on formula/constants, but the direction is not as universally exam\u2011stable as the post\u2011myopic excimer underestimation problem.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1436,
    "Name": "Post\u2011operative Diplopia Test",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 45\u2011year\u2011old woman presents with a divergent left eye. She had surgery as a small child although she is unclear which eye. Her vision is 6/6 in the right eye and 6/60 in the left eye. With the angle corrected whilst viewing through a prism she is aware of double vision. Which one of the following is NOT used as a post\u2011operative diplopia test?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cp style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003EHess chart.\u003C/span\u003E\u003C/p\u003E\u003Cp style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EA post\u2011operative diplopia test is essentially a\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003Eprism simulation\u003C/span\u003E\u0026nbsp;of the intended surgical alignment to see whether diplopia emerges when the deviation is neutralised, and this can be done using\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003Eloose prisms or a prism bar\u003C/span\u003E, or by giving a\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003Eprolonged trial with a Fresnel prism\u003C/span\u003E\u0026nbsp;to mimic the planned correction. A synoptophore can also be used in orthoptic practice to explore sensory status and alignment under dissociation and is part of the prism\u2011based toolkit used in strabismus assessment.\u0026nbsp;\u003C/p\u003E\u003Cp style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003EBy contrast, a Hess chart is a\u0026nbsp;\u003Cspan style=\u0022font-weight: 700;\u0022\u003Emapping tool for incomitant strabismus\u003C/span\u003E\u0026nbsp;(underaction/overaction across gaze positions) used to document and monitor motility patterns, not a prism\u2011simulation \u201Cwill you see double if we straighten you\u201D test, so it is not considered a post\u2011operative diplopia test.\u0026nbsp;\u003C/p\u003E\u003Cp style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1437,
    "Name": "Choroidal melanoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the MOST likely mechanism by which tumour cells spread in a 70\u2011year\u2011old man with malignant melanoma of the choroid?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EHaematological spread.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nChoroidal (uveal) melanoma classically metastasizes via the bloodstream because the uveal tract lacks true lymphatics, so lymphatic spread is not the dominant route in the way it is for many surface/epithelial malignancies.  This hematogenous tendency aligns with the well\u2011known metastatic pattern of uveal melanoma, where distant spread occurs predominantly to the liver, supporting blood\u2011borne dissemination rather than perineural or \u201Cnatural plane\u201D extension as the primary mechanism.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1438,
    "Name": "Glaucoma visual field patterns",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these scotomata is LEAST likely to be associated with glaucoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ETemporal wedge defect.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EArcuate scotomata, nasal steps, and paracentral scotomata are the classic nerve\u2011fibre\u2011bundle patterns of glaucomatous loss on standard automated perimetry, reflecting damage that respects the horizontal raphe and commonly presents as arcuate defects and nasal step changes, often with early paracentral involvement.  A temporal wedge defect can occur in glaucoma, but it is a less \u201Cclassic\u201D pattern on routine central field testing and is typically described as a far\u2011peripheral inferotemporal sector/wedge defect that may be missed unless the periphery is specifically tested, so it is the least likely option compared with the hallmark arcuate/nasal step/paracentral defects.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1439,
    "Name": "Systemic drugs reaching high intraocular levels",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ESystemically administered drugs achieve high intraocular concentrations if they have which ONE of the following?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EHigh lipid solubility.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003ESystemically administered drugs must cross the blood\u2013ocular barriers (blood\u2013aqueous and blood\u2013retinal barriers), which markedly restrict diffusion of many agents into the eye, so drugs that are more able to partition into and traverse lipid membranes are more likely to achieve higher intraocular levels.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;High protein binding works in the opposite direction because only the unbound fraction is available to diffuse across barriers, so strong protein affinity generally reduces the amount of free drug that can enter ocular tissues.\u003C/p\u003E\u003Cp\u003EHigh molecular weight also tends to limit penetration across biological barriers, making high intraocular concentrations less likely.\u003C/p\u003E\u003Cp\u003E\u201CLow pH\u201D by itself is not a useful determinant in this context; what matters more is the degree of ionisation at physiological pH (and membrane permeability/transport), not simply having an intrinsically low pH.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1440,
    "Name": "optic nerve sheath meningioma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40\u2011year\u2011old female in good general health presents with gradual painless loss of vision in her right eye over two months. Her acuity is 6/36 in the right eye and 6/6 in the left. She has a right relative afferent pupillary defect (RAPD) and fundus appearance is as shown. Which statement concerning radiological investigation is MOST likely to be correct?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-07-ff344038-e2b7-44c2-aaa4-0e0fbcfb7f1a.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ECT scan with contrast may show a \u201Ctram\u2011track\u201D sign within the orbit.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe fundus photo shows a swollen/abnormal optic disc with prominent dilated vessels on and around the disc that are typical of \u003Cstrong\u003Eoptociliary (retinochoroidal) shunt vessels\u003C/strong\u003E, a classic clue in compressive optic neuropathies and particularly optic nerve sheath meningioma in the right clinical context of painless progressive unilateral visual loss and RAPD.  Optic nerve sheath meningioma characteristically enhances \u003Cstrong\u003Earound\u003C/strong\u003E the optic nerve rather than within it, so with contrast imaging the enhancing sheath/tumor flanks the non\u2011enhancing optic nerve, creating the well\u2011known \u003Cstrong\u003E\u201Ctram\u2011track\u201D sign\u003C/strong\u003E on axial views (and a \u201Cdot/target\u201D sign on coronal views).  This is why the \u201CCT with contrast\u201D statement is the most likely correct option here; MRI is also excellent, but the option given is \u003Cstrong\u003EMRI without contrast\u003C/strong\u003E, which is specifically less suited to demonstrating the key enhancement pattern.  MRA is aimed at vascular disease (aneurysm/AVM) rather than a sheath tumor, and B\u2011scan ultrasound is not usually the defining diagnostic test compared with cross\u2011sectional orbital imaging that demonstrates the peri\u2011optic enhancement pattern.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1441,
    "Name": "Left occipito\u2011temporal glioma in a right\u2011handed patient ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a right\u2011handed patient with a left occipito\u2011temporal glioma which of these features is MOST likely to be found?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EHemianopic alexia.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIn a right\u2011handed person, language is most commonly left\u2011hemisphere dominant, and a lesion in the \u003Cstrong\u003Eleft occipito\u2011temporal region\u003C/strong\u003E is a classic setup for a reading disorder in which visual word information cannot be effectively processed by the dominant language network. Lesions involving the dominant occipital/occipito\u2011temporal region produce the syndrome of \u003Cstrong\u003Ealexia without agraphia (\u201Cpure alexia\u201D)\u003C/strong\u003E, typically accompanied by a \u003Cstrong\u003Eright homonymous hemianopia\u003C/strong\u003E, and clinically this often presents as marked difficulty reading despite preserved writing\u2014hence the expected finding is a form of alexia linked to the hemianopia.  A left homonymous hemianopia would imply a right retrochiasmal lesion, not a left occipito\u2011temporal one, so the hemianopia direction in that statement does not fit the lesion side.  See\u2011saw nystagmus is more characteristically associated with chiasmal/parasellar or related central lesions rather than a focal occipito\u2011temporal glioma, and a fixed dilated pupil suggests third nerve compression/uncal herniation rather than a localized occipito\u2011temporal cortical tumor presentation.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1442,
    "Name": "Dysphotopsia after cataract surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ERegarding dysphotopsia after cataract surgery which of the following statements is LEAST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ENegative dysphotopsia is relieved by pupillary constriction.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003ENegative dysphotopsia is classically perceived as a \u003Cstrong\u003Etemporal (often frontotemporal) crescent/arc-shaped shadow\u003C/strong\u003E, so that description is consistent with the usual symptom profile.  What makes the statement wrong is that negative dysphotopsia is typically \u003Cstrong\u003Eworse with a small pupil (pupillary constriction)\u003C/strong\u003E and \u003Cstrong\u003Eless noticeable when the pupil dilates\u003C/strong\u003E, which is why bright conditions (small pupil) often aggravate it.\u003C/p\u003E\u003Cp\u003EPositive dysphotopsia, in contrast, is described as \u003Cstrong\u003Ebright phenomena\u003C/strong\u003E such as streaks/arcs/rays (often triggered by \u003Cstrong\u003Eoblique or side light sources\u003C/strong\u003E) and is widely linked to \u003Cstrong\u003Eedge-related light effects\u003C/strong\u003E, particularly with \u003Cstrong\u003Esquare-edge IOL designs\u003C/strong\u003E that can promote internal reflections/glare.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1443,
    "Name": "Marfan syndrome inheritance risk",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has Marfan\u2019s syndrome and would like to know how likely it is that one of her children will inherit the condition. Her partner is not a member of her extended family. Which of the following options is the BEST estimate of the likelihood?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003E0.5\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EMarfan syndrome is inherited in an \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E pattern, meaning an affected individual typically carries one altered copy of the relevant gene and one normal copy, so \u003Cstrong\u003Eeach pregnancy has a 50% (1 in 2) chance\u003C/strong\u003E of the child inheriting the pathogenic variant and therefore the condition.  The fact that her partner is not from her extended family simply reduces the chance that the partner also has the same familial variant; assuming the partner is unaffected, the risk to each child remains \u003Cstrong\u003E50%\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1444,
    "Name": "Penicillin allergy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich ONE of the following drugs should NEVER be given to a patient with penicillin allergy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ECo\u2011amoxiclav.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ECo\u2011amoxiclav contains \u003Cstrong\u003Eamoxicillin\u003C/strong\u003E, which is a \u003Cstrong\u003Epenicillin (penicillin\u2011class / penicillin\u2011like \u03B2\u2011lactam)\u003C/strong\u003E, so in a patient labelled as penicillin\u2011allergic it is the one you should avoid.  In contrast, amikacin is an aminoglycoside (not a \u03B2\u2011lactam) and has no structural relationship to penicillin, so penicillin allergy does not automatically preclude its use.\u003C/p\u003E\u003Cp\u003ECefuroxime (a cephalosporin) and meropenem (a carbapenem) are \u03B2\u2011lactams but true cross\u2011reactivity with penicillin is generally \u003Cstrong\u003Elow\u003C/strong\u003E and depends mainly on side\u2011chain similarity rather than the \u03B2\u2011lactam ring itself; many guidelines therefore treat them as \u003Cem\u003Epotentially usable with appropriate clinical caution and history\u2011taking\u003C/em\u003E, rather than \u201Cnever.\u201D\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1445,
    "Name": "Immunological treatment of myasthenia gravis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u201CWith regards to the immunological treatment of myasthenia gravis, which of the following is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EAzathioprine may be used as a steroid\u2011sparing agent for disease control.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EAzathioprine is a well\u2011established long\u2011term immunosuppressant in myasthenia gravis and is commonly used alongside corticosteroids to achieve disease control while allowing steroid reduction (a steroid\u2011sparing strategy).\u003C/p\u003E\u003Cp\u003EIntravenous immunoglobulin is not typically used for \u201Cmild\u201D disease; it is mainly a short\u2011term, rapid immunomodulatory treatment used for severe or rapidly worsening weakness, peri\u2011operative bridging, or crisis/exacerbations rather than routine mild presentations.\u003C/p\u003E\u003Cp\u003EPlasma exchange is also a rapid \u201Crescue/bridge\u201D therapy with benefits that are short\u2011lived (weeks), so it does not confer long\u2011term remission on its own without ongoing immunosuppression.\u003C/p\u003E\u003Cp\u003EThymectomy has the strongest evidence base in non\u2011thymomatous acetylcholine receptor antibody\u2013positive generalized disease (improving outcomes and reducing steroid requirement); in seronegative disease, benefit is less certain and it is not the clear \u201Cmost likely correct\u201D statement in this set.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1446,
    "Name": "Effect of a single radial corneal suture on astigmatism",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EConsidering the effect of inserting or removing a single radial corneal suture upon refractive astigmatism, which of the following statements is MOST LIKELY to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EInsertion of a suture results in steepening of the corneal curvature in the meridian of the new suture.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EA single \u003Cstrong\u003Etight\u003C/strong\u003E radial corneal suture increases tensile force across that meridian, and the predictable topographic response is \u003Cstrong\u003Esteepening in the sutured meridian with coupling-related flattening 90 degrees away\u003C/strong\u003E, which is the principle surgeons exploit when adjusting or adding sutures to reduce post\u2011operative astigmatism.  By the same logic, removing (or significantly loosening) a previously tight suture tends to reduce that meridional steepening\u2014i.e., it \u003Cstrong\u003Eflattens the meridian of the removed suture\u003C/strong\u003E and causes a relative \u003Cstrong\u003Esteepening 90 degrees away\u003C/strong\u003E, so the \u201Cremoval causes steepening in the same meridian\u201D statement is the opposite of what is expected.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1447,
    "Name": "Follicular conjunctivitis \u002B preauricular/submandibular lymphadenopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 22\u2011year\u2011old female presents with a history of fever, and now has a follicular conjunctivitis. Examination reveals that the sub\u2011mandibular and the pre\u2011auricular lymph nodes are enlarged. Which of the following is least likely to be an association?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ESuccessful treatment with clindamycin.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003EParinaud oculoglandular syndrome\u003C/strong\u003E, most commonly due to \u003Cstrong\u003Ecat\u2011scratch disease (Bartonella henselae)\u003C/strong\u003E, which characteristically causes \u003Cstrong\u003Eunilateral granulomatous/follicular conjunctivitis with ipsilateral regional lymphadenopathy\u003C/strong\u003E (often preauricular and/or submandibular) and systemic symptoms such as fever.  Ocular Bartonella infection is well known to be associated with \u003Cstrong\u003Euveitis\u003C/strong\u003E and with \u003Cstrong\u003Eoptic nerve swelling\u003C/strong\u003E in the form of \u003Cstrong\u003Eneuroretinitis\u003C/strong\u003E (optic disc edema with later macular star), and Bartonella can also cause \u003Cstrong\u003Evasculitis that may be occlusive\u003C/strong\u003E, with reported cases including \u003Cstrong\u003Ecentral retinal artery/vein occlusion\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EBy contrast, \u003Cstrong\u003Eclindamycin is not a standard or typical effective therapy\u003C/strong\u003E for cat\u2011scratch disease/Parinaud oculoglandular syndrome; when antibiotics are used, guidance commonly cites \u003Cstrong\u003Eazithromycin\u003C/strong\u003E for uncomplicated CSD and other regimens (e.g., doxycycline \u00B1 rifampicin) for more significant ocular/systemic disease, making \u201Csuccessful treatment with clindamycin\u201D the least likely association in this context.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1448,
    "Name": "PEDIG occlusion dose",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAccording to Paediatric Eye Diseases Investigative Group guidelines, what patching regime would you MOST likely prescribe \u003Cstrong\u003Ewithout near tasks\u003C/strong\u003E for a 3\u2011year\u2011old child with the following VA: \u003Cstrong\u003ERVA LogMAR 0.1, LVA 0.7\u003C/strong\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ERight occlusion 6 hours per day.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ELogMAR \u003Cstrong\u003E0.7\u003C/strong\u003E corresponds to approximately \u003Cstrong\u003E20/100\u003C/strong\u003E, while logMAR \u003Cstrong\u003E0.1\u003C/strong\u003E corresponds to ~\u003Cstrong\u003E20/25\u003C/strong\u003E, so this is \u003Cstrong\u003Esevere amblyopia\u003C/strong\u003E by the commonly used PEDIG severity bands (severe \u2248 20/100\u201320/400).  PEDIG\u2019s key randomized trial in severe amblyopia compared \u003Cstrong\u003E6 hours/day\u003C/strong\u003E with full\u2011time patching and showed similar visual improvement, which is why 6 hours/day is the standard evidence\u2011based \u201Cpart\u2011time\u201D prescription for severe cases in this age group.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe \u201Cwithout near tasks\u201D wording doesn\u2019t force you to reduce or increase the prescribed hours in the PEDIG framework, because PEDIG also tested whether \u201Cnear\u201D activities add benefit to patching and found no meaningful advantage of near over distance activities when patching is prescribed (so the dose recommendation is still driven mainly by baseline severity rather than the activity type).\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1449,
    "Name": "Hysteresis principle",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following investigations utilises the principle of hysteresis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EOcular response analyser.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EHysteresis refers to a system showing different responses on \u201Cloading\u201D versus \u201Cunloading,\u201D and in the eye the classic clinical example is \u003Cstrong\u003Ecorneal hysteresis\u003C/strong\u003E, which reflects the cornea\u2019s viscoelastic damping.  The \u003Cstrong\u003EOcular Response Analyzer (ORA)\u003C/strong\u003E measures this by using an air\u2011puff to indent the cornea and recording two applanation events: one as the cornea moves \u003Cstrong\u003Einward\u003C/strong\u003E and one as it returns \u003Cstrong\u003Eoutward\u003C/strong\u003E; the \u003Cstrong\u003Edifference between the inward and outward applanation pressures\u003C/strong\u003E is the hysteresis value (corneal hysteresis).  In contrast, \u003Cstrong\u003EB\u2011scan ultrasonography\u003C/strong\u003E is based on acoustic reflection/echoes, \u003Cstrong\u003EERG\u003C/strong\u003E is based on retinal bioelectrical responses to light stimuli, and \u003Cstrong\u003ESD\u2011OCT\u003C/strong\u003E is based on optical interferometry\u2014none of which relies on a hysteresis loop phenomenon as the core measurement principle.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1450,
    "Name": "Jackson Cross Cylinder",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following statements MOST clearly describes a Jackson Cross Cylinder?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EA spherocylindrical lens in which the power of the sphere is half the power of the cylinder and of the opposite sign.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA Jackson cross cylinder is made from \u003Cstrong\u003Etwo equal but opposite cylinders oriented 90\u00B0 apart\u003C/strong\u003E, giving it \u003Cstrong\u003Ezero spherical equivalent\u003C/strong\u003E and allowing it to refine cylinder power/axis without shifting the circle of least confusion.  In spherocylindrical notation this is commonly written as \u003Cstrong\u003E\u002B0.25 / \u22120.50\u003C/strong\u003E or \u003Cstrong\u003E\u002B0.50 / \u22121.00\u003C/strong\u003E, which shows that the \u003Cstrong\u003Ecylinder magnitude is double the sphere magnitude\u003C/strong\u003E and the \u003Cstrong\u003Esigns are opposite\u003C/strong\u003E\u2014equivalently, the \u003Cstrong\u003Esphere is half the cylinder and of opposite sign\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1451,
    "Name": "pigmented conjunctival lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EYou are asked to see a 30\u2011year\u2011old woman with a slowly enlarging pigmented conjunctival lesion as shown in the photograph below. What is the MOST likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-09-5a3256a0-f052-4739-92f9-7c7951f17409.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThis is most consistent with \u003Cstrong\u003Econjunctival malignant melanoma\u003C/strong\u003E, because the lesion is \u003Cstrong\u003Ediscrete and nodular/elevated\u003C/strong\u003E with \u003Cstrong\u003Eprominent feeder vessels\u003C/strong\u003E and a history of \u003Cstrong\u003Eprogressive enlargement\u003C/strong\u003E, which are classic suspicious clinical features for conjunctival melanoma.  A conjunctival naevus is typically \u003Cstrong\u003Elong\u2011standing from childhood/early life\u003C/strong\u003E and often contains \u003Cstrong\u003Eintralesional cysts\u003C/strong\u003E, which supports a benign diagnosis rather than a newly enlarging nodular lesion.  Primary acquired melanosis is usually \u003Cstrong\u003Eflat, patchy pigmentation\u003C/strong\u003E rather than a raised mass (even though it can be a precursor lesion).  Lymphangioma/lymphangiectasia characteristically appears \u003Cstrong\u003Ecystic/transparent\u003C/strong\u003E (often \u201Cstring of pearls\u201D or cystic spaces), not as a solid pigmented nodule.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1452,
    "Name": "Posterior vitreous detachment",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPosterior vitreous detachment is typically present in which one of the following:\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EGiant retinal tear.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003Egiant retinal tear\u003C/strong\u003E is classically defined as a full\u2011thickness retinal break extending \u22653 clock hours \u003Cstrong\u003Ein the presence of a posteriorly detached vitreous\u003C/strong\u003E, so PVD is part of the typical setting rather than an incidental finding.  In \u003Cstrong\u003Eretinal dialysis\u003C/strong\u003E, the mechanism is different: the vitreous is typically still attached (including at the vitreous base), which is why these detachments can be slow and often demarcated, so a PVD is not the usual context. \u003Cstrong\u003ETraumatic macular holes\u003C/strong\u003E are also usually seen without a complete PVD\u2014EyeWiki notes that complete PVD is rare and the posterior vitreous remains adherent to the macula in the majority.  Finally, \u003Cstrong\u003Eatrophic round hole retinal detachments\u003C/strong\u003E (often in lattice) commonly occur in eyes with little vitreous degeneration and typically \u003Cstrong\u003Ewithout\u003C/strong\u003E PVD, reflecting their non\u2011tractional pathogenesis.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1453,
    "Name": " nedocromil sodium",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these types of drug is nedocromil sodium?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EMast cell stabiliser.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ENedocromil sodium acts by \u003Cstrong\u003Estabilising mast cells\u003C/strong\u003E and inhibiting mediator release (including histamine) involved in allergic reactions, which is why it is used for \u003Cstrong\u003Eitching associated with allergic conjunctivitis\u003C/strong\u003E as an ophthalmic preparation.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1454,
    "Name": "Blunt ocular trauma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following statements is MOST likely to be true following blunt trauma to the eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ESclera is thinnest behind rectus muscle insertions.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIn blunt trauma, ocular tissues fail preferentially at anatomical weak points, and the sclera has a well\u2011described thickness profile: it is \u003Cstrong\u003Ethickest near the optic nerve\u003C/strong\u003E and \u003Cstrong\u003Ethinnest just posterior to the rectus muscle insertions\u003C/strong\u003E, which is why ruptures from blunt trauma are commonly described at or just behind these insertions as well as at the limbus.  Bruch\u2019s membrane is not \u201Chighly elastic\u0022, in traumatic choroidal rupture the globe deformation causes the RPE\u2013Bruch complex to stretch and \u003Cstrong\u003Ebreak\u003C/strong\u003E, reflecting its limited tensile strength/elasticity rather than resilience.  Retinal detachment associated with retinal dialysis often \u003Cstrong\u003Eprogresses slowly\u003C/strong\u003E and diagnosis is frequently \u003Cstrong\u003Edelayed\u003C/strong\u003E, rather than presenting immediately, consistent with vitreous being typically still attached in these eyes.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1455,
    "Name": "Intermittent Exotropia Subtype ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 8\u2011year\u2011old child presents with strabismus. The findings are an exotropia, which measures 35 prism dioptres for distance and 15 prism dioptres for near. After 45 minutes of monocular occlusion the near deviation has increased to 30 prism dioptres. Which of the following is the MOST accurate diagnostic category?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ESimulated divergence excess exotropia.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA larger distance than near exodeviation initially suggests a divergence\u2011excess pattern, but the key step is reassessing the near angle after prolonged monocular occlusion to abolish tenacious proximal fusion. When the near deviation increases after occlusion so that the distance\u2013near difference becomes small (typically no longer meeting the \u226510 prism dioptre distance\u2011greater\u2011than\u2011near threshold), this fits the definition of pseudo/simulated divergence excess rather than true divergence excess. Here, the near angle rises from 15\u0394 to 30\u0394 after 45 minutes of occlusion, bringing it close to the distance angle of 35\u0394, which is exactly the pattern expected in simulated divergence excess.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1456,
    "Name": "Best IOP\u2011lowering response to argon laser trabeculoplasty (ALT)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following types of glaucoma is MOST likely to have the best intraocular pressure lowering response to Argon laser trabeculoplasty (ALT)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EPseudoexfoliative glaucoma\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EALT tends to work best when the \u003Cstrong\u003Etrabecular meshwork is densely pigmented\u003C/strong\u003E, because pigment facilitates absorption of laser energy and enhances the biological response that increases outflow. Eyes with \u003Cstrong\u003Epseudoexfoliation\u003C/strong\u003E commonly have \u003Cstrong\u003Eheavier trabecular pigmentation\u003C/strong\u003E and are classically described as responding well to trabeculoplasty.\u003C/p\u003E\n\u003Cp\u003EBy comparison, \u003Cstrong\u003Euveitic glaucoma\u003C/strong\u003E is not an ideal candidate because trabeculoplasty is generally \u003Cstrong\u003Eavoided in active inflammation\u003C/strong\u003E (and can exacerbate intraocular inflammation), and secondary glaucomas such as \u003Cstrong\u003Eaphakic/traumatic mechanisms\u003C/strong\u003E are described as \u003Cstrong\u003Eless responsive\u003C/strong\u003E than primary open\u2011angle/pigmentary/PEX patterns.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1457,
    "Name": "Contact lens\u2013related painful keratitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient, who wears contact lenses, has developed a painful keratitis. Which of the following MOST strongly supports a diagnosis of acanthamoeba keratitis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong style=\u0022\u0022\u003ELinear intrastromal infiltrates\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003ELinear intrastromal infiltrates represent \u003Cstrong\u003Eradial keratoneuritis / radial perineuritis\u003C/strong\u003E (perineural infiltrates tracking along corneal nerves), which is an \u003Cstrong\u003Eearly and characteristic\u003C/strong\u003E sign of Acanthamoeba keratitis and therefore the most supportive finding among the options.\u003C/p\u003E\n\u003Cp\u003EThe other findings listed are \u003Cstrong\u003Enon\u2011specific\u003C/strong\u003E and can occur with many causes of microbial keratitis or chronic inflammation. Corneal melting is more typical of severe bacterial/fungal disease and is not the key supportive clinical clue for Acanthamoeba, while neovascularisation and stromal haze/opacification can be secondary late sequelae of multiple keratitides rather than a distinguishing feature.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1458,
    "Name": "CRVO \u002B raised ESR \u002B raised gamma region on SPEP",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 67\u2011year\u2011old man presents with a three\u2011day history of blurred vision due to a central retinal vein occlusion in the right eye. Acuity is 6/18 right and 6/6 left. ESR is elevated at 98 and the gamma zone is elevated on serum protein electrophoresis. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EMultiple myeloma.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EAn elevated \u003Cstrong\u003Egamma region\u003C/strong\u003E on serum protein electrophoresis strongly points toward a \u003Cstrong\u003Emonoclonal gammopathy\u003C/strong\u003E, classically seen as a narrow spike in the gamma-globulin zone, and multiple myeloma is a key malignant cause of this pattern.  In the context of a retinal vein occlusion, paraproteinaemia can drive \u003Cstrong\u003Ehyperviscosity\u003C/strong\u003E and microvascular flow impairment, predisposing to venous stasis and retinal venous occlusion; CRVO has been reported in association with paraproteinaemias and multiple myeloma, including cases where electrophoresis demonstrates increased \u03B3\u2011globulins/paraprotein.  Although ESR can be markedly raised in many inflammatory and malignant states, the combination of a very high ESR with a raised gamma region on electrophoresis makes a plasma\u2011cell dyscrasia the most coherent single diagnosis from the list. \u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1459,
    "Name": "DVLA Group 2 driving standard",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFor a Group 2 Driving license the minimum requirement in the better eye is 6/7.5. What does the DVLA specify should be the minimum visual acuity in the worse eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003E6/60.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EFor \u003Cstrong\u003EGroup 2 (bus and lorry)\u003C/strong\u003E licensing, DVLA guidance states the visual acuity must be \u003Cstrong\u003Eat least 6/7.5 in the better eye\u003C/strong\u003E and \u003Cstrong\u003Eat least 6/60 in the poorer (worse) eye\u003C/strong\u003E, with correction if required (and if spectacles are used, there is also a \u002B8 dioptre limit).\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1460,
    "Name": "Post\u2011blunt trauma hypotony with shallow AC and resolving hyphaema ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient presents with blurred vision in one eye following blunt trauma one week previously. The visual acuity is 6/18 in that eye. The anterior chamber is shallow and there is a small resolving hyphaema. The intraocular pressure is recorded as 4 mmHg compared with 16 mmHg in the other eye. What is the MOST likely cause of the hypotony?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003ECyclodialysis cleft.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA cyclodialysis cleft is a \u003Cstrong\u003Edisinsertion of the ciliary body from the scleral spur\u003C/strong\u003E, creating a direct pathway between the \u003Cstrong\u003Eanterior chamber and the suprachoroidal space\u003C/strong\u003E, which markedly increases uveoscleral outflow and produces \u003Cstrong\u003Eprofound hypotony\u003C/strong\u003E.  This fits the clinical picture of \u003Cstrong\u003Every low IOP (4 mmHg)\u003C/strong\u003E shortly after blunt trauma with associated anterior segment signs such as a resolving hyphaema, and it is specifically highlighted as an important diagnosis to consider in \u003Cstrong\u003Enew\u2011onset hypotony after trauma\u003C/strong\u003E, even when the peripheral chamber is shallow and gonioscopic visualization can be difficult.  In contrast, angle recession is classically important because it predisposes to \u003Cstrong\u003Elater elevated IOP and secondary open\u2011angle glaucoma\u003C/strong\u003E, not marked early hypotony.\u003C/p\u003E\n\u003Cp\u003E\u003Cem style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1461,
    "Name": "Oculocardiac reflex",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to the oculo\u2011cardiac reflex, which of these statements is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u003C/strong\u003E \u003Cstrong\u003EIt can occur after peribulbar anaesthesia.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe oculocardiac reflex is a \u003Cstrong\u003Etrigeminovagal\u003C/strong\u003E reflex: the \u003Cstrong\u003Eafferent limb is via the trigeminal nerve (predominantly V1/ophthalmic division)\u003C/strong\u003E and the \u003Cstrong\u003Eefferent limb is via the vagus nerve\u003C/strong\u003E, producing bradycardia when the globe, conjunctiva, or extraocular muscles are manipulated.  Because it can be triggered by orbital manipulation and even regional blocks, it has been reported during or despite \u003Cstrong\u003Eperibulbar/retrobulbar-type regional anaesthesia\u003C/strong\u003E, and peribulbar anaesthesia does \u003Cstrong\u003Enot reliably abolish\u003C/strong\u003E the reflex once it is provoked by extraocular muscle traction.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe other statements are less likely to be correct because the reflex \u003Cstrong\u003Edoes not require an intact globe\u003C/strong\u003E (it can be elicited by manipulation of orbital contents, including after enucleation), it is generally \u003Cstrong\u003Emore prominent in children and tends to decrease with age rather than increase\u003C/strong\u003E, and the afferent limb is \u003Cstrong\u003Enot\u003C/strong\u003E the facial nerve (that description fits the corneal blink reflex instead).\u003C/p\u003E\u003Cp\u003E\u003Cem style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1462,
    "Name": "TASS",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is LEAST likely to be a complication of toxic anterior segment syndrome (TASS)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003ECorrect answer:\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EPeripheral corneal ulceration\u003C/strong\u003E\u003C/h3\u003E\n\u003Cp\u003EToxic anterior segment syndrome is a sterile, acute postoperative inflammatory reaction caused by exposure of intraocular tissues to toxic substances, so its complications are largely confined to the anterior segment and reflect intraocular damage rather than surface tissue necrosis. It can lead to marked anterior chamber inflammation with corneal oedema, secondary trabecular dysfunction with a significant rise in intraocular pressure, and iris injury that may result in atrophy with transillumination defects and an atonic, poorly reactive dilated pupil. Although macular oedema is not a defining feature, it can occur as a postoperative inflammatory sequela and is still more plausible than peripheral corneal ulceration, which typically implies corneal epithelial breakdown and stromal necrosis from infectious keratitis, exposure, neurotrophic disease, or immune-mediated peripheral ulcerative keratitis rather than a toxic intraocular anterior segment reaction.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1463,
    "Name": "Paradoxical pupil response",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to the paradoxical pupil response found in some inherited retinal conditions, which of the following statements is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: It is thought to be due to the unopposed effect of S cones in the retina\u003C/span\u003E\u003C/h3\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\n\u003Cp\u003EThe paradoxical pupil response described in some inherited retinal disorders is best explained by altered retinal photoreceptor signaling in which the usual balance of cone inputs is disrupted, leaving short-wavelength sensitive cone pathways relatively unopposed and capable of driving an atypical pupillary behavior. This is a retinal phenomenon rather than a near-response phenomenon, so attributing it to convergence in the dark does not fit the physiology of the pupillary light reflex pathway, and it is not primarily an iris autonomic problem such as denervation hypersensitivity, which would instead point toward post-ganglionic parasympathetic dysfunction and pharmacological supersensitivity rather than a stimulus-dependent paradoxical response. It is also not confined to laboratory-only detection, because the abnormality can be appreciated clinically with careful observation of pupillary behaviour to different light conditions and wavelengths in the appropriate retinal dystrophy context.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1464,
    "Name": "Number needed to treat",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA study comparing the use of Intravitreal ranibizumab (IVR) for the treatment of neovascular age-related macular degeneration (AMD), reports a number needed to treat of 3.13 when compared to sham treatment. Which of these statements is MOST likely to be justified based upon this information?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-size: 14px; line-height: 20px;\u0022\u003E\u003Cp style=\u0022font-weight: 400;\u0022\u003EA number needed to treat is the inverse of the absolute risk reduction and represents the average number of patients who must receive the intervention instead of control for one additional patient to achieve the specified outcome (or avoid one additional bad outcome) over the study time frame.  An NNT of 3.13 therefore means that treating about three patients with intravitreal ranibizumab rather than sham results in one additional patient meeting the study endpoint (here framed as vision retention), so the statement that best matches the meaning of NNT is the one expressing \u201Cabout three treated for one additional beneficial outcome.\u201D  Statements that describe \u201C3.13 times more likely\u201D are describing a relative measure such as a risk ratio or odds ratio, not an NNT, and a statement about how many received sham versus IVR is about allocation ratio rather than treatment effect.\u0026nbsp;\u003C/p\u003E\n\u003Cp style=\u0022\u0022\u003E\u003Cem style=\u0022\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/em\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/h3\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 11,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1465,
    "Name": "Abusive head trauma (RCOphth 2013)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to the suggested documentation of retinal haemorrhages in children with suspected abusive head trauma within The Royal College of Ophthalmologists\u2019 guideline on abusive head trauma (2013), which of the following descriptions is LEAST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: The depth of haemorrhages should be classified as either intraretinal or multilayered.\u003C/span\u003E\u003C/h3\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\n\u003Cp\u003EA key part of the 2013 RCOphth/RCPCH recommended proforma is to document retinal hemorrhages in a structured way that captures features with diagnostic value, including morphology, layer, location, and approximate burden; importantly, the \u201Cdepth/layer\u201D field is not restricted to only intraretinal versus multilayered, because the proforma explicitly prompts classification across preretinal, intraretinal, subretinal, and multilayered categories, so a statement limiting depth to just intraretinal or multilayered is incomplete and therefore least likely to be correct.  The other descriptions align with the same proforma: recording whether haemorrhages are white-centred is specifically prompted under morphology, location is explicitly separated into posterior pole defined in relation to zone 1 of ROP and the peripheral retina, and the number is categorised as few, many, or too numerous to count with indicative ranges, so these are consistent with the guideline\u2019s suggested documentation framework.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1466,
    "Name": "Drug toxicity: sudden bilateral central vision loss",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ESudden loss of central vision in both eyes is MOST likely due to treatment with which of the following?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Ethambutol.\u003C/span\u003E\u003C/h3\u003E\u003Ch3\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-size: 14px; line-height: 20px;\u0022\u003E\n\u003Cp style=\u0022font-weight: 400;\u0022\u003EEthambutol classically causes a \u003Cstrong\u003Etoxic optic neuropathy\u003C/strong\u003E that is \u003Cstrong\u003Ebilateral and fairly symmetric\u003C/strong\u003E, producing an \u003Cstrong\u003Eacute-to-subacute drop in central visual acuity\u003C/strong\u003E with \u003Cstrong\u003Ecentral or centrocaecal scotomas\u003C/strong\u003E and \u003Cstrong\u003Edyschromatopsia\u003C/strong\u003E (often red\u2013green), which fits the pattern of sudden bilateral central vision loss best. Tamoxifen toxicity is more typically a \u003Cstrong\u003Emaculopathy\u003C/strong\u003E with \u003Cstrong\u003Ecrystalline deposits\u003C/strong\u003E and foveal structural change that is usually \u003Cstrong\u003Emore insidious\u003C/strong\u003E rather than presenting as abrupt bilateral central acuity loss. Thioridazine is associated with a \u003Cstrong\u003Epigmentary retinopathy\u003C/strong\u003E and more \u003Cstrong\u003Egeneralised retinal dysfunction\u003C/strong\u003E, so symptoms and signs tend to reflect \u003Cstrong\u003Ediffuse retinal involvement\u003C/strong\u003E rather than a predominantly optic nerve pattern of central scotoma and dyschromatopsia. Vigabatrin toxicity characteristically causes \u003Cstrong\u003Ebilateral concentric peripheral field constriction\u003C/strong\u003E due to retinal toxicity, so the hallmark complaint is \u003Cstrong\u003Eprogressive \u201Ctunnel vision\u201D\u003C/strong\u003E rather than sudden central visual loss.\u003C/p\u003E\u003Cp style=\u0022\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/h3\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1467,
    "Name": "Uveitic glaucoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn glaucoma associated with uveitis, which of the following is least likely to be the cause of raised intraocular pressure?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Pigments deposit on the trabecular meshwork.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EIn uveitis-associated glaucoma, \u003Cstrong\u003Eraised intraocular pressure is most commonly driven by impaired aqueous outflow due to inflammatory mechanisms\u003C/strong\u003E rather than primary pigmentary obstruction, so pigment deposition is the least likely explanation in this context. \u003Cstrong\u003EPeripheral anterior synechiae can permanently close the angle and reduce trabecular access\u003C/strong\u003E, producing a sustained outflow block and chronic pressure elevation, particularly in recurrent or severe anterior uveitis. \u003Cstrong\u003ETrabeculitis causes functional shutdown of the trabecular meshwork\u003C/strong\u003E through inflammatory oedema and cellular dysfunction, giving a potentially marked pressure rise even when the angle is anatomically open, and this is a well-recognised mechanism in several uveitic entities. \u003Cstrong\u003EProteinaceous flare, inflammatory cells, and fibrin can physically clog the trabecular meshwork\u003C/strong\u003E, forming trabecular precipitates and debris-related obstruction that elevates pressure, especially in acute anterior chamber inflammation. By contrast, while pigment liberation from the iris can occur during inflammation, \u003Cstrong\u003Epigment deposition as the dominant mechanism is more characteristic of pigment dispersion or pseudoexfoliation syndromes\u003C/strong\u003E, not the typical pathophysiology of uveitic glaucoma, making it the least likely cause among the listed options.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 3,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1468,
    "Name": "Acute orbital inflammation with lid necrosis in a poorly controlled diabetic",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA poorly controlled diabetic patient develops acute orbital inflammation with proptosis. There is necrosis of the upper lid. Which of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Mucormycosis.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EIn a poorly controlled diabetic, especially in the setting of ketoacidosis, \u003Cstrong\u003Erhino\u2011orbito\u2011cerebral mucormycosis is the classic cause of rapidly progressive orbital inflammation with proptosis and tissue necrosis\u003C/strong\u003E, because the organism is \u003Cstrong\u003Eangioinvasive\u003C/strong\u003E, causing \u003Cstrong\u003Evascular thrombosis, ischemia, and \u201Cblack eschar\u201D necrosis\u003C/strong\u003E that can involve the nasal mucosa, palate, eyelids, and orbit with alarming speed. \u003Cstrong\u003EUpper lid necrosis\u003C/strong\u003E is a major clue pointing to this angioinvasive necrotising process rather than a purely inflammatory orbital cellulitis pattern. Aspergillosis can also be invasive in immunocompromised patients and can involve the orbit, but the most exam\u2011typical pairing of \u003Cstrong\u003Euncontrolled diabetes with fulminant necrosis\u003C/strong\u003E is mucormycosis rather than aspergillus. Granulomatosis with polyangiitis can cause orbital inflammation and necrotising disease, but it is usually framed by \u003Cstrong\u003Esystemic vasculitis features\u003C/strong\u003E and tends to be less \u201Cexplosively\u201D necrotic at the eyelid as a presenting hallmark compared with the classic rapidly progressive fungal angioinvasion seen in mucormycosis. Necrobiotic xanthogranuloma is typically a \u003Cstrong\u003Echronic\u003C/strong\u003E periocular infiltrative condition with \u003Cstrong\u003Eyellowish plaques/nodules\u003C/strong\u003E and association with paraproteinaemia, not an acute fulminant orbital process with lid necrosis.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1469,
    "Name": "Episcleritis with peripheral corneal ulcer, saddle nose, and valvular disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 23 year old woman presents to casualty with a history of recent episodes of redness of her eyes and some discomfort. On examination she has some episcleritis and one peripheral corneal ulcer. She has a saddle nose and is on the waiting list for an aortic valve replacement. She is taking prednisolone and etanercept. Her ESR is 72 mm/hr and her haemoglobin is 10.2 g/dl. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Relapsing polychondritis.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003ERelapsing polychondritis is the best fit because it is a \u003Cstrong\u003Esystemic, immune\u2011mediated inflammation targeting cartilaginous and proteoglycan\u2011rich tissues\u003C/strong\u003E, classically producing \u003Cstrong\u003Eauricular and nasal chondritis with collapse of the nasal bridge leading to a saddle\u2011nose deformity\u003C/strong\u003E, and it commonly causes ocular inflammation such as \u003Cstrong\u003Eepiscleritis and scleritis\u003C/strong\u003E, with the potential for \u003Cstrong\u003Eperipheral ulcerative keratitis\u003C/strong\u003E due to adjacent limbal vasculitis and collagenolysis. The history of \u003Cstrong\u003Esignificant cardiovascular involvement requiring aortic valve replacement\u003C/strong\u003E is also highly supportive, because relapsing polychondritis can involve the \u003Cstrong\u003Eaortic root and cardiac valves\u003C/strong\u003E, leading to regurgitation and progressive valvular disease in a subset of patients, and the raised inflammatory markers with anaemia fit a chronic systemic inflammatory process. Rheumatoid arthritis can certainly be associated with episcleritis and peripheral ulcerative keratitis, and biologic therapy such as etanercept is used in rheumatoid disease, but the combination of \u003Cstrong\u003Esaddle\u2011nose deformity from cartilage destruction\u003C/strong\u003E together with \u003Cstrong\u003Emajor valvular/aortic involvement at this young age\u003C/strong\u003E is much more characteristic of relapsing polychondritis than rheumatoid arthritis. Kawasaki disease is a childhood medium\u2011vessel vasculitis with mucocutaneous features and coronary artery involvement rather than destructive nasal cartilage disease and chronic episcleritis with peripheral corneal ulceration in adulthood. Dermatomyositis is primarily an inflammatory myopathy with characteristic skin findings and does not explain the hallmark combination of \u003Cstrong\u003Ecartilage collapse\u003C/strong\u003E and \u003Cstrong\u003Evalvular/aortic disease\u003C/strong\u003E alongside these ocular signs.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1470,
    "Name": "Acute red, photophobic eye with anterior and vitreous cells and a peripheral white patch",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 32 year old man presents with a sore, photophobic, red left eye with reduced vision. On examination he has both anterior chamber and vitreous cells and an extensive white patch in the peripheral retina. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Acute retinal necrosis.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EAcute retinal necrosis\u003C/strong\u003E is the best fit because the key pattern is \u003Cstrong\u003Ea painful red photophobic eye with both anterior uveitis and vitritis plus a confluent, pale-white area of peripheral necrotising retinitis\u003C/strong\u003E, which is the classic clinical constellation for this diagnosis and explains the reduced vision through intense intraocular inflammation and retinal involvement. This differs from \u003Cstrong\u003Epars planitis\u003C/strong\u003E, which is an intermediate uveitis characterised by \u003Cstrong\u003Evitreous cells with \u201Csnowballs/snowbanking\u201D\u003C/strong\u003E and often relatively less pain and photophobia, and it does not typically produce an \u003Cstrong\u003Eextensive, sharply abnormal white necrotic retinal patch\u003C/strong\u003E in the periphery. It also differs from \u003Cstrong\u003Eposterior scleritis\u003C/strong\u003E, where the dominant feature is usually \u003Cstrong\u003Esevere deep ocular pain\u003C/strong\u003E with posterior segment signs such as choroidal folds or exudative retinal detachment, and while some spill-over inflammation can occur, the hallmark is not a large peripheral necrotising retinal whitening. \u003Cstrong\u003ERecurrent toxoplasma chorioretinitis\u003C/strong\u003E can present with vitritis and a white retinitis focus, but it is classically a \u003Cstrong\u003Efocal necrotising retinochoroiditis often adjacent to an old pigmented scar\u003C/strong\u003E and more often posterior, rather than an \u003Cstrong\u003Eextensive peripheral confluent necrotic patch\u003C/strong\u003E accompanied by the intense pan-uveitic picture that strongly points to acute retinal necrosis.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1471,
    "Name": "Haemorrhagic retinal pigment epithelial detachment in a 35-year-old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 35 year old man presents with a haemorrhagic retinal pigment epithelial detachment and an acuity of 6/60. An image of his fundus is shown. Which ONE of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Sorsby\u2019s macular dystrophy.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA haemorrhagic retinal pigment epithelial detachment with marked central vision loss in a relatively young adult is most consistent with \u003Cstrong\u003Eearly-onset choroidal neovascularisation on a background of an inherited macular dystrophy\u003C/strong\u003E, and \u003Cstrong\u003ESorsby\u2019s macular dystrophy is classically a third-to-fifth decade condition in which choroidal neovascular membranes recur and are associated with haemorrhage and rapid central visual loss\u003C/strong\u003E.  This presentation is less consistent with acute posterior multifocal placoid pigment epitheliopathy because that disorder is characterised by \u003Cstrong\u003Emultiple creamy placoid lesions at the level of the retinal pigment epithelium in the posterior pole\u003C/strong\u003E, usually with a self-limited inflammatory course, and haemorrhagic pigment epithelial detachment would be an atypical framing for the primary diagnosis rather than the expected core finding.  It is also less consistent with birdshot retinopathy, which is a chronic posterior uveitis with \u003Cstrong\u003Emultiple cream-coloured choroidal lesions and vitritis\u003C/strong\u003E rather than an isolated haemorrhagic pigment epithelial detachment picture causing abrupt central acuity drop.  Punctate inner choroidopathy can certainly be complicated by \u003Cstrong\u003Echoroidal neovascularisation and pigment epithelial detachment with haemorrhage\u003C/strong\u003E, but it predominantly affects \u003Cstrong\u003Eyoung myopic women\u003C/strong\u003E and is typically described with multiple small punched-out yellow-white lesions in the posterior pole; therefore, in an exam stem emphasising a haemorrhagic pigment epithelial detachment in a 35-year-old man, the more characteristic \u201Cfit\u201D is Sorsby\u2019s macular dystrophy.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1472,
    "Name": "Episodic blurred vision with pain and tearing on waking in a hypermetropic 65-year-old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 65 year old hypermetropic woman (\u002B3.50 DS both eyes) gives a six month history of episodic blurred vision associated with ocular pain and epiphora. She has difficulty opening her eyes in the morning on awakening. On examination she has bilateral corneal guttata, anterior chamber depths of 3.0mm right and left eye and central corneal thickness of 530 microns right and left eye. The eyelids and conjunctiva appear normal. What is the MOST likely cause of her symptoms?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Recurrent corneal erosion syndrome.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003ERecurrent corneal erosion syndrome best explains this presentation because the defining clinical clue is \u003Cstrong\u003Edifficulty opening the eyes on awakening\u003C/strong\u003E, which reflects \u003Cstrong\u003Elid\u2013epithelium adhesion overnight followed by epithelial shear on first opening\u003C/strong\u003E, producing \u003Cstrong\u003Esudden pain, reflex tearing, and transient blur\u003C/strong\u003E from an irregular corneal surface. The episodic nature over months with \u003Cstrong\u003Epain and epiphora that are worst on waking\u003C/strong\u003E is far more characteristic of recurrent erosions than endothelial or glaucomatous mechanisms.\u0026nbsp;\u003C/p\u003E\u003Cp\u003EFuchs endothelial dystrophy can cause \u003Cstrong\u003Emorning blurred vision\u003C/strong\u003E due to overnight corneal hydration, and guttata may be present, but it typically produces \u003Cstrong\u003Ehaze/blur that improves as the day progresses\u003C/strong\u003E rather than the very specific \u003Cstrong\u003Emechanical \u201Ccan\u2019t open the eye on waking\u201D pain pattern\u003C/strong\u003E, and the \u003Cstrong\u003Enormal central corneal thickness\u003C/strong\u003E with no mention of stromal/epithelial edema makes decompensation less likely as the main driver.\u003C/p\u003E\u003Cp\u003EIntermittent angle closure glaucoma is suggested by hypermetropia, but it classically causes \u003Cstrong\u003Ehaloes, headache, nausea, and an attack pattern often precipitated by dim light\u003C/strong\u003E, and it does not explain \u003Cstrong\u003Erecurrent morning lid-opening pain\u003C/strong\u003E; in addition, the anterior chamber depth given is not markedly shallow and the external eye is described as normal, which is less consistent with symptomatic angle-closure episodes.\u003C/p\u003E\u003Cp\u003EStaphylococcal hypersensitivity would usually be accompanied by \u003Cstrong\u003Eblepharitis/meibomian disease and conjunctival hyperaemia\u003C/strong\u003E with peripheral corneal infiltrates, and the stem explicitly notes that \u003Cstrong\u003Eeyelids and conjunctiva appear normal\u003C/strong\u003E, making this the least fitting explanation for the symptom pattern.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
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  },
  {
    "Id": 1473,
    "Name": "NICE (Aug 2008; updated later) wet AMD",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to the National Institute for Health and Care Excellence (NICE) guidance issued in August 2008 (and updated in 2012) for treatment of wet age-related macular degeneration (AMD), which of these is LEAST likely to be a valid criterion for treatment with anti-VEGF agents?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Lesion size is less or equal to 4 disc areas in greatest linear dimension.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe NICE technology appraisal criteria for initiating anti\u2011VEGF therapy in wet AMD specify \u003Cstrong\u003Ea best\u2011corrected visual acuity between 6/12 and 6/96\u003C/strong\u003E, \u003Cstrong\u003Eno permanent structural damage to the central fovea\u003C/strong\u003E, \u003Cstrong\u003Eevidence of recent presumed disease progression\u003C/strong\u003E, and a \u003Cstrong\u003Emaximum lesion size of 12 disc areas in greatest linear dimension\u003C/strong\u003E, so a threshold of 4 disc areas is not the NICE anti\u2011VEGF cut\u2011off and is therefore the least likely to be valid.  The reason the 4 disc area figure appears as a distractor is that smaller lesion size limits have historically been used in other treatment contexts (classically photodynamic therapy eligibility discussions), whereas NICE\u2019s anti\u2011VEGF recommendation explicitly allows treatment up to 12 disc areas provided the other clinical criteria are met.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 1474,
    "Name": "Reverse pupil block during phaco",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring a phaco-emulsification procedure a patient develops \u201Creverse pupil block\u201D. Which of the following manoeuvres is MOST likely to be effective at preventing excessive depth of the anterior chamber?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Using a second instrument to lift the iris forward.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u201CReverse pupil block\u201D during phaco is essentially the iris being \u003Cstrong\u003Epushed posteriorly\u003C/strong\u003E because fluid/pressure in the anterior chamber cannot readily equilibrate across the pupil into the posterior chamber, producing a \u003Cstrong\u003Every deep anterior chamber\u003C/strong\u003E with a \u003Cstrong\u003Eback-bowed iris\u003C/strong\u003E and a tendency toward iris\u2013lens diaphragm retropulsion; therefore, the most effective immediate manoeuvre is to \u003Cstrong\u003Ebreak the block mechanically\u003C/strong\u003E by \u003Cstrong\u003Elifting the iris forward at the pupillary margin\u003C/strong\u003E, allowing pressure equalisation and rapid shallowing to a safer, more stable chamber.\u003C/p\u003E\u003Cp\u003EIntravenous mannitol is least relevant because it reduces vitreous volume and posterior segment pressure over time rather than correcting an acute intraoperative iris\u2013pupil pressure differential that is being maintained by the fluidics of the surgery.\u003C/p\u003E\u003Cp\u003EReducing the bottle height can lessen infusion pressure and may reduce the degree of deepening, but it does not directly relieve the fundamental \u201Cvalve\u201D effect at the pupil and is therefore less reliably effective as a single manoeuvre when the syndrome is established.\u0026nbsp;\u003C/p\u003E\u003Cp\u003EA surgical iridotomy can prevent or treat certain pupil block mechanisms in other settings, but in the acute phaco setting it is not the most practical or immediate solution compared with simply lifting the iris to equalise pressures and restore normal iris configuration.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
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  },
  {
    "Id": 1475,
    "Name": "Intracameral agents",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIntracameral use of which of the following is MOST likely to result in ocular toxicity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Gentamicin.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EIntracameral gentamicin is the most likely to cause ocular toxicity because \u003Cstrong\u003Eaminoglycosides are well recognized to be directly toxic to intraocular tissues\u003C/strong\u003E, particularly the \u003Cstrong\u003Ecorneal endothelium\u003C/strong\u003E and, if they reach the posterior segment, the \u003Cstrong\u003Eretina\u003C/strong\u003E, with reported severe complications after intraocular exposure.\u0026nbsp;\u003C/p\u003E\u003Cp\u003EIn contrast, ceftazidime is widely used intraocularly in endophthalmitis treatment with a comparatively safer ocular toxicity profile at appropriate doses, triamcinolone is commonly used intraocularly as an anti-inflammatory and to visualize vitreous with its main risks being \u003Cstrong\u003Esteroid-related pressure rise\u003C/strong\u003E and cataract rather than acute direct tissue toxicity, and trypan blue is routinely used for capsular staining in cataract surgery and is generally well tolerated when used at correct concentration and exposure time. \u003Cstrong\u003ETherefore, gentamicin is the option most associated with clinically significant ocular toxicity when placed intracamerally.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
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  },
  {
    "Id": 1476,
    "Name": "Aspirin and diabetic retinopathy progression",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich ONE of the following trials showed that aspirin has no clinically important effects on the progression of diabetic retinopathy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Early Treatment Diabetic Retinopathy Study (ETDRS).\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe key evidence comes from the \u003Cstrong\u003EEarly Treatment Diabetic Retinopathy Study\u003C/strong\u003E, in which \u003Cstrong\u003E3,711 patients\u003C/strong\u003E with mild-to-severe non\u2011proliferative or early proliferative diabetic retinopathy were randomized to \u003Cstrong\u003Easpirin 650 mg daily versus placebo\u003C/strong\u003E, and the study concluded that \u003Cstrong\u003Easpirin did not alter the course of diabetic retinopathy\u003C/strong\u003E, did \u003Cstrong\u003Enot prevent progression to high\u2011risk proliferative disease\u003C/strong\u003E, did \u003Cstrong\u003Enot reduce visual loss\u003C/strong\u003E, and did \u003Cstrong\u003Enot increase vitreous haemorrhage\u003C/strong\u003E, leading to the explicit conclusion that aspirin has \u003Cstrong\u003Eno clinically important beneficial (or harmful) effect\u003C/strong\u003E on retinopathy progression.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;By contrast, the \u003Cstrong\u003EDiabetes Control and Complications Trial\u003C/strong\u003E was fundamentally a trial of \u003Cstrong\u003Eintensive glycaemic control\u003C/strong\u003E in type 1 diabetes aimed at testing whether near\u2011normal glucose reduces microvascular complications rather than a trial designed to answer the aspirin question.\u003C/p\u003E\u003Cp\u003EThe \u003Cstrong\u003EUnited Kingdom Prospective Diabetes Study\u003C/strong\u003E addressed type 2 diabetes outcomes with \u003Cstrong\u003Eglycaemic and blood pressure control strategies\u003C/strong\u003E, not aspirin as the primary intervention for retinopathy progression.\u003C/p\u003E\u003Cp\u003EThe \u003Cstrong\u003EDAMAD\u003C/strong\u003E study did investigate antiplatelet therapy in early diabetic retinopathy and reported small changes in microaneurysm evolution, but its findings were not framed as the definitive \u201Cno clinically important effect\u201D conclusion that is classically attributed to the ETDRS aspirin component.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 4,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1477,
    "Name": "Progressive central reading difficulty in a young adult",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 25 year old man with no family history of eye disease presents with slowly progressive difficulties reading fine print. His fundal appearance and fluorescein angiograms are shown in the photographs. What is the MOST likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-12-4a8e2d3f-1a51-4f4a-b4aa-4319b5070251.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Stargardt disease.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA young adult with \u003Cstrong\u003Eslowly progressive loss of central reading ability\u003C/strong\u003E together with the typical appearance of \u003Cstrong\u003Eyellow-white macular/posterior pole flecks and silent choroid\u003C/strong\u003E\u0026nbsp;on colour imaging and a fluorescein angiogram pattern that is classically used to support this diagnosis is most consistent with Stargardt disease, which is the commonest inherited juvenile-onset macular dystrophy and often presents exactly with gradually worsening central vision and difficulty with fine print. This is much less consistent with acute multifocal placoid pigment epitheliopathy, which is an \u003Cstrong\u003Eacute inflammatory chorioretinopathy\u003C/strong\u003E presenting with \u003Cstrong\u003Esudden\u003C/strong\u003E visual disturbance and multiple placoid creamy lesions rather than an insidious course. It is also less consistent with dominant drusen, which typically has an \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E pattern with a suggestive family history and drusen configuration rather than a \u201Cflecked retina\u201D dystrophy presentation in a 25-year-old with progressive reading difficulty. Pseudo\u2011vitelliform degeneration tends to show a more \u003Cstrong\u003Efovea-centred vitelliform (\u2018egg-yolk\u2019) lesion\u003C/strong\u003E pattern and a different angiographic signature related to vitelliform material, rather than a flecked maculopathy phenotype typical of Stargardt disease.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
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  },
  {
    "Id": 1478,
    "Name": "Frisby stereotest",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ERegarding the test of visual function shown, which of the following statements is MOST likely to be correct?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-12-be3debd3-8fbe-4d20-8772-40a669b2b6a9.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: It can be affected by parallax cues.\u003C/span\u003E\u003C/h3\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\n\u003Cp\u003EThe device shown is a \u003Cstrong\u003EFrisby (real-depth) stereotest\u003C/strong\u003E, which presents stereoscopic disparity using \u003Cstrong\u003Ephysical separation of targets on different surfaces\u003C/strong\u003E and does \u003Cstrong\u003Enot\u003C/strong\u003E rely on polarizing spectacles; a key practical limitation is that if the plate or the patient\u2019s head is allowed to move, the target can become detectable through \u003Cstrong\u003Emotion parallax\u003C/strong\u003E, meaning the result can be contaminated by parallax cues rather than true binocular stereopsis.  This is why the statement about susceptibility to parallax is the most defensible. In contrast, the claim that it requires orthogonal polarizing lenses describes vectograph-based stereotests rather than Frisby, and the claim about testing only a small range is not a defining feature of this test compared with its well-known issue of monocular cue contamination if administered incorrectly.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1479,
    "Name": "PERG \u002B full-field VEP",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EUsing this investigation, what is the\u0026nbsp;\u003Cstrong\u003Emost likely clinical scenario\u003C/strong\u003E.\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-12-59913867-d2d8-4d4b-9103-a5b5cfee6cb7.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: A 30 year old female with acute left vision loss to 6/36 and a relative afferent pupillary defect (RAPD).\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003Ethis is a picture of\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Epattern ERG (PERG) and\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Efull-field VEP.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe VEP is abnormal because the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Emajor positive peak is delayed (prolonged peak time/latency)\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E and the response appears \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ereduced and temporally dispersed\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E compared with what is expected for a normal VEP and\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe PERG is abnormal because the N95 component is reduced, giving a reduced N95 amplitude (and therefore a reduced N95:P50 relationship).\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe key step is to interpret the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EVEP first\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E: a full-field VEP abnormality localises dysfunction \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Esomewhere along the retino\u2011cortical pathway\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, but crucially \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ea delayed or abnormal VEP is not specific for optic nerve disease because macular dysfunction can also produce VEP delay\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, so the VEP alone cannot tell you whether the problem is retinal (macular) or post\u2011retinal (optic nerve/visual pathway).  That is exactly why the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EPERG is paired\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E with the VEP: PERG provides an objective measure of \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Emacular/retinal ganglion cell\u2013related function\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, helping you decide whether the VEP abnormality is driven primarily by retinal (macular) dysfunction or by post\u2011retinal conduction abnormalities.\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EOnce you use that logic, the most coherent clinical scenario is an \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eacute optic neuropathy\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E picture: an \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003ERAPD\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E is a strong clinical sign of asymmetric afferent pathway dysfunction and is typical of optic neuritis/optic neuropathy, whereas a simple refractive change does not produce an RAPD.  The refractive scenario is therefore unlikely because a VEP abnormality driven by optics would not match the physiology and the acuity improving with a small plus lens points to refractive/latent hyperopia rather than a primary afferent defect. The elderly subretinal neovascular membrane option is less likely because a CNV-driven maculopathy would be expected to show a primary macular functional deficit that can account for VEP changes, whereas the overall logic of using PERG alongside VEP is to demonstrate that the VEP abnormality is \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Enot\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E simply macular in origin.  A retained ferrous intraocular foreign body with siderosis is less likely because it classically causes progressive retinal toxicity detectable on retinal electrophysiology rather than a presentation anchored by an acute afferent defect with RAPD.\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
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  },
  {
    "Id": 1480,
    "Name": "Abnormal head posture in right superior oblique palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat abnormal head position (AHP) would you expect to see in the presence of a RIGHT superior oblique palsy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Left head tilt, left face turn.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA right superior oblique palsy typically produces a \u003Cstrong\u003Eright hypertropia that worsens on right head tilt\u003C/strong\u003E because the weak superior oblique cannot generate normal \u003Cstrong\u003Eintorsion\u003C/strong\u003E during ipsilateral head tilt, so the vertical deviation increases; the compensatory posture is therefore a \u003Cstrong\u003Ehead tilt to the opposite side\u003C/strong\u003E to minimise the hypertropia and torsional diplopia. In addition, the vertical deviation is usually least in the gaze position where the affected eye is relatively \u003Cstrong\u003Eabducted\u003C/strong\u003E, so the patient adopts a \u003Cstrong\u003Eface turn that places the eyes into that more comfortable gaze\u003C/strong\u003E, which in a right superior oblique palsy is most commonly achieved by a \u003Cstrong\u003Eleft face turn\u003C/strong\u003E (placing the eyes into right gaze). Taken together, the classic compensatory AHP is \u003Cstrong\u003Eleft head tilt with left face turn\u003C/strong\u003E, whereas postures involving right head tilt would tend to exacerbate the deviation and are therefore less likely.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1481,
    "Name": "Pharmacological localization of Horner syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 52 year old patient presents with a 2mm left ptosis and ipsilateral miosed pupil. An apraclonidine test is positive and the pupil dilates by 2mm with 1% phenylephrine to which the contralateral pupil is unresponsive. Of these diagnoses, which is the MOST likely?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Carotid artery dissection.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003EA \u003Cstrong\u003Epositive apraclonidine test\u003C/strong\u003E supports Horner syndrome because \u003Cstrong\u003Edenervation hypersensitivity\u003C/strong\u003E allows apraclonidine\u2019s weak alpha\u20111 activity to \u003Cstrong\u003Edilate the affected miotic pupil and partially elevate the ptosis\u003C/strong\u003E, but this step \u003Cstrong\u003Econfirms Horner rather than localising the lesion\u003C/strong\u003E.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003EThe crucial localising clue is that the affected pupil \u003Cstrong\u003Edilates markedly with dilute phenylephrine (1%) while the normal pupil does not\u003C/strong\u003E, which indicates \u003Cstrong\u003Epostganglionic (third\u2011order) sympathetic denervation\u003C/strong\u003E because the iris dilator has become \u003Cstrong\u003Esupersensitive to adrenergic agonists\u003C/strong\u003E. \u003Cstrong\u003EPostganglionic Horner syndrome classically arises from internal carotid artery pathology\u003C/strong\u003E because the oculosympathetic fibres travel with the \u003Cstrong\u003Einternal carotid artery\u003C/strong\u003E into the cavernous sinus and orbit, making \u003Cstrong\u003Ecarotid artery dissection\u003C/strong\u003E the most likely diagnosis here.\u0026nbsp;\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003EBy contrast, an \u003Cstrong\u003Eapical lung tumour\u003C/strong\u003E and a \u003Cstrong\u003Ecervical rib\u003C/strong\u003E most typically affect the \u003Cstrong\u003Epreganglionic (second\u2011order) fibres\u003C/strong\u003E at the thoracic outlet, and an \u003Cstrong\u003EArnold\u2013Chiari malformation\u003C/strong\u003E would be expected to cause a \u003Cstrong\u003Ecentral (first\u2011order) Horner syndrome\u003C/strong\u003E, so these do not match the \u003Cstrong\u003Epostganglionic hypersensitivity pattern\u003C/strong\u003E implied by the phenylephrine response.\u003C/div\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-size: 14px; font-style: normal; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1482,
    "Name": "Child with bull\u2019s-eye maculopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA seven year old boy is referred with reduced visual acuity by his optometrist. His teachers have also noted that he is falling behind at school. His visual acuity is 6/36 in each eye. Fundoscopy shows a bilateral bull\u2019s eye maculopathy. An electroretinogram (ERG) shows a reduced b-wave and electro-oculography (EOG) is normal. Which one of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: large;\u0022\u003EAnswer: Juvenile neuronal ceroid lipofuscinosis (Batten\u2019s disease).\u003C/span\u003E\u003C/h3\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: large;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\n\u003Cp\u003EThe combination of \u003Cstrong\u003Eearly school-age bilateral visual loss\u003C/strong\u003E, a \u003Cstrong\u003Ebull\u2019s-eye maculopathy\u003C/strong\u003E, and evidence of \u003Cstrong\u003Einner retinal dysfunction on ERG\u003C/strong\u003E (classically an \u201Celectronegative\u201D pattern with a relatively reduced b-wave) strongly points to juvenile neuronal ceroid lipofuscinosis, and the fact that he is \u201Cfalling behind at school\u201D supports the expected \u003Cstrong\u003Eneurocognitive decline\u003C/strong\u003E that accompanies this disorder.  A \u003Cstrong\u003Enormal EOG\u003C/strong\u003E argues against a primary retinal pigment epithelium pump disorder as the dominant problem and is compatible with the retinal degeneration pattern described in CLN3-associated disease.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;Fabry disease would more typically be associated with corneal verticillata and vascular changes rather than a bull\u2019s-eye maculopathy with this electrophysiology pattern and early cognitive decline.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EHomocystinuria more classically causes ectopia lentis and high myopia with systemic thrombotic risk rather than this retinal dystrophy phenotype.\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;Zellweger syndrome is a severe peroxisomal disorder presenting in infancy with profound systemic features, making it very unlikely in a 7-year-old presenting primarily with school-age retinal degeneration.\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1483,
    "Name": "Myopic young woman with photopsias and posterior pole spots",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 35\u2011year\u2011old myopic woman presents with intermittent brief flashes of light in the central field of the left eye for three months (about once a week). Corrected VA is 6/9 with contact lenses; colour vision and visual fields are normal. Fundus shows multiple depigmented spots. Which is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EPunctate inner choroidopathy.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EPunctate inner choroidopathy (PIC)\u003C/strong\u003E best fits because it classically affects \u003Cstrong\u003Eyoung myopic women\u003C/strong\u003E, presents with \u003Cstrong\u003Ephotopsias\u003C/strong\u003E and \u003Cstrong\u003Esmall yellow\u2011white depigmented lesions at the posterior pole\u003C/strong\u003E, and early on may show \u003Cstrong\u003Enear\u2011normal acuity, color vision, and fields\u003C/strong\u003E. The lesions are inflammatory at the level of the choroid/outer retina and carry a risk of later \u003Cstrong\u003Echoroidal neovascularisation\u003C/strong\u003E, but the initial exam can otherwise be unremarkable\u2014exactly as described.\u003C/p\u003E\u003Cp\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EBig blind spot syndrome:\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E would give an \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eenlarged blind spot on perimetry\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E and often MEWDS\u2011like signs; the stem states \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Enormal visual fields\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, making this unlikely.\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EOptic neuritis:\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E typically causes \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Epain on eye movements, reduced color vision (red desaturation), RAPD, and central visual loss\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E rather than photopsias with discrete chorioretinal spots; here \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ecolor vision and fields are normal\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\u003Cp\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EStargardt disease:\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E a \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Emacular dystrophy\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E with \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Episciform flecks\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E and progressive central loss, usually beginning in the teens/early adulthood; \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ebrief intermittent photopsias\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E with otherwise normal colour vision/fields are not typical, and the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Efundus description (depigmented punctate spots)\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E is not characteristic.\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1484,
    "Name": "Diabetic foot infection with shock features",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 45\u2011year\u2011old man with type 2 diabetes mellitus has developed an infected left foot ulcer after minor trauma. He attends the eye clinic with loss of appetite, nausea and vomiting, polyuria and weight loss. On examination he is hypotensive with a tachycardia, cold extremities and peripheral cyanosis. Which of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ESepticaemia.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe presence of an \u003Cstrong\u003Eobvious infectious source (infected diabetic foot ulcer)\u003C/strong\u003E together with \u003Cstrong\u003Esystemic features of circulatory compromise\u2014hypotension, tachycardia, cold extremities and peripheral cyanosis\u2014most strongly indicates septicaemia (sepsis with shock)\u003C/strong\u003E as the unifying diagnosis.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;While \u003Cstrong\u003Ehyperglycaemia\u003C/strong\u003E can explain polyuria and weight loss, it \u003Cstrong\u003Edoes not cause cold, cyanotic peripheries with hypotension\u003C/strong\u003E, which are hallmarks of shock.\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;\u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EDiabetic ketoacidosis\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E may complicate infection in type 2 diabetes, but the stem does not give typical pointers such as \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EKussmaul respirations, fruity breath, marked dehydration with warm peripheries, or documented severe acidosis/ketonaemia\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E; instead, it emphasises \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ehaemodynamic instability from infection\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E. \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EHyponatraemia\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E might cause nausea or malaise, yet \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ecannot account for the profound shock physiology\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E described. In short, \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Einfected diabetic foot \u002B shock signs = septicaemia/septic shock\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E as the most likely\u2014and most urgent\u2014diagnosis.\u0026nbsp;\u003C/span\u003E\u003C/p\u003E\u003Cp\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1485,
    "Name": "Acute corneal hydrops in keratoconus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA twenty five year old patient who had previously refused treatment with collagen cross linking presents with an acutely painful left eye. The cornea is oedematous inferiorly although the upper part is clear. Which of the following treatment options is LEAST likely to play a role in treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EDescemet stripping endothelial keratoplasty.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Eacute corneal hydrops in keratoconus\u003C/strong\u003E, where a \u003Cstrong\u003Ebreak in Descemet membrane\u003C/strong\u003E\u0026nbsp;producing \u003Cstrong\u003Esectoral corneal oedema\u003C/strong\u003E and significant pain, often inferiorly. In that setting, measures that \u003Cstrong\u003Ereduce stromal oedema and promote reattachment/sealing of the Descemet break\u003C/strong\u003E can be helpful, so \u003Cstrong\u003Ehypertonic sodium chloride 5%\u003C/strong\u003E may reduce epithelial/stromal oedema symptomatically, and \u003Cstrong\u003Eanterior chamber gas (such as SF6)\u003C/strong\u003E can act as an internal tamponade to \u003Cstrong\u003Eoppose Descemet membrane and shorten the course of hydrops\u003C/strong\u003E in selected cases. If significant scarring, irregularity, or optical failure persists after resolution, \u003Cstrong\u003Epenetrating keratoplasty\u003C/strong\u003E can have a role as a definitive tectonic/optical rehabilitation option in advanced keratoconus.\u003C/p\u003E\u003Cp\u003EIn contrast, \u003Cstrong\u003EDescemet stripping endothelial keratoplasty is designed for primary endothelial failure\u003C/strong\u003E, and it is \u003Cstrong\u003Eleast relevant in acute hydrops\u003C/strong\u003E, because the fundamental problem is \u003Cstrong\u003Ea mechanical Descemet rupture in an ectatic cornea\u003C/strong\u003E, not isolated endothelial pump failure, so replacing endothelium alone would not address the underlying ectasia or the tear mechanism.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1486,
    "Name": "Hemifacial spasm",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of these is the MOST likely location of an aneurysm causing hemifacial spasm?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EAnterior inferior cerebellar artery\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EHemifacial spasm is most commonly caused by \u003Cstrong\u003Eneurovascular compression of the facial nerve at its root exit zone\u003C/strong\u003E in the cerebellopontine angle, and the arteries most often implicated are branches of the vertebrobasilar system rather than anterior circulation vessels. In large series and reference summaries, the \u003Cstrong\u003Eanterior inferior cerebellar artery is the commonest offending vessel\u003C/strong\u003E, followed by the \u003Cstrong\u003Eposterior inferior cerebellar artery\u003C/strong\u003E and then the vertebral artery, which is why an aneurysm arising from the anterior inferior cerebellar artery is the most likely to produce hemifacial spasm by compressing the facial nerve in this region. \u003Cstrong\u003ESupraclinoid carotid\u003C/strong\u003E and \u003Cstrong\u003Ebasilar tip\u003C/strong\u003E aneurysms are anatomically remote from the facial nerve root exit zone and are therefore much less likely to present with hemifacial spasm as the primary mechanism.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1487,
    "Name": "Proliferative vitreoretinopathy ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the MOST likely effect of proliferative vitreoretinopathy on a retinal break?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EEverting of the edge of the retinal break.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EIn PVR, \u003Cstrong\u003Ecellular proliferation on the retinal surfaces forms contractile epi\u2011 and subretinal membranes\u003C/strong\u003E that exert tangential traction on the retina; \u003Cstrong\u003Ethis traction \u201Crolls\u201D or everts the margins of a pre\u2011existing retinal break (fish\u2011mouth configuration)\u003C/strong\u003E, making it wider and more rigid and hampering successful re\u2011apposition with retinopexy and tamponade. \u003Cstrong\u003EBy contrast, operculation\u003C/strong\u003E\u0026nbsp;is an \u003Cstrong\u003Eacute vitreoretinal traction event\u003C/strong\u003E in which a plug of retina is avulsed and \u201Coperculated,\u201D typically \u003Cstrong\u003Ebefore\u003C/strong\u003E PVR develops; it is \u003Cstrong\u003Enot\u003C/strong\u003E a consequence of PVR scarring. \u003Cstrong\u003EA retinal pigmentary demarcation line\u003C/strong\u003E\u0026nbsp;indicates \u003Cstrong\u003Echronic rhegmatogenous retinal detachment\u003C/strong\u003E (the \u201Chigh\u2011water mark\u201D), \u003Cstrong\u003Enot\u003C/strong\u003E the contractile changes of PVR. \u003Cstrong\u003ETortuosity of surrounding vessels\u003C/strong\u003E\u0026nbsp;is \u003Cstrong\u003Enonspecific\u003C/strong\u003E and not the characteristic mechanical effect that PVR has on a break.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1488,
    "Name": "Immunosuppressive \u201Cdisease\u2011modifying\u201D drugs",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following disease modifying drugs is best described as an anti\u2011metabolite?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EMycophenolate mofetil.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EMycophenolate mofetil is best described as an \u003Cstrong\u003Eantimetabolite\u003C/strong\u003E because it inhibits \u003Cstrong\u003Einosine monophosphate dehydrogenase\u003C/strong\u003E, thereby blocking \u003Cstrong\u003Ede novo guanine nucleotide synthesis\u003C/strong\u003E and preferentially suppressing \u003Cstrong\u003ET\u2011 and B\u2011lymphocyte proliferation\u003C/strong\u003E, which rely heavily on this pathway. In contrast, ciclosporin and tacrolimus are \u003Cstrong\u003Ecalcineurin inhibitors\u003C/strong\u003E that reduce T\u2011cell activation by inhibiting calcineurin\u2011dependent transcription of cytokines such as IL\u20112, so they are not antimetabolites. Cyclophosphamide is an \u003Cstrong\u003Ealkylating agent\u003C/strong\u003E that crosslinks DNA and suppresses rapidly dividing immune cells, but it is mechanistically distinct from antimetabolites, which act by interfering with nucleotide synthesis pathways.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1489,
    "Name": "Scintillating scotoma in a young adult",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 22 year old man referred by an optometrist describes a transient visual disturbance where a blank area develops near fixation blocking out print when reading. It gradually enlarges and moves out to the edge of his field of vision and seems to have shimmering silvery edges. It gradually fades over 15 to 20 minutes and his vision returns to normal. He has had two or three similar episodes in the last six months. What is the MOST appropriate management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EReassurance\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis history is most characteristic of a \u003Cstrong\u003Emigraine visual aura (scintillating scotoma/fortification-type phenomenon)\u003C/strong\u003E: a \u003Cstrong\u003Epositive visual symptom\u003C/strong\u003E with \u003Cstrong\u003Eshimmering edges\u003C/strong\u003E that \u003Cstrong\u003Egradually expands and marches across the visual field\u003C/strong\u003E, then \u003Cstrong\u003Eresolves completely over 15\u201320 minutes\u003C/strong\u003E, and recurs in stereotyped fashion in a young person with otherwise normal vision between attacks. That time course and \u201Cmoving, shimmering\u201D quality strongly favours aura rather than an ischaemic event, because transient ischaemic attacks and amaurosis fugax are more often described as \u003Cstrong\u003Esudden-onset negative loss\u003C/strong\u003E (a curtain/grey-out), typically without scintillation, and the management would then pivot toward vascular risk evaluation, which is not the best fit here. Carotid ultrasound and low-dose aspirin are therefore not the most appropriate first steps for a classic migrainous aura pattern in a 22-year-old with no red-flag neurological features given. MRI brain imaging is generally reserved for \u003Cstrong\u003Eatypical\u003C/strong\u003E presentations such as persistent deficit, first-ever severe/new neurological symptoms, abnormal neurological examination, or unusual features suggesting an alternative diagnosis; in a typical recurrent visual aura with complete recovery and a classic spreading pattern, \u003Cstrong\u003Ereassurance and migraine-style counselling\u003C/strong\u003E is the most appropriate management.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1490,
    "Name": "Acute recurrent alternating anterior uveitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich one of the following is MOST commonly associated with acute bilateral, recurrent, alternating anterior uveitis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EHLA-B27 positivity\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Ch3\u003E\u003Cbr\u003E\u003C/h3\u003E\n\u003Cp\u003EAcute recurrent alternating anterior uveitis is most classically the pattern seen with HLA-B27\u2013associated acute anterior uveitis, which typically presents with sudden onset pain, photophobia, marked anterior chamber activity, a tendency to recur, and a characteristic behavior of affecting one eye at a time but alternating between eyes across episodes; it can appear bilateral over time because successive attacks occur in either eye rather than through simultaneous bilateral inflammation. Anterior segment ischaemia is usually a postoperative or vascular-compromise phenomenon linked to surgery on multiple rectus muscles or severe carotid/ocular ischemia and does not produce a stereotyped recurrent alternating acute uveitis pattern. Glaucomatocyclitic crisis is characterized by mild anterior uveitis with disproportionately raised intraocular pressure and recurrent unilateral attacks rather than alternating bilateral episodes. Sarcoidosis more commonly causes a chronic, granulomatous anterior uveitis with mutton-fat keratic precipitates, iris nodules, and a more persistent course, often with posterior segment involvement, rather than the classic acute recurrent alternating phenotype.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1491,
    "Name": "SRK/T A\u2011constant change",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient presents for cataract surgery. Biometry has been performed using the SRK T formula for a lens with an A constant of 118.5 and suggests a 22.0 Dioptre lens to achieve a desired post-operative refraction of emmetropia. The lens you wish to use has an A constant of 118.0. What power intraocular lens would be the MOST likely to achieve the desired post-operative refraction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003E21.5 D\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe key is what the \u003Cstrong\u003EA\u2011constant represents\u003C/strong\u003E: it is a lens-specific calibration term that primarily shifts the predicted \u003Cstrong\u003Eeffective lens position\u003C/strong\u003E, and changing it changes the IOL power needed to hit the same refractive target. A \u003Cstrong\u003Elower A\u2011constant\u003C/strong\u003E (118.0 instead of 118.5) corresponds to a prediction of a \u003Cstrong\u003Emore anterior effective lens position\u003C/strong\u003E, and for the same IOL power a more anterior lens position tends to produce a \u003Cstrong\u003Emore myopic outcome\u003C/strong\u003E, so to keep the target at \u003Cstrong\u003Eemmetropia\u003C/strong\u003E you typically choose a \u003Cstrong\u003Eslightly lower IOL power\u003C/strong\u003E. In practical exam terms, you adjust the IOL power by roughly the \u003Cstrong\u003Esame magnitude and direction\u003C/strong\u003E as the A\u2011constant change, so dropping the A\u2011constant by \u003Cstrong\u003E0.5\u003C/strong\u003E means dropping the IOL power by about \u003Cstrong\u003E0.5 D\u003C/strong\u003E, taking you from \u003Cstrong\u003E22.0 D to 21.5 D\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1492,
    "Name": "Diabetic retinopathy screening",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to Diabetic Retinopathy Screening, which of these statements is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EThere is a recognisable latent or pre-symptomatic stage of the disease.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EDiabetic retinopathy is a classic example of a condition with a \u003Cstrong\u003Elong recognisable pre-symptomatic phase\u003C/strong\u003E, because patients can develop detectable microvascular retinal changes for years before they notice symptoms, and this is precisely what makes population screening clinically valuable. The statement that most screened patients require treatment is incorrect because screening programmes primarily identify many individuals with no retinopathy or mild non-proliferative changes who do not need immediate intervention, with only a minority meeting thresholds for laser or intravitreal therapy at any one screening round. The claim that there is little published evidence of cost-effectiveness is also unlikely to be correct, as diabetic retinopathy screening is widely regarded as one of the more established and economically justified screening programmes due to prevention of avoidable sight loss and downstream costs. Finally, the statement about a WHO definition in 1978 is less likely to be the best answer because the classic public health framework for screening principles is usually attributed to earlier WHO-linked work on screening criteria rather than being uniquely anchored to that specific year, making it a weaker \u201Cmost likely\u201D statement compared with the clearly true point about a latent pre-symptomatic stage.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1493,
    "Name": "Vertical diplopia with enophthalmos and restricted vertical movements",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60 year old woman with vertical diplopia has a left hypertropia and reduced vertical movements of the left eye. She also has left enophthalmos. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EOrbital metastasis\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe key discriminator here is the combination of vertical diplopia with a hypertropia plus genuinely reduced vertical movements of the same eye and ipsilateral enophthalmos, which points to a restrictive orbital process rather than an isolated cranial nerve palsy. Orbital metastases can infiltrate extraocular muscles and orbital fat, producing mechanical restriction of elevation and/or depression, and some metastases\u2014classically scirrhous-type infiltration such as from breast carcinoma\u2014can cause fibrosis and volume contraction leading to enophthalmos rather than proptosis, making this the best overall fit.\u0026nbsp;\u003C/p\u003E\u003Cp\u003EA fourth nerve palsy typically causes a hypertropia with pattern-dependent incomitance and compensatory head tilt, but it does not usually produce true mechanical restriction on ductions or enophthalmos. A partially recovered third nerve palsy would more often be associated with a history of trauma and additional features such as ptosis, anisocoria, or a larger horizontal deviation, and enophthalmos is not characteristic. Thyroid eye disease most commonly causes proptosis and restrictive myopathy (often affecting elevation), so the restriction could fit, but the presence of enophthalmos makes thyroid eye disease much less likely than an infiltrative metastatic process.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1494,
    "Name": "Uveitis\u2013Glaucoma\u2013Hyphaema (UGH) syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to Uveitis Glaucoma Hyphaema (UGH) syndrome, which of the following statements is MOST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EUGH syndrome can occur with posterior chamber intraocular lenses.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EUGH syndrome is a \u003Cstrong\u003Emechanical complication\u003C/strong\u003E caused by \u003Cstrong\u003Echafing of intraocular lens components against the iris/ciliary body or angle\u003C/strong\u003E, leading to \u003Cstrong\u003Erecurrent anterior uveitis, intermittent hyphaema (or microhyphaema), and secondary IOP spikes/glaucoma\u003C/strong\u003E, so it is \u003Cstrong\u003Enot confined to anterior chamber lenses\u003C/strong\u003E and can occur with \u003Cstrong\u003Eposterior chamber IOLs\u003C/strong\u003E when they are malpositioned, placed in the sulcus with poor fit, tilted/decentred, or when haptics or optic edge rub the uveal tissues.\u003C/p\u003E\u003Cp\u003EThe other statements are less likely because the syndrome is often \u003Cstrong\u003Esymptomatic\u003C/strong\u003E with episodes of blurred vision, pain, photophobia, and red eye rather than being an incidental finding, and it is not predominantly driven by autoimmune predisposition but by \u003Cstrong\u003Erepetitive mechanical trauma\u003C/strong\u003E. The comparison with amaurosis fugax is also unreliable as a defining discriminator, because transient vision loss duration varies widely by cause, whereas UGH is best understood and identified by its \u003Cstrong\u003Erecurrent triad and mechanical IOL\u2013uveal irritation mechanism\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1495,
    "Name": "Opsoclonus\u2013myoclonus syndrome in infancy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 14 month old child presents with ataxia and \u201Cchaotic\u201D eye movements. What is the MOST likely underlying diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EOccult neuroblastoma.\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u201CChaotic\u201D multidirectional, high\u2011frequency saccadic eye movements in an infant strongly suggests \u003Cstrong\u003Eopsoclonus\u003C/strong\u003E, and when this is paired with \u003Cstrong\u003Eataxia\u003C/strong\u003E (often with myoclonus and irritability), the classic clinical constellation is \u003Cstrong\u003Eopsoclonus\u2013myoclonus syndrome\u003C/strong\u003E. In children, this syndrome is most commonly a \u003Cstrong\u003Eparaneoplastic autoimmune phenomenon\u003C/strong\u003E associated with \u003Cstrong\u003Eneuroblastoma\u003C/strong\u003E, which may be clinically occult at presentation, so the most appropriate underlying diagnosis among the options is occult neuroblastoma. The other choices are less likely because Aicardi syndrome is a congenital neurodevelopmental disorder classically associated with agenesis of the corpus callosum and chorioretinal lacunae rather than opsoclonus, Miller Fisher syndrome is typically an acute post\u2011infectious neuropathy with ophthalmoplegia, ataxia and areflexia rather than chaotic saccadic eye movements, and Wilms\u2019 tumour is not the characteristic neoplasm linked to opsoclonus\u2013myoclonus.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1496,
    "Name": "Gas-filled (post\u2011vitrectomy) eye",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following types of cataract is MOST likely to form in a gas filled (post\u2011vitrectomy) eye?\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EPosterior sub\u2011capsular\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA gas-filled post\u2011vitrectomy eye most characteristically develops a \u003Cstrong\u003Eposterior sub\u2011capsular cataract\u003C/strong\u003E because intraocular gas can promote \u003Cstrong\u003Eposterior lens changes\u003C/strong\u003E through \u003Cstrong\u003Ealtered lens metabolism and local dehydration/toxic effects at the posterior lens surface\u003C/strong\u003E, particularly when the gas bubble apposes the posterior lens region during postoperative positioning, leading to a \u003Cstrong\u003Erapidly symptomatic central posterior opacity\u003C/strong\u003E. \u003Cstrong\u003ENuclear sclerosis\u003C/strong\u003E is very common after vitrectomy in general due to increased intraocular oxygen exposure to the lens over time, but the question specifically highlights a \u003Cstrong\u003Egas-filled\u003C/strong\u003E eye, which classically points to \u003Cstrong\u003Eposterior sub\u2011capsular opacification\u003C/strong\u003E as the most likely pattern in that context. \u003Cstrong\u003EPosterior polar\u003C/strong\u003E cataract is a congenital/structural posterior capsular abnormality rather than an acquired post\u2011vitrectomy change, and \u003Cstrong\u003Ecortical\u003C/strong\u003E cataract is less characteristic of gas-related postoperative lens change.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1497,
    "Name": "Exercise\u2011induced transient central dimming",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 30 year old woman reports dimming and greyness of central vision in her right eye each time she attends her aerobics class. Her optic disc is a little pale, but there are no other findings. What is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer: Uhthoff phenomenon.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E Transient dimming or \u201Cgreying out\u201D of vision precipitated reproducibly by exercise is classic for Uhthoff phenomenon, in which a rise in core body temperature temporarily worsens conduction in previously demyelinated optic nerve fibres, producing brief visual deterioration; the subtly pale optic disc supports prior optic nerve injury, commonly from previous optic neuritis. Basilar migraine would more typically cause transient binocular visual symptoms with other brainstem features and does not characteristically recur only with exertion in one eye, while a carotico\u2011ophthalmic artery aneurysm would be expected to cause compressive neuro\u2011ophthalmic signs such as progressive field loss or ocular motor deficits rather than a temperature\u2011dependent reversible symptom. Visual obscurations from raised intracranial pressure are classically brief \u201Cgrey-outs\u201D triggered by posture or Valsalva and are associated with papilloedema rather than optic disc pallor, so that option is less fitting here.\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u0026nbsp;\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1498,
    "Name": "Congo red staining in corneal dystrophies",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn which of the following conditions is positively stained with Congo red?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ELattice dystrophy type 1\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003ECongo red is a histochemical stain that highlights \u003Cstrong\u003Eamyloid deposition\u003C/strong\u003E (classically showing \u003Cstrong\u003Eapple\u2011green birefringence under polarized light\u003C/strong\u003E), and among the listed corneal dystrophies the one defined by \u003Cstrong\u003Estromal amyloid\u003C/strong\u003E is \u003Cstrong\u003Elattice dystrophy type 1\u003C/strong\u003E, so it is the condition that would be \u003Cstrong\u003ECongo red positive\u003C/strong\u003E. Granular dystrophy is primarily a \u003Cstrong\u003Ehyaline (non\u2011amyloid) stromal deposition\u003C/strong\u003E disorder, macular dystrophy is a \u003Cstrong\u003Emucopolysaccharide/glycosaminoglycan stromal deposition\u003C/strong\u003E disorder, and Schnyder dystrophy is characterized by \u003Cstrong\u003Echolesterol/lipid deposition\u003C/strong\u003E within the cornea, so none of these would be expected to stain positively with Congo red in the way lattice dystrophy does.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1499,
    "Name": "Suspected intraocular foreign body after high\u2011velocity injury",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 20 year old mechanic feels something hit his right eye, and presents with 6/12 visual acuity, subconjunctival and vitreous haemorrhage, and low IOP. What is the MOST appropriate investigation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ECT scan of the orbits\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis presentation is highly suspicious for a \u003Cstrong\u003Ehigh\u2011velocity metallic intraocular foreign body and/or an open\u2011globe injury\u003C/strong\u003E, because\u0026nbsp;\u003Cstrong\u003Esubconjunctival haemorrhage\u003C/strong\u003E, \u003Cstrong\u003Evitreous haemorrhage\u003C/strong\u003E, and especially \u003Cstrong\u003Elow intraocular pressure\u003C/strong\u003E strongly suggest \u003Cstrong\u003Eglobe penetration/rupture with uveal wound leak\u003C/strong\u003E rather than an isolated superficial injury. In that setting, the most appropriate investigation is a \u003Cstrong\u003Enon\u2011contrast CT orbit\u003C/strong\u003E, as it is the best first\u2011line imaging test to detect and localise an \u003Cstrong\u003EIOFB\u003C/strong\u003E (particularly metallic) and associated orbital injury, while \u003Cstrong\u003EMRI is contraindicated\u003C/strong\u003E if a metallic foreign body is possible due to the risk of movement/heating. \u003Cstrong\u003EOcular ultrasound\u003C/strong\u003E can be helpful for vitreoretinal assessment when the globe is intact, but with suspected open globe and low IOP it is \u003Cstrong\u003Erelatively contraindicated\u003C/strong\u003E because probe pressure may worsen extrusion; \u003Cstrong\u003EOCT of the optic nerve\u003C/strong\u003E is not relevant to the acute trauma question and will not address the key diagnostic priority of excluding an IOFB/open globe.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1500,
    "Name": "Recurrent submacular haemorrhage with ICG nodular hyperfluorescence",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 73 year old patient presents with recurrent acute sub-macular haemorrhage. Indocyanine Green Angiography (ICG) demonstrates sub-retinal nodular fluorescence appearing within five minutes and persisting to the late phase. What is the MOST appropriate treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EPhotodynamic therapy (PDT) or verteporfin treatment\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe ICG description of an early-appearing subretinal nodular hyperfluorescent lesion that persists into the late phases in an elderly patient with recurrent acute submacular haemorrhage is most typical of polypoidal choroidal vasculopathy, where ICG highlights the polypoidal aneurysmal dilatations and branching vascular network far better than fluorescein angiography.\u003C/p\u003E\u003Cp\u003EIn this setting, verteporfin photodynamic therapy is the most appropriate treatment because it directly targets and closes the polypoidal lesions responsible for recurrent bleeding, thereby reducing rebleeding risk and improving anatomical control, whereas observation risks further haemorrhagic episodes and irreversible macular damage. Focal thermal laser is generally avoided for macular/subfoveal lesions due to scarring and poor visual outcomes, and while intravitreal anti-VEGF can be helpful\u2014particularly for associated exudation or the branching vascular network\u2014it is less reliably effective at inducing complete polyp closure when used alone in the classic exam framing, making PDT the best single choice here.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1501,
    "Name": "Visual acuity assessment in a 10\u2011month\u2011old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich is MOST likely to be an appropriate test for visual acuity in a ten month old child?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EForced choice preferential looking (using a grating pattern).\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EIn a 10\u2011month\u2011old infant, the most appropriate visual acuity assessment is one that does not require naming, matching, or reliable symbol recognition, and forced\u2011choice preferential looking with grating targets is designed exactly for this developmental stage by exploiting an infant\u2019s natural preference to look at a patterned stimulus rather than a blank field, allowing estimation of acuity without language or formal cooperation. Cardiff cards can also be used in infants and are a reasonable alternative because they use a preferential looking principle with vanishing optotypes, but forced\u2011choice grating methods are generally the most directly suitable and widely used approach at this age. In contrast, crowded Kay pictures and the Sheridan\u2013Gardiner test depend on picture/letter recognition or matching and typically require an older, more cooperative child, making them less appropriate for a 10\u2011month\u2011old.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1502,
    "Name": "Orbital cellulitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is MOST likely to be the commonest cause of orbital cellulitis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EInfection of the sinuses\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EOrbital cellulitis most commonly arises by \u003Cstrong\u003Econtiguous spread from adjacent paranasal sinus infection\u003C/strong\u003E, particularly from the \u003Cstrong\u003Eethmoid sinuses\u003C/strong\u003E, because the \u003Cstrong\u003Elamina papyracea is thin\u003C/strong\u003E and valveless venous channels facilitate extension of infection into the orbit, making sinusitis the dominant aetiology in typical presentations. Dacryocystitis usually causes a more anterior, medial preseptal infection centred on the lacrimal sac and is less often the primary driver of true postseptal orbital cellulitis, while dental, otitic, and facial skin infections can certainly spread but are overall less frequent than sinus-derived disease. Orbital trauma with fracture or a retained foreign body is an important cause to consider\u2014especially in specific histories\u2014but it is not the commonest cause across the general population compared with sinus infection.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1503,
    "Name": "Corneal topography pattern",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the MOST likely diagnosis based upon this topography image?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-14-5befa56a-1639-4f15-a367-282307fa4c0a.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong style=\u0022\u0022\u003EPellucid marginal degeneration\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis topography is most characteristic of \u003Cstrong\u003Epellucid marginal degeneration\u003C/strong\u003E because it shows \u003Cstrong\u003Einferior peripheral corneal steepening\u003C/strong\u003E with a relatively \u003Cstrong\u003Eflatter central cornea\u003C/strong\u003E, producing the classic \u003Cstrong\u003E\u201Ccrab-claw/kissing-doves\u201D pattern\u003C/strong\u003E that reflects \u003Cstrong\u003Ehigh against-the-rule astigmatism\u003C/strong\u003E driven by a \u003Cstrong\u003Ethin band of inferior cornea\u003C/strong\u003E rather than a focal cone. In contrast, \u003Cstrong\u003Ekeratoconus\u003C/strong\u003E usually shows a more \u003Cstrong\u003Elocalized cone-like area of steepening\u003C/strong\u003E (often inferotemporal) with an \u003Cstrong\u003Easymmetric bow-tie and skewed axes\u003C/strong\u003E, rather than broad inferior peripheral \u201Cclaws.\u201D \u003Cstrong\u003EPost\u2013extracapsular cataract extraction astigmatism\u003C/strong\u003E is typically a \u003Cstrong\u003Emore regular, symmetric bow-tie\u003C/strong\u003E pattern consistent with surgically induced regular astigmatism, not the distinctive peripheral inferior steepening pattern seen here. \u003Cstrong\u003EPost-LASIK\u003C/strong\u003E topography most often demonstrates a \u003Cstrong\u003Ecentral flattening ablation zone\u003C/strong\u003E (often with a ring-like transition), rather than isolated \u003Cstrong\u003Einferior peripheral steepening\u003C/strong\u003E with central relative sparing.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1504,
    "Name": "Retinal arteriovenous anastomosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich one of the following retinal vascular abnormalities is MOST likely to represent an arteriovenous anastomosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ERacemose haemangioma\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA retinal \u003Cstrong\u003Earteriovenous anastomosis\u003C/strong\u003E implies a \u003Cstrong\u003Edirect artery-to-vein communication without an intervening capillary bed\u003C/strong\u003E, and the classic retinal lesion that represents this is a \u003Cstrong\u003Eracemose haemangioma\u003C/strong\u003E, which is essentially a congenital \u003Cstrong\u003Eretinal arteriovenous malformation\u003C/strong\u003E with markedly dilated, tortuous vessels that shunt blood directly from artery to vein. By contrast, a \u003Cstrong\u003Ecapillary haemangioma\u003C/strong\u003E and an \u003Cstrong\u003Eoptic nerve haemangioblastoma\u003C/strong\u003E are vascular tumours characterized by a \u003Cstrong\u003Ecapillary-rich network\u003C/strong\u003E (typically with prominent feeder and draining vessels) rather than a direct AV shunt, and a \u003Cstrong\u003Ecavernous haemangioma\u003C/strong\u003E is composed of \u003Cstrong\u003Ethin-walled saccular venous \u201Ccaverns\u201D\u003C/strong\u003E with sluggish flow rather than an arteriovenous connection.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1505,
    "Name": "Uveitis investigations",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPatients with uveitis are frequently investigated for underlying conditions. In the following scenarios which is MOST likely to have the greatest positive predictive value?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EANA in a child with uveitis and an inflamed knee\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EPositive predictive value rises when the test is applied in a setting with a high pre-test probability, and the scenario that most strongly concentrates pre-test probability is a child with uveitis plus a clearly inflammatory large joint problem such as an inflamed knee, because that combination immediately makes juvenile idiopathic arthritis the leading systemic association and ANA positivity meaningfully supports that diagnostic pathway and risk phenotype.\u0026nbsp;\u003C/p\u003E\u003Cp\u003EBy contrast, ACE is an imperfect marker with limited specificity and is not made \u201Chigh PPV\u201D simply by a normal lung function test, anti-cardiolipin testing is not a typical high-yield discriminator for vitritis presentations, and HLA\u2011B27 can be associated with hypopyon anterior uveitis but the added history of recurrent mouth ulcers points more toward Beh\u00E7et disease (which is not defined by HLA\u2011B27), so that pairing is less coherent and therefore less predictive than the child-with-arthritis scenario.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1506,
    "Name": "Canaliculitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following treatments is the Most effective treatment for canaliculitis:\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ESurgery to the canaliculus and irrigation with topical antibiotics\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003ECanaliculitis most often persists because \u003Cstrong\u003Einfective concretions and debris within the canaliculus act as a protected nidus\u003C/strong\u003E, so purely medical therapy frequently fails to eradicate the source even if symptoms temporarily improve. The most effective approach is therefore \u003Cstrong\u003Eprocedural removal of canalicular contents (canaliculotomy with curettage/expression) followed by irrigation and topical antibiotics\u003C/strong\u003E, which directly clears the obstructing/infected material and reduces recurrence. Massage and warm compresses may help surface drainage but usually do not eliminate intraluminal concretions, oral antibiotics have limited penetration into the canalicular lumen and cannot reliably clear the debris-based nidus, and topical steroids risk masking infection and worsening persistence if used without definitive source control.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1507,
    "Name": "Incidental orbital cavernous haemangioma with stable longstanding visual loss",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 55 year old man with multiple sclerosis was referred to you after he was incidentally found to have a cavernous haemangioma in his left orbital apex from an MRI scan. He has had poor vision in his left eye for the past two years and had attributed it to his previous \u201Coptic neuritis\u201D. He does not complain of any recent change in his vision. What would be the MOST appropriate management in this case?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EObserve with frequent clinic review\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EAn incidental orbital cavernous haemangioma at the orbital apex in a patient with \u003Cstrong\u003Eno recent visual change\u003C/strong\u003E and \u003Cstrong\u003Elongstanding stable poor vision already attributed to optic neuritis\u003C/strong\u003E is most appropriately managed conservatively, because many orbital cavernous haemangiomas are \u003Cstrong\u003Eslow-growing and benign\u003C/strong\u003E, and intervention is usually reserved for cases with \u003Cstrong\u003Eprogressive visual decline, increasing optic nerve compression, or symptomatic progression\u003C/strong\u003E.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;In an orbital apex location, surgery carries \u003Cstrong\u003Ehigher risk\u003C/strong\u003E due to proximity to the optic nerve and extraocula muscles, so proceeding straight to excision without evidence of progression is unlikely to be justified. Medical therapy such as propranolol is not a standard effective treatment for adult orbital cavernous haemangioma, and stereotactic radiotherapy is typically considered only in selected situations where there is progressive compression and surgery is unsuitable, rather than for an incidental, stable lesion. \u003Cstrong\u003ETherefore, careful observation with regular clinical review is the best approach.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1508,
    "Name": "RCOphth hydroxychloroquine/chloroquine retinopathy monitoring",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ERegarding the RCOphth clinical guidelines on Hydroxychloroquine and chloroquine monitoring, which is the MOST likely recommendation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EAll patients who have been taking chloroquine should be monitored within 1 year of starting treatment\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe RCOphth updated guidance recognises that \u003Cstrong\u003Echloroquine is more retinotoxic than hydroxychloroquine\u003C/strong\u003E and therefore recommends that \u003Cstrong\u003Emonitoring for all chloroquine users begins after one year of therapy\u003C/strong\u003E, using appropriate retinal imaging tests, which makes the one\u2011year chloroquine statement the best match.  The six\u2011month chloroquine statement is not the recommended threshold in the guideline, so it is less likely to be correct.  The hydroxychloroquine statements are also less likely because RCOphth recommends \u003Cstrong\u003Eannual monitoring after five years for most hydroxychloroquine users\u003C/strong\u003E, with earlier commencement around one year reserved for those with \u003Cstrong\u003Eadditional risk factors\u003C/strong\u003E (such as high dose, renal impairment, or tamoxifen use), so routine monitoring within one year or within three years for all hydroxychloroquine users does not reflect the guideline\u2019s main recommendation.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1509,
    "Name": "Aberrant regeneration of the third nerve",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe following are features of Aberrant regeneration of third nerve except\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EAbduction on attempted upgaze\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EAberrant regeneration (oculomotor synkinesis) is caused by \u003Cstrong\u003Emisdirection of regenerating third\u2011nerve fibres\u003C/strong\u003E, producing \u003Cstrong\u003Eparadoxical co\u2011contraction\u003C/strong\u003E and characteristic synkinetic signs: the pupil may \u003Cstrong\u003Econstrict on attempted adduction\u003C/strong\u003E (pseudo\u2013Argyll Robertson pattern), the upper lid may \u003Cstrong\u003Eelevate or retract on attempted downgaze or adduction\u003C/strong\u003E (pseudo\u2013von Graefe), and there can be \u003Cstrong\u003Eadduction during attempted vertical gaze\u003C/strong\u003E with co\u2011contraction that may even produce \u003Cstrong\u003Eglobe retraction on attempted upgaze/downgaze\u003C/strong\u003E.  In contrast, \u003Cstrong\u003Eabduction on attempted upgaze\u003C/strong\u003E does not fit the physiology of third\u2011nerve misdirection, because the classic horizontal synkinesis in this condition is \u003Cstrong\u003Einappropriate adduction\u003C/strong\u003E during vertical gaze rather than abduction.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1510,
    "Name": "Infant \u201Cwhite lump\u201D at the limbus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA six month old boy presents as his parents have noticed a \u201Clump on the eye\u201D. You observe the white, solid lesion shown in the photograph. What is the MOST likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-15-001f417e-b8d8-4ba1-a64c-daad47ea3fb6.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ELimbal dermoid (epibulbar choristoma)\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis is most consistent with a \u003Cstrong\u003Elimbal dermoid\u003C/strong\u003E, because the lesion appears \u003Cstrong\u003Econgenital/early-onset\u003C/strong\u003E, \u003Cstrong\u003Ewhite and solid\u003C/strong\u003E, and sits at the \u003Cstrong\u003Einferior limbal/peripheral corneal region\u003C/strong\u003E, which is the classic location and look for an \u003Cstrong\u003Eepibulbar choristoma containing skin-like tissue\u003C/strong\u003E that can be noticed by parents as a \u201Clump\u201D in infancy; these lesions are typically \u003Cstrong\u003Ewell-circumscribed, non-infective, and non-fluctuant\u003C/strong\u003E, and may induce \u003Cstrong\u003Eastigmatism\u003C/strong\u003E if they encroach on the cornea.\u003C/p\u003E\u003Cp\u003EA conjunctival inclusion cyst is usually \u003Cstrong\u003Etranslucent and cystic\u003C/strong\u003E, often following trauma or surgery, rather than a solid white plaque-like mass in a 6\u2011month\u2011old. Phlyctenular disease is an \u003Cstrong\u003Einflammatory hypersensitivity reaction\u003C/strong\u003E that tends to be \u003Cstrong\u003Ered, irritated, photophobic\u003C/strong\u003E, and associated with \u003Cstrong\u003Elimbal injection\u003C/strong\u003E and episodic inflammation rather than a stable, solid congenital-appearing lump. Corneal keloid is an uncommon \u003Cstrong\u003Efibroproliferative scar mass\u003C/strong\u003E that usually follows \u003Cstrong\u003Etrauma, surgery, or significant inflammation\u003C/strong\u003E, and the history and age here fit far better with a \u003Cstrong\u003Edevelopmental choristoma\u003C/strong\u003E than an acquired scarring process.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1511,
    "Name": "Vernal keratoconjunctivitis (Horner\u2013Trantas dots)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn eight year old boy presents with this clinical appearance. If the white lesions were to be submitted for histological examination which of the following immune cells would be MOST likely to predominate?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-15-2ca5f742-d355-43c6-b80d-ddd4d2af9642.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EEosinophils\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe image shows multiple white limbal dots consistent with \u003Cstrong\u003EHorner\u2013Trantas dots\u003C/strong\u003E, a classic sign of \u003Cstrong\u003Evernal keratoconjunctivitis\u003C/strong\u003E, which is an allergic, Th2\u2011predominant ocular surface disease. These dots represent accumulations of inflammatory debris at the limbus in which \u003Cstrong\u003Eeosinophils\u003C/strong\u003E are prominent, reflecting the allergic/eosinophil\u2011driven nature of the condition; therefore, eosinophils would be the predominant immune cells on histology. Neutrophils would be more typical of acute bacterial infection, lymphocytes predominate in many chronic non\u2011allergic inflammatory processes, and plasma cells are seen in chronic conjunctival inflammation but are not the hallmark cell type for Horner\u2013Trantas dots in vernal disease.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1512,
    "Name": "GMC social media guidance",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following would NOT breach GMC guidance on appropriate use of social media?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EUsing a professional social media website (not open to the public) to discuss a patient\u2019s care (with no identifiable features)\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe only scenario that can be compatible with GMC expectations is using a \u003Cstrong\u003Eprofessional, non\u2011public platform\u003C/strong\u003E to discuss care \u003Cstrong\u003Ewithout sharing any identifiable patient information\u003C/strong\u003E, because the guiding principles are to \u003Cstrong\u003Emaintain patient confidentiality\u003C/strong\u003E, \u003Cstrong\u003Erespect privacy\u003C/strong\u003E, and \u003Cstrong\u003Ebehave professionally online\u003C/strong\u003E; a closed professional environment with robust anonymization is the closest match to those requirements.  The other scenarios are more likely to breach guidance because giving advice publicly while identifying yourself as a doctor yet remaining anonymous undermines \u003Cstrong\u003Eaccountability and trust\u003C/strong\u003E expected in professional communications, failing to disclose a financial/employment interest when commenting on a procedure is a clear \u003Cstrong\u003Econflict\u2011of\u2011interest transparency\u003C/strong\u003E problem, and replying to a patient via a private profile risks \u003Cstrong\u003Eboundary blurring\u003C/strong\u003E and unstructured clinical advice outside appropriate professional channels.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 7,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1513,
    "Name": "Headache \u002B bilateral uveitis \u002B retinal periphlebitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 24 year old man presents with headache, bilateral uveitis and a periphlebitis. Which of the following is the MOST likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003EBeh\u00E7et\u2019s disease\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis combination most strongly supports Beh\u00E7et\u2019s disease because it classically causes a \u003Cstrong\u003Ebilateral, relapsing panuveitis\u003C/strong\u003E with \u003Cstrong\u003Eretinal vasculitis\u003C/strong\u003E that commonly manifests as \u003Cstrong\u003Eperiphlebitis (venous sheathing and inflammation)\u003C/strong\u003E, and the associated \u003Cstrong\u003Eheadache\u003C/strong\u003E fits with systemic inflammatory activity and the possibility of neurological involvement in the Beh\u00E7et spectrum.\u003C/p\u003E\u003Cp\u003E\u0026nbsp;Acute retinal necrosis is usually dominated by a unilateral, rapidly progressive necrotising retinitis with intense vitritis rather than a primary picture of bilateral uveitis with periphlebitis. Sympathetic ophthalmia requires a preceding penetrating ocular injury or intraocular surgery to trigger bilateral granulomatous uveitis, which is not suggested by the stem. Vogt\u2013Koyanagi\u2013Harada syndrome can present with headache and bilateral granulomatous uveitis, but it is more characteristically associated with diffuse choroiditis and exudative retinal detachments rather than a retinal periphlebitis-led vasculitic phenotype, making Beh\u00E7et\u2019s disease the best single fit here.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1514,
    "Name": "HSV stromal keratitis with endotheliitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 30 year old man known to have recurrent herpes simplex keratitis presents with a 2 week history of reduced vision and a sore eye. He had been on prophylactic oral acyclovir but had discontinued this in error. On examination he has a moderate injection, an area of stromal thickening with localised endotheliitis and 1\u002B of anterior chamber cells. Which of the following is the most widely accepted combination of therapeutic agents in this case?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ESystemic acyclovir, topical steroid only\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003EHSV immune stromal keratitis with associated endotheliitis and mild anterior uveitis\u003C/strong\u003E, where the key pathology is \u003Cstrong\u003Estromal and endothelial inflammation\u003C/strong\u003E rather than active epithelial viral replication, so the cornerstone of management is a \u003Cstrong\u003Etopical corticosteroid to suppress the immune-mediated corneal inflammation\u003C/strong\u003E, but it must be given with \u003Cstrong\u003Eantiviral cover\u003C/strong\u003E to prevent worsening or reactivation of HSV; in practice, that antiviral cover is very commonly provided as \u003Cstrong\u003Esystemic acyclovir\u003C/strong\u003E (especially here, given he stopped prophylaxis and now has a significant inflammatory recurrence).\u003C/p\u003E\u003Cp\u003EAdding topical acyclovir on top of adequate systemic antiviral therapy is generally not essential in a case without epithelial ulceration, while systemic steroids are not the standard first-line for localised HSV stromal/endothelial disease and would be reserved for selected severe uveitic/systemic situations under specialist guidance; finally, any regimen that omits topical steroid fails to address the main driver of the reduced vision and stromal thickening, and risks persistent scarring and decompensation.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1515,
    "Name": "Periocular keratoacanthoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWith regard to peri-ocular keratoacanthoma which of the following is LEAST likely to be correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: \u003Cstrong\u003ERapid growth suggests the lesion is more likely to be an SCC\u003C/strong\u003E\u003C/span\u003E\u003C/h3\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cstrong\u003E\u003Cbr\u003E\u003C/strong\u003E\u003C/span\u003E\u003C/div\u003E\n\u003Cp\u003EPeriocular keratoacanthoma is a crateriform lesion that characteristically undergoes a phase of \u003Cstrong\u003Erapid growth over weeks\u003C/strong\u003E, and this rapid growth history is actually one of the clinical clues that points toward keratoacanthoma rather than making squamous cell carcinoma more likely, even though the key practical problem is that keratoacanthoma and well\u2011differentiated squamous cell carcinoma can overlap clinically and histologically.  Because of this uncertainty and the clinically important risk that a lesion labelled \u201Ckeratoacanthoma\u201D may prove to be invasive squamous cell carcinoma, periocular lesions are generally managed with \u003Cstrong\u003Edefinitive excision and margin control\u003C/strong\u003E to secure diagnosis and treatment, and this approach is explicitly recommended in periocular series.  It is also plausible that a periocular keratoacanthoma may be mistaken clinically for other common lid tumours, including nodular basal cell carcinoma.\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;A similar question appeared in a previous FRCOphth part 2 written exam.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1516,
    "Name": "Hypertropia in Adduction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child is brought in because the parent noticed that one eye occasionally \u201Cfloats upward.\u201D On examination you find a left hypertropia, and it becomes most noticeable when the child looks to the right. During an alternate cover test, when the left eye is uncovered it makes a corrective downward movement to re-fixate. When the left eye is covered, the right eye moves upward.\u003Cbr\u003EWhich diagnosis best accounts for this pattern?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer: Left inferior oblique overaction .\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\nThe \u003Cstrong\u003Eleft hypertropia is most evident in right gaze\u003C/strong\u003E, which places the \u003Cstrong\u003Eleft eye in adduction\u003C/strong\u003E\u2014the position where the \u003Cstrong\u003Einferior oblique acts as an elevator\u003C/strong\u003E\u2014so \u003Cstrong\u003Eoveraction makes the left eye drift upward\u003C/strong\u003E. On alternate cover testing, the \u003Cstrong\u003Edownward refixation of the left eye when uncovered\u003C/strong\u003E indicates it had \u003Cstrong\u003Eelevated under cover\u003C/strong\u003E, and the \u003Cstrong\u003Eupward shift of the right eye when the left is covered\u003C/strong\u003E reflects a \u003Cstrong\u003Eyoked, compensatory response consistent with Hering\u2019s law\u003C/strong\u003E. Therefore, the findings are best explained by \u003Cstrong\u003Eleft inferior oblique overaction\u003C/strong\u003E.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1517,
    "Name": "Earliest sign of malignant hyperthermia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EYou are preparing for strabismus surgery in a child who has a family history suggesting susceptibility to malignant hyperthermia. Which clinical/monitoring change is typically the first clue that malignant hyperthermia is developing during anesthesia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: E\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003Elevation of end-tidal carbon dioxide concentration\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003EMalignant hyperthermia causes a \u003Cstrong\u003Esudden hypermetabolic state in skeletal muscle\u003C/strong\u003E, leading to \u003Cstrong\u003Erapid CO\u2082 overproduction\u003C/strong\u003E. In the operating room, the earliest and most reliable clue is often a \u003Cstrong\u003Eprogressive, unexplained increase in end\u2011tidal CO\u2082 despite adequate ventilation\u003C/strong\u003E (often accompanied by \u003Cstrong\u003Eearly tachycardia\u003C/strong\u003E).\u003C/p\u003E\n\u003Cp\u003EA rise in body temperature is a \u003Cstrong\u003Elate finding\u003C/strong\u003E, because the patient may generate excess heat early but \u003Cstrong\u003Emeasurable hyperthermia typically appears after CO\u2082 and cardiovascular changes\u003C/strong\u003E. Myoglobinuria is also \u003Cstrong\u003Elater\u003C/strong\u003E, reflecting \u003Cstrong\u003Erhabdomyolysis\u003C/strong\u003E after sustained muscle breakdown, so it is not usually the first sign. Muscle rigidity can occur early (classically \u003Cstrong\u003Emasseter spasm\u003C/strong\u003E or generalized rigidity), but \u003Cstrong\u003Eend\u2011tidal CO\u2082 elevation is usually detected first\u003C/strong\u003E because it is continuously monitored and reflects the earliest physiologic shift toward hypercarbia and increased metabolic demand.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1518,
    "Name": "Binocular diplopia: most affected EOM",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 42-year-old woman has had binocular double vision for several weeks, and an external photograph is provided. Which extraocular muscle is most likely involved in the underlying condition?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Inferior rectus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe findings are most consistent with \u003Cstrong\u003Ethyroid eye disease\u003C/strong\u003E, a common cause of \u003Cstrong\u003Ebinocular diplopia in adults\u003C/strong\u003E due to \u003Cstrong\u003Erestrictive involvement of extraocular muscles\u003C/strong\u003E. The typical pattern of muscle involvement is: \u003Cstrong\u003Einferior rectus most commonly\u003C/strong\u003E, then \u003Cstrong\u003Emedial rectus\u003C/strong\u003E, followed by \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E, and \u003Cstrong\u003Elateral rectus least often\u003C/strong\u003E. Because the \u003Cstrong\u003Einferior rectus\u003C/strong\u003E is frequently affected, patients often develop \u003Cstrong\u003Erestriction of elevation\u003C/strong\u003E and diplopia related to that limitation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1519,
    "Name": "Pediatric CN VI palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about sixth cranial nerve palsy in children is not correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ETrue sixth nerve palsy in childhood is \u003Cstrong\u003Eseen more often in older children than in newborns/infants\u003C/strong\u003E, so saying it is more frequent in infancy is incorrect. A compensatory head turn can help maintain \u003Cstrong\u003Esingle binocular vision\u003C/strong\u003E, which is \u003Cstrong\u003Eprotective against amblyopia\u003C/strong\u003E by reducing constant suppression. Also, a meaningful proportion of children with an apparent sixth nerve palsy can have an \u003Cstrong\u003Eintracranial cause\u003C/strong\u003E, so \u003Cstrong\u003Eneuroimaging is often warranted\u003C/strong\u003E depending on the clinical context. In infants especially, many \u201Ccongenital sixth nerve palsy\u201D presentations are actually \u003Cstrong\u003Einfantile (congenital) esotropia with cross-fixation\u003C/strong\u003E, which can \u003Cstrong\u003Emimic an abduction limitation\u003C/strong\u003E, so checking \u003Cstrong\u003Etrue ductions\u003C/strong\u003E is important.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1520,
    "Name": "Amblyopia and crowding on HOTV testing",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old has reduced acuity in one eye measured using matching single bracketed HOTV. Considering how this testing method influences amblyopic vision, does the measured acuity in the weaker eye tend to be accurate, underestimated, or overestimated?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAmblyopia is associated with \u003Cstrong\u003Ecrowding (contour interaction)\u003C/strong\u003E, meaning vision often looks \u003Cstrong\u003Ebetter when letters are presented alone\u003C/strong\u003E than when they are surrounded by other letters or \u201Ccrowding bars.\u201D If testing uses \u003Cstrong\u003Eisolated single optotypes without surrounding contours\u003C/strong\u003E, acuity can be \u003Cstrong\u003Eartificially better (overestimated)\u003C/strong\u003E in amblyopia. Here, the optotypes are \u003Cstrong\u003Esingle but bracketed\u003C/strong\u003E, which intentionally adds \u003Cstrong\u003Econtour bars to simulate crowding\u003C/strong\u003E, making the measurement \u003Cstrong\u003Ecloser to what line testing would reveal\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EAlso, because the child is using a \u003Cstrong\u003Ematching method\u003C/strong\u003E, the result does not depend on \u003Cstrong\u003Eknowing or naming letters\u003C/strong\u003E, so poor letter knowledge is not the reason for reduced acuity.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1521,
    "Name": "Congenital glaucoma: risk to offspring",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient who has congenital glaucoma is considering having children. No other relatives are affected, and the partner has no history of congenital glaucoma. What is the estimated chance that a child will also have congenital glaucoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E2%\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWhen an individual has primary congenital glaucoma and there is \u003Cstrong\u003Eno additional family history\u003C/strong\u003E (and the partner is unaffected), the \u003Cstrong\u003Eempiric risk\u003C/strong\u003E for an affected child is \u003Cstrong\u003Eabout 2%\u003C/strong\u003E. This estimate comes from published observational data and is also summarized in the BCSC text, which states that \u003Cstrong\u003Eif no other family history of primary congenital glaucoma exists, the chance of an affected parent having an affected child is approximately 2%\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1522,
    "Name": "Parks 3-step",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 55-year-old has a right hypertropia. On Parks\u2013Bielschowsky 3-step testing, the vertical deviation increases in left gaze and with a left head tilt. Which extraocular muscle weakness best fits this pattern?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELeft superior rectus weakness.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EA right hypertropia limits the possibilities to muscles that would normally \u003Cstrong\u003Edepress the right eye\u003C/strong\u003E or \u003Cstrong\u003Eelevate the left eye\u003C/strong\u003E. When the hypertropia becomes larger in \u003Cstrong\u003Eleft gaze\u003C/strong\u003E, the pattern narrows to two main candidates: a muscle that primarily acts in that gaze position. The added clue is the \u003Cstrong\u003Eleft head tilt\u003C/strong\u003E, which drives the left eye to \u003Cstrong\u003Eintort\u003C/strong\u003E; vertical deviations that worsen with head tilt point to a problem in the muscles responsible for torsional stabilization in that eye. Because \u003Cstrong\u003Esuperior rectus and superior oblique are intorters\u003C/strong\u003E, worsening with \u003Cstrong\u003Eleft tilt\u003C/strong\u003E indicates deficient \u003Cstrong\u003Eleft-eye intorsion/elevation control\u003C/strong\u003E, identifying the \u003Cstrong\u003Eleft superior rectus\u003C/strong\u003E as the paretic muscle.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1523,
    "Name": "Stage 3 ROP definition",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich description best matches stage 3 retinopathy of prematurity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ERidge with extraretinal fibrovascular proliferation.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EStage 3 ROP is defined by a \u003Cstrong\u003Eridge\u003C/strong\u003E at the junction of vascularized and avascular retina with \u003Cstrong\u003Efibrovascular tissue proliferating beyond the retina (extraretinal)\u003C/strong\u003E. This distinguishes it from earlier stages, where there is either a \u003Cstrong\u003Eflat demarcation line\u003C/strong\u003E (stage 1) or a \u003Cstrong\u003Eraised ridge with or without small tufts\u003C/strong\u003E but without true extraretinal proliferation (stage 2). Retinal detachment corresponds to later disease, with \u003Cstrong\u003Esubtotal detachment in stage 4\u003C/strong\u003E (and \u003Cstrong\u003Etotal detachment in stage 5\u003C/strong\u003E).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1524,
    "Name": "Angle of vertical recti to visual axis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat angle do the superior and inferior rectus muscles make relative to the eye\u2019s visual axis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E23 degrees.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe superior and inferior rectus muscles do not run exactly along the visual axis; instead, they travel from the \u003Cstrong\u003Eannulus of Zinn\u003C/strong\u003E in a slightly outward (lateral) direction, creating an angle of \u003Cstrong\u003Eabout 23\u00B0\u003C/strong\u003E with the visual axis. This is commonly contrasted with the oblique muscles, which have a larger relationship angle to the visual axis of \u003Cstrong\u003Eabout 51\u00B0\u003C/strong\u003E, helping explain differences in their secondary/tertiary actions.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1525,
    "Name": "IO palsy vs Brown syndrome: key differences",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a left hypertropia and the right eye shows limited elevation in adduction on left gaze. Which statement is wrong when trying to tell inferior oblique palsy apart from Brown syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe statement that a V\u2011pattern occurs in inferior oblique palsy is incorrect.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EBoth conditions can look similar because each can cause \u003Cstrong\u003Elimited elevation in adduction\u003C/strong\u003E. The separation point is whether the problem is \u003Cstrong\u003Erestrictive\u003C/strong\u003E (Brown syndrome) or \u003Cstrong\u003Eparetic\u003C/strong\u003E (inferior oblique palsy). Brown syndrome is due to \u003Cstrong\u003Erestriction at the trochlea\u2013superior oblique tendon complex\u003C/strong\u003E, so it typically shows \u003Cstrong\u003Epositive forced ductions\u003C/strong\u003E, \u003Cstrong\u003Eminimal/absent superior oblique overaction\u003C/strong\u003E, \u003Cstrong\u003Eno significant torsion\u003C/strong\u003E, and a \u003Cstrong\u003Enegative head\u2011tilt test\u003C/strong\u003E; it often produces a \u003Cstrong\u003EV\u2011pattern\u003C/strong\u003E because the restricted eye cannot elevate in adduction and tends to drift outward in upgaze.\u003C/p\u003E\n\u003Cp\u003EInferior oblique palsy is a true weakness, so forced ductions are \u003Cstrong\u003Enegative\u003C/strong\u003E, and secondary changes are common\u2014especially \u003Cstrong\u003Esuperior oblique overaction\u003C/strong\u003E, which produces \u003Cstrong\u003Eintorsion\u003C/strong\u003E and tends to create an \u003Cstrong\u003EA\u2011pattern\u003C/strong\u003E, with a \u003Cstrong\u003Epositive head\u2011tilt test\u003C/strong\u003E. Therefore, attributing a \u003Cstrong\u003EV\u2011pattern\u003C/strong\u003E to inferior oblique palsy is the incorrect distinguishing feature.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1526,
    "Name": "Intermittent exotropia vs \u201Clazy eye\u201D patching",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 12-year-old boy has a two-year history of intermittent exotropia that has become constant over the last six months. On exam his visual acuity is 20/20 in the right eye and 20/20\u22122 in the left eye, with a 30\u2011prism\u2011diopter exotropia in primary gaze and freely alternating fixation (refraction \u002B1.00 sphere in both eyes; stereoacuity 40 seconds of arc with prism correction). His father notices the small acuity difference and asks whether patching would help a \u201Clazy eye.\u201D What is the most appropriate response?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPatching is not indicated here; management should focus on the manifest exotropia (surgical consideration).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis history fits a deviation that began around age 10, meaning binocular vision development during early childhood was likely \u003Cstrong\u003Enormal\u003C/strong\u003E, with the exotropia initially \u003Cstrong\u003Eintermittent/controlled\u003C/strong\u003E. A small inter-eye acuity difference such as 20/20 versus 20/20-2 typically \u003Cstrong\u003Edoes not meet common clinical thresholds for unilateral amblyopia\u003C/strong\u003E, which is usually defined as a \u003Cstrong\u003Edifference of at least two lines\u003C/strong\u003E on best-corrected acuity testing. Because the problem is now a \u003Cstrong\u003Emanifest exotropia\u003C/strong\u003E, the priority is restoring comfortable alignment and binocular function; \u003Cstrong\u003Estrabismus surgery can address the constant deviation\u003C/strong\u003E and reduce reliance on prisms.\u003C/p\u003E\n\u003Cp\u003EThe PEDIG patching data applies to children who truly have \u003Cstrong\u003Eamblyopia\u003C/strong\u003E; in this scenario, the child\u2019s findings are more consistent with \u003Cstrong\u003Estrabismus control failure\u003C/strong\u003E rather than amblyopia needing patch therapy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1527,
    "Name": "Christmas tree cataract \u002B paresthesias",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-year-old is referred because of an abnormal red reflex in both eyes. Slit-lamp exam shows bilateral lens opacities like those pictured. The child frequently reports tingling in the hands, feet, and around the mouth, yet is doing very well academically. Which underlying disorder best explains this presentation?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-bcbf324b-3f5a-431e-a8f8-c739d2460a22.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Hypoparathyroidism.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe slit-lamp photo shows a \u003Cstrong\u003E\u201CChristmas tree\u201D cataract\u003C/strong\u003E (multicolored, sparkling crystalline flecks). This cataract pattern is classically associated with \u003Cstrong\u003Ehypoparathyroidism\u003C/strong\u003E and can also be seen with \u003Cstrong\u003Emyotonic dystrophy\u003C/strong\u003E, so you must use the systemic clues to choose between them. The child\u2019s \u003Cstrong\u003Eperioral and distal tingling\u003C/strong\u003E strongly suggests \u003Cstrong\u003Ehypocalcemia\u003C/strong\u003E, which is a hallmark consequence of \u003Cstrong\u003Elow parathyroid hormone\u003C/strong\u003E. Hypocalcemia can also cause \u003Cstrong\u003Etetany\u003C/strong\u003E and classic bedside signs such as \u003Cstrong\u003EChvostek\u003C/strong\u003E (facial twitch with tapping) and \u003Cstrong\u003ETrousseau\u003C/strong\u003E (carpal spasm with BP cuff). Importantly, children with hypoparathyroidism typically have \u003Cstrong\u003Enormal intelligence\u003C/strong\u003E, matching the history.\u003C/p\u003E\n\u003Cp\u003EMyotonic dystrophy would be suggested instead by \u003Cstrong\u003Emyotonia (delayed relaxation, e.g., difficulty releasing a grip)\u003C/strong\u003E and other systemic/ocular features like \u003Cstrong\u003Eptosis, external ophthalmoplegia, pigmentary retinopathy, and cardiac conduction issues\u003C/strong\u003E, rather than prominent hypocalcemic paresthesias. Lowe syndrome has a different typical cataract morphology (often described as \u003Cstrong\u003Ethin discoform\u003C/strong\u003E), and sarcoidosis does not fit the combination of \u003Cstrong\u003EChristmas tree cataract \u002B hypocalcemic symptoms\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1528,
    "Name": "Failure of fetal fissure closure",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich condition results from incomplete closure of the embryonic (fetal) fissure during eye development?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Microphthalmos with cyst.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis is a \u003Cstrong\u003Ecoloboma-spectrum anomaly\u003C/strong\u003E caused by \u003Cstrong\u003Efailure of the embryonic (fetal) fissure to close\u003C/strong\u003E, which leaves a defect in the ocular wall. Through this defect, \u003Cstrong\u003Eneuroectoderm can herniate outward\u003C/strong\u003E, forming a \u003Cstrong\u003Ecolobomatous cyst\u003C/strong\u003E, and the globe is typically \u003Cstrong\u003Emicrophthalmic\u003C/strong\u003E. The cyst is usually \u003Cstrong\u003Einferonasal\u003C/strong\u003E, so it may present as a \u003Cstrong\u003Evisible/palpable mass under or behind the lower eyelid\u003C/strong\u003E, and the associated coloboma often involves the \u003Cstrong\u003Eoptic disc\u003C/strong\u003E with variable extension into the \u003Cstrong\u003Echoroid/retina\u003C/strong\u003E. Like other coloboma-related conditions, it can be associated with \u003Cstrong\u003Esystemic syndromes\u003C/strong\u003E (so a general/systemic evaluation may be warranted).\u003C/p\u003E\n\u003Cp\u003EThe other listed conditions are not due to fissure-closure failure: \u003Cstrong\u003EBergmeister papilla\u003C/strong\u003E and \u003Cstrong\u003Epersistent fetal vasculature\u003C/strong\u003E reflect \u003Cstrong\u003Epersistence of the fetal hyaloid system\u003C/strong\u003E, and \u003Cstrong\u003Enanophthalmos\u003C/strong\u003E is a \u003Cstrong\u003Esmall eye without a coloboma/cyst mechanism\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1529,
    "Name": "ARC and paradoxical diplopia after ET surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 45-year-old with long-standing esotropia is found to have anomalous retinal correspondence on pre-op testing, and you plan bilateral medial rectus recessions. What postoperative visual symptom may occur soon after surgery?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Crossed diplopia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn long\u2011standing esotropia, the visual system may develop \u003Cstrong\u003Eanomalous retinal correspondence (ARC)\u003C/strong\u003E to \u003Cstrong\u003Emaintain single binocular vision despite misalignment\u003C/strong\u003E by \u201Cremapping\u201D which retinal points correspond between the two eyes. If surgery corrects the \u003Cstrong\u003Emeasured\u003C/strong\u003E esotropia to orthotropia, the \u003Cstrong\u003Esensory adaptation can persist temporarily\u003C/strong\u003E, so the patient may \u003Cem\u003Eperceive\u003C/em\u003E the eyes as now being \u003Cstrong\u003Eovercorrected toward exotropia\u003C/strong\u003E relative to their adapted straight-ahead. That mismatch between the new motor alignment and the old sensory map produces \u003Cstrong\u003Eparadoxical diplopia\u003C/strong\u003E, and because the perceived state is \u003Cstrong\u003Eexotropic\u003C/strong\u003E, the doubling pattern is \u003Cstrong\u003Ecrossed diplopia\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1530,
    "Name": "CN IV palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 35-year-old develops diplopia after head trauma. He has a left hypertropia that increases in right gaze and with left head tilt; the primary-position hypertropia measures 10 prism diopters and torsion is minimal on double Maddox rod testing. What is the most appropriate initial surgical approach?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELeft inferior oblique weakening.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis motility pattern localizes to a \u003Cstrong\u003Eleft superior oblique (CN IV) palsy\u003C/strong\u003E: the hypertropia worsens in \u003Cstrong\u003Econtralateral gaze (right gaze)\u003C/strong\u003E and with \u003Cstrong\u003Eipsilateral head tilt (left tilt)\u003C/strong\u003E, which is the classic Parks/Bielschowsky pattern. Surgical planning is guided mainly by the \u003Cstrong\u003Eprimary-position vertical deviation\u003C/strong\u003E. With a primary-position hypertropia of \u003Cstrong\u003E10 prism diopters (\u226415)\u003C/strong\u003E, the standard initial procedure is \u003Cstrong\u003Eweakening of the ipsilateral inferior oblique\u003C/strong\u003E, which reduces the hypertropia in adduction and improves the typical gaze/tilt incomitance.\u003C/p\u003E\n\u003Cp\u003EMore extensive surgery is generally reserved for larger deviations: when the primary-position hypertropia is \u003Cstrong\u003E\u0026gt;15 prism diopters\u003C/strong\u003E, a common strategy is combining \u003Cstrong\u003Eipsilateral inferior oblique weakening\u003C/strong\u003E with \u003Cstrong\u003Econtralateral inferior rectus recession\u003C/strong\u003E to address the larger vertical misalignment. \u003Cstrong\u003ESuperior oblique tendon tuck\u003C/strong\u003E is typically considered when there is \u003Cstrong\u003Edemonstrable tendon laxity\u003C/strong\u003E or when the clinical picture suggests underaction that is best addressed by tightening, rather than as the first step for a small primary deviation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1531,
    "Name": "Infantile esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 7\u2011month\u2011old has had constant inward eye deviation for two months. Vision assessment shows CSM in the right eye and UC/US/UM in the left eye, and cycloplegic refraction is \u002B4.00 sphere in both eyes. What is the usual sequence of management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EStart with spectacles and amblyopia therapy (patch the better-seeing eye), then proceed to medial rectus recessions.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis child has \u003Cstrong\u003Esignificant hyperopia\u003C/strong\u003E and the left eye\u2019s fixation behavior (UC/US/UM) indicates \u003Cstrong\u003Ereduced visual function consistent with amblyopia risk\u003C/strong\u003E compared with the right eye (CSM). The standard approach is to optimize the sensory inputs before surgery: prescribe \u003Cstrong\u003Efull hyperopic correction\u003C/strong\u003E and treat amblyopia by \u003Cstrong\u003Epatching the better eye\u003C/strong\u003E to drive use of the weaker eye. Once vision is improved and more balanced, strabismus surgery is performed to align the eyes; operating before correcting \u003Cstrong\u003Erefractive error and amblyopia\u003C/strong\u003E increases the chance of an \u003Cstrong\u003Eunstable or suboptimal functional outcome\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EQuick interpretation of the fixation notation: \u003Cstrong\u003ECSM\u003C/strong\u003E suggests \u003Cstrong\u003Ecentral, steady fixation that is maintained\u003C/strong\u003E, whereas \u003Cstrong\u003EUC/US/UM\u003C/strong\u003E suggests \u003Cstrong\u003Euncentered, unsteady fixation that is not maintained\u003C/strong\u003E, supporting the need for \u003Cstrong\u003Eamblyopia therapy\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1532,
    "Name": "CN III palsy surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn strabismus caused by a third cranial nerve palsy, several operations may be used to improve alignment. Which listed approach is not an appropriate corrective option?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELarge lateral rectus recession with fixation of the globe to the lateral orbital periosteum.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn third nerve palsy, the typical resting position is a large \u003Cstrong\u003Eexotropia\u003C/strong\u003E (often with vertical/torsional components) because \u003Cstrong\u003Emedial rectus and other third-nerve muscles are weak\u003C/strong\u003E while the \u003Cstrong\u003Elateral rectus remains unopposed\u003C/strong\u003E. Surgical strategies therefore aim to \u003Cstrong\u003Ereduce abducting force\u003C/strong\u003E (e.g., large lateral rectus weakening or disinsertion/anchoring) and, when needed, provide \u003Cstrong\u003Eadditional adducting support\u003C/strong\u003E (e.g., large medial rectus strengthening or globe fixation toward the nasal side).\u003C/p\u003E\n\u003Cp\u003EFixing the globe to the \u003Cstrong\u003Elateral\u003C/strong\u003E orbital periosteum would pull/hold the eye \u003Cstrong\u003Eoutward\u003C/strong\u003E, which would \u003Cstrong\u003Eworsen exotropia rather than correct it\u003C/strong\u003E. If periosteal fixation is used as part of management, it is directed \u003Cstrong\u003Enasally\u003C/strong\u003E to help counter the abducting tendency after lateral rectus weakening.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1533,
    "Name": "Convergence insufficiency",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 11-year-old has headaches with near work. Alignment is normal at distance, but there is a 15\u2206 exophoria at near and a remote near point of convergence (18 cm). Cycloplegic refraction shows minimal hyperopia (\u002B0.25 OU). Which listed option is not an appropriate treatment approach?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPrescription of additional plus power beyond refractive error correction.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is classic for \u003Cstrong\u003Econvergence insufficiency\u003C/strong\u003E: symptoms with near tasks, \u003Cstrong\u003Egreater exophoria at near than distance\u003C/strong\u003E, and a \u003Cstrong\u003Ereceded near point of convergence\u003C/strong\u003E. Appropriate treatments aim to \u003Cstrong\u003Eincrease fusional convergence ability\u003C/strong\u003E and \u003Cstrong\u003Ebring the near point of convergence closer\u003C/strong\u003E, which is why \u003Cstrong\u003Econvergence exercises/vision therapy\u003C/strong\u003E (e.g., pencil push-ups and stereograms) are used; base-out prism can also be used as a \u003Cstrong\u003Etraining tool to stimulate convergence demand\u003C/strong\u003E in selected therapy setups.\u003C/p\u003E\n\u003Cp\u003EIn contrast, giving extra plus power reduces the need to accommodate, and because \u003Cstrong\u003Eaccommodation normally drives accommodative convergence\u003C/strong\u003E, extra plus tends to \u003Cstrong\u003Edecrease convergence drive\u003C/strong\u003E, potentially \u003Cstrong\u003Eworsening near exophoria and symptoms\u003C/strong\u003E rather than improving them.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1534,
    "Name": "Kestenbaum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with congenital nystagmus has a longstanding right head turn and is planned for a Kestenbaum procedure. The planned amounts are right medial rectus recession 7.0 mm, left medial rectus resection 8.4 mm, left lateral rectus recession 9.8 mm, and the right lateral rectus resection is unknown. What should the missing right lateral rectus resection value be?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E11.2 mm.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn the Kestenbaum (Kestenbaum\u2013Anderson) approach, the goal is to \u003Cstrong\u003Erotate the eyes toward the direction of the head turn\u003C/strong\u003E to bring the \u003Cstrong\u003Enull point closer to primary position\u003C/strong\u003E. A key planning rule is to keep the \u003Cstrong\u003Etotal surgical \u201Cdose\u201D balanced between the two eyes\u003C/strong\u003E so that both eyes rotate by a similar amount.\u003C/p\u003E\n\u003Cp\u003EHere, the left eye total is \u003Cstrong\u003E8.4 mm \u002B 9.8 mm = 18.2 mm\u003C/strong\u003E. The right eye must match this total, and it already has \u003Cstrong\u003E7.0 mm\u003C/strong\u003E assigned to the right medial rectus recession. Therefore, the remaining amount for the right lateral rectus resection is \u003Cstrong\u003E18.2 \u2212 7.0 = 11.2 mm\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1535,
    "Name": "Dissociated nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich condition is most classically linked to dissociated nystagmus (nystagmus seen predominantly in the abducting eye)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EInternuclear ophthalmoplegia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EDissociated nystagmus\u003C/strong\u003E refers to an oscillation that is \u003Cstrong\u003Emost prominent in the abducting eye during attempted horizontal gaze\u003C/strong\u003E. This pattern is classically seen in \u003Cstrong\u003Einternuclear ophthalmoplegia (INO)\u003C/strong\u003E because INO results from a lesion in the \u003Cstrong\u003Emedial longitudinal fasciculus (MLF)\u003C/strong\u003E, disrupting the normal linkage between \u003Cstrong\u003Eabducens output in one eye and medial rectus activation in the fellow eye\u003C/strong\u003E. The consequence is \u003Cstrong\u003Eimpaired adduction in the affected eye\u003C/strong\u003E and \u003Cstrong\u003Eabducting \u201Cnystagmus\u201D of the fellow eye\u003C/strong\u003E, which may represent \u003Cstrong\u003Esaccadic intrusions rather than a true nystagmus\u003C/strong\u003E. INO is most often due to \u003Cstrong\u003Edemyelination\u003C/strong\u003E (especially in younger patients) or \u003Cstrong\u003Ebrainstem ischemia/stroke\u003C/strong\u003E (more common in older patients).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1536,
    "Name": "Uncooperative child: screening for misalignment",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old will not fixate on a near target during your exam. Which test is not suitable for screening ocular misalignment in this situation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Cover\u2013uncover test.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn this scenario the limiting factor is \u003Cstrong\u003Epoor/unstable fixation\u003C/strong\u003E. The cover\u2013uncover test (and especially the alternate cover test) depends on the child \u003Cstrong\u003Econtinuously fixating a single target\u003C/strong\u003E so you can detect a \u003Cstrong\u003Etrue refixation movement\u003C/strong\u003E when the cover is placed and removed. If the child keeps looking away, you can\u2019t be sure whether any eye movement you see is due to \u003Cstrong\u003Estrabismus\u003C/strong\u003E, \u003Cstrong\u003Erandom searching/saccades\u003C/strong\u003E, or \u003Cstrong\u003Eattention shifts\u003C/strong\u003E, so the test becomes \u003Cstrong\u003Eunreliable\u003C/strong\u003E and can easily miss or falsely suggest a deviation.\u003C/p\u003E\n\u003Cp\u003EBy contrast, the other options are useful precisely because they \u003Cstrong\u003Edo not require sustained attention to an accommodative target\u003C/strong\u003E:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EHirschberg test\u003C/strong\u003E uses the \u003Cstrong\u003Ecorneal light reflex (first Purkinje image)\u003C/strong\u003E. You shine a penlight and simply observe whether the reflexes are \u003Cstrong\u003Esymmetric\u003C/strong\u003E and approximately centered in each pupil. Even if the child only looks toward the light briefly, you can still screen for misalignment. A common clinical estimate is that \u003Cstrong\u003E~1 mm of reflex decentration corresponds to ~15 prism diopters\u003C/strong\u003E. So a reflex near the pupillary margin (roughly 2 mm from center in a 4 mm pupil) suggests \u003Cstrong\u003E~30 PD\u003C/strong\u003E, mid-iris (~4 mm) suggests \u003Cstrong\u003E~60 PD\u003C/strong\u003E, and near the limbus (~6 mm) suggests \u003Cstrong\u003E~90 PD\u003C/strong\u003E. The key point is that Hirschberg is mainly a \u003Cstrong\u003Escreening/rough estimation\u003C/strong\u003E tool, not a precise measurement.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EKrimsky test\u003C/strong\u003E is essentially \u201CHirschberg plus prism.\u201D You still use the corneal light reflex, but you add a prism bar and adjust prism strength until the reflex becomes \u003Cstrong\u003Ecentered\u003C/strong\u003E in the deviating eye. This gives a \u003Cstrong\u003Ebetter quantification\u003C/strong\u003E than Hirschberg in a child who won\u2019t cooperate for cover testing. It\u2019s still imperfect (head turns, intermittent fixation, and variable attention can affect accuracy), but it is often the \u003Cstrong\u003Ebest practical way\u003C/strong\u003E to estimate the deviation in an uncooperative child.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EBruckner test\u003C/strong\u003E uses a direct ophthalmoscope to compare the \u003Cstrong\u003Ered reflex brightness\u003C/strong\u003E of both eyes simultaneously. If the eyes are misaligned (or if there is significant anisometropia/amblyopia risk), the reflexes become \u003Cstrong\u003Easymmetric\u003C/strong\u003E, and the deviating/non-fixating eye often shows a \u003Cstrong\u003Ebrighter, lighter reflex\u003C/strong\u003E. This makes Bruckner very helpful as a \u003Cstrong\u003Equick screen\u003C/strong\u003E in toddlers; however, it \u003Cstrong\u003Edoes not measure the angle\u003C/strong\u003E of deviation\u2014its strength is detection rather than quantification.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1537,
    "Name": "Moebius syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old has never shown facial smiling since birth. Examination shows bilateral failure of abduction with mild limitation of adduction in both eyes. Which diagnosis best fits this presentation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMoebius syndrome.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EMoebius syndrome is defined by congenital palsies of \u003Cstrong\u003Ecranial nerve VI\u003C/strong\u003E and \u003Cstrong\u003Ecranial nerve VII\u003C/strong\u003E. \u003Cstrong\u003EFacial nerve (VII) palsy\u003C/strong\u003E explains the history of a child who has \u003Cstrong\u003Enever smiled\u003C/strong\u003E and has a characteristic \u003Cstrong\u003E\u201Cmask-like\u201D facial expression\u003C/strong\u003E. \u003Cstrong\u003EAbducens (VI) palsy\u003C/strong\u003E explains the \u003Cstrong\u003Ebilateral loss of abduction\u003C/strong\u003E. Some patients also show \u003Cstrong\u003Emild adduction limitation\u003C/strong\u003E due to associated ocular motor dysinnervation or concomitant involvement of other cranial nerve pathways, and this can appear \u003Cstrong\u003Eless severe with convergence\u003C/strong\u003E. Moebius syndrome may also be accompanied by \u003Cstrong\u003Elimb anomalies (e.g., clubfoot), craniofacial/orofacial abnormalities, and chest-wall defects\u003C/strong\u003E, which can help support the diagnosis when present.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1538,
    "Name": "Periocular dermatitis from cycloplegic drops",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old with JIA-associated uveitis is using steroid and cycloplegic drops and develops marked periocular irritation with an eczematous allergic dermatitis around one eye. Which drop is the most likely culprit?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAtropine 1%.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EPeriocular \u201Ceczema-like\u201D inflammation in a child on drops is most consistent with \u003Cstrong\u003Eallergic contact dermatitis\u003C/strong\u003E from a topical ophthalmic medication. \u003Cstrong\u003EAtropine is a well-recognized trigger of eyelid/periocular allergic contact dermatitis\u003C/strong\u003E, and it may be due to the active drug itself or to components/preservatives that contact the periocular skin.  A recent ophthalmic report also describes periocular dermatitis findings occurring after atropine exposure around the eye region, reinforcing that this reaction can occur clinically.\u003C/p\u003E\n\u003Cp\u003EScopolamine can cause systemic \u003Cstrong\u003ECNS effects such as drowsiness\u003C/strong\u003E (and other anticholinergic effects), but that profile does not specifically match \u201Csevere periocular allergic dermatitis\u201D as the key clue in this vignette.  Steroid drops (prednisolone or fluorometholone) are more often used to \u003Cstrong\u003Etreat\u003C/strong\u003E ocular surface inflammation rather than being the classic cause of this periocular allergic pattern.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1539,
    "Name": "Ectopia lentis \u002B DVT",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 17-year-old teenager presents to your clinic with the slit-lamp finding as shown in the photograph. He has a personal caregiver because of his intellectual disability and also has a history of deep vein thrombosis. Which of the following would be the most appropriate treatment of this patient\u0027s systemic disorder?\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-106752c7-d86c-4bfd-bc5c-cbb3f601098b.png\u0022\u003E\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cp style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003EThe combination of \u003Cstrong\u003Eectopia lentis\u003C/strong\u003E, \u003Cstrong\u003Eintellectual disability\u003C/strong\u003E, and \u003Cstrong\u003Ethrombotic events (e.g., DVT)\u003C/strong\u003E is most consistent with \u003Cstrong\u003Ehomocystinuria\u003C/strong\u003E, classically due to \u003Cstrong\u003Ecystathionine \u03B2\u2011synthase deficiency\u003C/strong\u003E. The key management goal is to \u003Cstrong\u003Elower homocysteine levels\u003C/strong\u003E, because elevated homocysteine drives the \u003Cstrong\u003Ehypercoagulable risk\u003C/strong\u003E and contributes to systemic complications. Treatment therefore includes \u003Cstrong\u003Erestricting methionine intake\u003C/strong\u003E (to reduce precursor load) and giving \u003Cstrong\u003Epyridoxine (B6)\u003C/strong\u003E in patients who are responsive, often alongside \u003Cstrong\u003Efolate support\u003C/strong\u003E to optimize homocysteine metabolism. Early treatment can \u003Cstrong\u003Esubstantially reduce the risk of thrombosis\u003C/strong\u003E and improve long\u2011term outcomes, even though it is not a complete \u201Ccure.\u201D\u003C/p\u003E\n\u003Cp\u003EThe other options fit different disorders: \u003Cstrong\u003Eblood pressure/aortic management\u003C/strong\u003E aligns more with connective tissue aortopathy; \u003Cstrong\u003Ecysteamine\u003C/strong\u003E treats cystinosis; and a \u003Cstrong\u003Elow\u2011lysine diet\u003C/strong\u003E is used for conditions such as glutaric acidemia type I rather than this presentation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1540,
    "Name": "OKN drum in horizontal nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 1-year-old with congenital horizontal nystagmus needs an estimate of visual acuity using an OKN drum. Given the existing horizontal eye movements, what is the correct way to use the OKN drum to assess vision?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ERotate the OKN drum vertically (up or down).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe OKN drum is meant to trigger an \u003Cstrong\u003Eoptokinetic response\u003C/strong\u003E\u2014a pattern of \u003Cstrong\u003Eslow tracking\u003C/strong\u003E in the direction of the moving stripes with \u003Cstrong\u003Efast corrective \u201Crefixation\u201D jerks\u003C/strong\u003E in the opposite direction. In a child who already has \u003Cstrong\u003Ehorizontal nystagmus\u003C/strong\u003E, rotating the drum horizontally can make the OKN response \u003Cstrong\u003Ehard to recognize\u003C/strong\u003E, because the induced movements can be \u003Cstrong\u003Emasked by the baseline horizontal oscillations\u003C/strong\u003E. Rotating the drum \u003Cstrong\u003Evertically\u003C/strong\u003E avoids that overlap and makes it easier to detect a \u003Cstrong\u003Eclear vertical OKN response\u003C/strong\u003E. If a vertical OKN response is present, it generally indicates that vision is \u003Cstrong\u003Eat least around 20/400 or better\u003C/strong\u003E (a coarse screening threshold rather than a precise acuity measurement).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1541,
    "Name": "S1 hemangioma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3\u2011month\u2011old has a large facial capillary hemangioma in the segment 1 distribution causing significant ptosis (MRD \u22121). What is the most appropriate next step in management?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-a2c28c57-0393-4295-8037-aaf523511f8a.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMRI and MRA of the brain.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EA large segmental facial hemangioma in the \u003Cstrong\u003Esegment 1 (frontotemporal) distribution\u003C/strong\u003E raises concern for \u003Cstrong\u003EPHACE syndrome\u003C/strong\u003E, in which \u003Cstrong\u003Earterial cerebrovascular anomalies\u003C/strong\u003E can coexist with the cutaneous lesion. Because \u003Cstrong\u003Epropranolol can lower blood pressure\u003C/strong\u003E, starting it before defining the cerebral vasculature can be risky if the child has \u003Cstrong\u003Estenosis, hypoplasia, or other cerebrovascular abnormalities\u003C/strong\u003E, since reduced perfusion may precipitate ischemic complications. The safest \u201Cnext step\u201D is therefore \u003Cstrong\u003Eneurovascular imaging (MRI/MRA)\u003C/strong\u003E to evaluate for associated intracranial/arterial abnormalities; once this risk is assessed, hemangioma-directed therapy (often beta\u2011blocker treatment) can be pursued more safely.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1542,
    "Name": "Infected dacryocystocele",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a 1-week-old with an infected congenital dacryocystocele, which management option should be avoided?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-7cb7fb1e-5453-41c8-b33f-e6a7c6225d6c.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EExternal skin incision to decompress the sac.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EAn infected congenital dacryocystocele is typically due to \u003Cstrong\u003Eobstruction at the distal nasolacrimal duct with distention of the lacrimal sac\u003C/strong\u003E, often accompanied by an \u003Cstrong\u003Eintranasal cyst\u003C/strong\u003E under the inferior turbinate. When infection is present, treatment focuses on \u003Cstrong\u003Esystemic antibiotics\u003C/strong\u003E and \u003Cstrong\u003Erelieving the obstruction at its anatomic site\u003C/strong\u003E, most commonly with \u003Cstrong\u003Enasolacrimal duct probing\u003C/strong\u003E, sometimes combined with \u003Cstrong\u003Eendoscopic intranasal cyst management\u003C/strong\u003E when a nasal component contributes to persistent blockage or respiratory issues.\u003C/p\u003E\n\u003Cp\u003EAn external cut-down through the skin over the lacrimal sac is avoided because it does not address the underlying distal obstruction and carries a significant risk of creating a \u003Cstrong\u003Epersistent cutaneous lacrimal fistula\u003C/strong\u003E, which can become a chronic drainage problem.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1543,
    "Name": "Pediatric TED",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn children with thyroid eye disease, which clinical feature is much less common than it is in adults?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EExtraocular muscle fibrosis.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EPediatric thyroid eye disease is generally \u003Cstrong\u003Eless frequent and typically milder\u003C/strong\u003E than adult disease, so children more often show \u003Cstrong\u003Esoft-tissue signs\u003C/strong\u003E such as \u003Cstrong\u003Eproptosis\u003C/strong\u003E, \u003Cstrong\u003Eupper lid retraction\u003C/strong\u003E, \u003Cstrong\u003Elid lag\u003C/strong\u003E, and \u003Cstrong\u003Eperiorbital fullness/edema\u003C/strong\u003E. In contrast, the more advanced \u201Cburned-out\u201D manifestations seen in adults\u2014particularly \u003Cstrong\u003Erestrictive myopathy from extraocular muscle fibrosis\u003C/strong\u003E\u2014are \u003Cstrong\u003Euncommon in children\u003C/strong\u003E, which is why significant motility restriction is less typical in pediatric TED.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1544,
    "Name": "Upper eyelid coloboma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA newborn has a congenital eyelid coloboma. In the syndrome most commonly linked to this type of eyelid defect, what additional eye finding would you expect?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-ff784fd0-b830-457d-a84e-23683c045d33.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELimbal (epibulbar) dermoid.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EAn \u003Cstrong\u003Eupper eyelid coloboma\u003C/strong\u003E is classically associated with \u003Cstrong\u003EGoldenhar syndrome (oculo\u2011auriculo\u2011vertebral spectrum)\u003C/strong\u003E. One of the most typical accompanying ocular findings in this syndrome is an \u003Cstrong\u003Eepibulbar/limbal dermoid\u003C/strong\u003E, often located at the inferotemporal limbus. Goldenhar can also present with other ocular features such as \u003Cstrong\u003Emicrophthalmia, coloboma involving other ocular structures, strabismus, and refractive error\u003C/strong\u003E, but the \u201Cclassic\u201D paired finding tested most often is the \u003Cstrong\u003Elimbal dermoid\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EA helpful distinction is that \u003Cstrong\u003Elower eyelid colobomas\u003C/strong\u003E are more classically associated with \u003Cstrong\u003ETreacher\u2011Collins syndrome\u003C/strong\u003E, whereas \u003Cstrong\u003Eupper eyelid colobomas\u003C/strong\u003E point you toward \u003Cstrong\u003EGoldenhar/OAV spectrum\u003C/strong\u003E\u2014and that is why the expected ocular association is the \u003Cstrong\u003Elimbal dermoid\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1545,
    "Name": "Congenital ptosis: amblyopia mechanism",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old has a longstanding droopy right upper eyelid consistent with congenital ptosis. Which type of amblyopia is most commonly responsible for reduced vision in this situation?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-787b2683-280e-46e1-8cb6-fb4ac832b1db.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAnisometropic amblyopia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn congenital ptosis, reduced vision is most often due to \u003Cstrong\u003Erefractive causes\u003C/strong\u003E, particularly \u003Cstrong\u003Eanisometropia and associated astigmatism\u003C/strong\u003E, rather than true deprivation. \u003Cstrong\u003EOcclusion (deprivation) amblyopia is uncommon\u003C/strong\u003E unless the lid physically blocks the visual axis for a substantial portion of the time. Even when ptosis looks significant, many children adopt a \u003Cstrong\u003Ecompensatory chin-up posture\u003C/strong\u003E that helps maintain a usable visual axis and reduces the risk of deprivation amblyopia.\u003C/p\u003E\n\u003Cp\u003EAnother key point is that congenital ptosis is frequently associated with \u003Cstrong\u003Epersistent astigmatism\u003C/strong\u003E, and this refractive component can remain \u003Cstrong\u003Eeven after ptosis repair\u003C/strong\u003E. For that reason, management should not stop at surgery: \u003Cstrong\u003Eaccurate refraction with appropriate spectacle correction\u003C/strong\u003E and \u003Cstrong\u003Econtinued amblyopia treatment when indicated\u003C/strong\u003E are necessary to optimize visual outcomes.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1546,
    "Name": "Axenfeld\u2013Rieger syndrome gene association",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 18-year-old has anterior segment findings consistent with the condition shown and is being treated for glaucoma in both eyes. Which gene mutation best explains this ocular syndrome?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-54f41ea2-1285-4f38-8edf-9c9ff160c624.png\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-3e1917ea-78da-4a02-ae2b-1bf9e36b9031.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPITX2.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe ocular findings described are characteristic of \u003Cstrong\u003EAxenfeld\u2013Rieger syndrome\u003C/strong\u003E, which features \u003Cstrong\u003Eanterior segment dysgenesis\u003C/strong\u003E such as \u003Cstrong\u003Eposterior embryotoxon\u003C/strong\u003E, \u003Cstrong\u003Eiris strands bridging to the angle\u003C/strong\u003E, and \u003Cstrong\u003Epupillary displacement (corectopia)\u003C/strong\u003E, often accompanied by \u003Cstrong\u003Eearly-onset glaucoma\u003C/strong\u003E due to \u003Cstrong\u003Eangle abnormalities\u003C/strong\u003E. Axenfeld\u2013Rieger syndrome is most commonly \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E, and a major gene associated with this phenotype is \u003Cstrong\u003EPITX2\u003C/strong\u003E (with \u003Cstrong\u003EFOXC1\u003C/strong\u003E also classically implicated, though it is not one of the listed choices).\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003EHere are the conditions classically linked to the \u003Cem\u003Eother\u003C/em\u003E gene options:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMYOC (myocilin)\u003C/strong\u003E \u2192 most strongly associated with \u003Cstrong\u003Ejuvenile\u2011onset open\u2011angle glaucoma (JOAG)\u003C/strong\u003E and can also be seen in \u003Cstrong\u003Eadult primary open\u2011angle glaucoma\u003C/strong\u003E.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EOPTN (optineurin)\u003C/strong\u003E \u2192 associated with \u003Cstrong\u003Eopen\u2011angle glaucoma\u003C/strong\u003E, particularly forms described as \u003Cstrong\u003Enormal\u2011tension glaucoma susceptibility\u003C/strong\u003E, and certain pathogenic variants (e.g., E50K) are well known in inherited glaucoma literature.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EOPA1\u003C/strong\u003E \u2192 classically causes \u003Cstrong\u003Eautosomal dominant optic atrophy (DOA / \u201CKjer\u201D optic atrophy)\u003C/strong\u003E and can present as \u003Cstrong\u003EDOA\u2011plus\u003C/strong\u003E with extra\u2011ocular neurologic features in some carriers.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1547,
    "Name": "INO",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 33-year-old woman with neurologic symptoms has slow adduction of the right eye on exam, consistent with internuclear ophthalmoplegia. Which statement about this condition is true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe abducting eye shows horizontal nystagmus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EInternuclear ophthalmoplegia results from a \u003Cstrong\u003Emedial longitudinal fasciculus (MLF) lesion\u003C/strong\u003E, which disrupts the normal linkage between \u003Cstrong\u003Eabduction of one eye and adduction of the fellow eye\u003C/strong\u003E during horizontal gaze. This produces \u003Cstrong\u003Eslow or limited adduction\u003C/strong\u003E of the affected eye and a compensatory \u003Cstrong\u003Eabducting (dissociated) nystagmus\u003C/strong\u003E in the fellow eye when looking to the opposite side. The lesion localizes \u003Cstrong\u003Eto the same side as the adduction deficit\u003C/strong\u003E, and \u003Cstrong\u003Econvergence is typically preserved\u003C/strong\u003E, so adduction improves when the patient converges. Medial rectus fibrosis is not the usual mechanism here; the problem is \u003Cstrong\u003Ecentral internuclear signaling\u003C/strong\u003E, not primary extraocular muscle scarring.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1548,
    "Name": "Kestenbaum\u2013Anderson for nystagmus head turn",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old with congenital nystagmus uses a large left head turn to reduce the nystagmus, and prism glasses were not tolerated. Which surgical option can be used to lessen this compensatory head turn?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EIn congenital nystagmus, a head turn usually reflects a \u003Cstrong\u003Enull zone\u003C/strong\u003E where the nystagmus intensity is lowest and vision is best. The purpose of the Kestenbaum\u2013Anderson procedure is to \u003Cstrong\u003Eshift the null zone toward primary position\u003C/strong\u003E, so the child no longer needs a large compensatory head posture to see clearly. For a \u003Cstrong\u003Eleft head turn\u003C/strong\u003E, the eyes are surgically rotated \u003Cstrong\u003Eto the left\u003C/strong\u003E, achieved by combining \u003Cstrong\u003Eweakening (recession) of the left medial rectus and right lateral rectus\u003C/strong\u003E with \u003Cstrong\u003Estrengthening (resection) of the left lateral rectus and right medial rectus\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EA different strategy sometimes used is \u003Cstrong\u003Erecession of all four horizontal rectus muscles posterior to the equator\u003C/strong\u003E to dampen nystagmus, but placing them \u003Cstrong\u003Eanterior\u003C/strong\u003E to the equator is not the intended approach for that alternative technique.\u003C/p\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003ESo,\u003C/span\u003EThe appropriate operation is the \u003Cstrong\u003EKestenbaum\u2013Anderson pattern that rotates the eyes toward the left\u003C/strong\u003E to bring the \u003Cstrong\u003Enull zone\u003C/strong\u003E closer to primary position and reduce the head turn.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1549,
    "Name": "Marfan ectopia lentis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 8-year-old with Marfan syndrome has marked lens subluxation with minimal zonular support. Glasses or other refractive correction does not provide acceptable vision, and lensectomy is planned. Which option is the least suitable intraocular lens or visual rehabilitation approach in this child?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ETraditional anterior chamber intraocular lens.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn a child with Marfan-related ectopia lentis, the capsule\u2013zonule complex is often \u003Cstrong\u003Etoo unstable to support a standard posterior chamber IOL\u003C/strong\u003E, so management frequently aims for the safest long-term optical plan. Many pediatric surgeons prefer to leave the child \u003Cstrong\u003Eaphakic initially\u003C/strong\u003E and achieve good vision with \u003Cstrong\u003Econtact lenses (often best quality)\u003C/strong\u003E or aphakic spectacles, because these options avoid implant-related risks while the eye is still growing and the child will need long-term follow-up.\u003C/p\u003E\n\u003Cp\u003EWhen an IOL is considered without capsular support, \u003Cstrong\u003Eiris-fixated\u003C/strong\u003E and \u003Cstrong\u003Escleral-fixated\u003C/strong\u003E lenses are possible, but in children there is ongoing concern about \u003Cstrong\u003Elong-term complications\u003C/strong\u003E such as \u003Cstrong\u003Ecorneal endothelial cell loss\u003C/strong\u003E, \u003Cstrong\u003Elens dis-enclavation (iris-claw)\u003C/strong\u003E, \u003Cstrong\u003Esuture-related failure/breakage\u003C/strong\u003E, and the need for reoperation over decades.\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003Etraditional anterior chamber IOL\u003C/strong\u003E is generally viewed as the poorest choice in this age group because it sits close to the cornea and angle, increasing the risk of \u003Cstrong\u003Echronic endothelial trauma and progressive cell loss\u003C/strong\u003E, as well as other anterior segment complications over a long lifetime.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1550,
    "Name": "Intermittent exotropia: type of suppression",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 48-year-old has a recorded intermittent exotropia of 30 prism diopters, demonstrates good stereopsis (40 seconds of arc), and reports no history of diplopia. Which type of suppression is most likely present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EFacultative suppression.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis pattern fits an intermittent deviation where binocular function is still strong: \u003Cstrong\u003Egood stereoacuity implies the visual system can fuse when the eyes are aligned\u003C/strong\u003E. The lack of diplopia suggests that when the eye drifts out, the patient briefly uses \u003Cstrong\u003Ea suppression mechanism to avoid double vision\u003C/strong\u003E, but that suppression must \u003Cstrong\u003Eturn off when alignment is restored\u003C/strong\u003E, otherwise stereo would be consistently poor. That \u201Con only when misaligned\u201D behavior defines \u003Cstrong\u003Efacultative suppression\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EIn contrast, \u003Cstrong\u003Eobligatory suppression is present all the time\u003C/strong\u003E (even when the eyes are straight), which would be expected to \u003Cstrong\u003Edegrade binocular vision\u003C/strong\u003E and is more in line with persistent sensory loss such as amblyopia. \u201CCentral\u201D and \u201Cperipheral\u201D describe \u003Cem\u003Ewhere\u003C/em\u003E suppression occurs (to prevent confusion versus diplopia), but the key clue here is the \u003Cem\u003Eintermittent\u003C/em\u003E nature with preserved stereo\u2014pointing to \u003Cstrong\u003Esuppression that is conditional, not constant\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1551,
    "Name": "One-eye surgery for 20\u0394 partially accommodative esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old with partially accommodative esotropia has a residual 20 prism diopters of esotropia at distance despite full cycloplegic correction, and amblyopia has already been treated. The parent will only consent to surgery on one eye. Using the provided surgical dosage table, what is the most appropriate surgical plan?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-19-c11978b8-605b-4a1d-9a57-619772deb8dc.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EA unilateral recess\u2013resect procedure: medial rectus recession 3.5 mm plus lateral rectus resection 5.0 mm in the same eye.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe child has \u003Cstrong\u003Ea true residual 20\u0394 esotropia\u003C/strong\u003E even with full cycloplegic correction, so surgery should target \u003Cstrong\u003Ethe nonaccommodative (residual) component\u003C/strong\u003E. The dosage chart provided is for \u003Cstrong\u003Ebilateral\u003C/strong\u003E surgery: for 20\u0394, it shows \u003Cstrong\u003E3.5 mm recession of both medial recti\u003C/strong\u003E or \u003Cstrong\u003E5.0 mm resection of both lateral recti\u003C/strong\u003E. If you perform only one of those bilateral plans on a single eye, you would expect \u003Cstrong\u003Eroughly half the intended effect\u003C/strong\u003E, leaving a substantial residual deviation.\u003C/p\u003E\n\u003Cp\u003EWhen only one eye can be operated, the standard way to approximate the bilateral \u201Cdose\u201D is a \u003Cstrong\u003Eone-eye recess\u2013resect\u003C/strong\u003E: combine \u003Cstrong\u003Ea medial rectus recession\u003C/strong\u003E (to weaken the adducting pull) with \u003Cstrong\u003Ea lateral rectus resection\u003C/strong\u003E (to strengthen the abducting pull) in the same eye. Using the table values for a 20\u0394 target, pairing \u003Cstrong\u003E3.5 mm medial rectus recession\u003C/strong\u003E with \u003Cstrong\u003E5.0 mm lateral rectus resection\u003C/strong\u003E effectively \u201Cadds\u201D the corrective effect from each muscle so the combined result is designed to address \u003Cstrong\u003Ethe full 20\u0394\u003C/strong\u003E rather than half.\u003C/p\u003E\n\u003Cp\u003EAlso, simply \u201Csplitting the difference\u201D into equal recession and resection amounts is not ideal because \u003Cstrong\u003Erecessions and resections do not produce identical prism-diopter effects per millimeter\u003C/strong\u003E, and \u003Cstrong\u003Emedial vs lateral rectus dose\u2013response differs\u003C/strong\u003E, so averaging risks \u003Cstrong\u003Esystematic under- or overcorrection\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1552,
    "Name": "Blood supply to extraocular muscles",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich option most accurately describes how the ophthalmic (and related) arterial branches supply the extraocular muscles?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe lateral muscular branch of the ophthalmic artery supplies the lateral rectus, superior rectus, superior oblique, and levator palpebrae.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe ophthalmic artery gives off \u003Cstrong\u003Emuscular branches\u003C/strong\u003E that feed the extraocular muscles. A useful way to remember the split is: \u003Cstrong\u003Ethe lateral muscular branch supplies the \u201Clateral/superior\u201D group (lateral rectus, superior rectus, superior oblique, and levator)\u003C/strong\u003E, while \u003Cstrong\u003Ethe medial muscular branch supplies the \u201Cmedial/inferior\u201D group (medial rectus, inferior rectus, and inferior oblique)\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EThis matters clinically because the rectus muscles also contribute \u003Cstrong\u003Eanterior ciliary arteries\u003C/strong\u003E, which are a major component of \u003Cstrong\u003Eanterior segment perfusion\u003C/strong\u003E. The \u003Cstrong\u003Esuperior and inferior recti\u003C/strong\u003E (not the medial and lateral recti as a pair) are typically emphasized as carrying a large share of this anterior segment contribution, which is why operating on multiple rectus muscles\u2014especially several in the same eye\u2014raises concern for anterior segment ischemia.\u003C/p\u003E\n\u003Cp\u003EFinally, the infraorbital artery contribution is more relevant to the \u003Cstrong\u003Einferior rectus and inferior oblique\u003C/strong\u003E, not the superior oblique and lateral rectus, making that pairing incorrect.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1553,
    "Name": "Visual axis definition",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly defines the eye\u2019s visual axis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAn imaginary line connecting the fixation point and the fovea.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Evisual axis\u003C/strong\u003E represents the line of sight used for fixation: it links the \u003Cstrong\u003Eobject being looked at (fixation point)\u003C/strong\u003E to the \u003Cstrong\u003Efovea\u003C/strong\u003E, where the sharpest vision occurs. This is why it is the most relevant \u201Caxis\u201D for describing alignment and where the eye is actually aimed during viewing.\u003C/p\u003E\n\u003Cp\u003EBy contrast, the statement describing a line through the optical centers corresponds to the \u003Cstrong\u003Eoptical axis\u003C/strong\u003E, which is an anatomic/optical reference line through the eye\u2019s refracting elements rather than the line used for fixation. The statement describing a line perpendicular to the cornea through the pupil center defines the \u003Cstrong\u003Epupillary axis\u003C/strong\u003E. The remaining statement does not correspond to a standard ocular axis used in clinical optics.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1554,
    "Name": "Kawasaki disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA hospitalized 4-year-old has fever, bilateral red eyes with photophobia, fissured lips, and redness of the palms and soles, suggesting a systemic inflammatory syndrome. Which test is most crucial for guiding management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EEchocardiography.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003EKawasaki disease\u003C/strong\u003E, a \u003Cstrong\u003Emedium\u2011vessel vasculitis\u003C/strong\u003E in children. The management priority is evaluating for \u003Cstrong\u003Ecoronary artery involvement\u003C/strong\u003E, because the most serious complications are \u003Cstrong\u003Ecoronary artery dilation/aneurysms\u003C/strong\u003E and associated cardiac morbidity. A \u003Cstrong\u003E2\u2011D echocardiogram\u003C/strong\u003E is therefore essential early to assess the coronary arteries and guide urgency and follow\u2011up.\u003C/p\u003E\n\u003Cp\u003EOcular inflammation can occur (including \u003Cstrong\u003Econjunctival injection\u003C/strong\u003E and sometimes \u003Cstrong\u003Eanterior uveitis\u003C/strong\u003E), but these findings are typically \u003Cstrong\u003Enot the main determinant of systemic risk\u003C/strong\u003E. The life\u2011threatening concern is \u003Cstrong\u003Ecardiac\u003C/strong\u003E, so the most important test is \u003Cstrong\u003Eechocardiography\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1555,
    "Name": "CN III divisions: who innervates what?",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly describes how the oculomotor nerve divides and which extraocular muscles each division supplies?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ECN III splits into upper and lower divisions; the upper division supplies levator palpebrae and superior rectus, while the lower division supplies medial rectus, inferior rectus, and inferior oblique.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe oculomotor nerve divides in the orbit into \u003Cstrong\u003Etwo branches\u003C/strong\u003E with a predictable pattern. The \u003Cstrong\u003Eupper division\u003C/strong\u003E supplies \u003Cstrong\u003Elevator palpebrae superioris\u003C/strong\u003E and \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E. The \u003Cstrong\u003Elower division\u003C/strong\u003E supplies \u003Cstrong\u003Emedial rectus\u003C/strong\u003E, \u003Cstrong\u003Einferior rectus\u003C/strong\u003E, and \u003Cstrong\u003Einferior oblique\u003C/strong\u003E. A useful extra clinical detail is that the \u003Cstrong\u003Eparasympathetic fibers to the pupil (sphincter pupillae) and accommodation (ciliary muscle)\u003C/strong\u003E travel with the \u003Cstrong\u003Elower-division pathway\u003C/strong\u003E, classically alongside the branch going to the \u003Cstrong\u003Einferior oblique\u003C/strong\u003E via the ciliary ganglion.\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-02-19-5ef25595-1aef-4c93-9e8d-929ebb0125da.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1556,
    "Name": "Neonatal chlamydial conjunctivitis: treatment",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 7-day-old newborn has bilateral mucous discharge with papillary conjunctival inflammation and pseudomembranes, and there are strong maternal risk factors for sexually transmitted infection. What is the most appropriate treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EOral macrolide antibiotic.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Eneonatal chlamydial conjunctivitis\u003C/strong\u003E (ophthalmia neonatorum due to \u003Cstrong\u003EChlamydia trachomatis\u003C/strong\u003E): onset around \u003Cstrong\u003Ethe first 1\u20132 weeks of life\u003C/strong\u003E, \u003Cstrong\u003Emucopurulent discharge\u003C/strong\u003E, and a \u003Cstrong\u003Epapillary\u003C/strong\u003E conjunctival response; \u003Cstrong\u003Epseudomembranes\u003C/strong\u003E can appear in more significant cases. \u003Cstrong\u003EPremature rupture of membranes\u003C/strong\u003E increases the chance of earlier exposure, so symptoms can show up sooner than the typical window.\u003C/p\u003E\n\u003Cp\u003EThe key management point is that treatment should be \u003Cstrong\u003Esystemic\u003C/strong\u003E, not just topical, because chlamydial infection in neonates can involve more than the eyes and is associated with \u003Cstrong\u003Epneumonia\u003C/strong\u003E and \u003Cstrong\u003Eotitis media\u003C/strong\u003E. Therefore, a \u003Cstrong\u003Esystemic macrolide (classically oral erythromycin)\u003C/strong\u003E is used rather than topical therapy alone.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are not appropriate:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ETopical erythromycin alone may reduce surface bacterial load but \u003Cstrong\u003Edoes not adequately treat or prevent systemic disease\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003EObservation fits \u003Cstrong\u003Echemical conjunctivitis\u003C/strong\u003E, which typically occurs very early and resolves quickly, not at 7 days with this inflammatory picture.\u003C/li\u003E\n\u003Cli\u003ETrifluridine is an antiviral used for \u003Cstrong\u003Eherpetic\u003C/strong\u003E eye disease, which more often presents later and with different clues (e.g., vesicular skin lesions or corneal involvement).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1557,
    "Name": "Sensory nystagmus patterns vs visual acuity",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn congenital sensory nystagmus, which sequence of nystagmus patterns generally corresponds to the lowest to highest visual acuity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ESearching nystagmus \u0026lt; pendular nystagmus \u0026lt; jerk nystagmus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn congenital sensory nystagmus, the waveform often reflects how much usable foveal vision the child has. \u003Cstrong\u003ESearching nystagmus\u003C/strong\u003E tends to occur when vision is \u003Cstrong\u003Every poor\u003C/strong\u003E (often \u003Cstrong\u003Eworse than 20/200\u003C/strong\u003E), because fixation is unstable and the eyes appear to \u201Csearch\u201D for a target. \u003Cstrong\u003EPendular nystagmus\u003C/strong\u003E is common and is more typical when vision is \u003Cstrong\u003Eat least about 20/200 in one eye\u003C/strong\u003E, representing a middle range of acuity. \u003Cstrong\u003EJerk nystagmus\u003C/strong\u003E is generally linked with the \u003Cstrong\u003Ebest acuity\u003C/strong\u003E among these patterns (often around \u003Cstrong\u003E20/60\u201320/100\u003C/strong\u003E), because there is usually a more effective fixation strategy (including brief periods of better foveation).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1558,
    "Name": "Orbital subperiosteal abscess with optic nerve compromise",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old develops rapid unilateral eyelid swelling after recent dental work. Exam shows reduced vision in the affected eye, a clear afferent pupillary defect, proptosis, and restricted eye movements. CT confirms a large lateral orbital subperiosteal abscess. What is the most appropriate management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EImmediate drainage of the subperiosteal abscess with intravenous antibiotics.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis child has multiple high-risk features that indicate \u003Cstrong\u003Eurgent surgical drainage rather than observation\u003C/strong\u003E. The most important red flag is \u003Cstrong\u003Eoptic nerve compromise\u003C/strong\u003E demonstrated by \u003Cstrong\u003Ereduced visual acuity and a definite afferent pupillary defect\u003C/strong\u003E, meaning vision-threatening pressure/inflammation is already present. The abscess is also \u003Cstrong\u003Elarge\u003C/strong\u003E and located \u003Cstrong\u003Elaterally (nonmedial)\u003C/strong\u003E, which is less likely to resolve reliably with antibiotics alone. In addition, a \u003Cstrong\u003Erecent dental source\u003C/strong\u003E increases concern for \u003Cstrong\u003Eanaerobic and mixed flora\u003C/strong\u003E, making the infection more aggressive and less predictable with conservative therapy. Finally, his age (10 years) falls into the group with \u003Cstrong\u003Ehigher likelihood of refractory pathogens\u003C/strong\u003E and a lower threshold for operative management.\u003C/p\u003E\n\u003Cp\u003EOral antibiotics alone are inadequate for an orbital abscess. Delaying drainage for a trial period risks progression to \u003Cstrong\u003Eworsening optic neuropathy\u003C/strong\u003E and potential \u003Cstrong\u003Eintracranial extension\u003C/strong\u003E. Adding systemic corticosteroids up front is not the priority in an active abscess because the immediate goal is \u003Cstrong\u003Esource control\u003C/strong\u003E plus \u003Cstrong\u003Ebroad intravenous antimicrobial coverage\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1559,
    "Name": "Latent nystagmus: waveform \u002B head turn",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4-year-old with congenital esotropia reads better binocularly (20/25) than with either eye covered (20/60). He develops horizontal jerk nystagmus only during monocular occlusion and makes compensatory head turns depending on which eye is covered. What waveform is typical for this nystagmus, and which direction does he turn his head when the right eye is occluded?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EExponential decrease in slow-phase velocity; head turn to the left.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis pattern is classic for \u003Cstrong\u003Elatent nystagmus\u003C/strong\u003E: vision is \u003Cstrong\u003Ebetter with both eyes open\u003C/strong\u003E and the nystagmus \u003Cstrong\u003Eappears only when one eye is occluded\u003C/strong\u003E. The hallmark waveform is an \u003Cstrong\u003Eexponentially decreasing slow phase\u003C/strong\u003E, which contrasts with congenital motor nystagmus where the slow phase typically \u003Cstrong\u003Eincreases\u003C/strong\u003E over time.\u003C/p\u003E\n\u003Cp\u003EWhen one eye is covered in latent nystagmus, the \u003Cstrong\u003Efast phase beats toward the eye that is not occluded\u003C/strong\u003E. So with the \u003Cstrong\u003Eright eye occluded\u003C/strong\u003E, the \u003Cstrong\u003Eleft eye is the viewing eye\u003C/strong\u003E and the jerk beats \u003Cstrong\u003Eto the left\u003C/strong\u003E. To reduce the nystagmus (use the \u201Cnull\u201D), the child positions gaze so the viewing eye is in the more favorable direction; here that means he prefers to look \u003Cstrong\u003Eto the right\u003C/strong\u003E with the left eye (adducting it), which is achieved by turning the head \u003Cstrong\u003Eto the left\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EFinal sentence:\u003C/strong\u003E The correct combination is \u003Cstrong\u003Eexponential decrease in slow-phase velocity\u003C/strong\u003E with a \u003Cstrong\u003Eleft head turn\u003C/strong\u003E when the \u003Cstrong\u003Eright eye is occluded\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1560,
    "Name": "Superior segmental optic nerve hypoplasia: key maternal association",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old frequently trips over objects on the ground. Examination shows bilaterally thin superior optic disc rims with prominent peripapillary atrophy, and visual field testing demonstrates inferior field loss in both eyes. Which maternal condition is most classically linked to this finding?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Maternal diabetes.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Esuperior segmental optic nerve hypoplasia\u003C/strong\u003E, a variant of optic nerve hypoplasia where the \u003Cstrong\u003Esuperior neuroretinal rim is underdeveloped\u003C/strong\u003E, producing \u003Cstrong\u003Ecorresponding inferior visual field defects\u003C/strong\u003E\u2014which explains why the child bumps into objects at his feet. The finding of \u003Cstrong\u003Ethin superior rims with marked peripapillary changes\u003C/strong\u003E fits this pattern, and it is \u003Cstrong\u003Eclassically associated with children of diabetic mothers\u003C/strong\u003E, although sporadic cases can occur.\u003C/p\u003E\n\u003Cp\u003EOther maternal exposures (such as certain drugs/toxins) have been reported in association with optic nerve hypoplasia more broadly, but the \u003Cstrong\u003Emost characteristic association for superior segmental involvement\u003C/strong\u003E is \u003Cstrong\u003Ematernal diabetes\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1561,
    "Name": "Dacryocystocele with feeding difficulty",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA newborn has a bluish swelling just nasal to the lower eyelid near the medial canthus, without fever or skin redness. The infant also has feeding difficulty with grunting. What is the best next management step?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u0026nbsp;\u003Cimg src=\u0022/upload-2026-02-22-a4cc3aec-ddc4-4e5a-ad9d-ec580023d95d.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EImmediate lacrimal probing, with ENT endoscopic management if needed.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation most strongly fits a \u003Cstrong\u003Econgenital dacryocystocele\u003C/strong\u003E, caused by \u003Cstrong\u003Enasolacrimal duct obstruction with distention of the lacrimal sac\u003C/strong\u003E, often accompanied by a \u003Cstrong\u003Edistal intranasal cyst\u003C/strong\u003E. The key management-changing clue is the report of \u003Cstrong\u003Efeeding difficulty and grunting\u003C/strong\u003E, which raises concern for \u003Cstrong\u003Epartial nasal airway obstruction\u003C/strong\u003E from the intranasal component. Because newborns are \u003Cstrong\u003Eobligate nasal breathers\u003C/strong\u003E, even partial blockage can produce \u003Cstrong\u003Erespiratory distress during feeding\u003C/strong\u003E. In this setting, management should be \u003Cstrong\u003Eurgent decompression\u003C/strong\u003E: \u003Cstrong\u003Enasolacrimal probing\u003C/strong\u003E to relieve the obstruction, and if there is a significant nasal cyst or persistent obstruction, \u003Cstrong\u003Eendoscopic marsupialization by ENT\u003C/strong\u003E is added to definitively open the intranasal blockage.\u003C/p\u003E\n\u003Cp\u003EImaging can be helpful when the diagnosis is unclear or when alternative lesions are suspected, but here the priority is addressing \u003Cstrong\u003Efunctional airway compromise\u003C/strong\u003E. Conservative measures (massage \u00B1 antibiotics) are reasonable only when there is \u003Cstrong\u003Eno infection and no respiratory compromise\u003C/strong\u003E; delaying intervention in a symptomatic newborn risks worsening breathing/feeding issues. Routine incision/drainage as if all cases are occultly infected is not appropriate, especially when the exam suggests \u003Cstrong\u003Eno cellulitis\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1562,
    "Name": "Medial rectus recession amount for 15\u0394 esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 1-year-old with esotropia has cross-fixation and measures 15 prism diopters at both distance and near. What is the typical average bilateral medial rectus recession amount per eye for this deviation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E3.0 mm in each eye (bilateral medial rectus recessions).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EFor infantile or early-onset esotropia, surgical dosing is commonly guided by standard recession tables. A deviation of \u003Cstrong\u003E15 prism diopters\u003C/strong\u003E is considered a \u003Cstrong\u003Esmall-angle esotropia\u003C/strong\u003E, and the typical bilateral plan is \u003Cstrong\u003Eabout 3 mm recession of each medial rectus\u003C/strong\u003E. The logic is dose\u2013response: \u003Cstrong\u003Esmaller angles require smaller recessions\u003C/strong\u003E, while larger deviations progressively require \u003Cstrong\u003Elarger medial rectus recessions\u003C/strong\u003E (often exceeding \u003Cstrong\u003E5 mm\u003C/strong\u003E for large angles). Cross-fixation supports that the deviation is clinically meaningful, but it \u003Cstrong\u003Edoes not change the basic recession amount\u003C/strong\u003E for a measured 15\u0394 in a standard dosing approach.\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-02-22-c27aa6eb-1ae7-4f84-a650-ff3105442325.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1563,
    "Name": "Refractive accommodative esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old has progressively increasing inward deviation over 3 months. Exam shows about 20\u0394 esotropia at both distance and near, and cycloplegic refraction is \u002B4.00 sphere in each eye. What is the most appropriate initial management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPrescribe the full cycloplegic hyperopic correction (\u002B4.00 sphere OU).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis pattern fits \u003Cstrong\u003Erefractive accommodative esotropia\u003C/strong\u003E: onset in the typical age range, \u003Cstrong\u003Emoderate hyperopia\u003C/strong\u003E, and an esotropia that is \u003Cstrong\u003Esimilar at distance and near\u003C/strong\u003E. The key mechanism is that excessive accommodation needed to overcome hyperopia drives \u003Cstrong\u003Eaccommodative convergence\u003C/strong\u003E, pulling the eyes inward. Providing the \u003Cstrong\u003Efull cycloplegic refraction\u003C/strong\u003E reduces the accommodative demand and therefore \u003Cstrong\u003Ereduces the convergence trigger\u003C/strong\u003E, often improving or resolving the deviation.\u003C/p\u003E\n\u003Cp\u003EOver-plussing beyond the measured cycloplegic refraction is not routine because it can blur distance vision and is not necessary to address the mechanism when the cycloplegic measurement already captures the needed correction. Undercorrecting (\u201Cleaving some accommodation stimulus\u201D) risks \u003Cstrong\u003Epersistent esotropia\u003C/strong\u003E and may jeopardize binocular development.\u003C/p\u003E\n\u003Cp\u003EBifocals are mainly used when there is a \u003Cstrong\u003Enear\u2013distance disparity\u003C/strong\u003E consistent with a \u003Cstrong\u003Ehigh AC/A ratio\u003C/strong\u003E (near deviation much larger than distance). Here, the deviation is essentially the same at distance and near, so an executive bifocal is not the appropriate first step. Alongside glasses, the clinician should still watch for and treat \u003Cstrong\u003Eamblyopia\u003C/strong\u003E if present.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1564,
    "Name": "Optical penalization in amblyopia therapy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich option describes optical penalization as a method used to treat amblyopia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPrescribing a high plus lens to the sound eye to intentionally blur it for amblyopia treatment.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EOptical penalization means \u003Cstrong\u003Ereducing the visual performance of the better-seeing (sound) eye using optics\u003C/strong\u003E, so the child is encouraged to \u003Cstrong\u003Euse the amblyopic eye\u003C/strong\u003E, especially for near tasks. A \u003Cstrong\u003Ehigh plus lens\u003C/strong\u003E placed over an emmetropic sound eye creates \u003Cstrong\u003Eintentional blur (most noticeably at near)\u003C/strong\u003E by shifting the focal point, which \u201Cpenalizes\u201D the sound eye without using an occlusive patch.\u003C/p\u003E\n\u003Cp\u003EPRK is a refractive surgical procedure and is not a penalization strategy. Over-minus lenses are used to stimulate accommodation and convergence in intermittent exotropia management, not to penalize the sound eye. A high minus contact lens over an emmetropic sound eye would tend to increase accommodative demand and does not serve the goal of \u003Cstrong\u003Eblurring the sound eye to promote amblyopic-eye use\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1565,
    "Name": "Methotrexate in children",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old with oligoarticular juvenile idiopathic arthritis is doing well on weekly oral methotrexate. What is the most common adverse effect of methotrexate in children?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EGastrointestinal disturbance.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWith weekly \u003Cstrong\u003Eoral methotrexate\u003C/strong\u003E, the most frequent problem in children is \u003Cstrong\u003Egastrointestinal intolerance\u003C/strong\u003E\u2014typically \u003Cstrong\u003Enausea, abdominal discomfort, vomiting, or diarrhea\u003C/strong\u003E. This is common enough that clinicians often reduce symptoms by using \u003Cstrong\u003Efolic acid supplementation\u003C/strong\u003E and, if intolerance persists, switching from oral to \u003Cstrong\u003Esubcutaneous/intramuscular dosing\u003C/strong\u003E, which can be better tolerated in some patients.\u003C/p\u003E\n\u003Cp\u003EBy contrast, \u003Cstrong\u003Ehepatic toxicity\u003C/strong\u003E, \u003Cstrong\u003Einterstitial pneumonitis\u003C/strong\u003E, and \u003Cstrong\u003Emyelosuppression\u003C/strong\u003E are important but \u003Cstrong\u003Emuch less common\u003C/strong\u003E (though potentially serious), which is why routine monitoring is done even when the child feels well.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1566,
    "Name": "Parinaud (dorsal midbrain) syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old has months of restricted eye movements. Exam shows impaired upgaze with \u201Csinking\u201D of the eyes on attempted upgaze, and pupils that respond better to near than to light. What is the most likely underlying cause?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPinealoma.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe findings point to \u003Cstrong\u003Edorsal midbrain (Parinaud) syndrome\u003C/strong\u003E, suggested by \u003Cstrong\u003Eupgaze limitation (especially saccades)\u003C/strong\u003E, \u003Cstrong\u003Elight\u2013near dissociation\u003C/strong\u003E, and \u003Cstrong\u003Econvergence\u2013retraction movements\u003C/strong\u003E on attempted upgaze (the \u201Ceyes sink in\u201D description). In children, the most characteristic structural cause is a \u003Cstrong\u003Epineal region mass\u003C/strong\u003E, which compresses the dorsal midbrain/pretectal area and produces this classic pattern.\u003C/p\u003E\n\u003Cp\u003EThe other listed causes are less typical for this age/presentation: \u003Cstrong\u003Emidbrain infarction\u003C/strong\u003E is more characteristic in older patients, \u003Cstrong\u003Emultiple sclerosis\u003C/strong\u003E is a more common cause in young adults, and \u003Cstrong\u003Ecraniopharyngioma\u003C/strong\u003E is a suprasellar tumor classically linked to optic chiasm/visual field endocrine issues rather than the classic dorsal midbrain gaze palsy pattern.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1567,
    "Name": "4\u2011PD base\u2011out test",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4-year-old undergoes the 4\u2011prism\u2011diopter base\u2011out test. When the prism is placed in front of the right eye, the left eye abducts; when the same prism is placed in front of the left eye, neither eye moves. What diagnosis best explains this pattern?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMonofixation syndrome.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe 4\u2011PD base\u2011out test checks whether the visual system can detect a small induced disparity and then respond with \u003Cstrong\u003Ea version movement followed by a fusional vergence (refixation) movement\u003C/strong\u003E. In a normal binocular system, placing a 4\u2011PD base\u2011out prism before either eye triggers \u003Cstrong\u003Ea conjugate shift of the eyes\u003C/strong\u003E to pick up the displaced image, followed by \u003Cstrong\u003Ea corrective convergence movement\u003C/strong\u003E to re-establish single binocular fixation.\u003C/p\u003E\n\u003Cp\u003EThis child\u2019s asymmetric response suggests a \u003Cstrong\u003Esmall central suppression scotoma\u003C/strong\u003E in one eye with \u003Cstrong\u003Eperipheral fusion\u003C/strong\u003E preserved\u2014classic for monofixation. When the prism is placed before the eye with intact fixation, the fellow eye may show an initial movement (indicating the system detected image displacement), but when the prism is placed before the eye with the suppression scotoma, \u003Cstrong\u003Ethere is no drive to move\u003C/strong\u003E, because the displaced image falls into the suppressed central area and is effectively \u201Cignored.\u201D That is why you can see \u003Cstrong\u003Emovement in one testing position but no movement when the prism is switched to the other eye\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EThis pattern is not explained by simple accommodative esotropia, and it is not a normal response. Isolated amblyopia can reduce responses, but the hallmark here is \u003Cstrong\u003Eselective non-response tied to one eye consistent with a suppression scotoma\u003C/strong\u003E, which is the defining sensory feature of monofixation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1568,
    "Name": "Inferior oblique: tertiary action",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring surgery to weaken an overacting inferior oblique muscle, which movement would be reduced that corresponds specifically to this muscle\u2019s tertiary action?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELess abduction.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe inferior oblique has three actions: \u003Cstrong\u003Eprimary extorsion\u003C/strong\u003E, \u003Cstrong\u003Esecondary elevation\u003C/strong\u003E, and \u003Cstrong\u003Etertiary abduction\u003C/strong\u003E. When you weaken the inferior oblique to treat inferior oblique overaction, you reduce the muscle\u2019s overall effect, including its \u003Cstrong\u003Etertiary action\u003C/strong\u003E. Since the tertiary action of the inferior oblique is \u003Cstrong\u003Eabduction\u003C/strong\u003E, the expected effect on that specific action is \u003Cstrong\u003Ereduced abduction\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1569,
    "Name": "Craniosynostosis (Apert): common strabismus pattern",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn craniosynostosis syndromes such as Apert syndrome, which A/V pattern deviation is seen most often?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: V-pattern exotropia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn craniosynostosis syndromes (such as Apert), the strabismus pattern is strongly influenced by the \u003Cstrong\u003Eabnormal orbital anatomy\u003C/strong\u003E. These children often have \u003Cstrong\u003Ewide\u2011spaced orbits (hypertelorism)\u003C/strong\u003E and \u003Cstrong\u003Eshallow, dysmorphic orbits with abnormal orbital size/shape\u003C/strong\u003E. The shallow orbits can be associated with \u003Cstrong\u003Eproptosis\u003C/strong\u003E and, more importantly for motility, \u003Cstrong\u003Emalposition and altered pull directions of the extraocular muscles\u003C/strong\u003E. Because the bony orbit and muscle paths are distorted, the eyes frequently drift \u003Cstrong\u003Emore outward in upgaze\u003C/strong\u003E, producing a \u003Cstrong\u003EV\u2011pattern exotropia\u003C/strong\u003E, and this is commonly accompanied by \u003Cstrong\u003Einferior oblique overaction\u003C/strong\u003E (which further increases divergence in upgaze).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1570,
    "Name": "Infantile esotropia: amblyopia likelihood",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 8\u2011month\u2011old appears to have infantile (congenital) esotropia, and the deviation seems similar regardless of which eye is fixing. Which statement about amblyopia is most likely true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAmblyopia in neither eye.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWhen the deviation is \u003Cstrong\u003Ecomitant and the child alternates fixation\u003C/strong\u003E, each eye gets used often enough that \u003Cstrong\u003Eone eye is not consistently suppressed\u003C/strong\u003E, so amblyopia is less likely. Amblyopia is more expected when there is \u003Cstrong\u003Efixation preference\u003C/strong\u003E\u2014for example, if one eye is consistently the deviating/non\u2011fixing eye over time.\u003C/p\u003E\n\u003Cp\u003EInfants with long\u2011standing esotropia may also show \u003Cstrong\u003Ecross\u2011fixation\u003C/strong\u003E, where the adducting eye is used to look into the opposite temporal field. This can \u003Cstrong\u003Emimic an abduction limitation\u003C/strong\u003E, but true abduction can usually be demonstrated using \u003Cstrong\u003Edoll\u2019s head (vestibulo\u2011ocular) maneuvers\u003C/strong\u003E or by \u003Cstrong\u003Ebriefly occluding one eye while checking ductions\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1571,
    "Name": "Allergic conjunctivitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 11-year-old with weeks of itchy eyes is started on lodoxamide 0.1% for allergic conjunctivitis. The parent calls the next day upset because there is no symptomatic relief. What is the most appropriate counseling/management response?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003ELodoxamide is primarily a \u003Cstrong\u003Emast\u2011cell stabilizer\u003C/strong\u003E, so it is \u003Cstrong\u003Enot expected to give immediate relief\u003C/strong\u003E\u2014its benefit builds over \u003Cstrong\u003Eseveral days\u003C/strong\u003E because it works by \u003Cstrong\u003Epreventing mediator release\u003C/strong\u003E rather than quickly blocking histamine that is already driving itching.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ESwitching from one pure mast\u2011cell stabilizer to another (e.g., cromolyn) doesn\u2019t solve the parent\u2019s \u201Cnext-day\u201D concern because it has a similar \u003Cstrong\u003Edelayed onset\u003C/strong\u003E profile. Jumping straight to a topical steroid (e.g., loteprednol) is generally unnecessary for a mild presentation and carries \u003Cstrong\u003Esteroid risks\u003C/strong\u003E (IOP rise, cataract, infection risk) that are not justified when a safer, effective anti-allergy drop can address symptoms.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1572,
    "Name": "Dominant optic atrophy (Kjer)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old girl is referred to your office after failing a school vision screening. Her best corrected visual acuity is 20/50 OD and 20/40 OS. Her mom states that her vision seems to have gotten slowly worse over the past couple of years. There is no afferent pupillary defect. She does not display any nystagmus. Her dilated fundus exam is seen in the photo above. You perform a neurological exam which is completely normal. Which of the following is true regarding this girl\u0027s most likely ocular condition?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-23-ea117311-3fd5-48bc-a69d-76754a64965b.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EIt is associated with blue\u2013yellow (tritan) dyschromatopsia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe history and disc appearance fit \u003Cstrong\u003Edominant optic atrophy (Kjer optic atrophy)\u003C/strong\u003E: \u003Cstrong\u003Eslowly progressive bilateral vision loss\u003C/strong\u003E, typically \u003Cstrong\u003Emild to moderate\u003C/strong\u003E, often with \u003Cstrong\u003Etemporal disc pallor\u003C/strong\u003E and a characteristic excavation appearance, and usually \u003Cstrong\u003Eno nystagmus\u003C/strong\u003E. A classic functional clue is \u003Cstrong\u003Eblue\u2013yellow (tritan) color vision deficiency\u003C/strong\u003E, and long-term vision is often \u003Cstrong\u003Erelatively preserved\u003C/strong\u003E compared with more severe hereditary optic atrophies. This condition is commonly linked to \u003Cstrong\u003EOPA1 mutations\u003C/strong\u003E and follows an \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E inheritance pattern.\u003C/p\u003E\n\u003Cp\u003EThe other statements match different entities: an \u003Cstrong\u003Eautosomal recessive optic atrophy\u003C/strong\u003E tends to present \u003Cstrong\u003Eearlier\u003C/strong\u003E with \u003Cstrong\u003Emore severe vision loss\u003C/strong\u003E (often with nystagmus in a subset), and \u003Cstrong\u003Ematernal-only transmission\u003C/strong\u003E points toward \u003Cstrong\u003Emitochondrial inheritance\u003C/strong\u003E (as in Leber hereditary optic neuropathy), which more often affects \u003Cstrong\u003Eyoung males\u003C/strong\u003E rather than a girl with a long, gradual course.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003EBehr optic atrophy is another hereditary optic atrophy which is much rarer than the above diseases. Its clinical features are: onset of vision loss in early childhood (i.e. \u0026lt;10 years old), ataxia, intellectual disability, and urinary incontinence.\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1573,
    "Name": "3\u2011step test: localizing a left hypertropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 33-year-old develops diplopia after head trauma. Motility measurements show a left hypertropia that becomes larger in left gaze and also increases with a left head tilt. Based on the Parks\u2013Bielschowsky three-step test, what is the most likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ERight inferior oblique palsy.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe pattern localizes using the \u003Cstrong\u003EParks\u2013Bielschowsky 3\u2011step test\u003C/strong\u003E:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EStep 1: A \u003Cstrong\u003Eleft hypertropia\u003C/strong\u003E limits the possibilities to muscles that normally \u003Cstrong\u003Edepress the left eye\u003C/strong\u003E or \u003Cstrong\u003Eelevate the right eye\u003C/strong\u003E (because weakness in those actions allows the left eye to sit higher).\u003C/li\u003E\n\u003Cli\u003EStep 2: The hypertropia is \u003Cstrong\u003Eworse in left gaze\u003C/strong\u003E, which further narrows the problem to the pair of candidates whose vertical action is most relevant in that gaze position.\u003C/li\u003E\n\u003Cli\u003EStep 3: The hypertropia is \u003Cstrong\u003Eworse with left head tilt\u003C/strong\u003E, which identifies the muscle that fails when the eyes are challenged by the torsional demand produced by that head tilt. Putting these together points most strongly to \u003Cstrong\u003Eweakness of the right inferior oblique\u003C/strong\u003E.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1574,
    "Name": "High AC/A accommodative ET: traditional medication risk",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EA 3-year-old has intermittent esotropia that is larger at near than distance and has a high AC/A ratio. The parent refuses spectacles. Which medication has historically been used to reduce the convergence component, and what major serious adverse effect must be warned about?\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EEchothiophate iodide\u003C/strong\u003E, with the key serious risk being \u003Cstrong\u003Eprolonged paralysis during general anesthesia (especially with succinylcholine)\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EEchothiophate is a \u003Cstrong\u003Elong\u2011acting anticholinesterase\u003C/strong\u003E that increases acetylcholine at the neuromuscular and muscarinic synapses. In this setting, it is used to create \u003Cstrong\u003Echronic miosis and increased ciliary muscle tone\u003C/strong\u003E, which can \u003Cstrong\u003Ereduce accommodative effort\u003C/strong\u003E and thereby \u003Cstrong\u003Ereduce accommodative convergence\u003C/strong\u003E, helping children whose esotropia is driven by a \u003Cstrong\u003Ehigh AC/A ratio\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EThe most important safety issue is systemic cholinesterase inhibition: echothiophate can \u003Cstrong\u003Eprolong the action of depolarizing neuromuscular blockers\u003C/strong\u003E, so a child exposed to \u003Cstrong\u003Esuccinylcholine\u003C/strong\u003E may have \u003Cstrong\u003Eunexpectedly prolonged apnea/paralysis\u003C/strong\u003E. This is why families must be told to \u003Cstrong\u003Ealert anesthesiologists\u003C/strong\u003E if the child ever needs surgery. A notable additional adverse effect is \u003Cstrong\u003Eiris cyst formation\u003C/strong\u003E, which may be mitigated by \u003Cstrong\u003Ephenylephrine co\u2011administration\u003C/strong\u003E in some regimens.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1575,
    "Name": "Sturge\u2013Weber: red fundus and brain association",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old has a unilateral port-wine\u2013type facial lesion and a fundus that looks noticeably redder in one eye, along with a stroke-like episode after minor head trauma. Which intracranial abnormality is most likely associated with this syndrome?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-23-bf33205d-45a1-4454-8ad9-cf6ad714b64c.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELeptomeningeal vascular malformation.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe unilateral \u201Credder/pinker\u201D fundus strongly suggests a \u003Cstrong\u003Ediffuse choroidal hemangioma\u003C/strong\u003E, and when this occurs together with a facial \u003Cstrong\u003Eport\u2011wine stain\u003C/strong\u003E (especially around the eyelid), the classic diagnosis is \u003Cstrong\u003ESturge\u2013Weber syndrome\u003C/strong\u003E. The neurological hallmark of this syndrome is a \u003Cstrong\u003Eleptomeningeal vascular malformation (leptomeningeal angioma)\u003C/strong\u003E, which can lead to \u003Cstrong\u003Eseizures, stroke\u2011like episodes, and progressive neurologic deficits\u003C/strong\u003E, and is often associated with \u003Cstrong\u003Ecortical/subcortical calcifications\u003C/strong\u003E on imaging. The history of a stroke\u2011like event after seemingly minor head trauma fits this pattern of fragile/abnormal vascular perfusion.\u003C/p\u003E\n\u003Cp\u003EA practical clinical implication is that these children can also develop \u003Cstrong\u003Eglaucoma on the same side as the facial lesion\u003C/strong\u003E, due to either \u003Cstrong\u003Eangle dysgenesis (earlier presentation)\u003C/strong\u003E or \u003Cstrong\u003Eelevated episcleral venous pressure (later presentation)\u003C/strong\u003E, so eye pressure monitoring is important in follow-up.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1576,
    "Name": "Longest extraocular muscle tendon",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the listed extraocular muscles, which one has the longest tendon?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ELevator.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Elevator palpebrae superioris\u003C/strong\u003E is one of the muscles with a notably long tendon; among the options provided, it has the \u003Cstrong\u003Elongest tendon\u003C/strong\u003E. In contrast, the rectus muscles listed have \u003Cstrong\u003Eshorter tendons\u003C/strong\u003E compared with the levator. A useful related fact is that the \u003Cstrong\u003Esuperior oblique\u003C/strong\u003E (not listed here) has an even longer tendon overall, which is why it is often cited as having the longest tendon among the extraocular muscles.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1577,
    "Name": "ROP screening: preferred dilating drop",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring an ROP screening exam in the NICU, which dilating drop is most routinely recommended for this very young age group?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ECyclopentolate 0.5%.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EFor ROP screening, many neonatal protocols use \u003Cstrong\u003Ecyclopentolate 0.5%\u003C/strong\u003E (often paired with \u003Cstrong\u003Ephenylephrine 2.5%\u003C/strong\u003E) because it achieves reliable dilation while aiming to limit systemic adverse effects in premature infants. \u003Cbr\u003E\nThis age group is especially vulnerable to systemic absorption from eye drops, so practice guidelines commonly prefer \u003Cstrong\u003Elower concentrations/regimens\u003C/strong\u003E and careful administration (e.g., minimizing excess drops, nasolacrimal occlusion) to reduce complications.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1578,
    "Name": "Blepharophimosis syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 11-year-old girl has lifelong \u201Csleepy-looking\u201D eyelids, and her father appears to have the same inherited eyelid condition. Which systemic problem can be associated with this disorder?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-23-cf8f42f8-0656-41f7-a22a-82f96405b5a4.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPremature ovarian failure.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Eblepharophimosis\u2013ptosis\u2013epicanthus inversus syndrome (BPES)\u003C/strong\u003E, an \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E eyelid disorder characterized by \u003Cstrong\u003Enarrowed horizontal palpebral fissures (blepharophimosis)\u003C/strong\u003E, \u003Cstrong\u003Eptosis\u003C/strong\u003E, \u003Cstrong\u003Etelecanthus\u003C/strong\u003E, and \u003Cstrong\u003Eepicanthus inversus\u003C/strong\u003E. BPES has two clinical subtypes: \u003Cstrong\u003Eone form is associated with premature ovarian insufficiency\u003C/strong\u003E, which can lead to \u003Cstrong\u003Ereduced fertility/infertility\u003C/strong\u003E and earlier loss of ovarian function. Because the condition can be transmitted through an affected father, a clear family history like this supports an inherited BPES pattern, and the most important systemic association to remember is \u003Cstrong\u003Epremature ovarian failure\u003C/strong\u003E (in the subtype that includes ovarian involvement).\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003ETo connect the \u003Cem\u003Eother listed findings\u003C/em\u003E with their more typical syndromic associations:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPreauricular skin tags\u003C/strong\u003E \u2192 commonly seen in \u003Cstrong\u003EGoldenhar syndrome / oculo\u2011auriculo\u2011vertebral spectrum\u003C/strong\u003E, often along with epibulbar dermoids and vertebral anomalies.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAtrioventricular septal defect\u003C/strong\u003E \u2192 strongly associated with \u003Cstrong\u003EDown syndrome (trisomy 21)\u003C/strong\u003E and is one of its most common congenital heart lesions.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EProximal muscle weakness\u003C/strong\u003E \u2192 classically points toward \u003Cstrong\u003Emyotonic dystrophy type 2 (proximal myotonic myopathy)\u003C/strong\u003E or other proximal myopathies; myotonic dystrophy is a multisystem muscular dystrophy family with characteristic muscle weakness patterns.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1579,
    "Name": "Apert syndrome: \u201CEXCEPT\u201D feature",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with a congenital skull deformity is suspected to have Apert syndrome. Which listed feature does not support this diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAbsence of syndactyly.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EApert syndrome is a craniosynostosis syndrome in which \u003Cstrong\u003Esyndactyly is a hallmark finding\u003C/strong\u003E, often severe enough to produce a \u003Cstrong\u003E\u201Cmitten hand\u201D\u003C/strong\u003E appearance when multiple digits are fused. Because \u003Cstrong\u003Edigit fusion is expected\u003C/strong\u003E, stating that syndactyly is absent argues against Apert and therefore is the \u201CEXCEPT\u201D feature.\u003C/p\u003E\n\u003Cp\u003EOther findings can occur in Apert and therefore support the diagnosis: \u003Cstrong\u003Eautosomal dominant inheritance\u003C/strong\u003E is typical for many craniosynostosis syndromes, \u003Cstrong\u003Edevelopmental delay/intellectual impairment\u003C/strong\u003E can be present, and \u003Cstrong\u003Einternal organ malformations (including cardiac defects)\u003C/strong\u003E may occur as part of the syndrome spectrum. A useful comparator is that \u003Cstrong\u003ECrouzon syndrome\u003C/strong\u003E classically has craniosynostosis \u003Cstrong\u003Ewithout limb anomalies\u003C/strong\u003E, which helps explain why lack of syndactyly points away from Apert.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1580,
    "Name": "Gonococcal conjunctivitis in a child",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-year-old has two days of severe bilateral purulent conjunctivitis with copious green discharge, and Gram stain shows gram-negative diplococci. What is the most appropriate management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer:\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Efrequent saline lavage, ceftriaxone, and referral to child protective services\u003C/span\u003E\u003C/span\u003E\u003C/p\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\n\u003Cp\u003EThis presentation strongly suggests \u003Cstrong\u003Egonococcal conjunctivitis\u003C/strong\u003E, which is an \u003Cstrong\u003Eocular emergency\u003C/strong\u003E because it can progress rapidly and become vision-threatening if corneal involvement develops. The cornerstone of management is \u003Cstrong\u003Esystemic therapy with ceftriaxone\u003C/strong\u003E plus \u003Cstrong\u003Ecopious saline irrigation\u003C/strong\u003E to reduce bacterial load and discharge.\u003C/p\u003E\n\u003Cp\u003EIn a prepubertal child, gonococcal infection is \u003Cstrong\u003Enot typical from casual contact\u003C/strong\u003E, so clinicians must treat this as a \u003Cstrong\u003Epossible sexually transmitted infection\u003C/strong\u003E and ensure \u003Cstrong\u003Eimmediate child-safety evaluation through the appropriate protection services and multidisciplinary team\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003ETopical-only regimens (such as erythromycin) are \u003Cstrong\u003Einsufficient\u003C/strong\u003E for gonococcal disease, and oral macrolides are aimed more at chlamydial infection rather than gonorrhea. Partner treatment language applies to sexually active patients, but in this scenario the priority is \u003Cstrong\u003Esystemic treatment, safety assessment, and reporting through the proper channels\u003C/strong\u003E. If corneal disease appears, \u003Cstrong\u003Eadd intensive topical therapy\u003C/strong\u003E guided by the treating team.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1581,
    "Name": "Emmetropization and childhood hyperopia trend",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA healthy 3-year-old has \u002B2.00 D hyperopia in both eyes, normal acuity, and straight eyes. The parents ask how this refractive error typically changes as the child grows. What is the best counseling statement?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EHyperopia often increases until about age 6\u20138, then gradually decreases toward emmetropia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EChildren are typically \u003Cstrong\u003Ehyperopic early in life\u003C/strong\u003E because the eye starts with a \u003Cstrong\u003Eshorter axial length\u003C/strong\u003E and different optical proportions. As the eye grows through early childhood, hyperopia can \u003Cstrong\u003Eincrease and reach a peak around school age (roughly 6\u20138 years)\u003C/strong\u003E. After that, normal growth tends to produce a \u003Cstrong\u003Emyopic shift toward emmetropia\u003C/strong\u003E\u2014the process called \u003Cstrong\u003Eemmetropization\u003C/strong\u003E, where the refractive state moves closer to plano over time.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1582,
    "Name": "Post\u2011strabismus conjunctival granuloma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child is 9 months after bilateral medial rectus recession. A localized conjunctival \u201Clump\u201D has been present for about 8 weeks near the prior surgical site. What is the most appropriate management?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-23-be331e83-81f9-4813-885d-d302a57123b8.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ETopical steroids.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis lesion is most consistent with a \u003Cstrong\u003Epost\u2011strabismus conjunctival granuloma\u003C/strong\u003E, commonly a \u003Cstrong\u003Eforeign\u2011body (suture) granuloma\u003C/strong\u003E arising at or near the muscle reattachment site. These appear as a \u003Cstrong\u003Elocalized, raised, mildly inflamed mass\u003C/strong\u003E and are often related to a chronic reaction to suture material. First\u2011line treatment is \u003Cstrong\u003Etopical anti\u2011inflammatory therapy\u003C/strong\u003E, because many cases \u003Cstrong\u003Eshrink or resolve with topical steroids\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EExcision is generally reserved for lesions that \u003Cstrong\u003Efail to regress\u003C/strong\u003E, \u003Cstrong\u003Erecur\u003C/strong\u003E, or remain \u003Cstrong\u003Esymptomatic/persistent\u003C/strong\u003E despite adequate topical therapy. Mitomycin C is not a routine treatment for this postoperative granuloma, and simple observation risks prolonged irritation when a low\u2011risk medical option is usually effective.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1583,
    "Name": "Epiretinal membrane",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 65-year-old patient undergoes pars plana vitrectomy (PPV) for an epiretinal membrane. What is the approximate risk of developing a visually significant cataract within 2 years following surgery?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe most common complication after pars plana vitrectomy in phakic patients over 50 years is development of a visually significant \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enuclear sclerotic cataract\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAccording to the BCSC Retina text, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emore than 90% of eyes\u003C/b\u003E\u003C/span\u003E in patients over 50 years will develop a visually significant cataract within \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2 years\u003C/b\u003E\u003C/span\u003E of vitrectomy.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe mechanism is thought to relate to:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIncreased intraocular oxygen tension after removal of the vitreous gel\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOxidative damage to the crystalline lens nucleus\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAdditional long-term risk after vitrectomy includes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eopen-angle glaucoma (~10-20%)\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFurther reading:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.ajo.com/article/S0002-9394(06)00254-6/fulltext\u0022 target=\u0022_blank\u0022\u003EOpen Angle Glaucoma After Vitrectomy by Stanley Chang\u003C/a\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EDr. Stanley Chang\u2019s work demonstrated:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHigher mean IOP in vitrectomized eyes compared with fellow eyes (19.5 \u00B1 2.7 mmHg vs 14.3 \u00B1 3.0 mmHg; p = 0.0001).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIn eyes developing glaucoma post-vitrectomy, the interval to diagnosis was longer in phakic eyes (45.95 \u00B1 44.79 months) than in nonphakic eyes (18.39 \u00B1 13.76 months; p = 0.0115), suggesting the crystalline lens may be relatively protective.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EEyes already treated for glaucoma preoperatively required more medications post-vitrectomy (2.9 \u00B1 1.2 vs 2.00 \u00B1 1.4; p = 0.0215).\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1584,
    "Name": "ROP",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA pediatrician refers a newborn infant to the Ophthalmology clinic to rule out retinopathy of prematurity (ROP). The baby is currently 2 weeks old with a postconceptional age of 29 weeks. When should the first dilated fundus examination be performed?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EROP screening timing is based on:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPostnatal age\u003C/b\u003E\u003C/span\u003E (4-6 weeks after birth), OR\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003E31-33 weeks postmenstrual/postconceptional age\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E,\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EWhichever is later\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis infant is:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E2 weeks postnatal age\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E29 weeks postconceptional age\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe first screening should therefore occur at:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E4-6 weeks postnatal age \u2192 which would be \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2-4 weeks from now\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EImmediate screening is not indicated because:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERetinal vascularization has not yet progressed sufficiently to detect clinically meaningful ROP at 29 weeks postconceptional age.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EFurther reading:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.sciencedirect.com/science/article/pii/S0378378223000117\u0022 target=\u0022_blank\u0022\u003EUK screening and treatment of retinopathy of prematurity Updated 2022 Guidelines\u003C/a\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1585,
    "Name": "Papilloedema investigations",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 5-year-old girl presents with bilateral blurry vision. Fundus examination in both eyes shows severe bilateral optic disc edema with associated retinal changes as illustrated. What is the most important next diagnostic step?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-24-f6a3e388-7357-42c2-b5aa-42b5d67eaa5e.png\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe fundus photograph demonstrates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebilateral severe optic disc edema\u003C/b\u003E\u003C/span\u003E, consistent with possible \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epapilledema\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EBilateral disc edema in a child must be assumed to represent raised intracranial pressure until proven otherwise.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EUrgent neuroimaging is required before any lumbar puncture.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMRI brain\u003C/b\u003E\u003C/span\u003E is necessary to exclude:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EIntracranial mass lesions\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EHydrocephalus\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EMeningoencephalitis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EMRV (magnetic resonance venography)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is essential to exclude:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECerebral venous sinus thrombosis\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EAlthough infections (e.g., Bartonella, Toxoplasma) and inflammatory causes (e.g., sarcoidosis) can cause optic disc edema, they do not take priority over ruling out life-threatening intracranial pathology.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EERG is not helpful in evaluating optic disc edema or papilledema.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.medlink.com/media/jrp4\u0022 target=\u0022_blank\u0022\u003EPapilledema with macular star figure\u003C/a\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1586,
    "Name": "Bilateral vs unilateral SO palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is not typical when comparing findings in bilateral versus unilateral superior oblique palsy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EUnilateral cases usually have at least 15 degrees of excyclotorsion.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn superior oblique palsy, \u003Cstrong\u003Elarge excyclotorsion strongly suggests bilateral involvement\u003C/strong\u003E, not unilateral. \u003Cstrong\u003EUnilateral cases typically have minimal torsion\u003C/strong\u003E (often only a few degrees) and often show \u003Cstrong\u003Elittle or no V\u2011pattern\u003C/strong\u003E, whereas \u003Cstrong\u003Ebilateral palsy\u003C/strong\u003E is more likely to produce a \u003Cstrong\u003Esignificant V\u2011pattern\u003C/strong\u003E and \u003Cstrong\u003Egreater excyclotorsion (commonly \u0026gt;10\u00B0)\u003C/strong\u003E. A classic clue for bilateral disease is the \u201Calternating\u201D head\u2011tilt pattern: \u003Cstrong\u003Eright hypertropia on right head tilt and left hypertropia on left head tilt\u003C/strong\u003E, reflecting involvement of both superior obliques.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1587,
    "Name": "Maddox rod in esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has a large esotropia when not wearing glasses. A Maddox rod is placed in front of the left eye to measure the horizontal deviation. What relative position of the red line compared with the white light would the child report?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: The child would report a \u003Cstrong\u003Ered vertical line to the left of the white light\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003ETo measure a horizontal deviation with a Maddox rod, the rod is oriented horizontally so it produces a \u003Cstrong\u003Evertical red line\u003C/strong\u003E, allowing you to judge horizontal separation between the red line (seen by the eye behind the Maddox rod) and the white light (seen by the fellow eye). In an \u003Cstrong\u003Eesotropia\u003C/strong\u003E, the diplopia pattern is \u003Cstrong\u003Euncrossed\u003C/strong\u003E, meaning each eye\u2019s perceived image stays on its own side of space. Because the Maddox rod is over the \u003Cstrong\u003Eleft eye\u003C/strong\u003E, the red line corresponds to the left eye\u2019s perception, so it will be perceived \u003Cstrong\u003Eto the left\u003C/strong\u003E of the white light seen by the right eye.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1588,
    "Name": "Marcus Gunn jaw-winking: involved nerve",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4-month-old has mild congenital ptosis with eyelid elevation triggered by jaw movements during bottle feeding. Which nerve is classically aberrantly connected with the superior division of CN III in this condition?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ECranial nerve V3 (mandibular division of the trigeminal nerve).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is typical of \u003Cstrong\u003EMarcus\u2013Gunn jaw-winking (trigemino-oculomotor synkinesis)\u003C/strong\u003E, where \u003Cstrong\u003Ejaw movement triggers involuntary elevation of the ptotic eyelid\u003C/strong\u003E. The classic mechanism is an \u003Cstrong\u003Eaberrant connection between motor fibers of the mandibular division of CN V (V3)\u003C/strong\u003E and the \u003Cstrong\u003Elevator palpebrae superioris pathway carried by the superior division of CN III\u003C/strong\u003E, leading to \u003Cstrong\u003Eco-contraction during chewing/sucking\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EThe other trigeminal divisions listed (V1 and V2) are \u003Cstrong\u003Epurely sensory\u003C/strong\u003E, so they are not the typical motor pathway responsible for the synkinetic eyelid movement. CN VII is the motor nerve to \u003Cstrong\u003Eorbicularis oculi\u003C/strong\u003E (eyelid closure), not levator elevation, so it does not match the characteristic \u201Cjaw-wink\u201D pattern.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1589,
    "Name": "Preferential looking card",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EA preverbal 1-year-old is being assessed for visual acuity using a preferential-looking method shown in the image. Which type of visual acuity card is being used?\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-02-24-efee0630-ed39-4fc5-b843-804f32094c6f.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ETeller card.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EA Teller preferential-looking card has \u003Cstrong\u003Etwo fields\u003C/strong\u003E\u2014one side contains \u003Cstrong\u003Ehigh-contrast grating stripes\u003C/strong\u003E and the other side is \u003Cstrong\u003Eblank/gray\u003C/strong\u003E. The examiner watches whether the child \u003Cstrong\u003Econsistently looks toward the grating side\u003C/strong\u003E, indicating the stripes are being detected. By presenting \u003Cstrong\u003Eprogressively finer gratings\u003C/strong\u003E, you identify the finest stripe width the child can reliably detect, which provides an \u003Cstrong\u003Eestimate of visual acuity\u003C/strong\u003E in a nonverbal child.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; font-style: normal; font-weight: 400; line-height: 20px;\u0022\u003E\u003Cp style=\u0022font-size: 14px;\u0022\u003EHere\u2019s a quick summary of the \u003Cstrong\u003Eother choices\u003C/strong\u003E\u0026nbsp;):\u003C/p\u003E\n\u003Ch3 style=\u0022\u0022\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E* Tumbling E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul style=\u0022font-size: 14px;\u0022\u003E\n\u003Cli\u003EUses the letter \u003Cstrong\u003E\u201CE\u201D\u003C/strong\u003E shown in different orientations (up, down, left, right).\u003C/li\u003E\n\u003Cli\u003EThe child either \u003Cstrong\u003Epoints\u003C/strong\u003E to match the direction or \u003Cstrong\u003Estates\u003C/strong\u003E the direction.\u003C/li\u003E\n\u003Cli\u003EBest for children who \u003Cstrong\u003Ecan understand directions\u003C/strong\u003E but may not know letters (often older preschool age and above).\u003C/li\u003E\n\u003C/ul\u003E\n\u003Ch3 style=\u0022font-size: 14px;\u0022\u003E*Allen card\u003C/h3\u003E\n\u003Cul style=\u0022font-size: 14px;\u0022\u003E\n\u003Cli\u003EUses \u003Cstrong\u003Esimple picture optotypes\u003C/strong\u003E (common objects) to measure recognition acuity.\u003C/li\u003E\n\u003Cli\u003EDesigned for young children who can \u003Cstrong\u003Ename\u003C/strong\u003E or \u003Cstrong\u003Ematch\u003C/strong\u003E pictures.\u003C/li\u003E\n\u003Cli\u003ELess precise than standardized letter-based charts, but useful when the child can\u2019t do letters yet.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Ch3 style=\u0022font-size: 14px;\u0022\u003E* HOTV card\u003C/h3\u003E\n\u003Cul style=\u0022font-size: 14px;\u0022\u003E\n\u003Cli\u003EUses only the letters \u003Cstrong\u003EH, O, T, V\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003ECan be done as \u003Cstrong\u003Ematching\u003C/strong\u003E (child points to the same letter on a handheld card) or \u003Cstrong\u003Enaming\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003EVery common for preschool children because it\u2019s \u003Cstrong\u003Emore standardized\u003C/strong\u003E than picture charts and doesn\u2019t require knowing the full alphabet.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1590,
    "Name": "Worth 4-dot in monofixation syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old with prior strabismus surgery is tested with the Worth 4-dot. If the child has monofixation syndrome, what pattern of responses is expected at distance versus near?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EDistance: 2 or 3 lights; near: 4 lights.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EMonofixation syndrome is characterized by \u003Cstrong\u003Ea small central suppression scotoma\u003C/strong\u003E with \u003Cstrong\u003Epreserved peripheral fusion\u003C/strong\u003E. At \u003Cstrong\u003Edistance\u003C/strong\u003E, the Worth 4-dot image is more likely to fall \u003Cstrong\u003Ewithin the central suppression zone\u003C/strong\u003E, so the child may report \u003Cstrong\u003Esuppression\u003C/strong\u003E and see only \u003Cstrong\u003E2 or 3 lights\u003C/strong\u003E. At \u003Cstrong\u003Enear\u003C/strong\u003E, the target subtends a larger visual angle and is more likely to project \u003Cstrong\u003Eoutside the central scotoma\u003C/strong\u003E, allowing \u003Cstrong\u003Eperipheral fusion\u003C/strong\u003E, so the child typically reports seeing \u003Cstrong\u003Eall 4 lights\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1591,
    "Name": "Accommodative esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old with accommodative esotropia has moderate hyperopia on cycloplegic refraction and is prescribed the full correction. The parent asks whether the child will keep needing the same glasses strength over the next few years. What is the most accurate counseling statement?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EYour child\u0027s prescription will likely increase in power over the next 2 to 3 years.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn early childhood, hyperopia often \u003Cstrong\u003Eincreases until it peaks around school age (roughly 5\u20137 years)\u003C/strong\u003E as the eye continues its growth and refractive development. Because this child is only 2 years old, it is reasonable to counsel that the measured hyperopic prescription may \u003Cstrong\u003Eincrease over the next few years\u003C/strong\u003E, so the glasses strength may need to be updated. Later, as emmetropization progresses, the hyperopia may \u003Cstrong\u003Egradually decrease\u003C/strong\u003E, and some children can be carefully reduced (\u201Cweaned\u201D) from full plus over time, but this is typically considered \u003Cstrong\u003Eafter the peak years\u003C/strong\u003E and only if alignment remains stable.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1592,
    "Name": "Paralytic incomitant horizontal strabismus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFor an incomitant horizontal deviation caused by a weak horizontal muscle that still has some remaining function, what single surgical approach is most commonly chosen first?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EWeakening of the direct antagonist muscle.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWhen a weak horizontal muscle still has \u003Cstrong\u003Esome residual function\u003C/strong\u003E, the main problem is often the \u003Cstrong\u003Eunopposed pull and secondary tightness/contracture of its antagonist\u003C/strong\u003E, which mechanically prevents the weak muscle from working effectively. \u003Cstrong\u003EWeakening the antagonist reduces this restraining force\u003C/strong\u003E, improves the eye\u2019s ability to rotate toward the weak muscle\u2019s field, and typically \u003Cstrong\u003Epreserves better motility\u003C/strong\u003E than trying to \u201Cforce\u201D alignment by strengthening the weak muscle alone.\u003C/p\u003E\n\u003Cp\u003EA pure strengthening procedure on the weak muscle may not truly restore lost innervation; instead it can act like a \u003Cstrong\u003Etight tether\u003C/strong\u003E, risking \u003Cstrong\u003Erestriction\u003C/strong\u003E and limiting versions without reliably correcting the incomitance. Transposition procedures are generally reserved for situations where the muscle is \u003Cstrong\u003Eessentially nonfunctional\u003C/strong\u003E (complete palsy) and you need to recruit other muscles to substitute for the lost action. Operating on the contralateral eye can help in selected incomitance patterns, but it is \u003Cstrong\u003Enot the usual first single move\u003C/strong\u003E when the key issue is an antagonist that is overpowering a partially functioning muscle.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1593,
    "Name": "Notation for intermittent near esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old has an intermittent esotropia seen at near fixation. Which abbreviation correctly documents this deviation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003Enswer: \u003Cstrong\u003EE\u0027(T)\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EE\u003C/strong\u003E denotes \u003Cstrong\u003Eesophoria/esotropia direction (eso)\u003C/strong\u003E, and \u003Cstrong\u003E(T)\u003C/strong\u003E indicates the deviation is \u003Cstrong\u003Eintermittent\u003C/strong\u003E (only manifest some of the time). The \u003Cstrong\u003Eprime symbol (\u0027)\u003C/strong\u003E specifies \u003Cstrong\u003Enear fixation\u003C/strong\u003E. Putting these together, \u003Cstrong\u003EE\u0027(T)\u003C/strong\u003E correctly communicates \u003Cstrong\u003Eintermittent esotropia at near\u003C/strong\u003E.\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cstrong\u003EE(T)\u003C/strong\u003E means an \u003Cstrong\u003Eintermittent esotropia\u003C/strong\u003E but doesn\u2019t specify whether it\u2019s at near or distance, \u003Cstrong\u003EE\u2032\u003C/strong\u003E indicates an \u003Cstrong\u003Eeso deviation at near\u003C/strong\u003E but doesn\u2019t convey intermittency (often interpreted as a near \u003Cstrong\u003Ephoria\u003C/strong\u003E), and \u003Cstrong\u003EET\u2032\u003C/strong\u003E specifies a \u003Cstrong\u003Econstant near esotropia\u003C/strong\u003E (a near tropia present all the time).\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1594,
    "Name": "Maximizing superior rectus primary action",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen testing the superior rectus muscle, which eye position best isolates and maximizes its primary action?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAbduct the eye about 23\u00B0 from primary position.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Eprimary action of the superior rectus is elevation\u003C/strong\u003E. Because the superior rectus does not pull exactly along the visual axis in primary position (its line of pull is angled), placing the eye in about \u003Cstrong\u003E23\u00B0 of abduction\u003C/strong\u003E aligns the muscle\u2019s pull more directly with the visual axis. This makes the superior rectus act as the \u003Cstrong\u003Emost effective elevator\u003C/strong\u003E, allowing you to best assess its primary action.\u003C/p\u003E\n\u003Cp\u003EIn contrast, moving the eye far into adduction would increase the relative contribution of the muscle\u2019s \u003Cstrong\u003Etorsional component (intorsion)\u003C/strong\u003E rather than pure elevation, and \u201C67\u00B0 adduction\u201D is also not a practical physiologic position for standard clinical testing.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1595,
    "Name": "Head tilt test: primary IO overaction vs bilateral SO palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical exam finding best distinguishes bilateral primary oblique overaction from bilateral weakness of the opposing oblique muscle?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: Head tilt test.\u003C/p\u003E\n\u003Cp\u003EThe key discriminator is how the \u003Cstrong\u003Evertical deviation changes with head tilt\u003C/strong\u003E. In \u003Cstrong\u003Ebilateral superior oblique palsy\u003C/strong\u003E, the Bielschowsky head-tilt response typically shows \u003Cstrong\u003Ealternating hypertropias\u003C/strong\u003E: \u003Cstrong\u003Eright hypertropia on right tilt\u003C/strong\u003E and \u003Cstrong\u003Eleft hypertropia on left tilt\u003C/strong\u003E, because tilting recruits torsional demands that expose weakness of each superior oblique on its respective side. In contrast, \u003Cstrong\u003Eprimary inferior oblique overaction\u003C/strong\u003E is not driven by a superior oblique weakness, so the \u003Cstrong\u003Ehead-tilt\u2013induced hypertropia is usually small or negligible\u003C/strong\u003E (often without the classic alternating pattern).\u003C/p\u003E\n\u003Cp\u003EThe other options are less specific for this particular distinction: \u003Cstrong\u003Esubjective torsion\u003C/strong\u003E can be absent or unreliable due to \u003Cstrong\u003Esensory adaptation\u003C/strong\u003E; a \u003Cstrong\u003E\u0026gt;10\u0394 up/down gaze difference\u003C/strong\u003E can signal a pattern deviation but does not reliably tell you whether it is primary overaction versus secondary to antagonist palsy; and \u003Cstrong\u003Elarge vertical fusional amplitudes\u003C/strong\u003E are more helpful for separating long-standing/congenital from acute causes rather than distinguishing these two mechanisms.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1596,
    "Name": "Most common site of limbal dermoid",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhere on the limbus do limbal dermoids most commonly occur?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EInferotemporal limbus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003ELimbal dermoids are congenital choristomas that most often arise at the \u003Cstrong\u003Einferotemporal limbus\u003C/strong\u003E, classically at the corneoscleral junction. This location is also clinically useful because limbal dermoids are commonly associated with \u003Cstrong\u003Eoculo\u2011auriculo\u2011vertebral spectrum (Goldenhar syndrome)\u003C/strong\u003E, where ocular surface dermoids may coexist with craniofacial/auricular anomalies. A simple way to remember the site is that \u003Cstrong\u003Einferotemporal\u003C/strong\u003E is the limbal quadrant closest to the ear region, which is frequently involved in Goldenhar-spectrum disorders.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1597,
    "Name": "Congenital CN IV palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 12-year-old is being evaluated for a trochlear nerve palsy. Which finding would argue against a congenital (long-standing) trochlear nerve palsy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ESmall vertical fusional amplitudes.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003ECongenital trochlear nerve palsy is typically long-standing, so patients often develop \u003Cstrong\u003Ecompensatory mechanisms\u003C/strong\u003E over time. One common clue is a \u003Cstrong\u003Ehead tilt present in old photographs\u003C/strong\u003E, showing the abnormal posture existed for years. Long-term head tilt can also produce \u003Cstrong\u003Efacial asymmetry\u003C/strong\u003E from chronic posture during growth. Importantly, because the deviation has been present for a long time, these patients often develop \u003Cstrong\u003Elarge vertical fusional amplitudes\u003C/strong\u003E (they can \u201Cfuse through\u201D a larger vertical misalignment), which is a classic feature supporting a congenital palsy.\u003C/p\u003E\n\u003Cp\u003EBy contrast, \u003Cstrong\u003Esmall vertical fusional amplitudes\u003C/strong\u003E fit better with an \u003Cstrong\u003Eacquired\u003C/strong\u003E vertical deviation, where the patient has not had time to adapt and therefore cannot compensate well. Lack of recent head trauma may be reassuring, but it does not outweigh the key physiologic point that congenital cases usually show \u003Cstrong\u003Elarge\u003C/strong\u003E, not small, vertical fusional ranges.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1598,
    "Name": "Aniridia: characteristic corneal change",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old with bilateral reduced vision and horizontal jerk nystagmus has minimal visible iris tissue on exam. Which corneal finding is most classically associated with this condition?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-24-b0f06b84-3e89-473c-8440-90035166153e.png\u0022\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ECorneal opacification.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Eaniridia\u003C/strong\u003E, where the iris is \u003Cstrong\u003Ehypoplastic rather than truly absent\u003C/strong\u003E and patients commonly have \u003Cstrong\u003Efoveal hypoplasia and nystagmus\u003C/strong\u003E, leading to reduced visual acuity. The corneal complication most characteristic of aniridia is a progressive \u003Cstrong\u003Eaniridia-associated keratopathy\u003C/strong\u003E, driven by \u003Cstrong\u003Elimbal stem cell deficiency\u003C/strong\u003E. Over time, this causes \u003Cstrong\u003Econjunctivalization, superficial vascularization, recurrent epithelial breakdown, and scarring\u003C/strong\u003E, which clinically appears as \u003Cstrong\u003Eprogressive corneal opacification\u003C/strong\u003E and can further reduce vision.\u003C/p\u003E\n\u003Cp\u003EThe other options fit different corneal disease patterns: \u003Cstrong\u003Eapical thinning with pain\u003C/strong\u003E suggests ectatic disease (e.g., keratoconus/hydrops), \u003Cstrong\u003Esevere corneal hypoesthesia\u003C/strong\u003E points toward neurotrophic causes, and \u003Cstrong\u003Ediffuse microcystic edema\u003C/strong\u003E is more typical of acute endothelial decompensation or acute IOP-related corneal edema rather than the classic long-term corneal problem in aniridia.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1599,
    "Name": "Over-elevation in adduction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn an incomitant vertical deviation, which condition would not produce overelevation of the adducted eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBrown syndrome.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EOverelevation in adduction\u003C/strong\u003E is most often linked to \u003Cstrong\u003Einferior oblique overaction\u003C/strong\u003E, commonly seen as a secondary finding when the \u003Cstrong\u003Esuperior oblique is weak\u003C/strong\u003E (so the eye elevates excessively in adduction). It can also be seen in settings where an apparent \u201Cupshoot\u201D in adduction becomes more noticeable, such as \u003Cstrong\u003Elarge-angle exotropia with a V-pattern tendency\u003C/strong\u003E, and craniofacial/orbital dysmorphism can predispose to \u003Cstrong\u003Eoblique dysfunction or pulley-related abnormalities\u003C/strong\u003E that mimic these patterns.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBrown syndrome is the opposite problem\u003C/strong\u003E: it is a \u003Cstrong\u003Emechanical restriction of elevation in adduction\u003C/strong\u003E (classically involving the superior oblique tendon\u2013trochlea complex), so instead of an upshoot you expect a \u003Cstrong\u003Elimitation of upgaze in adduction\u003C/strong\u003E and often an appearance of \u003Cstrong\u003Erelative overdepression in adduction\u003C/strong\u003E, not overelevation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1600,
    "Name": "Definition of a phoria",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly defines a phoria?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EA latent deviation that becomes apparent when fusional control is disrupted.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003Ephoria\u003C/strong\u003E is a \u003Cstrong\u003Elatent (hidden) misalignment\u003C/strong\u003E that is normally \u003Cstrong\u003Ekept in check by binocular fusion\u003C/strong\u003E, so the eyes appear straight under ordinary binocular viewing. When fusion is \u003Cstrong\u003Ebroken\u003C/strong\u003E\u2014for example during \u003Cstrong\u003Ecover testing\u003C/strong\u003E\u2014the latent deviation \u003Cstrong\u003Eshows itself\u003C/strong\u003E, because the fusional mechanism is no longer holding the eyes aligned.\u003C/p\u003E\n\u003Cp\u003EBy contrast, a \u003Cstrong\u003Etropia\u003C/strong\u003E is a \u003Cstrong\u003Emanifest deviation\u003C/strong\u003E that is present even when both eyes are open, because fusion cannot fully control it. An intermittently manifest deviation under binocular conditions would be described as an \u003Cstrong\u003Eintermittent tropia\u003C/strong\u003E, not a phoria.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1601,
    "Name": "Lisch nodules and NF1",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA boy\u2019s slit-lamp exam shows multiple small iris lesions as shown in the photo. Which associated systemic/ocular statement is most likely true?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-24-750192d5-a8c6-4992-a165-4fac0f1ffa9b.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThis boy is at higher risk for pilocytic astrocytomas of the optic nerve.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe photo shows \u003Cstrong\u003Emultiple iris melanocytic hamartomas (Lisch nodules)\u003C/strong\u003E, which are a classic ocular sign used in diagnosing \u003Cstrong\u003Eneurofibromatosis type 1 (NF1)\u003C/strong\u003E. \u003Cbr\u003E\nNF1 is strongly associated with \u003Cstrong\u003Eoptic pathway gliomas\u003C/strong\u003E, and these are most commonly \u003Cstrong\u003Epilocytic astrocytomas\u003C/strong\u003E occurring in childhood. \u003Cbr\u003E\nTherefore, the most likely true statement is that the child has increased risk of \u003Cstrong\u003Epilocytic astrocytoma involving the optic pathway/optic nerve\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPosterior subcapsular cataracts\u003C/strong\u003E are classically linked to \u003Cstrong\u003Eneurofibromatosis type 2 (NF2)\u003C/strong\u003E rather than NF1.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESpontaneous hyphema\u003C/strong\u003E is a classic association of \u003Cstrong\u003Ejuvenile xanthogranuloma (JXG)\u003C/strong\u003E involving the iris, not Lisch nodules.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003ENF1 is typically \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E, not autosomal recessive.\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1602,
    "Name": "Forceps Descemet tears",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn an infant with a Descemet membrane tear from forceps delivery, what is the most common reason for persistent long-term visual loss?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAmblyopia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EForceps-related \u003Cstrong\u003EDescemet membrane breaks\u003C/strong\u003E can cause \u003Cstrong\u003Eacute stromal/epithelial corneal edema\u003C/strong\u003E, but in many infants this corneal haze \u003Cstrong\u003Eimproves as endothelial function stabilizes\u003C/strong\u003E. The bigger long-term problem is that the scar/irregularity often induces \u003Cstrong\u003Esignificant astigmatism and anisometropia\u003C/strong\u003E, creating a chronic blur in one eye during the critical period of visual development. That sustained image degradation most commonly leads to \u003Cstrong\u003Erefractive amblyopia\u003C/strong\u003E, which becomes the main driver of lasting reduced vision unless it\u2019s detected early and treated with \u003Cstrong\u003Efull cycloplegic correction \u00B1 occlusion/penalization therapy\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are less likely as the \u003Cem\u003Emajor\u003C/em\u003E long-term cause:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECorneal edema:\u003C/strong\u003E usually \u003Cstrong\u003Etransient\u003C/strong\u003E; persistent edema can occur if endothelial damage is severe, but it is not the typical main reason for long-term loss compared with amblyopia.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESecondary glaucoma:\u003C/strong\u003E not a classic primary sequela of isolated Descemet tears from forceps; it can occur in other anterior segment/angle disorders but is not the usual outcome here.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHyphema:\u003C/strong\u003E may occur with significant birth trauma but is typically \u003Cstrong\u003Eacute\u003C/strong\u003E and not the usual cause of permanent visual deficit in this scenario.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1603,
    "Name": "Monocular elevation deficiency (MED)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has monocular elevation deficiency of the left eye with a large hypotropia and chin-up posture. Forced duction testing shows no restriction. Which surgical procedure is most appropriate?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EKnapp procedure.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EMonocular elevation deficiency (formerly \u201Cdouble elevator palsy\u201D) has two main mechanisms:\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003ERestrictive\u003C/strong\u003E: a \u003Cstrong\u003Etight inferior rectus\u003C/strong\u003E mechanically prevents elevation.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EParetic\u003C/strong\u003E: \u003Cstrong\u003Eweakness of the elevators\u003C/strong\u003E (superior rectus and/or inferior oblique) due to dysinnervation.\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cp\u003E\u003Cstrong\u003EForced duction testing is the key fork in the road.\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EIf forced ductions are positive (restriction present)\u003C/strong\u003E \u2192 treat the restriction first, typically with \u003Cstrong\u003Einferior rectus recession\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIf forced ductions are negative (no restriction)\u003C/strong\u003E \u2192 the problem is most consistent with \u003Cstrong\u003Eelevator weakness\u003C/strong\u003E, and the preferred approach is a \u003Cstrong\u003Etransposition procedure\u003C/strong\u003E to \u201Cborrow\u201D vertical elevating force from functioning muscles.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThat is exactly what the \u003Cstrong\u003EKnapp procedure\u003C/strong\u003E does: it \u003Cstrong\u003Etransposes the medial and lateral rectus muscles superiorly\u003C/strong\u003E (toward the superior rectus insertion) to augment elevation and improve the hypotropia and chin-up posture in the \u003Cstrong\u003Enon-restrictive\u003C/strong\u003E form of MED.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are wrong:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHarada\u2013Ito\u003C/strong\u003E: designed to treat \u003Cstrong\u003Etorsional diplopia/excyclotorsion\u003C/strong\u003E (selective anterior superior oblique tendon tightening), not a primary elevation deficit.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior oblique spacer\u003C/strong\u003E: used for \u003Cstrong\u003EBrown syndrome\u003C/strong\u003E (restriction of elevation in adduction due to tight SO tendon\u2013trochlea complex), not MED.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior rectus recession\u003C/strong\u003E: correct \u003Cstrong\u003Eonly if the inferior rectus is tight\u003C/strong\u003E (positive forced ductions). Here forced ductions are negative, so IR recession is not the best match.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1604,
    "Name": "Cogan lid twitch",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 45-year-old with one week of diplopia has a characteristic upper lid \u201Ctwitch\u201D/overshoot when returning to primary gaze after looking down. Which test would confirm the suspected diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAnti\u2011MuSK antibody test.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe \u201Covershoot\u201D of the upper lid when returning to primary gaze after sustained downgaze is \u003Cstrong\u003ECogan lid twitch\u003C/strong\u003E, a classic bedside sign of \u003Cstrong\u003Eocular myasthenia gravis (OMG)\u003C/strong\u003E. OMG causes \u003Cstrong\u003Efatigable weakness\u003C/strong\u003E of extraocular muscles (diplopia) and often eyelid muscles (ptosis), and confirmation is supported by \u003Cstrong\u003Emyasthenia autoantibody testing\u003C/strong\u003E. Among the options, \u003Cstrong\u003Eanti\u2011MuSK antibodies\u003C/strong\u003E are a recognized confirmatory serologic test for myasthenia.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EMRI/MRA Circle of Willis: aimed at aneurysm/vascular lesions; that would fit a painful CN III palsy workup, not a \u003Cstrong\u003Efatigable ocular motility disorder with Cogan lid twitch\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003EAnti\u2011thyrotropin receptor antibodies: support \u003Cstrong\u003Ethyroid eye disease\u003C/strong\u003E, which is typically restrictive and non\u2011fatigable, and does not produce Cogan lid twitch.\u003C/li\u003E\n\u003Cli\u003EEKG: not a diagnostic test for the cause of this ocular sign (though systemic MG can have other evaluations, EKG is not confirmatory for OMG).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1605,
    "Name": "CN VI palsy: why secondary deviation \u003E primary deviation",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a right abducens (CN VI) palsy. The deviation is smaller when the left (normal) eye fixates and larger when the right (paretic) eye fixates. What principle explains this?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe secondary deviation is larger than the primary deviation because of Hering\u2019s law.\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPrimary deviation\u003C/strong\u003E is measured while the \u003Cstrong\u003Enormal (left) eye fixates\u003C/strong\u003E; the paretic right eye is allowed to assume its underacting position, so the deviation you measure is relatively smaller.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESecondary deviation\u003C/strong\u003E is measured while the \u003Cstrong\u003Eparetic (right) eye fixates\u003C/strong\u003E. To force the weak right lateral rectus to abduct enough to fixate, the brain increases innervation to that muscle.\u003C/li\u003E\n\u003Cli\u003EBy \u003Cstrong\u003EHering\u2019s law of equal innervation\u003C/strong\u003E, the increased drive sent to the weak right lateral rectus is \u003Cstrong\u003Ealso sent to its yoke muscle\u003C/strong\u003E in the fellow eye (the \u003Cstrong\u003Eleft medial rectus\u003C/strong\u003E). That extra left medial rectus activation pulls the left eye further inward, making the measured misalignment \u003Cstrong\u003Elarger\u003C/strong\u003E.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1606,
    "Name": "Orbital rhabdomyosarcoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich finding is least likely to be a presenting feature of orbital rhabdomyosarcoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-size: 14px; font-weight: 400; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPain.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EOrbital rhabdomyosarcoma most often presents with \u003Cstrong\u003Erapid-onset proptosis\u003C/strong\u003E and \u003Cstrong\u003Eglobe displacement\u003C/strong\u003E due to \u003Cstrong\u003Emass effect\u003C/strong\u003E, frequently accompanied by \u003Cstrong\u003Eeyelid edema and conjunctival chemosis\u003C/strong\u003E from orbital congestion. \u003Cstrong\u003EPain is comparatively uncommon\u003C/strong\u003E at presentation and tends to occur only in a minority of cases (for example, if there is secondary inflammation or significant pressure effects), making it the \u003Cstrong\u003Eleast likely\u003C/strong\u003E among the listed options.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/h3\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1607,
    "Name": "Extraocular muscle innervation",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about extraocular muscle innervation is incorrect?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003Ethe nerves to the recti and superior oblique enter at two\u2011thirds of the distance from origin to insertion.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EFor the \u003Cstrong\u003Erectus muscles and the superior oblique\u003C/strong\u003E, the motor nerves typically enter the muscle belly \u003Cstrong\u003Emuch closer to the origin\u2014about the posterior one\u2011third\u003C/strong\u003E, not two\u2011thirds of the way toward the insertion. This is why \u003Cstrong\u003Eanterior segment surgery near the insertion is unlikely to injure these motor nerves\u003C/strong\u003E, whereas a deep posterior instrument/needle can.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are true:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECN IV lies outside the muscle cone\u003C/strong\u003E, so a standard retrobulbar block (within the cone) is \u003Cstrong\u003Eless likely\u003C/strong\u003E to affect superior oblique function. (Not impossible if the needle/volume tracks unusually, but the anatomic principle is correct.)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior oblique nerve injury can cause pupillary abnormalities\u003C/strong\u003E because the \u003Cstrong\u003Eparasympathetic fibers destined for the ciliary ganglion\u003C/strong\u003E travel with the \u003Cstrong\u003Einferior division of CN III\u003C/strong\u003E and run with the branch that supplies the \u003Cstrong\u003Einferior oblique\u003C/strong\u003E\u2014so injury can produce a \u003Cstrong\u003Epersistently dilated pupil\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EThe nerve to the inferior oblique enters laterally\u003C/strong\u003E as it crosses near the inferior rectus region, making the \u201Clateral entry\u201D description correct.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1608,
    "Name": "Oculocardiac reflex: highest-risk muscle",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring strabismus surgery, traction on which extraocular muscle most commonly triggers the oculocardiac reflex?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMedial rectus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Eoculocardiac reflex\u003C/strong\u003E is a trigemino\u2011vagal reflex: \u003Cstrong\u003Etraction on an extraocular muscle\u003C/strong\u003E (or pressure on the globe) sends afferent signals via the \u003Cstrong\u003Etrigeminal nerve (V1)\u003C/strong\u003E to the brainstem, which then triggers increased \u003Cstrong\u003Evagal output\u003C/strong\u003E, producing \u003Cstrong\u003Ebradycardia\u003C/strong\u003E and in severe cases \u003Cstrong\u003Earrhythmias or asystole\u003C/strong\u003E. \u003Cstrong\u003EMedial rectus traction\u003C/strong\u003E is classically the most likely to provoke this reflex during strabismus surgery.\u003C/p\u003E\n\u003Cp\u003EIf bradycardia occurs, the immediate first step is to \u003Cstrong\u003Estop traction/release the muscle\u003C/strong\u003E, and if significant or persistent, treat with an anticholinergic such as \u003Cstrong\u003EIV atropine\u003C/strong\u003E (and optimize oxygenation/anesthetic depth).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1609,
    "Name": "Phakomatoses: tumor suppressor gene \u201CNOT\u201D question",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed condition is not typically caused by a tumor suppressor gene mutation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EEncephalotrigeminal angiomatosis (Sturge\u2013Weber syndrome).\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EVon Recklinghausen disease = Neurofibromatosis type 1 (NF1)\u003C/strong\u003E, which is caused by mutation of \u003Cstrong\u003ENF1\u003C/strong\u003E, a classic \u003Cstrong\u003Etumor suppressor\u003C/strong\u003E gene.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EVon Hippel\u2013Lindau disease\u003C/strong\u003E is due to mutation in \u003Cstrong\u003EVHL\u003C/strong\u003E, also a \u003Cstrong\u003Etumor suppressor\u003C/strong\u003E gene.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ERetinoblastoma\u003C/strong\u003E is the prototype \u003Cstrong\u003Etumor suppressor\u003C/strong\u003E disease (mutation in \u003Cstrong\u003ERB1\u003C/strong\u003E).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EEncephalotrigeminal angiomatosis = Sturge\u2013Weber syndrome\u003C/strong\u003E is typically a \u003Cstrong\u003Esporadic vascular malformation syndrome\u003C/strong\u003E, not classically grouped with inherited tumor suppressor gene disorders.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1610,
    "Name": "TAO restrictive esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with thyroid-associated orbitopathy has horizontal diplopia and a CT showing extraocular muscle enlargement. The motility grid shows esotropia that is largest in right gaze and smaller in primary and left gaze. Which strabismus surgery plan is most appropriate?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-24-8d58201b-5e3e-4e79-b8db-b7f6e0f114a8.png\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-24-8cb4f6da-d2a1-4cbf-a8cd-e42bd69e218d.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ERight medial rectus recession.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn thyroid-associated orbitopathy, the misalignment is typically \u003Cstrong\u003Erestrictive\u003C/strong\u003E, not paretic. The enlarged, fibrotic muscle \u003Cstrong\u003Etethers the globe toward its field of action\u003C/strong\u003E, and the deviation becomes worse when the patient tries to look \u003Cstrong\u003Eaway\u003C/strong\u003E from the restricted muscle.\u003C/p\u003E\n\u003Cp\u003EHere, the esotropia is \u003Cstrong\u003Emuch larger in right gaze\u003C/strong\u003E than in primary and left gaze. Right gaze requires \u003Cstrong\u003Eabduction of the right eye\u003C/strong\u003E. A tight \u003Cstrong\u003Eright medial rectus\u003C/strong\u003E limits right eye abduction, so when the patient attempts right gaze the right eye cannot abduct adequately and the measured \u003Cstrong\u003Eesotropia increases\u003C/strong\u003E, matching the grid pattern. Therefore, the correct surgical strategy is to \u003Cstrong\u003Erecess (weaken) the tight, restricted muscle\u003C/strong\u003E, which is the \u003Cstrong\u003Eright medial rectus\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EWhy the other choices are wrong:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ERight lateral rectus resection\u003C/strong\u003E and \u003Cstrong\u003Ebilateral lateral rectus resection\u003C/strong\u003E are \u003Cstrong\u003Estrengthening\u003C/strong\u003E procedures. In restrictive TAO strabismus, \u003Cstrong\u003Eresection is generally avoided\u003C/strong\u003E because it can worsen restriction and create unpredictable outcomes; the main goal is to \u003Cstrong\u003Erelease restriction\u003C/strong\u003E, not \u201Cboost\u201D the antagonist.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELeft medial rectus recession\u003C/strong\u003E would address a left medial rectus restriction pattern (typically making deviation worse in left gaze), which does \u003Cstrong\u003Enot\u003C/strong\u003E fit this grid where the deviation is worst in \u003Cstrong\u003Eright\u003C/strong\u003E gaze.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1611,
    "Name": "AKC vs VKC",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical feature most helps tell atopic keratoconjunctivitis apart from vernal keratoconjunctivitis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAKC also involves the inferior palpebral conjunctiva.\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAKC classically involves the lower lid (inferior palpebral/tarsal) conjunctiva\u003C/strong\u003E and can have more chronic, year\u2011round disease tied to atopic dermatitis. This lower-lid involvement is a useful \u201Cexam differentiator.\u201D\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EVKC more classically targets the upper tarsus (giant papillae) and/or limbus\u003C/strong\u003E, often in a seasonal pattern.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are less helpful:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESeasonality\u003C/strong\u003E is more characteristic of \u003Cstrong\u003EVKC\u003C/strong\u003E, not AKC.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIntense itching and redness\u003C/strong\u003E occur in \u003Cstrong\u003Eboth\u003C/strong\u003E AKC and VKC.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EMale predominance\u003C/strong\u003E is more typical of \u003Cstrong\u003EVKC\u003C/strong\u003E (often boys/young males).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1612,
    "Name": "Avoiding anterior segment ischemia while correcting hypertropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn elderly diabetic patient will only allow surgery on one eye. You plan a lateral rectus recession and medial rectus resection for a large exotropia, and you also want to address a right hypertropia. Which additional procedure is least likely to cause anterior segment ischemia while also helping the hypertropia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EInferior oblique myectomy.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAnterior segment ischemia risk rises when multiple rectus muscles are operated in the same eye\u003C/strong\u003E, because the anterior segment circulation is largely supported by anterior ciliary arteries traveling with the rectus muscles. In an \u003Cstrong\u003Eelderly diabetic\u003C/strong\u003E (vascular risk), doing surgery on a third rectus muscle in the same sitting is particularly undesirable.\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior rectus recession\u003C/strong\u003E and \u003Cstrong\u003Einferior rectus resection\u003C/strong\u003E can help a hypertropia, but each would make this a \u003Cstrong\u003Ethree-rectus operation\u003C/strong\u003E in one eye (lateral rectus \u002B medial rectus \u002B another rectus), \u003Cstrong\u003Eincreasing ischemia risk\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior oblique tenotomy\u003C/strong\u003E weakens a depressor/intorter; weakening it would typically \u003Cstrong\u003Eworsen a hypertropia\u003C/strong\u003E rather than treat it.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior oblique myectomy\u003C/strong\u003E is an \u003Cstrong\u003Eoblique muscle procedure\u003C/strong\u003E, so it \u003Cstrong\u003Edoes not add another rectus muscle\u003C/strong\u003E to the operation (therefore \u003Cstrong\u003Eminimizing anterior segment ischemia risk\u003C/strong\u003E) and it can \u003Cstrong\u003Ereduce a hypertropia\u003C/strong\u003E when the inferior oblique is contributing (e.g., overelevation in adduction).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1613,
    "Name": "Post\u2011trauma depression deficit without entrapment",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old has facial trauma with reduced depression of the right eye. Forced ductions are negative and CT shows no muscle entrapment. What is the best management approach?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EObservation.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWith a depression deficit after trauma, the first task is to decide whether this is \u003Cstrong\u003Erestrictive entrapment\u003C/strong\u003E (which needs urgent release) or a \u003Cstrong\u003Eparetic/contusional weakness\u003C/strong\u003E (which often improves spontaneously). The key findings here are \u003Cstrong\u003Enegative forced ductions\u003C/strong\u003E and \u003Cstrong\u003Eno entrapment on CT\u003C/strong\u003E, which strongly support \u003Cstrong\u003Einferior rectus weakness/contusion\u003C/strong\u003E rather than mechanical tethering. In that setting, the most appropriate initial strategy is \u003Cstrong\u003Ewatchful waiting\u003C/strong\u003E, because post-traumatic muscle/nerve dysfunction frequently \u003Cstrong\u003Erecovers over time\u003C/strong\u003E as edema and neuropraxia resolve.\u003C/p\u003E\n\u003Cp\u003EImmediate exploration is reserved for scenarios suggesting \u003Cstrong\u003Etrue entrapment\u003C/strong\u003E (restriction on forced ductions, classic trapdoor fracture with oculocardiac symptoms, or imaging/clinical evidence of incarceration). Steroids are not the routine first-line solution when the primary issue is an isolated motility weakness without restriction. Definitive strabismus surgery (such as strengthening the depressed action or weakening the antagonist) is typically deferred until the deviation is \u003Cstrong\u003Estable\u003C/strong\u003E and \u003Cstrong\u003Espontaneous recovery has plateaued\u003C/strong\u003E, commonly over a period of months.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1614,
    "Name": "Facial angiofibromas",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has facial lesions as shown. Which retinal lesion is classically associated with the underlying syndrome?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-25-35be0a37-00c9-4b93-99b5-5bdb4ebbcfa3.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ERetinal astrocytoma.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe facial lesion shown is most consistent with \u003Cstrong\u003Efacial angiofibromas (formerly \u201Cadenoma sebaceum\u201D)\u003C/strong\u003E, which are a classic cutaneous manifestation of \u003Cstrong\u003Etuberous sclerosis complex (TSC)\u003C/strong\u003E. TSC is a phakomatosis characterized by hamartomas in multiple organs, and the characteristic retinal lesion is the \u003Cstrong\u003Eretinal astrocytic hamartoma (retinal astrocytoma)\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are less fitting:\u003C/strong\u003E capillary hemangioma is more typical of infantile hemangioma syndromes; cavernous hemangioma can be sporadic or associated with cerebral cavernous malformations; and proliferative retinal vasculopathy is not the classic retinal hallmark of TSC.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1615,
    "Name": "A\u2011pattern XT",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn an A\u2011pattern exotropia (with mild excyclotorsion) managed using a recess\u2013resect procedure, how should the horizontal rectus muscles be vertically transposed?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMedial rectus resection displaced superiorly \u002B lateral rectus recession displaced inferiorly.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EFor \u003Cstrong\u003EA\u2011pattern\u003C/strong\u003E deviations, the goal of vertical transposition of the horizontal recti is to shift the horizontal muscle vectors in a way that \u003Cstrong\u003Ereduces the greater deviation in upgaze\u003C/strong\u003E (the \u201CA\u201D opens superiorly). The classic rule is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003E\u201CMALE\u201D = Medials to the Apex, Laterals to the Empty space.\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EIn an \u003Cstrong\u003EA\u2011pattern\u003C/strong\u003E, the \u003Cstrong\u003Eapex is superior\u003C/strong\u003E (the narrow part of the \u201CA\u201D is in downgaze and the wider part is in upgaze).\u003C/li\u003E\n\u003Cli\u003ETherefore, place the \u003Cstrong\u003Emedial rectus (strengthening/resection) superiorly\u003C/strong\u003E (toward the apex) and place the \u003Cstrong\u003Elateral rectus (weakening/recession) inferiorly\u003C/strong\u003E (toward the \u201Cempty/open\u201D part).\u003C/li\u003E\n\u003Cli\u003EThis combination both addresses the exotropia (recess\u2013resect) and collapses the A\u2011pattern by appropriate vertical offsets.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1616,
    "Name": "Partially accommodative ET",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old with moderate hyperopia has an esotropia that improves but does not fully resolve with full cycloplegic correction (residual 25\u0394 at distance and near). Before bilateral medial rectus recessions, what is the best counseling about the goal of surgery?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe objective of this surgery is to produce straight eyes with glasses on.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis child has \u003Cstrong\u003Epartially accommodative esotropia\u003C/strong\u003E: full hyperopic correction reduces the deviation (from 45\u0394 to 25\u0394), but a \u003Cstrong\u003Eresidual non-accommodative component\u003C/strong\u003E remains. \u003Cstrong\u003EStrabismus surgery in this setting targets that residual deviation while the child is wearing the full plus correction.\u003C/strong\u003E It is \u003Cstrong\u003Enot\u003C/strong\u003E intended to \u201Ccure\u201D the refractive error or eliminate the need for glasses. After surgery, the child typically \u003Cstrong\u003Estill needs the hyperopic spectacles\u003C/strong\u003E to keep the accommodative component controlled and to maintain alignment.\u003C/p\u003E\n\u003Cp\u003EWhy the other choices are wrong:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ESaying the child won\u2019t need glasses after surgery is incorrect because the underlying hyperopia and accommodative component persist.\u003C/li\u003E\n\u003Cli\u003EThe goal is not straight eyes with glasses off; removing glasses would reintroduce accommodative demand and likely bring back a larger esotropia.\u003C/li\u003E\n\u003Cli\u003EBifocals are used mainly for \u003Cstrong\u003Ehigh AC/A (near deviation \u0026gt; distance)\u003C/strong\u003E; here distance and near residual deviations are the same (25\u0394 and 25\u0394\u2032), so bifocals are not the expected next step.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1617,
    "Name": "PHACES (S1 hemangioma \u002B morning glory)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2\u2011month\u2011old has a large segment 1 facial hemangioma (\u0026gt;5 cm) and morning glory disc anomaly. What associated abnormality is most likely on further workup?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EIpsilateral cerebrovascular abnormalities.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003EA large \u003Cstrong\u003Esegment 1 (frontotemporal) facial hemangioma\u003C/strong\u003E in an infant strongly suggests \u003Cstrong\u003EPHACES syndrome\u003C/strong\u003E, a neurocutaneous association defined by:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EP\u003C/strong\u003Eosterior fossa malformations\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EH\u003C/strong\u003Eemangioma (typically large, segmental facial)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA\u003C/strong\u003Erterial anomalies (especially cervicocerebral)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EC\u003C/strong\u003Eardiac defects (and/or coarctation)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EE\u003C/strong\u003Eye abnormalities\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ES\u003C/strong\u003Eternal clefting / supraumbilical raphe\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003Cp\u003Ethe \u201CA\u201D stands for \u003Cstrong\u003Earterial abnormalities\u003C/strong\u003E, and segment 1 hemangiomas are particularly linked to \u003Cstrong\u003Eipsilateral cerebrovascular anomalies\u003C/strong\u003E such as \u003Cstrong\u003Earterial hypoplasia, stenosis/occlusion, aberrant arterial origin, progressive vasculopathy, or aneurysms\u003C/strong\u003E. The added finding of \u003Cstrong\u003Emorning glory disc anomaly\u003C/strong\u003E is an important \u003Cstrong\u003Eeye abnormality\u003C/strong\u003E that further supports PHACES and increases the need for \u003Cstrong\u003Eneurovascular imaging\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are less likely:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EDilated/tortuous episcleral vessels\u003C/strong\u003E is more suggestive of conditions with elevated episcleral venous pressure (e.g., certain glaucomas/vascular syndromes).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EChoroidal hemangioma\u003C/strong\u003E is classically linked with \u003Cstrong\u003ESturge\u2013Weber syndrome.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EVentral/midline cleft\u003C/strong\u003E and cardiac defects can occur in PHACES, but \u003Cstrong\u003Esegment 1\u003C/strong\u003E hemangiomas most characteristically point to \u003Cstrong\u003Earterial/cerebrovascular abnormalities\u003C/strong\u003E on the same side.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1618,
    "Name": "Duane syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is false about Duane syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EIn most anatomical and imaging studies, the nucleus of the third cranial nerve is absent.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EDuane syndrome is a congenital cranial dysinnervation disorder primarily involving the abducens system.\u003C/strong\u003E The classic neuroanatomy is \u003Cstrong\u003Eabsent or hypoplastic CN VI (abducens) nucleus/nerve\u003C/strong\u003E, with \u003Cstrong\u003Eaberrant innervation of the lateral rectus by branches of CN III\u003C/strong\u003E, leading to co-contraction of medial and lateral rectus on attempted adduction and the characteristic \u003Cstrong\u003Eglobe retraction and palpebral fissure narrowing\u003C/strong\u003E. Therefore, saying the \u003Cstrong\u003ECN III nucleus is absent\u003C/strong\u003E is the incorrect statement; it is the \u003Cstrong\u003ECN VI nucleus/nerve\u003C/strong\u003E that is typically absent/hypoplastic.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1619,
    "Name": "PEDIG ATS: what helps in stable residual amblyopia?",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn children with stable residual amblyopia despite standard treatment, which PEDIG Amblyopia Treatment Study strategy has been shown to produce a meaningful additional improvement in visual acuity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EIncreased patching to 6 hours in patients previously patching 2 hours per day.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EStable residual amblyopia\u003C/strong\u003E means the child has already had an initial response to treatment (glasses \u00B1 patching/atropine) but then \u003Cstrong\u003Eplateaus\u003C/strong\u003E. In PEDIG\u2019s ATS work, the approach that consistently produced \u003Cstrong\u003Estatistically significant additional gain\u003C/strong\u003E was \u003Cstrong\u003Eescalating patching from 2 hours/day to 6 hours/day\u003C/strong\u003E in children who were still amblyopic despite 2-hour patching. This makes sense clinically: if the child is plateaued on a low \u201Cdose,\u201D increasing the \u201Cdose\u201D can recruit more improvement before considering more invasive or less proven add-ons.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options don\u2019t best fit ATS evidence for improved acuity:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ELevodopa \u002B carbidopa\u003C/strong\u003E was studied as an adjunct but did \u003Cstrong\u003Enot\u003C/strong\u003E show a clinically meaningful advantage over placebo in the relevant ATS trial population.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAdding a plano lens to atropine penalization\u003C/strong\u003E may increase blur in the sound eye, but the study results did \u003Cstrong\u003Enot\u003C/strong\u003E demonstrate a clearly significant benefit over atropine alone for stable residual amblyopia.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1620,
    "Name": "Congenital (infantile) esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6\u2011month\u2011old has congenital/infantile esotropia. Which associated finding is commonly seen with this condition?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: Latent nystagmus.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EInfantile (congenital) esotropia\u003C/strong\u003E is classically associated with the \u201Cinfantile strabismus complex,\u201D which commonly includes \u003Cstrong\u003Elatent nystagmus (fusion maldevelopment nystagmus), dissociated vertical deviation (DVD), and inferior oblique overaction\u003C/strong\u003E, along with cross-fixation. Because the deviation begins early (by ~6 months), binocular fusion development is disrupted, making \u003Cstrong\u003Elatent nystagmus\u003C/strong\u003E a frequent accompanying finding.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHigh refractive error (\u0026gt; \u002B4.00 D OU):\u003C/strong\u003E Infantile esotropia usually has \u003Cstrong\u003Elow to moderate hyperopia\u003C/strong\u003E; marked hyperopia with ET is more suggestive of \u003Cstrong\u003Erefractive accommodative esotropia\u003C/strong\u003E rather than true infantile ET.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA-pattern:\u003C/strong\u003E When a pattern is present in infantile esotropia, it is more often a \u003Cstrong\u003EV-pattern\u003C/strong\u003E due to \u003Cstrong\u003Einferior oblique overaction\u003C/strong\u003E, not an A-pattern.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESmall angle (\u0026lt;15 PD):\u003C/strong\u003E Infantile esotropia is typically a \u003Cstrong\u003Elarge-angle, constant deviation\u003C/strong\u003E (often ~35\u201350 PD or more), not a small-angle deviation.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1621,
    "Name": "Aphakic glaucoma risk",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich child has the greatest risk of developing aphakic glaucoma after pediatric cataract surgery?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E10-year-old child with microcornea who underwent cataract surgery at age 1 year.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe two strongest predictors for aphakic (post\u2013congenital cataract surgery) glaucoma are:\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003EYounger age at surgery\u003C/strong\u003E, especially surgery performed in \u003Cstrong\u003Einfancy/first year of life\u003C/strong\u003E, and\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAbnormal anterior segment anatomy\u003C/strong\u003E, with \u003Cstrong\u003Emicrocornea\u003C/strong\u003E being a classic high\u2011risk marker.\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy this option is highest risk:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EInfant surgery\u003C/strong\u003E: The earlier the cataract is removed, the higher the long-term glaucoma risk\u2014often presenting \u003Cstrong\u003Eyears later\u003C/strong\u003E, so a 10\u2011year\u2011old who had surgery at \u003Cstrong\u003E1 year\u003C/strong\u003E is in the window where glaucoma can manifest.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EMicrocornea\u003C/strong\u003E: A smaller cornea often signals broader anterior segment dysgenesis/angle vulnerability, which increases the likelihood of later aqueous outflow problems and glaucoma.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1622,
    "Name": "40\u0394 basic exotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a comitant, freely alternating exotropia measuring 40 prism diopters at both distance and near on repeat exams. Which surgical plan most appropriately corrects this deviation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBilateral lateral rectus recession of 8 mm.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA 40\u0394 exotropia is a moderate-to-large deviation, and standard \u201Cvirgin muscle\u201D dosing typically requires a large bilateral weakening of the lateral recti (often around 8\u20139 mm each).\u003C/strong\u003E A bilateral plan is preferred because it is \u003Cstrong\u003Esymmetric\u003C/strong\u003E, tends to be \u003Cstrong\u003Emore predictable\u003C/strong\u003E for comitant deviations, and avoids creating excessive unilateral limitation in abduction that can happen with very large single-muscle surgery.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other plans are less appropriate:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EBilateral lateral rectus recession of 5 mm\u003C/strong\u003E is usually appropriate for smaller exotropias; for 40\u0394 it would be expected to \u003Cstrong\u003Eundercorrect\u003C/strong\u003E (insufficient weakening).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EBilateral medial rectus resection of 5 mm\u003C/strong\u003E strengthens adduction bilaterally and can correct exotropia, but for a typical \u201Cbasic\u201D 40\u0394 deviation, surgeons more commonly start with \u003Cstrong\u003Ebilateral lateral rectus recessions\u003C/strong\u003E as the primary symmetric weakening approach; resections can be used in other strategies but this option is not the best \u201Cstandard\u201D match here.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EUnilateral lateral rectus recession of 12 mm\u003C/strong\u003E is an unusually large single-muscle recession and risks \u003Cstrong\u003Esignificant abduction limitation\u003C/strong\u003E and postoperative incomitance; large deviations are generally managed by operating on \u003Cstrong\u003Etwo horizontal muscles\u003C/strong\u003E rather than pushing one muscle to an extreme dose.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1623,
    "Name": "Oblique muscles: anatomy \u201CEXCEPT\u201D question",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about the superior and inferior oblique muscles is not correct?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBoth the superior and inferior oblique muscles pass closer to the globe than their respective recti muscles.\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior oblique:\u003C/strong\u003E its tendon passes through the trochlea and then courses \u003Cstrong\u003Eclose to the globe\u003C/strong\u003E, and clinically it\u2019s often described as passing closer to the globe than the \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior oblique:\u003C/strong\u003E however, \u003Cstrong\u003Edoes not\u003C/strong\u003E pass closer to the globe than the \u003Cstrong\u003Einferior rectus\u003C/strong\u003E\u2014it runs \u003Cstrong\u003Emore inferiorly (farther from the globe) relative to the inferior rectus\u003C/strong\u003E.\u003Cbr\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EOrigins:\u003C/strong\u003E the superior oblique originates near the sphenoid (not from the annulus of Zinn) and the inferior oblique originates from the anterior medial orbital floor (also not the annulus) .\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1624,
    "Name": "Skull base suture fusion ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPremature closure of sutures at the skull base leads to which craniofacial abnormality?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMidface hypoplasia.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EPremature fusion of \u003Cstrong\u003Eskull base sutures\u003C/strong\u003E primarily affects \u003Cstrong\u003Efacial growth\u003C/strong\u003E, especially the \u003Cstrong\u003Emaxilla and midface\u003C/strong\u003E, producing \u003Cstrong\u003Emidface hypoplasia\u003C/strong\u003E (a retruded midface). In contrast, premature fusion of the \u003Cstrong\u003Ecalvarial sutures\u003C/strong\u003E (coronal, sagittal, metopic, lambdoid) alters the \u003Cstrong\u003Eshape of the cranial vault\u003C/strong\u003E, producing head-shape deformities such as \u003Cstrong\u003Eplagiocephaly\u003C/strong\u003E or \u003Cstrong\u003Escaphocephaly\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EHypertelorism and telecanthus are \u003Cstrong\u003Edistance descriptors\u003C/strong\u003E rather than primary \u201Ccranial malformation names\u201D:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHypertelorism\u003C/strong\u003E = increased bony orbital separation / increased interpupillary distance.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ETelecanthus\u003C/strong\u003E = increased distance between the \u003Cstrong\u003Emedial canthi\u003C/strong\u003E (can be due to hypertelorism or soft-tissue causes).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1625,
    "Name": "Monofixation syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical finding would essentially exclude (rule out) monofixation syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E60 seconds of arc of stereoacuity.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EMonofixation syndrome is a sensory adaptation characterized by \u003Cstrong\u003Eperipheral fusion with a central suppression scotoma\u003C/strong\u003E, meaning the patient generally lacks \u003Cstrong\u003Ebifoveal (bimacular) fusion\u003C/strong\u003E. As a result, stereoacuity is usually \u003Cstrong\u003Ereduced (coarse)\u003C/strong\u003E\u2014commonly in the \u003Cstrong\u003Ehundreds to thousands of seconds of arc\u003C/strong\u003E, not fine stereopsis. Therefore, \u003Cstrong\u003E60 arcsec\u003C/strong\u003E implies \u003Cstrong\u003Egood/fine stereopsis\u003C/strong\u003E, which essentially \u003Cstrong\u003Erules out monofixation syndrome\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EWhy the other choices fit monofixation rather than exclude it:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPeripheral fusion\u003C/strong\u003E is actually a defining feature of monofixation.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAbsence of bimacular fusion\u003C/strong\u003E is expected because of the central scotoma.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESeeing only 2 lights at distance on Worth 4-dot\u003C/strong\u003E can occur because the distance target projects more centrally and falls within the suppression zone, leading to a non-fusion response; near testing often improves because the stimulus subtends a larger angle and can be fused peripherally.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1626,
    "Name": "Mechanical origin of the superior rectus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich structure functions as the mechanical (functional) origin of the superior rectus muscle?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EDense collagen surrounding extraocular muscles.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003EThe \u003Cstrong\u003Esuperior rectus is a rectus muscle\u003C/strong\u003E, and the rectus muscles do not behave mechanically as if they \u201Cpull\u201D directly from their anatomic origin at the annulus of Zinn. Instead, their effective line of action is guided by a \u003Cstrong\u003Efibroelastic pulley system\u003C/strong\u003E\u2014rings/sleeves of \u003Cstrong\u003Edense connective tissue\u003C/strong\u003E surrounding each rectus muscle. These pulleys act as the \u003Cstrong\u003Efunctional (mechanical) origin\u003C/strong\u003E because they redirect and stabilize the muscle path, largely determining the direction of force applied to the globe during eye movements.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are not correct:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETrochlea\u003C/strong\u003E is the functional pulley/mechanical origin of the \u003Cstrong\u003Esuperior oblique\u003C/strong\u003E, not the superior rectus.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELockwood\u2019s ligament\u003C/strong\u003E is the main suspensory ligament of the globe and is more relevant to the \u003Cstrong\u003Einferior rectus/inferior oblique complex\u003C/strong\u003E and lower lid support, not the superior rectus\u2019 mechanical origin.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhitnall\u2019s ligament\u003C/strong\u003E is a key support structure for the \u003Cstrong\u003Elevator palpebrae superioris\u003C/strong\u003E (acts as a sling/pulley for the levator), not for the superior rectus.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1627,
    "Name": "Longest extraocular muscle overall",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen you include both the muscle belly and the tendon, which extraocular muscle is the longest overall?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ESuperior oblique.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe superior oblique has the \u003Cstrong\u003Elongest tendon\u003C/strong\u003E among the extraocular muscles, and when you add tendon length to the muscle belly, it becomes the \u003Cstrong\u003Elongest overall\u003C/strong\u003E. The \u003Cstrong\u003Elevator\u003C/strong\u003E also has a long tendon (aponeurosis), making it a close second, but the superior oblique still wins on total length.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1628,
    "Name": "Worth 4\u2011dot",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child sees only 2 dots on Worth 4\u2011dot at distance but sees all 4 dots at near (red filter OD, green filter OS). What diagnosis does this pattern indicate, and which eye is amblyopic?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMonofixation syndrome with OS being the amblyopic/suppressed eye.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EHere\u2019s the logic using the Worth\u20114\u2011Dot principles:\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhy this is monofixation syndrome\u003C/strong\u003E\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cul\u003E\n\u003Cli\u003EIn \u003Cstrong\u003Emonofixation syndrome\u003C/strong\u003E, the patient has \u003Cstrong\u003Eperipheral fusion\u003C/strong\u003E but a \u003Cstrong\u003Esmall central suppression scotoma\u003C/strong\u003E (no true bifoveal fusion).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAt distance (10 ft)\u003C/strong\u003E, the 4\u2011dot target subtends a \u003Cstrong\u003Esmall visual angle\u003C/strong\u003E, so its image tends to fall \u003Cstrong\u003Ewithin the central suppression zone\u003C/strong\u003E \u2192 the child reports \u003Cstrong\u003Esuppression\u003C/strong\u003E (seeing fewer than 4 dots).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAt near (2 ft)\u003C/strong\u003E, the same target subtends a \u003Cstrong\u003Elarger visual angle\u003C/strong\u003E, so more of the stimulus falls \u003Cstrong\u003Eoutside\u003C/strong\u003E the central suppression scotoma \u2192 the child can use \u003Cstrong\u003Eperipheral fusion\u003C/strong\u003E and reports \u003Cstrong\u003E4 dots\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhich eye is suppressed/amblyopic? (OS)\u003C/strong\u003E\u003Cbr\u003E\nWith \u003Cstrong\u003Ered over the right eye\u003C/strong\u003E and \u003Cstrong\u003Egreen over the left eye\u003C/strong\u003E:\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cul\u003E\n\u003Cli\u003ESeeing \u003Cstrong\u003Eonly 2 dots\u003C/strong\u003E at distance implies the child is seeing \u003Cstrong\u003Eonly the red\u2011filter eye\u2019s perception\u003C/strong\u003E (the \u003Cstrong\u003Ewhite\u003C/strong\u003E dot appears red through the red lens, plus the red dot itself), meaning the \u003Cstrong\u003Eleft eye (green lens, OS)\u003C/strong\u003E is being suppressed at distance.\u003C/li\u003E\n\u003Cli\u003ETherefore, the \u003Cstrong\u003Esuppressed eye is OS\u003C/strong\u003E, which corresponds to the \u003Cstrong\u003Eamblyopic/suppressed eye\u003C/strong\u003E in the answer choices.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhy \u201Cnormal W4D with dense amblyopia\u201D is not the best fit\u003C/strong\u003E\u003Cbr\u003E\nA \u201Cnormal\u201D Worth\u20114\u2011Dot response is \u003Cstrong\u003E4 dots at both distance and near\u003C/strong\u003E (stable fusion). This child shows \u003Cstrong\u003Edistance suppression\u003C/strong\u003E but \u003Cstrong\u003Enear fusion\u003C/strong\u003E, which is the classic monofixation pattern rather than a normal response.\u003C/li\u003E\u003C/ol\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1629,
    "Name": "Septo\u2011optic dysplasia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 1\u2011year\u2011old has unilateral poor vision with an optic nerve abnormality on fundus exam, and MRI shows absence of the septum pellucidum. Which pituitary hormone abnormality is most commonly seen in this condition?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-26-12b6ba18-e80c-4346-9b3d-cb2047da83b0.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EGrowth hormone (GH).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis picture \u002B MRI clue points to \u003Cstrong\u003Esepto\u2011optic dysplasia (SOD / de Morsier syndrome)\u003C/strong\u003E, defined by \u003Cstrong\u003Eoptic nerve hypoplasia\u003C/strong\u003E with a \u003Cstrong\u003Emidline brain defect\u003C/strong\u003E (classically \u003Cstrong\u003Eabsent septum pellucidum\u003C/strong\u003E) and frequent \u003Cstrong\u003Ehypothalamic\u2011pituitary dysfunction\u003C/strong\u003E. In SOD, the \u003Cstrong\u003Emost common endocrine abnormality is growth hormone deficiency\u003C/strong\u003E, which can make a child appear \u201Csickly\u201D due to poor growth and broader hypopituitarism risk.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are less likely as the \u003Cem\u003Emost common\u003C/em\u003E:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETSH\u003C/strong\u003E and \u003Cstrong\u003EACTH\u003C/strong\u003E deficiencies can occur and are clinically important (especially ACTH because of hypoglycemia/adrenal crisis risk), but they are \u003Cstrong\u003Enot the most frequent\u003C/strong\u003E deficiency in SOD.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EADH\u003C/strong\u003E deficiency (central diabetes insipidus) can occur, but it is \u003Cstrong\u003Eless common\u003C/strong\u003E than GH deficiency.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1630,
    "Name": "Normal timing of infant eye contact",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA healthy full-term 2\u2011week\u2011old isn\u2019t making eye contact or reacting to facial expressions yet. What is the best reassurance/counseling response?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EDo not worry. Your baby will not make eye contact with you until she is at least 6 weeks old.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EAt \u003Cstrong\u003E2 weeks\u003C/strong\u003E, a full\u2011term newborn\u2019s vision and social engagement are still immature. Newborns can see \u003Cstrong\u003Elight, shapes, and faces\u003C/strong\u003E but their vision is \u003Cstrong\u003Eblurry\u003C/strong\u003E and their ability to sustain purposeful gaze is limited in the early weeks.  Intentional, consistent \u003Cstrong\u003Eeye contact\u003C/strong\u003E is commonly expected around \u003Cstrong\u003E6\u20138 weeks\u003C/strong\u003E of age, making reassurance the most appropriate response here.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe other options are inappropriate as first responses in an otherwise healthy 2\u2011week\u2011old: a routine dilated exam or neuroimaging is not the initial step when the timeline is still within normal developmental range, and waiting until \u003Cstrong\u003E4 months\u003C/strong\u003E is too late for this milestone.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1631,
    "Name": "Central vs peripheral fusion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly describes how receptive field size affects central (foveal) versus peripheral fusion?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EThe area in the peripheral retina has a large receptive field and thus objects can be dissimilar in size and shape and still be seen singly.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy this is true:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECentral (foveal) fusion\u003C/strong\u003E demands extremely precise matching because foveal receptive fields are \u003Cstrong\u003Esmall\u003C/strong\u003E and spatial resolution is high. That means the two eyes\u2019 images must be \u003Cstrong\u003Every similar\u003C/strong\u003E (fine detail, contour, size/shape) to be fused into one percept.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPeripheral fusion\u003C/strong\u003E is more \u201Cforgiving\u201D because receptive fields in the peripheral retina are \u003Cstrong\u003Elarger\u003C/strong\u003E and spatial resolution is lower. With larger receptive fields, the visual system can tolerate \u003Cstrong\u003Emore mismatch\u003C/strong\u003E between the two eyes\u2019 images (differences in size/shape/position) and still maintain single vision.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1632,
    "Name": "JIA-associated uveitic glaucoma with band keratopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 10-year-old with the corneal abnormality shown in the photo above and has a history of joint pains affecting both knees and wrists, has severe glaucoma (IOP ~40) despite maximal medical therapy including oral CAI. Which intervention best controls IOP?\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-02-26-b90d7379-9e18-45f1-88cf-c804bf9f9fab.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBaerveldt glaucoma drainage implant.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe corneal photo is consistent with band keratopathy\u003C/strong\u003E, which in a 10-year-old plus knee/wrist arthralgias strongly points toward \u003Cstrong\u003EJIA-associated chronic anterior uveitis\u003C/strong\u003E. \u003Cstrong\u003EUveitic glaucoma\u003C/strong\u003E in children can be aggressive and may be due to \u003Cstrong\u003Etrabecular damage from chronic inflammation\u003C/strong\u003E, \u003Cstrong\u003Esteroid response\u003C/strong\u003E, and/or sequelae of repeated intraocular inflammation. An IOP of ~40 mmHg \u003Cstrong\u003Edespite maximal drops and oral CAI\u003C/strong\u003E indicates that medication escalation is unlikely to achieve safe long-term control.\u003C/p\u003E\n\u003Cp\u003EIn pediatric uveitic glaucoma, \u003Cstrong\u003Efiltering surgery (trabeculectomy or ExPress-type bleb surgery) has a high failure risk\u003C/strong\u003E because uveitic eyes\u2014especially in children\u2014tend to \u003Cstrong\u003Escar aggressively\u003C/strong\u003E, causing \u003Cstrong\u003Erapid bleb failure\u003C/strong\u003E and poor durability of pressure control. Similarly, \u003Cstrong\u003Eangle surgery (goniotomy/trabeculotomy)\u003C/strong\u003E can work in select pediatric glaucomas, but in established \u003Cstrong\u003Euveitic/secondary glaucomas\u003C/strong\u003E with marked IOP elevation on maximal meds, it is often \u003Cstrong\u003Eless predictable\u003C/strong\u003E as a definitive solution.\u003C/p\u003E\n\u003Cp\u003ETherefore, when the goal is \u003Cstrong\u003Ethe best chance of sustained IOP control\u003C/strong\u003E, many specialists favor a \u003Cstrong\u003Eglaucoma drainage device\u003C/strong\u003E (e.g., \u003Cstrong\u003EBaerveldt\u003C/strong\u003E, Ahmed, Molteno), and among the provided options the best match is the \u003Cstrong\u003EBaerveldt implant\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EKey perioperative counseling/management point: \u003Cstrong\u003Einflammation control is critical\u003C/strong\u003E. \u003Cstrong\u003EActive uveitis increases postoperative complication risk\u003C/strong\u003E, especially hypotony and scarring, so surgery is ideally timed when inflammation is quiet and may be accompanied by \u003Cstrong\u003Eperioperative \u201Cstress-dose\u201D steroids/immunosuppression\u003C/strong\u003E to reduce postoperative inflammatory complications.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1633,
    "Name": "Wilson disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich test is best for diagnosing Wilson disease early in a child?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003ESerum copper and ceruloplasmin.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWilson disease is a disorder of copper handling, so the earliest reliable clue comes from abnormal copper/ceruloplasmin biochemistry rather than late physical signs.\u003C/strong\u003E In many children\u2014especially those presenting early\u2014\u003Cstrong\u003EKayser\u2013Fleischer rings may be absent\u003C/strong\u003E, and even when present they tend to correlate more with advanced copper deposition (classically neurologic involvement) rather than being the best \u003Cem\u003Eearly\u003C/em\u003E screening tool.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not the best \u201Cearly\u201D method:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECT of the brain:\u003C/strong\u003E brain imaging may be normal early and is not a screening/confirmatory test for Wilson disease.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EKayser\u2013Fleischer ring detection:\u003C/strong\u003E helpful and classic, but \u003Cstrong\u003Enot sensitive for early pediatric disease\u003C/strong\u003E (can appear later or be absent in purely hepatic presentations).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EUrinary copper excretion:\u003C/strong\u003E can be useful and is often part of the workup, but for the \u201Cbest early method\u201D, \u003Cstrong\u003Eserum ceruloplasmin (and copper studies) are the first-line biochemical screen\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1634,
    "Name": "Brown syndrome vs inferior rectus restriction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has limited elevation of the right eye in adduction, and forced ductions show restriction. Which maneuver best helps you tell Brown syndrome (superior oblique tendon restriction) apart from inferior rectus restriction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EWorsened restriction on retropulsion.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBoth inferior rectus restriction and Brown syndrome can cause \u201Cpoor elevation in adduction,\u201D so you need a maneuver that selectively stresses the suspected structure.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBrown syndrome is essentially a mechanical problem of the superior oblique tendon\u2013trochlea complex\u003C/strong\u003E (a \u201Ctight\u201D tendon that won\u2019t glide). \u003Cstrong\u003EWhen you retropulse the globe (push it posteriorly), you effectively increase tension on the superior oblique tendon\u003C/strong\u003E, which \u003Cstrong\u003Eaccentuates the restriction\u003C/strong\u003E of elevation in adduction if Brown syndrome is the cause. That is why \u003Cstrong\u003Erestriction worsening with retropulsion\u003C/strong\u003E points toward \u003Cstrong\u003EBrown syndrome\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EIn contrast, \u003Cstrong\u003Einferior rectus restriction is a rectus tightness problem\u003C/strong\u003E, and the classic way to stress the rectus muscles during forced duction is not retropulsion; it\u2019s maneuvers that alter the rectus \u201Ctethering\u201D mechanics (often evaluated by testing restriction patterns in the opposite direction of the suspected restriction and by assessing behavior with proptosis vs retropulsion). \u003Cstrong\u003ERetropulsion specifically is the discriminating stressor for the oblique tendon mechanism\u003C/strong\u003E, so it favors Brown syndrome over inferior rectus restriction.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1635,
    "Name": "Complete CN VI palsy (6 months)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 56-year-old has a traumatic right CN VI palsy with complete loss of right lateral rectus function persisting for 6 months. What is the most appropriate management now?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EVertical muscle transposition surgery.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EIn a CN VI palsy, management depends on whether there is \u003Cstrong\u003Eresidual lateral rectus function\u003C/strong\u003E:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EIf there is some residual function\u003C/strong\u003E, a common strategy is \u003Cstrong\u003Eweakening the antagonist medial rectus\u003C/strong\u003E (recession) and \u003Cstrong\u003Estrengthening the lateral rectus\u003C/strong\u003E (resection) to rebalance forces and improve alignment. That works because the lateral rectus can still contribute something when you \u201Chelp it\u201D mechanically.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIf there is total paralysis (no meaningful lateral rectus function)\u003C/strong\u003E, then resecting the lateral rectus alone (or even doing a big MR recession \u002B LR resection) cannot reliably restore abduction, because you cannot \u201Cresect\u201D function into a completely denervated muscle. In that setting, the most effective approach is to \u003Cstrong\u003Erecruit other muscles to substitute for abduction\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThat is exactly what \u003Cstrong\u003Evertical rectus transposition (VRT)\u003C/strong\u003E procedures do: they shift the vertical recti (superior and inferior rectus) toward the lateral rectus to create an \u003Cstrong\u003Eabducting vector\u003C/strong\u003E, improving primary position alignment and expanding the field of single binocular vision.\u003C/p\u003E\n\u003Cp\u003ECommon examples include:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHummelsheim\u003C/strong\u003E (split-tendon transposition of vertical recti toward LR)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EJensen\u003C/strong\u003E (muscle union/suture technique)\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EFoster augmentation\u003C/strong\u003E (full-tendon transposition with posterior fixation/augmentation to increase abducting effect)\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EWhy the other choices are less appropriate here:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EBotulinum toxin to the medial rectus\u003C/strong\u003E can be useful earlier (to reduce contracture and sometimes help alignment), but at \u003Cstrong\u003E6 months with persistent total palsy\u003C/strong\u003E, it is usually not definitive by itself.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELarge MR recession \u002B LR resection\u003C/strong\u003E is best when some LR function remains; with \u003Cstrong\u003Etotal LR paralysis\u003C/strong\u003E, it\u2019s typically insufficient compared with transposition.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELarge LR resection only\u003C/strong\u003E is the least effective in complete palsy for the same reason (no innervation \u2192 no true abducting force).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1636,
    "Name": "Post-op nausea in a 2\u2011year\u2011old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAfter strabismus surgery, a nauseated 2\u2011year\u2011old needs an antiemetic. Which option is contraindicated due to a serious age-related safety risk?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EPromethazine.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EPromethazine (Phenergan) is \u003Cstrong\u003Econtraindicated in children under 2 years\u003C/strong\u003E because of the risk of \u003Cstrong\u003Epotentially fatal respiratory depression\u003C/strong\u003E\u2014a risk serious enough to warrant a \u003Cstrong\u003Eboxed warning\u003C/strong\u003E and explicit age-based contraindication in labeling.\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EOndansetron\u003C/strong\u003E is commonly used for pediatric postoperative nausea/vomiting and is widely recommended as first-line in many pediatric recovery protocols (with typical cautions like QT risk in susceptible patients).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EMetoclopramide\u003C/strong\u003E can be used but carries risks like extrapyramidal symptoms; it is not the classic strict age-based \u201Cdo not use\u201D choice in this question stem.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDiphenhydramine\u003C/strong\u003E is not a standard first-line antiemetic, but it is not the key contraindicated drug in a 2\u2011year\u2011old the way promethazine is.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 5,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1637,
    "Name": "Red-glass test: \u201Cpinkish\u201D single light",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring the red-glass test in an adult with exotropia, the patient reports seeing one \u201Cpinkish\u201D light instead of two. What does this indicate?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EHarmonious ARC.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhat the red-glass test is checking:\u003C/strong\u003E It helps detect \u003Cstrong\u003Eanomalous retinal correspondence (ARC)\u003C/strong\u003E so you can anticipate \u003Cstrong\u003Epost\u2011operative diplopia risk\u003C/strong\u003E in long\u2011standing strabismus. You place the \u003Cstrong\u003Ered filter over the fixating (non-deviating) eye\u003C/strong\u003E, shine a white light, and ask what the patient sees.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EHow to interpret \u201Cpinkish single light\u201D:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EIf the patient reports a \u003Cstrong\u003Esingle \u201Cpink\u201D light\u003C/strong\u003E, it means the \u003Cstrong\u003Ered-filter image and the white/green image are perceived as superimposed\u003C/strong\u003E\u2014the brain is matching the two eyes\u2019 images as if they correspond, \u003Cstrong\u003Edespite the measured exotropia\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003EThat pattern is classic for \u003Cstrong\u003Eharmonious ARC\u003C/strong\u003E, where the sensory adaptation fully compensates for the deviation so that the patient maintains \u003Cstrong\u003Esingle vision without separation\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy it is not the other choices:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuppression\u003C/strong\u003E would typically produce \u003Cstrong\u003Eone light\u003C/strong\u003E of the color corresponding to the \u003Cstrong\u003Enon-suppressed eye\u003C/strong\u003E (not a blended \u201Cpink\u201D superimposition), because one eye\u2019s input is being ignored.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EUnharmonious ARC\u003C/strong\u003E is when the patient sees \u003Cstrong\u003Etwo lights\u003C/strong\u003E, but the separation is \u003Cstrong\u003Eless than the measured deviation\u003C/strong\u003E (partial sensory adaptation).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPseudoharmonious ARC\u003C/strong\u003E is a special situation where the test result may appear \u201Charmonious\u201D due to testing conditions (e.g., certain prism/measurement setups), but it does not represent true harmonious correspondence in everyday viewing.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1638,
    "Name": "Corneal clouding",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the listed systemic diseases is most strongly associated with prominent corneal clouding?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EScheie syndrome.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EScheie syndrome is part of mucopolysaccharidosis type I (MPS I)\u003C/strong\u003E (\u03B1\u2011L\u2011iduronidase deficiency), a group in which \u003Cstrong\u003Eglycosaminoglycans (GAGs) accumulate in the cornea\u003C/strong\u003E, leading to \u003Cstrong\u003Eclassically significant corneal clouding\u003C/strong\u003E (often more consistently emphasized in MPS I than in many other metabolic disorders). \u003Cstrong\u003EThis makes Scheie the best choice in terms of both frequency and clinically meaningful corneal haze among the options.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHunter syndrome (MPS II)\u003C/strong\u003E: classically \u003Cstrong\u003Edoes not have corneal clouding\u003C/strong\u003E. Ocular findings are more often pigmentary retinopathy/optic nerve issues rather than prominent corneal haze.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EKrabbe disease\u003C/strong\u003E: a leukodystrophy (galactocerebrosidase deficiency) where major findings are neurologic (irritability, spasticity, developmental regression). \u003Cstrong\u003ECorneal clouding is not a classic hallmark.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EGaucher disease\u003C/strong\u003E: lipid storage disease (glucocerebrosidase deficiency) with hepatosplenomegaly, cytopenias, bone crises; ocular findings are not typically dominated by severe corneal clouding.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1639,
    "Name": "Type 1 Duane syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn type 1 Duane retraction syndrome with a significant compensatory face turn, what is the most commonly performed surgical procedure?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EMedial rectus recession on the involved side.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EType 1 Duane syndrome is characterized by abduction limitation (an \u201Cabduction deficit\u201D), often with esotropia in primary position and a face turn toward the involved side to place the eyes in a gaze position where alignment is better.\u003C/strong\u003E The surgical goal in a symptomatic patient is to \u003Cstrong\u003Ereduce the abnormal head posture\u003C/strong\u003E and \u003Cstrong\u003Eimprove primary position alignment\u003C/strong\u003E, while also minimizing the hallmark co\u2011contraction phenomenon that causes globe retraction.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ERecessing the medial rectus on the involved side is the most commonly used first procedure\u003C/strong\u003E because it \u003Cstrong\u003Ereduces the esotropic pull\u003C/strong\u003E in primary position and \u003Cstrong\u003Ereduces the drive for adduction\u003C/strong\u003E, which can also lessen the degree of co\u2011contraction and retraction on attempted adduction. In practical terms, it\u2019s the most standard, broadly applicable operation for the typical \u201Cesotropic Duane\u201D presentation with a face turn.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other procedures are not preferred as the \u201Cmost often used\u201D option:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ELateral rectus resection on the involved side\u003C/strong\u003E tends to be avoided because strengthening the lateral rectus in Duane can \u003Cstrong\u003Eexacerbate co\u2011contraction and globe retraction\u003C/strong\u003E and may worsen abnormal upshoots/downshoots.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EOperating on the uninvolved eye\u2019s horizontal muscles\u003C/strong\u003E is not the classic first-line approach for type 1 Duane with face turn; the main problem is usually the \u003Cstrong\u003Eprimary position eso/head posture driven by the involved side mechanics\u003C/strong\u003E, so treatment is typically directed to the involved side first.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1640,
    "Name": "Panum\u2019s fusional area:",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly describes how Panum\u2019s fusional area relates to whether a 3\u2011D object is seen singly or double?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EA 3-dimensional object is seen as a double image if any part of it falls outside of Panum\u2019s area.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EPanum\u2019s fusional area\u003C/strong\u003E is the tolerance zone around corresponding retinal points where \u003Cstrong\u003Esmall retinal disparities can still be fused into single vision\u003C/strong\u003E. A \u003Cstrong\u003E3\u2011D object has depth\u003C/strong\u003E, so different parts of it project with different disparities. If \u003Cstrong\u003Eany portion\u003C/strong\u003E of that object produces a disparity \u003Cstrong\u003Ebeyond\u003C/strong\u003E Panum\u2019s fusional limits, that portion cannot be fused and is perceived as \u003Cstrong\u003Ediplopic\u003C/strong\u003E (even if other parts of the object remain fused).\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1641,
    "Name": "Gaze-evoked nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EA child has a right-beating jerk nystagmus that becomes stronger when she looks to the right and lessens when she looks to the left. Which named \u201Claw\u201D describes this pattern?\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EAlexander\u2019s law.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAlexander\u2019s law states that jerk nystagmus increases in intensity when gaze is directed toward the fast phase (the direction of the jerk).\u003C/strong\u003E\u003Cbr\u003E\nHere, the nystagmus is \u003Cstrong\u003Eright-beating\u003C/strong\u003E (fast phase to the right), so it \u003Cstrong\u003Eworsens in right gaze\u003C/strong\u003E and \u003Cstrong\u003Eimproves in left gaze\u003C/strong\u003E\u2014a classic Alexander\u2019s law pattern.\u003C/p\u003E\n\u003Cp\u003EWhy the other options are not the best fit:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EListing\u2019s law\u003C/strong\u003E and \u003Cstrong\u003EDonder\u2019s law\u003C/strong\u003E are rules about \u003Cstrong\u003Etorsion and eye orientation\u003C/strong\u003E in different gaze positions (how the eye \u201Cchooses\u201D a unique torsional position for a given direction of gaze), not about nystagmus intensity changing with gaze direction.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESherrington\u2019s law\u003C/strong\u003E is \u003Cstrong\u003Ereciprocal innervation\u003C/strong\u003E (when an agonist contracts, its antagonist relaxes). It explains normal muscle coordination and is famously violated in some dysinnervation syndromes (e.g., co-contraction), but it does not describe gaze-dependent nystagmus intensity.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1642,
    "Name": "ROP screening: who qualifies when course is stable?",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EIn clinically stable newborns, which criterion best identifies those who should undergo ROP screening?\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBorn at gestational age of 30 weeks or earlier.\u003C/strong\u003E\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe classic screening thresholds used in many guidelines are birth weight \u22641500 g or gestational age \u226430 weeks, plus selected higher\u2011GA/higher\u2011BW infants only if their clinical course is unstable or high risk.\u003C/strong\u003E \u003Cbr\u003E\nBecause the stem explicitly says \u003Cstrong\u003Eassume all newborns are clinically stable\u003C/strong\u003E, the \u201Cextra\u201D group (1500\u20132000 g or \u0026gt;30 weeks) does \u003Cstrong\u003Enot\u003C/strong\u003E apply, so the best match among the choices is the \u003Cstrong\u003Egestational age cutoff of \u226430 weeks\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EBirth weight \u22642000 g\u003C/strong\u003E: some guidelines include \u003Cstrong\u003Eselected\u003C/strong\u003E infants between 1500\u20132000 g only when they are \u003Cstrong\u003Ehigh risk/unstable\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EBirth weight \u22642500 g\u003C/strong\u003E: this is \u003Cstrong\u003Etoo broad\u003C/strong\u003E and would greatly overscreen; it is not part of standard ROP screening criteria in settings with developed neonatal care\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EGestational age \u226432 weeks\u003C/strong\u003E: standard criteria emphasize \u003Cstrong\u003E\u226430 weeks\u003C/strong\u003E (with selective screening above that only if high risk).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1643,
    "Name": "Spasmus nutans: expected associated finding",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 1-year-old has head nodding with fine, high-frequency, asymmetric horizontal nystagmus and otherwise normal ocular exam. What additional finding would you expect with the most likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EStiff neck (torticollis).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThis presentation is most consistent with \u003Cstrong\u003Espasmus nutans\u003C/strong\u003E, which classically includes the triad of \u003Cstrong\u003Ehead nodding\u003C/strong\u003E, \u003Cstrong\u003Emonocular/asymmetric nystagmus\u003C/strong\u003E, and \u003Cstrong\u003Etorticollis (abnormal head posture that can look like a stiff neck)\u003C/strong\u003E. \u003Cstrong\u003EThe \u201Cshimmering,\u201D low-amplitude, high-frequency, asymmetric nystagmus with head nodding\u003C/strong\u003E is the key pattern that points to this diagnosis.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other findings are not expected:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAlternating nystagmus with either eye occluded\u003C/strong\u003E points more toward \u003Cstrong\u003Elatent/manifest latent nystagmus\u003C/strong\u003E associated with early-onset strabismus, not the spasmus nutans triad.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA null point in primary gaze\u003C/strong\u003E is more typical of \u003Cstrong\u003Einfantile nystagmus syndrome\u003C/strong\u003E (congenital motor nystagmus) with a gaze position that dampens the oscillation, often producing a consistent compensatory head posture rather than the classic spasmus nutans triad.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPersistence until adolescence\u003C/strong\u003E is not typical for spasmus nutans, which is usually \u003Cstrong\u003Ebenign and self-limited\u003C/strong\u003E, commonly resolving in early childhood.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1644,
    "Name": "Craniosynostosis growth rule",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn craniosynostosis, which \u201Claw\u201D describes the principle that skull growth is restricted perpendicular to the fused suture and continues mainly parallel to it?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EVirchow\u2019s law\u003C/strong\u003E explains the predictable head shapes seen in craniosynostosis: when a suture fuses early, skull growth is \u003Cstrong\u003Erestricted perpendicular\u003C/strong\u003E to that suture and compensates \u003Cstrong\u003Eparallel\u003C/strong\u003E to it, producing characteristic deformities\u2014e.g., \u003Cstrong\u003Esagittal synostosis \u2192 scaphocephaly (long, narrow head)\u003C/strong\u003E, \u003Cstrong\u003Eunicoronal synostosis \u2192 anterior plagiocephaly (asymmetric frontal/orbital shape)\u003C/strong\u003E, \u003Cstrong\u003Ebicoronal synostosis \u2192 brachycephaly (short, broad head)\u003C/strong\u003E, \u003Cstrong\u003Emetopic synostosis \u2192 trigonocephaly (triangular forehead)\u003C/strong\u003E, and \u003Cstrong\u003Elambdoid synostosis \u2192 posterior plagiocephaly.\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003E\u003Cbr\u003E\u003C/strong\u003E\u003C/div\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESherrington\u2019s law\u003C/strong\u003E = reciprocal innervation of agonist/antagonist muscles (extraocular muscle physiology), not skull growth.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHering\u2019s law\u003C/strong\u003E = equal innervation to yoke muscles, also extraocular muscle physiology.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EKestenbaum\u003C/strong\u003E refers to a \u003Cstrong\u003Estrabismus procedure\u003C/strong\u003E for nystagmus-related head posture, not a cranial growth law.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1645,
    "Name": "BoTox in extraocular muscle: duration \u002B effect",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with a CN VI palsy, if botulinum toxin A is injected into the medial rectus, how long does the paralysis typically last and what happens to the muscle?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003E5\u20138 weeks; will lengthen the muscle.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBotulinum toxin A causes chemodenervation of the injected extraocular muscle\u003C/strong\u003E, with clinical onset usually within \u003Cstrong\u003E2\u20134 days\u003C/strong\u003E. \u003Cstrong\u003EDuring the period of paralysis, the medial rectus effectively \u201Crelaxes,\u201D allowing it to lengthen\u003C/strong\u003E, which helps reduce its restrictive pull in a sixth nerve palsy (i.e., helps counteract the esotropic tendency from an unopposed medial rectus). \u003Cstrong\u003EIn extraocular muscles, the typical functional duration is about 5\u20138 weeks\u003C/strong\u003E, which is \u003Cstrong\u003Eshorter\u003C/strong\u003E than the duration seen when BoTox is used in facial muscles such as the orbicularis (often \u003Cstrong\u003E~3 months or longer\u003C/strong\u003E).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1646,
    "Name": "CN III palsy: primary goal of strabismus surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a chronic pupil-involving third nerve palsy with significant hypotropia and marked loss of elevation/adduction. What is the main goal of strabismus surgery in this setting?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBinocular function in primary position and in slight downgaze for reading.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIn long-standing, complete or near-complete CN III palsy, surgery cannot truly \u201Crestore\u201D the missing muscle innervation\u003C/strong\u003E, so attempts to regain \u003Cstrong\u003Eall ductions\u003C/strong\u003E or recreate normal \u003Cstrong\u003Erotational forces\u003C/strong\u003E are unrealistic. \u003Cstrong\u003EThe practical surgical aim is to expand the patient\u2019s field of single binocular vision where it matters most functionally\u003C/strong\u003E\u2014straight ahead (\u003Cstrong\u003Eprimary position\u003C/strong\u003E) and the \u003Cstrong\u003Ereading position\u003C/strong\u003E (typically \u003Cstrong\u003Eslight downgaze\u003C/strong\u003E). This is why surgeons prioritize alignment that reduces diplopia in these key gaze positions rather than chasing full motility restoration.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1647,
    "Name": " Krimsky test",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA preverbal toddler with dense amblyopia in the left eye has poor fixation, so cover\u2013uncover testing cannot reliably measure the strabismus. You shine a penlight at both eyes and see the corneal light reflex is decentered. You want to quantify the deviation by placing prisms in front of one eye until the corneal reflex is centered and symmetric. Which test are you performing?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Krimsky test.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBruckner test:\u003C/strong\u003E \u003Cstrong\u003EUse a direct ophthalmoscope to view both red reflexes at the same time.\u003C/strong\u003E You are mainly judging \u003Cstrong\u003Esymmetry and brightness\u003C/strong\u003E of the reflexes to screen for problems such as \u003Cstrong\u003Estrabismus, anisometropia, or media opacity (e.g., cataract)\u003C/strong\u003E. A noticeably \u003Cstrong\u003Ebrighter reflex in one eye\u003C/strong\u003E can suggest \u003Cstrong\u003Estrabismus in that eye\u003C/strong\u003E (often because \u003Cstrong\u003Efoveation/angle changes alter the reflected light pattern\u003C/strong\u003E).\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EHirschberg test:\u003C/strong\u003E \u003Cstrong\u003EUse a penlight and observe where the corneal light reflex falls relative to the pupil.\u003C/strong\u003E This is a \u003Cstrong\u003Erough estimate\u003C/strong\u003E of ocular misalignment (not a precise measurement). \u003Cstrong\u003ECentered reflex \u2248 straight eyes; decentered reflex \u2248 strabismus\u003C/strong\u003E, and the farther the reflex is displaced, the larger the deviation.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EKrimsky test:\u003C/strong\u003E \u003Cstrong\u003EThis is the Hirschberg test plus prisms.\u003C/strong\u003E Instead of just estimating, you \u003Cstrong\u003Eplace prisms in front of one eye and increase prism power until the corneal light reflex becomes centered and symmetric\u003C/strong\u003E between the two eyes. The prism amount required to \u201Cre-center\u201D the reflex gives a \u003Cstrong\u003Equantified measurement\u003C/strong\u003E of the deviation. This is especially useful when the patient \u003Cstrong\u003Ecannot reliably fixate\u003C/strong\u003E (e.g., \u003Cstrong\u003Edense amblyopia, low vision, or very young children\u003C/strong\u003E), where cover testing is unreliable.\u003C/p\u003E\n\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1648,
    "Name": "Dystopia canthorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has dystopia canthorum (lateral displacement of the medial canthi). Which syndrome is this finding classically specific for?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EWaardenburg syndrome.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EDystopia canthorum\u003C/strong\u003E refers to \u003Cstrong\u003Elateral displacement of the medial canthi\u003C/strong\u003E (often with lateral displacement of the lacrimal puncta). Clinically, a helpful way to visualize it is that an imaginary line drawn between the \u003Cstrong\u003Eupper and lower puncta\u003C/strong\u003E may \u003Cstrong\u003Ecross the cornea\u003C/strong\u003E, reflecting that the medial canthal complex has shifted laterally. This finding is a classic hallmark of \u003Cstrong\u003EWaardenburg syndrome\u003C/strong\u003E, particularly the subtype that features dystopia canthorum.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not correct:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMarfan syndrome\u003C/strong\u003E is classically linked to \u003Cstrong\u003Eectopia lentis\u003C/strong\u003E and systemic connective tissue features, not dystopia canthorum.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EStickler syndrome\u003C/strong\u003E is associated with \u003Cstrong\u003Ehigh myopia, retinal detachment risk, and craniofacial anomalies\u003C/strong\u003E (e.g., Pierre Robin sequence), not a \u201Cspecific\u201D dystopia canthorum sign.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHallermann\u2013Streiff syndrome\u003C/strong\u003E features \u003Cstrong\u003Ecraniofacial dysplasia with microphthalmia and dental anomalies\u003C/strong\u003E, but dystopia canthorum is not its defining specific marker.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1649,
    "Name": "Bangerter foils as amblyopia therapy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich item is actually used to treat amblyopia rather than to test binocular function?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EBangerter foil.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBangerter foils are a form of optical penalization.\u003C/strong\u003E They are \u003Cstrong\u003Egraded translucent filters\u003C/strong\u003E that stick onto the spectacle lens of the \u003Cstrong\u003Esound (non-amblyopic) eye\u003C/strong\u003E, creating a controlled amount of blur so the child is encouraged to use the amblyopic eye. The level of blur can be titrated by choosing different foil densities, making them useful when a child \u003Cstrong\u003Ecannot tolerate patching\u003C/strong\u003E or \u003Cstrong\u003Eatropine penalization\u003C/strong\u003E, especially in \u003Cstrong\u003Emild to moderate amblyopia\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are not amblyopia therapy:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ESynoptophore\u003C/strong\u003E is primarily an \u003Cstrong\u003Eassessment/orthoptic training tool\u003C/strong\u003E for binocular vision (fusion, suppression, stereopsis) rather than a standard amblyopia \u201Cpenalization\u201D treatment.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EBagolini lenses\u003C/strong\u003E are used to \u003Cstrong\u003Eevaluate sensory fusion and suppression\u003C/strong\u003E under near-natural viewing conditions; they\u2019re a \u003Cstrong\u003Etest\u003C/strong\u003E, not a treatment.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWorth 4-dot flashlight\u003C/strong\u003E is a \u003Cstrong\u003Efusion/suppression test\u003C/strong\u003E (near/distance responses), not an amblyopia treatment.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1650,
    "Name": "ROP look-alikes: IP and FEVR",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich two conditions most closely mimic the retinal appearance of retinopathy of prematurity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EAnswer: \u003Cstrong\u003EIncontinentia pigmenti and familial exudative vitreoretinopathy (FEVR).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EBoth \u003Cstrong\u003EIP\u003C/strong\u003E and \u003Cstrong\u003EFEVR\u003C/strong\u003E can produce a retinal picture that strongly resembles ROP because they share the key anatomic problem of \u003Cstrong\u003Eincomplete peripheral retinal vascularization\u003C/strong\u003E with subsequent \u003Cstrong\u003Eneovascularization\u003C/strong\u003E, \u003Cstrong\u003Efibrovascular proliferation\u003C/strong\u003E, \u003Cstrong\u003Etraction\u003C/strong\u003E, and potential \u003Cstrong\u003Eretinal detachment\u003C/strong\u003E\u2014the same pathway that drives severe ROP.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EHow to distinguish them from true ROP (high-yield clues):\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EFEVR\u003C/strong\u003E is a \u003Cstrong\u003Egenetic disorder of retinal vascular development\u003C/strong\u003E (often autosomal dominant) that can look very similar to ROP, but \u003Cstrong\u003Eprematurity is not required\u003C/strong\u003E. A full-term child (or a \u201Cnormal pregnancy\u201D history) with a ROP-like fundus should make you think of \u003Cstrong\u003EFEVR\u003C/strong\u003E; \u003Cstrong\u003Efamily screening\u003C/strong\u003E can be helpful because expressivity is variable and relatives may have subtle findings.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIncontinentia pigmenti (Bloch\u2013Sulzberger)\u003C/strong\u003E is \u003Cstrong\u003EX-linked dominant\u003C/strong\u003E and classically has \u003Cstrong\u003Eskin findings\u003C/strong\u003E (staged lesions progressing to hyperpigmented streaks/whorls), plus possible \u003Cstrong\u003ECNS features\u003C/strong\u003E (e.g., seizures, developmental issues). The eye findings can mirror ROP because of peripheral nonperfusion and secondary neovascular changes.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EUsher syndrome\u003C/strong\u003E is primarily a \u003Cstrong\u003Eretinal dystrophy (retinitis pigmentosa) \u002B hearing loss\u003C/strong\u003E, not a peripheral avascular \u201CROP-like\u201D vasoproliferative retinopathy.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPHPV (persistent fetal vasculature)\u003C/strong\u003E is a \u003Cstrong\u003Edevelopmental failure of hyaloid regression\u003C/strong\u003E causing leukocoria/microphthalmia and a fibrovascular stalk\u2014its anatomy and retinal appearance are \u003Cstrong\u003Enot the classic ROP pattern\u003C/strong\u003E of peripheral avascular retina with neovascular ridge/tractional changes.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1651,
    "Name": "Downbeat nystagmus in primary gaze ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 13-year-old has had progressively noticeable abnormal eye movements for about six months. On straight-ahead fixation, there is a jerk nystagmus whose fast phase beats downward. The patient tends to hold the head with the chin lowered, which seems to reduce the oscillations. The remainder of the eye exam is unremarkable. What is the most likely underlying cause?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Arnold\u2013Chiari malformation.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EA jerk nystagmus with a downward fast phase in primary (straight-ahead) gaze is classic for downbeat nystagmus.\u003C/strong\u003E Downbeat nystagmus most strongly points to dysfunction at the \u003Cstrong\u003Ecervicomedullary junction\u003C/strong\u003E and/or the \u003Cstrong\u003Evestibulocerebellum (especially the cerebellar flocculus).\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EArnold\u2013Chiari (classically Chiari I) involves downward displacement of the cerebellar tonsils through the foramen magnum,\u003C/strong\u003E which can disrupt these pathways and produce \u003Cstrong\u003Edownbeat nystagmus.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA compensatory head posture (often chin-down) may lessen symptoms\u003C/strong\u003E by moving gaze into a position where the nystagmus is reduced (a \u201Cnull\u201D zone), so that behavioral clue supports a chronic central pattern rather than an isolated ocular problem.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are less likely\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ENeuroblastoma\u003C/strong\u003E is classically linked to \u003Cstrong\u003Eopsoclonus\u003C/strong\u003E (chaotic, rapid, multidirectional saccades) rather than a steady downbeat jerk nystagmus in primary gaze.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPinealoma\u003C/strong\u003E more commonly causes \u003Cstrong\u003Edorsal midbrain (Parinaud) syndrome\u003C/strong\u003E\u2014problems with upgaze and characteristic convergence\u2013retraction phenomena\u2014rather than primary-position downbeat nystagmus.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECraniopharyngioma\u003C/strong\u003E is a parasellar/suprasellar lesion and is more often associated with \u003Cstrong\u003Esee-saw\u2013type ocular oscillations\u003C/strong\u003E or visual field/endocrine manifestations, not the typical downbeat pattern.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1652,
    "Name": "Ectopia lentis et pupillae",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old is evaluated for \u201Csmall pupils.\u201D Examination shows bilaterally small pupils that are decentered toward the superotemporal quadrant. Both crystalline lenses are also partially dislocated (subluxed). If ectopia lentis et pupillae is suspected, in which direction should the lens displacement occur?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: inferonasally.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EIn ectopia lentis et pupillae, the lens and the pupil are typically displaced in opposite directions.\u003C/strong\u003E The pupil is eccentrically positioned because of developmental abnormalities of the iris and zonular apparatus, and the lens tends to shift away from the direction of the pupil decentration.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: 700;\u0022\u003EReported inheritance is most often autosomal recessive, though autosomal dominant inheritance with reduced penetrance has also been described.\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u0026nbsp;Associated ocular findings can include\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: 700;\u0022\u003Epoor dilation, persistent pupillary membrane, iris transillumination defects, early cataract formation, secondary glaucoma, high myopia, and increased risk of retinal detachment.\u003C/span\u003E\u003C/p\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe pupils are displaced superotemporally in both eyes, so the lenses should be displaced inferonasally\u003C/strong\u003E (the opposite quadrant).\u003C/p\u003E\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1653,
    "Name": "Fresnel prisms to reduce a nystagmus-related head turn",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4-year-old with congenital nystagmus is brought in because of a pronounced abnormal head posture. The caregiver prefers a non-surgical option. Examination shows the child consistently turns the head to the left to lessen the nystagmus. How should horizontal Fresnel prisms be oriented on each eye to help reduce the left head turn?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: base-in prism over the right eye; base-out prism over the left eye.\u003C/span\u003E\u003C/h3\u003E\n\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EExplanation:\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EStep 1: Identify the null zone from the head posture\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA left face turn usually means the eyes are being placed in right gaze to reach the \u201Cnull zone\u201D (the gaze position where nystagmus intensity is lowest).\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ESo, a left head turn \u2192 null zone in right gaze.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EStep 2: How prisms help in congenital nystagmus\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EYoked prisms are used to shift the visual scene toward the null zone so the child can keep the head straighter while still benefiting from the reduced nystagmus.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA practical rule: orient the prisms so the prism apices point toward the null zone.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EBecause a prism displaces the image toward its apex, placing the apex toward the null zone moves the target into that preferred gaze position.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EStep 3: Apply this to a right-gaze null zone\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ERight-gaze null zone means both prism apices must point to the patient\u2019s right (in real-world coordinates).\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ERight eye:\u003C/strong\u003E the apex must point temporally (to the right) \u2192 \u003Cstrong\u003Ebase-in\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELeft eye:\u003C/strong\u003E the apex must point nasally (also to the right) \u2192 \u003Cstrong\u003Ebase-out\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003ETherefore, the correct setup is base-in on the right eye and base-out on the left eye.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EIf the head turn is large or prism management is insufficient, surgical approaches (e.g., Kestenbaum\u2013Anderson-type procedures) can rotate the eyes so primary gaze aligns closer to the null zone, reducing the need for an abnormal head posture.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1654,
    "Name": "Monocular oscillopsia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old has chronic diplopia and describes a sensation that the visual world \u201Cshimmers\u201D or \u201Cmoves,\u201D and this persists even when the left eye is covered. Which management option would NOT be an appropriate treatment for the problem described?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Harada\u2013Ito procedure.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe key clue is \u201Coscillation\u201D that continues when one eye is closed, which indicates monocular oscillopsia.\u003C/strong\u003E That strongly suggests an abnormal movement of a single eye rather than a purely binocular misalignment complaint. \u003Cstrong\u003EA classic cause is superior oblique myokymia\u003C/strong\u003E, where \u003Cstrong\u003Eintermittent, small-amplitude, high-frequency torsional (and sometimes vertical) micro-movements\u003C/strong\u003E occur in one eye, often in an otherwise neurologically normal person. These brief torsional bursts create the subjective sense that the environment is vibrating or moving.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy most listed treatments are appropriate\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETopical timolol\u003C/strong\u003E can reduce symptoms in some patients because \u003Cstrong\u003Ebeta-blockade may dampen the abnormal muscle activity\u003C/strong\u003E and lessen the frequency/intensity of the oscillations.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESystemic anticonvulsants (for example carbamazepine or phenytoin)\u003C/strong\u003E are commonly used because \u003Cstrong\u003Esuperior oblique myokymia behaves like an episodic hyperexcitability phenomenon\u003C/strong\u003E, and membrane-stabilizing agents can suppress attacks.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior oblique tendon weakening (often tenotomy/tenectomy) with simultaneous inferior oblique weakening\u003C/strong\u003E is a recognized surgical strategy when medical therapy fails, aiming to \u003Cstrong\u003Ereduce the torsional oscillations and balance the vertical/torsional forces\u003C/strong\u003E.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy Harada\u2013Ito is the exception\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EHarada\u2013Ito is primarily a torsion-correcting procedure for symptomatic excyclotorsion, typically in a trochlear (fourth nerve) palsy scenario.\u003C/strong\u003E It works by \u003Cstrong\u003Eadvancing/strengthening the anterior fibers of the superior oblique tendon to address torsional misalignment\u003C/strong\u003E, and it has \u003Cstrong\u003Elimited impact on vertical deviation\u003C/strong\u003E.\u003Cbr\u003E\nIn contrast, \u003Cstrong\u003Esuperior oblique myokymia is not mainly a static torsional misalignment problem\u2014it is an episodic torsional \u201Ctremor-like\u201D movement disorder of the muscle.\u003C/strong\u003E Therefore, \u003Cstrong\u003EHarada\u2013Ito does not target the underlying mechanism and is not considered an appropriate intervention for the oscillopsia described.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1655,
    "Name": "CN VI palsy vs Duane syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement does not help differentiate an abducens (CN VI) palsy from Duane syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: The statement that CN VI palsy usually has little to no esotropia in primary gaze.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ECN VI palsy weakens the lateral rectus, so abduction is limited and the affected eye drifts inward. As a result, a noticeable esotropia in primary position is expected, often roughly matching the severity of the abduction deficit.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EDuane syndrome, in contrast, often has only a small primary-position deviation (sometimes none), with its hallmark findings appearing on attempted adduction due to co-contraction and misinnervation.\u003C/strong\u003E\u003Cbr\u003E\nSo, saying that \u003Cstrong\u003ECN VI palsy lacks significant primary-position esotropia\u003C/strong\u003E is \u003Cstrong\u003Enot\u003C/strong\u003E a feature of CN VI palsy and therefore \u003Cstrong\u003Edoes not\u003C/strong\u003E serve as a distinguishing sign\u2014making it the exception.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EWhy the other statements DO distinguish CN VI palsy from Duane syndrome\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAbsence of upshoots/downshoots:\u003C/strong\u003E \u003Cstrong\u003EIn CN VI palsy, the main issue is abduction weakness without the classic \u201Cslippage\u201D phenomena. Duane syndrome can show dramatic upshoots or downshoots on adduction from tight lateral rectus and co-contraction.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENo globe retraction on adduction:\u003C/strong\u003E \u003Cstrong\u003EGlobe retraction is a signature clue for Duane syndrome (co-contraction of medial and lateral rectus on adduction), whereas CN VI palsy does not produce retraction.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENo palpebral fissure narrowing with attempted adduction:\u003C/strong\u003E \u003Cstrong\u003EBecause the globe retracts in Duane syndrome, the eyelid fissure typically narrows on adduction; CN VI palsy lacks this finding.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1656,
    "Name": "Earliest clinical sign of anterior segment ischemia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 72-year-old with hypertension and diabetes undergoes a rectus transposition procedure to treat exotropia secondary to a third nerve palsy. When more than two rectus muscles are operated on, a sight-threatening complication can occur. What is the earliest clinical sign of that complication?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: anterior chamber cells and flare.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis scenario is most concerned with anterior segment ischemia (ASI).\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EASI becomes more likely when surgery involves multiple rectus muscles (classically three or more), especially in older patients or those with vascular risk factors such as diabetes and hypertension.\u003C/strong\u003E The key anatomic reason is that \u003Cstrong\u003Ea large portion of the anterior segment blood supply comes from the anterior ciliary arteries, which run with the rectus muscles; operating on several recti can reduce perfusion to the iris/ciliary body/anterior segment.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EEarliest sign:\u003C/strong\u003E \u003Cstrong\u003EAnterior chamber inflammation (cells and flare) is typically the first detectable finding\u003C/strong\u003E, reflecting early ischemic injury to the iris and ciliary body with breakdown of the blood\u2013aqueous barrier. This can appear before corneal changes or pupil abnormalities.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not the earliest\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECorneal epithelial edema\u003C/strong\u003E is a later manifestation, generally occurring after ischemia has progressed enough to impair endothelial function and corneal clarity.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDescemet membrane folds\u003C/strong\u003E also tend to appear after significant corneal edema develops, so they are usually a subsequent sign rather than the first clue.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPupil irregularity\u003C/strong\u003E (from iris ischemia/atrophy and sphincter dysfunction) is classically associated with ASI but is typically a more advanced finding compared with early anterior chamber reaction.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical pearl:\u003C/strong\u003E In suspected ASI, clinicians also watch for \u003Cstrong\u003Epain, photophobia, decreased vision, sluggish pupil responses, hypotony, corneal edema, and progressive iris atrophy\u003C/strong\u003E, with risk rising as the number of operated rectus muscles increases and in patients with systemic vasculopathy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1657,
    "Name": "Cyclic esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about cyclic esotropia is incorrect?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: The claim that extraocular muscle surgery is usually not curative.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ECyclic esotropia is an uncommon type of intermittent strabismus in which patients alternate between \u201Cstraight\u201D periods and periods of manifest esotropia in a predictable cycle (classically every other day, i.e., about 48 hours).\u003C/strong\u003E Because of this alternating pattern, \u003Cstrong\u003Enon-surgical treatments often give inconsistent results.\u003C/strong\u003E However, \u003Cstrong\u003Estrabismus surgery directed at the measured deviation on the esotropic days is generally the most reliable and is often curative\u003C/strong\u003E, which is the opposite of what the incorrect statement suggests.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other statements are true\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETypical cycle ~48 hours:\u003C/strong\u003E \u003Cstrong\u003EMany cases follow an every-other-day pattern.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EBinocular function on straight days:\u003C/strong\u003E \u003Cstrong\u003EWhen alignment is orthotropic (or close to it), binocular single vision and fusion are often possible.\u003C/strong\u003E On esotropic days, \u003Cstrong\u003Efusion is frequently lost\u003C/strong\u003E, commonly due to \u003Cstrong\u003Esuppression\u003C/strong\u003E (especially in younger children).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPatching may convert it to constant esotropia:\u003C/strong\u003E \u003Cstrong\u003EOcclusion can disrupt sensory adaptation and may \u201Cbreak\u201D the cycle\u003C/strong\u003E, occasionally resulting in \u003Cstrong\u003Ea persistent, manifest esotropia\u003C/strong\u003E rather than alternating straight/strabismic days.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EExtra clinical pearl (helps the concept stick)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EOn strabismic days, younger children often suppress to avoid diplopia; older children who cannot suppress as easily may complain of diplopia during the esotropic phase.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1658,
    "Name": "Botulinum toxin A",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EBotulinum toxin type A produces muscle weakness by preventing release of which neurotransmitter at the neuromuscular junction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: acetylcholine.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBoNT-A causes chemodenervation by blocking acetylcholine release at the neuromuscular junction.\u003C/strong\u003E Botulinum toxin A enters cholinergic nerve terminals and \u003Cstrong\u003Ecleaves SNARE proteins (classically SNAP-25), which are required for synaptic vesicles to fuse with the presynaptic membrane.\u003C/strong\u003E Without vesicle fusion, \u003Cstrong\u003Eacetylcholine cannot be released\u003C/strong\u003E, so the muscle fiber is not stimulated and becomes functionally weakened/paralyzed.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other neurotransmitters are incorrect\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ENorepinephrine\u003C/strong\u003E is mainly used by \u003Cstrong\u003Epostganglionic sympathetic neurons\u003C/strong\u003E and is not the primary transmitter at skeletal muscle NMJs.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDopamine\u003C/strong\u003E is primarily a \u003Cstrong\u003Ecentral nervous system\u003C/strong\u003E neurotransmitter (and a precursor to norepinephrine), not the key transmitter for skeletal NMJ transmission.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESerotonin\u003C/strong\u003E is chiefly involved in \u003Cstrong\u003Ecentral neurotransmission\u003C/strong\u003E and enteric signaling; it is not the transmitter responsible for skeletal muscle activation at the NMJ.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical duration pearl (cleaned and clarified)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe functional effect typically lasts longer in facial muscles like the orbicularis (often \u22653 months) and tends to be shorter in extraocular muscles (commonly ~5\u20138 weeks),\u003C/strong\u003E reflecting differences in muscle physiology, dosing, and reinnervation dynamics.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1659,
    "Name": "JIA subtypes",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong common juvenile idiopathic arthritis (JIA) subtypes, arrange the following conditions from the highest to the lowest likelihood of developing uveitis:\u0026nbsp;\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003EAnswer\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EAnswer: Oligoarticular JIA \u0026gt; RF-negative polyarticular JIA \u0026gt; systemic JIA (Still disease).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EJuvenile idiopathic arthritis is the leading systemic condition associated with pediatric uveitis, most often presenting as chronic anterior uveitis.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe risk of uveitis is not equal across JIA subtypes\u2014oligoarticular disease carries the highest risk (between the mentioned types), RF-negative polyarticular disease has an intermediate risk, and systemic JIA has a very low risk.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EOligoarticular JIA is classically the subtype most linked to chronic anterior uveitis, with reported rates often in the ~10\u201330% range.\u003C/strong\u003E This category is typically defined by \u003Cstrong\u003Earthritis lasting more than 6 weeks with involvement of four or fewer joints during the first 6 months.\u003C/strong\u003E Serologically, \u003Cstrong\u003Erheumatoid factor is usually negative\u003C/strong\u003E, and \u003Cstrong\u003EANA positivity is common\u003C/strong\u003E, which correlates with a higher uveitis risk in many children.\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ERF-negative polyarticular JIA can also be associated with anterior uveitis, but overall less frequently than oligoarticular disease.\u003C/strong\u003E A commonly cited figure is \u003Cstrong\u003Earound ~10%\u003C/strong\u003E in some cohorts, making it a reasonable \u201Cmiddle\u201D option among the three listed conditions.\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EUveitis is uncommon in systemic JIA compared with other subtypes.\u003C/strong\u003E Systemic JIA is characterized by systemic inflammation (fevers, rash, etc.), but \u003Cstrong\u003Eit rarely produces the classic chronic anterior uveitis pattern seen in oligoarticular/ANA-positive disease\u003C/strong\u003E, so it belongs at the bottom of the frequency list.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1660,
    "Name": "Orbital fat prolapse during strabismus surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring strabismus surgery for a 6-year-old with exotropia, an unintended rent occurs in Tenon\u2019s capsule and orbital fat herniates into the surgical field. What is the most appropriate management at this moment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EOrbital fat appearing in a strabismus case usually means the posterior Tenon\u2019s barrier has been breached. If the fat is left prolapsed, it can heal to the sclera or extraocular muscles and form restrictive scar tissue.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThis postoperative restriction is known as fat adherence (adherence) syndrome and can lead to limited ductions and new or worsening motility problems.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe practical goal in the operating room is to remove the exposed fat that could scar to ocular tissues and then restore the tissue plane.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ETherefore, the preferred approach is to carefully trim/excise the prolapsed orbital fat (rather than leaving it exposed) and then close the Tenon\u2019s capsule tear using absorbable sutures to prevent further fat herniation and minimize future adhesions.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1661,
    "Name": "Infant with enlarged corneas and corneal haze",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-month-old is brought in because the eyes appear unusually large. Penlight examination shows bilateral findings consistent with corneal clouding, and both corneas measure 13.5 mm horizontally. The irides look normal. There is a family history of a similar eye problem in a close relative. Which gene mutation is most consistent with the diagnosis in this infant?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-05-82cb8047-c725-4783-858c-9e736c6392ef.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: GLC3B\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe combination of \u201Cbig-looking eyes,\u201D very large corneal diameters (13.5 mm in a 2\u2011month-old), and a hazy/irregular corneal light reflex strongly indicates primary congenital glaucoma (PCG) with corneal edema.\u003C/strong\u003E \u003Cstrong\u003EIn infants, elevated intraocular pressure can stretch the cornea and globe (buphthalmos) and cause corneal edema, which is why the corneal reflex looks irregular and the cornea appears cloudy.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EPrimary congenital glaucoma is often sporadic, but familial cases occur and are linked to mutations in the \u201CGLC3\u201D group (classically including CYP1B1/GLC3A, and also GLC3B and GLC3C).\u003C/strong\u003E Since the listed choices include \u003Cstrong\u003EGLC3B\u003C/strong\u003E, that is the best match for PCG among the options provided.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong :\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPITX2\u003C/strong\u003E is classically associated with \u003Cstrong\u003EAxenfeld\u2013Rieger spectrum\u003C/strong\u003E, an anterior segment dysgenesis condition that can lead to secondary glaucoma, but it does not best explain the classic PCG picture of markedly enlarged infant corneas with diffuse corneal edema.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EGLC1A (MYOC)\u003C/strong\u003E is associated with \u003Cstrong\u003Ejuvenile-onset open-angle glaucoma\u003C/strong\u003E, typically presenting later (childhood/adolescence) and not with buphthalmos/corneal enlargement in early infancy.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELOXL1\u003C/strong\u003E is strongly associated with \u003Cstrong\u003Epseudoexfoliation glaucoma\u003C/strong\u003E, a condition of older adults rather than infants.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1662,
    "Name": "Familial aniridia: expected associated finding",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old has had nystagmus since early infancy, reduced vision in both eyes, and very little visible iris tissue bilaterally. The same iris abnormality is present in the child\u2019s parent and two siblings. Which additional finding is most likely in this child?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Photosensitivity.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe clinical picture is most consistent with aniridia, which typically includes bilateral iris hypoplasia, foveal hypoplasia (driving reduced visual acuity), and early-onset nystagmus.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EWhen aniridia is familial (multiple affected first-degree relatives), it most often reflects a heritable PAX6-related condition rather than a sporadic contiguous gene deletion.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EWith little to no iris tissue, excessive light enters the eye, so photophobia/photosensitivity is a very common symptom.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\nWilms tumor and nephroblastoma refer to the same pediatric renal malignancy. The key discriminator is inheritance pattern: familial aniridia (typically isolated PAX6 mutation) is not associated with a substantially increased Wilms tumor risk compared with the general population.\u003Cbr\u003E\nIn contrast, sporadic aniridia can be due to larger deletions involving the WT1 region (classically the WAGR spectrum), and that subgroup carries a meaningful Wilms tumor risk\u2014hence the emphasis on genetic testing and tumor surveillance in apparently sporadic cases.\u003Cbr\u003E\nBecause this case is strongly familial, the \u201Ctumor risk\u201D association is less likely than a direct optical symptom such as photosensitivity.\u003C/p\u003E\u003Cp\u003E\nMyelinated retinal nerve fiber layer is an incidental fundus finding that can be linked to refractive amblyopia, but it is not a typical association of aniridia. Aniridia is more classically associated with glaucoma, cataract, optic nerve hypoplasia, and later corneal changes from limbal stem cell deficiency rather than myelinated nerve fibers.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1663,
    "Name": "Cerebral visual impairment (CVI)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about cerebral visual impairment is true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Optic nerve cupping may be seen in premature infants.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ECerebral visual impairment refers to visual dysfunction caused by injury to the visual pathways behind the lateral geniculate nucleus (retrogeniculate), and the term \u201Ccerebral\u201D is preferred because both cortical and subcortical damage can produce the same functional visual problems.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EIn premature infants, periventricular leukomalacia is a major cause of cerebral visual impairment and can be associated with optic nerve structural changes, including optic disc cupping that can resemble glaucomatous cupping.\u003C/strong\u003E Importantly, this cupping occurs from neurodevelopmental/white-matter injury effects on the optic pathways rather than from elevated intraocular pressure.\u003C/p\u003E\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1664,
    "Name": "Planning a unilateral recess\u2013resect for a 40\u0394 alternating exotropia ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EA 20-year-old has an untreated alternating exotropia measuring 40 prism diopters. You plan a unilateral recess\u2013resect procedure on the left eye. Using the general Parks dosing approach, which combination of medial rectus strengthening and lateral rectus weakening is most reasonable?\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Left medial rectus resection 6 mm with left lateral rectus recession 8 mm.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EThese problems usually assess three ideas rather than exact memorized millimeters:\u003C/strong\u003E\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhich muscles to target for an exotropia\u003C/strong\u003E,\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhich action to take on each muscle (strengthen vs weaken)\u003C/strong\u003E, and\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhether the deviation size calls for a small vs large dose.\u003C/strong\u003E\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cp\u003E\u003Cstrong\u003EStep 1 \u2014 Pick the correct \u201Cdirection\u201D of surgery for exotropia\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EIn exotropia, the eye is deviated outward, so the standard recess\u2013resect strategy is:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EStrengthen the medial rectus (resection)\u003C/strong\u003E to increase adduction pull, and\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWeaken the lateral rectus (recession)\u003C/strong\u003E to reduce abduction pull.\u003Cbr\u003E\nAll proposed plans follow this basic pairing, so the decision hinges on the amount.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EStep 2 \u2014 Remember that the lateral rectus generally needs a larger millimeter dose\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EFor horizontal surgery, equal millimeter changes do not produce equal effects across muscles.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe lateral rectus typically requires a larger recession than the medial rectus requires resection to achieve a comparable overall correction\u003C/strong\u003E, so a sensible plan usually shows a \u003Cstrong\u003Ebigger number on the lateral rectus\u003C/strong\u003E than on the medial rectus.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EStep 3 \u2014 Scale the dose to the deviation size (40\u0394 is \u201Clarge\u201D)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA 40\u0394 exotropia is well beyond a small-angle deviation, so a minimal recess\u2013resect (such as ~3\u20134 mm on each muscle) would be under-dosed.\u003C/strong\u003E\u003Cbr\u003E\nA more appropriate plan should reflect a \u003Cstrong\u003Esubstantial\u003C/strong\u003E lateral rectus recession paired with a \u003Cstrong\u003Emoderate-to-large\u003C/strong\u003E medial rectus resection\u2014commonly in the range of \u003Cstrong\u003Eabout 8 mm recession on the lateral rectus with about 6 mm resection on the medial rectus\u003C/strong\u003E for a unilateral approach.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EWhy the other plans are not reasonable:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPlans with very small amounts (around 3\u20134 mm)\u003C/strong\u003E are \u003Cstrong\u003Etoo conservative\u003C/strong\u003E for a 40\u0394 deviation and would be expected to leave a significant residual exotropia.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA plan where the medial rectus resection exceeds the lateral rectus recession\u003C/strong\u003E is generally \u003Cstrong\u003Eless consistent with typical horizontal dose-response behavior\u003C/strong\u003E, where the lateral rectus often needs the larger millimeter change.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA plan that reverses the \u201Cbigger LR, smaller MR\u201D relationship\u003C/strong\u003E tends to be less aligned with the usual Parks-style proportional thinking for unilateral recess\u2013resect in moderate-to-large exotropia.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1665,
    "Name": "Congenital NLDO at 18 months despite massage",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 18\u2011month\u2011old has had tearing from presumed congenital nasolacrimal duct obstruction since early infancy. The family has performed consistent Crigler massage for about a year, but the child still has epiphora. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Probing.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EPersistent tearing at 18 months despite adequate conservative care suggests that spontaneous resolution is less likely, so the next standard step is to mechanically open the obstruction.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EPrimary probing of the nasolacrimal duct is typically the first interventional treatment\u003C/strong\u003E and can often be performed as an office procedure in select children (or under anesthesia depending on age/cooperation and local practice). \u003Cstrong\u003EWhen done properly, probing has a high success rate, commonly reported around the 80\u201390% range in uncomplicated cases\u003C/strong\u003E, which is why it is the preferred next step after massage fails.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIf symptoms remain after initial probing, escalation options include a repeat probing, silicone intubation.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EDacryocystorhinostomy (DCR) is generally reserved for refractory cases\u003C/strong\u003E because it is more invasive and usually considered only after less invasive procedures have not worked.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1666,
    "Name": "Congenital visual loss: which condition shows an early abnormal fundus?",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn an infant with reduced vision present since birth, which diagnosis is most likely to show an abnormal fundus examination when evaluated during the first few months of life?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: De Morsier syndrome (septo-optic dysplasia).\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EKey idea:\u003C/strong\u003E \u003Cstrong\u003EAmong these conditions, septo\u2011optic dysplasia is the one in which the eye exam can reveal a structural abnormality immediately\u2014classically optic nerve hypoplasia\u2014so the fundus can look abnormal very early in life.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\n\u003Cstrong\u003ESepto\u2011optic dysplasia (De Morsier syndrome) is a congenital disorder involving midline brain development issues with unilateral or bilateral optic nerve hypoplasia.\u003C/strong\u003E Because the optic nerve is underdeveloped from birth, \u003Cstrong\u003Ethe optic discs may appear small and pale with a \u201Cdouble\u2011ring\u201D sign, making the fundus abnormal even in the first months.\u003C/strong\u003E \u003Cstrong\u003ENystagmus often becomes more obvious around 1\u20134 months as fixation pathways mature, but the optic nerve abnormality is present from the start.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are less likely to show an abnormal fundus in the first months\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAchromatopsia:\u003C/strong\u003E \u003Cstrong\u003EThis is a cone dysfunction syndrome (often described as rod monochromatism) causing poor central vision, photophobia, reduced/absent color vision, and nystagmus.\u003C/strong\u003E However, \u003Cstrong\u003Ethe retinal appearance in early infancy is typically normal\u003C/strong\u003E, and diagnosis often relies on \u003Cstrong\u003EERG demonstrating absent or markedly reduced cone responses.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELeber congenital amaurosis:\u003C/strong\u003E \u003Cstrong\u003EThis is a severe inherited retinal dystrophy affecting rods and cones.\u003C/strong\u003E Although visual behavior is markedly reduced and pupils may be sluggish, \u003Cstrong\u003Ethe fundus can look deceptively normal early on\u003C/strong\u003E, with more classic pigmentary/atrophic changes (vessel attenuation, optic disc pallor, pigment migration) developing later in many genotypes. \u003Cstrong\u003EERG is often crucial early.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECortical visual impairment:\u003C/strong\u003E \u003Cstrong\u003EThe problem is retro\u2011geniculate (brain/visual pathway) rather than primary retinal disease, so the ocular structures and fundus are usually normal.\u003C/strong\u003E In some cases of very early severe injury, \u003Cstrong\u003Esecondary optic pallor can eventually occur via trans\u2011synaptic degeneration\u003C/strong\u003E, but \u003Cstrong\u003Ethat is not the typical early fundus finding within the first few months\u003C/strong\u003E, and many infants still have a normal-appearing fundus initially.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1667,
    "Name": "Infantile spasms \u002B chorioretinal lacunae: expected systemic finding",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-month-old infant is evaluated for infantile spasms. Fundus examination shows multiple oval, pale chorioretinal lesions consistent with the appearance in the image. Which additional abnormality is most likely to be found during further evaluation?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-05-a5b55168-0cd2-443f-beba-1b8bb0927c04.png\u0022\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Absence (agenesis) of the corpus callosum on MRI.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe fundus photo shows characteristic chorioretinal lacunae\u2014well-known for Aicardi syndrome.\u003C/strong\u003E \u003Cstrong\u003EWhen chorioretinal lacunae occur in an infant with infantile spasms, Aicardi syndrome becomes the unifying diagnosis.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EAicardi syndrome classically presents with a triad: chorioretinal lacunae, agenesis of the corpus callosum, and infantile spasms.\u003C/strong\u003E \u003Cstrong\u003EBecause corpus callosum agenesis is a core feature of the syndrome, brain MRI most often demonstrates partial or complete absence of the corpus callosum.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EAdditional supportive findings can include optic nerve and retinal anomalies (for example colobomas) and small eyes, along with neurodevelopmental delay.\u003C/strong\u003E \u003Cstrong\u003EThe condition is typically described as X-linked dominant and usually not compatible with survival in most 46,XY individuals (rare exceptions such as XXY can occur).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are less likely\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPositive Toxocara ELISA\u003C/strong\u003E fits ocular toxocariasis, which more often produces a unilateral inflammatory mass-like picture (posterior pole granuloma or peripheral granuloma) and may cause leukocoria.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENeuronal lipofuscin deposits\u003C/strong\u003E point toward neuronal ceroid lipofuscinosis (Batten disease). \u003Cstrong\u003EThat disorder can involve seizures and progressive neurodegeneration, but it typically presents later and is associated with retinal degeneration/optic atrophy and markedly abnormal ERG rather than classic chorioretinal lacunae in early infancy.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EA mutation on chromosome 22\u003C/strong\u003E is commonly tested in association with neurofibromatosis type 2. \u003Cstrong\u003ENF2 is characterized by bilateral vestibular schwannomas and other tumors/cataracts, not the distinctive lacunae-plus-infantile-spasms pattern.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1668,
    "Name": "Strabismus procedure with the highest vision threat if perforation happens",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the following strabismus operations, which one carries the greatest risk to central vision if an intraoperative complication (such as scleral perforation) occurs?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Inferior oblique advancement.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe key complication being tested is scleral perforation and the potential for retinal injury.\u003C/strong\u003E \u003Cstrong\u003EThe procedure that becomes most dangerous to visual acuity is the one performed closest to the posterior pole\u2014because an accidental full-thickness pass risks damaging the macula, which is critical for central vision.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EInferior oblique advancement is a \u201Cstrengthening/anteriorization/advancement-type\u201D operation that requires reattaching the inferior oblique more posteriorly and/or in a location that brings the surgical field closer to the posterior segment than typical weakening procedures.\u003C/strong\u003E \u003Cstrong\u003EThat posterior (and relatively deep) working location increases the chance that an unintended perforation could involve the posterior retina, and therefore the macula, leading to a much greater threat to best-corrected visual acuity (for example macular hemorrhage, chorioretinal scar, or retinal detachment involving the posterior pole).\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1669,
    "Name": "Oculocerebrorenal (Lowe) syndrome ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4\u2011month\u2011old has poor visual tracking since birth. The child had marked hypotonia at birth, severe growth failure, and urine studies showing renal tubular dysfunction (renal tubular acidosis, hypokalemia, hypercalciuria, and aminoaciduria). This constellation suggests a specific systemic syndrome. Which congenital cataract morphology is most characteristic of that syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: disciform (membranous) cataracts.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis presentation is most consistent with Lowe syndrome (oculocerebrorenal syndrome): a disorder combining ocular disease, neurodevelopmental hypotonia, and proximal renal tubular dysfunction (Fanconi-type features).\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe urinalysis pattern\u2014aminoaciduria, renal tubular acidosis, hypokalemia, and hypercalciuria\u2014strongly points to a proximal tubulopathy, which explains failure to thrive and can contribute to rickets/poor growth.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIn Lowe syndrome, the classic ocular hallmark is dense congenital cataracts that are commonly described as disciform or \u201Cmembranous.\u201D\u003C/strong\u003E These cataracts are often present early and are a key reason infants have poor fixation/visual behavior from birth.\u003Cbr\u003E\n\u003Cstrong\u003EAdditional high-yield ocular associations include an increased risk of glaucoma in infancy and surface abnormalities (such as conjunctival/corneal scarring),\u003C/strong\u003E but the cataract type asked here is the disciform/membranous pattern.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other cataract types are less appropriate\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAnterior subcapsular cataracts\u003C/strong\u003E are more classically linked to \u003Cstrong\u003Elens trauma or chronic inflammation and certain dermatologic associations (for example severe atopy).\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECerulean (\u201Cblue\u2011dot\u201D) cataracts\u003C/strong\u003E are typically \u003Cstrong\u003Esmall peripheral cortical opacities\u003C/strong\u003E that are often minimally symptomatic.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPosterior subcapsular cataracts\u003C/strong\u003E are commonly associated with \u003Cstrong\u003Esteroid exposure, inflammation, radiation, and some retinal dystrophies.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1670,
    "Name": "Microcornea: diagnostic size cutoff in newborns",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat horizontal corneal diameter is commonly used as the cutoff to label a newborn as having microcornea?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Horizontal corneal diameter less than 9 mm.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EMicrocornea refers to a cornea that is abnormally small in diameter but otherwise typically clear and of near-normal thickness.\u003C/strong\u003E In practice, the most commonly used definition is \u003Cstrong\u003Ea horizontal corneal diameter below 9 mm in a newborn.\u003C/strong\u003E As children grow, the threshold is sometimes expressed differently (for example, \u003Cstrong\u003Ebelow about 10 mm by around 2 years of age\u003C/strong\u003E), reflecting the expected increase in corneal diameter with age.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy this cutoff matters clinically\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA small cornea often accompanies a smaller overall eye (short axial length), which frequently produces hyperopia.\u003C/strong\u003E The anterior segment can also be crowded, which increases susceptibility to \u003Cstrong\u003Eangle-closure mechanisms\u003C/strong\u003E. Even when angle closure is not present, \u003Cstrong\u003Eglaucoma risk can still be higher than in the general population\u003C/strong\u003E, so these children warrant careful long-term monitoring of intraocular pressure, optic nerves, and anterior chamber configuration.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EMicrocornea may be seen alongside other congenital ocular disorders such as \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Epersistent fetal vasculature (PFV/PHPV), coloboma, and nanophthalmos\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, so it should prompt a broader anatomic evaluation (corneal clarity, anterior segment depth, lens status, axial length, and posterior segment assessment when possible).\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
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  },
  {
    "Id": 1671,
    "Name": " SUN grading of anterior chamber cells and flare (pediatric uveitis)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old has band keratopathy in both eyes. Anterior chamber assessment shows 30 cells in a 1 mm \u00D7 1 mm slit beam in the right eye, and the iris details look hazy. In the left eye there are 20 cells in the same field, and there is only a mild haze while iris details remain clearly visible. Using SUN terminology, how should the cell and flare grades be documented for each eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Right eye: 3\u002B cell, 3\u002B flare | Left eye: 2\u002B cell, 1\u002B flare.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EStep 1 \u2014 Grade the cells (SUN, 1 mm \u00D7 1 mm field):\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ESUN cell grades are based on the number of cells per 1\u00D71 mm slit beam: 16\u201325 cells = 2\u002B, 26\u201350 cells = 3\u002B, and \u0026gt;50 = 4\u002B.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ERight eye has 30 cells \u2192 falls in 26\u201350 \u2192 3\u002B cells.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ELeft eye has 20 cells \u2192 falls in 16\u201325 \u2192 2\u002B cells.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EStep 2 \u2014 Grade the flare (SUN):\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ESUN flare grading is based on clarity of iris/lens details: 1\u002B = faint flare, 2\u002B = moderate (details still clear), 3\u002B = marked (details hazy), 4\u002B = intense with fibrin/plastic aqueous.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ERight eye: \u201Cview of the iris is hazy\u201D \u2192 marked flare \u2192 3\u002B flare.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ELeft eye: \u201Cfaint haze but iris details clearly visible\u201D \u2192 faint flare \u2192 1\u002B flare.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1672,
    "Name": "See-saw nystagmus in a child",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 14-year-old has had unusual rhythmic eye movements for three months. Examination shows a pendular pattern in which one eye moves upward with inward torsion while the other simultaneously moves downward with outward torsion. In children, which lesion most commonly explains this finding?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Craniopharyngioma.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis eye movement pattern is classic for see-saw nystagmus.\u003C/strong\u003E \u003Cstrong\u003EIn see-saw nystagmus, the two eyes move in opposite vertical directions while torsion also occurs in opposite directions (one eye elevates and intorts while the other depresses and extorts), giving a \u201Cteeter-totter\u201D appearance.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe most typical neuroanatomic source is a lesion around the parasellar region and/or the midbrain.\u003C/strong\u003E \u003Cstrong\u003EIn pediatric patients, craniopharyngioma is a common parasellar mass and is therefore a classic association with see-saw nystagmus.\u003C/strong\u003E \u003Cstrong\u003EBecause craniopharyngiomas can compress the optic chiasm, they may also produce bitemporal hemianopic visual field loss.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EManagement focuses on treating the underlying cause.\u003C/strong\u003E \u003Cstrong\u003EDefinitive therapy is directed at the responsible lesion (often surgical removal/management).\u003C/strong\u003E \u003Cstrong\u003ESymptom-reducing medications such as baclofen or clonazepam may lessen the oscillations in some cases, but they do not replace lesion-directed treatment.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ENeuroblastoma is most strongly linked to opsoclonus\u003C/strong\u003E (chaotic, rapid, multidirectional saccadic bursts).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECerebellar tumor or infarct more commonly produces other nystagmus patterns\u003C/strong\u003E (for example downbeat, upbeat, or periodic alternating nystagmus depending on the region involved).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EWhipple disease is not a typical pediatric cause of see-saw nystagmus\u003C/strong\u003E and is classically associated with systemic infectious features; it is not the high-yield lesion-location match for this specific ocular motor finding.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1673,
    "Name": "Neonatal conjunctivitis prophylaxis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAcross different countries, several agents are used to prevent neonatal conjunctivitis (ophthalmia neonatorum). Which option is not used for prophylaxis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: PHMB eye drops.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EPHMB (polyhexamethylene biguanide) is primarily an anti-amoebic medication used in the treatment of Acanthamoeba keratitis, not as routine newborn prophylaxis. Because its standard clinical role is therapeutic for corneal infection rather than preventive neonatal care, it is the \u201Cexception\u201D among the listed options.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other listed agents can be used for prophylaxis\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EErythromycin ophthalmic ointment is the standard prophylactic medication used in many settings (notably in the United States) to reduce the risk of neonatal conjunctivitis, especially gonococcal disease.\u003C/li\u003E\n\u003Cli\u003ESilver nitrate was historically the classic prophylactic agent (\u201CCred\u00E9 prophylaxis\u201D). It is effective at preventing gonococcal ophthalmia, but it does not reliably prevent chlamydial conjunctivitis and can cause chemical conjunctivitis.\u003C/li\u003E\n\u003Cli\u003EPovidone\u2013iodine drops have been used as a low-cost prophylaxis option in resource-limited settings and have broad antimicrobial activity, making it a practical alternative in some regions.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1674,
    "Name": "Inferior oblique anatomy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement about the inferior oblique extraocular muscle is incorrect?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer:\u0026nbsp;\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px; font-weight: bold;\u0022\u003EThe inferior oblique arises from the ethmoid bone.\u003C/span\u003E\u003C/p\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe inferior oblique does not originate from the ethmoid.\u003C/strong\u003E \u003Cstrong\u003EIt originates anteriorly from the periosteum of the maxillary bone on the orbital floor, just lateral to the nasolacrimal fossa.\u003C/strong\u003E Because of this anterior\u2013inferomedial origin, the muscle then courses posterolaterally beneath the inferior rectus toward its scleral insertion.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other statements are true\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe course relative to the inferior rectus is a common point of confusion, but it is correct that the inferior oblique passes \u201Cinferior/external\u201D to the inferior rectus (farther from the globe).\u003C/strong\u003E In practical terms, the inferior oblique is in a more superficial plane than the inferior rectus as it sweeps laterally and posteriorly.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIts insertion is also correctly described as being under the lateral rectus and relatively posterior on the globe, in the vicinity of the macular/posterior pole region.\u003C/strong\u003E This posterior insertion location is one reason posterior passes during certain inferior oblique procedures can carry a higher risk of visually significant complications if a scleral perforation occurs.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EInnervation is correctly stated as coming from the inferior division of cranial nerve III.\u003C/strong\u003E The inferior oblique shares this division with the medial rectus and inferior rectus (and the parasympathetic fibers to the pupil travel with the inferior division as well).\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EQuick memory anchor (high-yield)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EInferior oblique: \u201Cmaxillary origin, under/behind IR plane, inserts posterolateral under LR, innervated by inferior division of III.\u201D\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1675,
    "Name": "Brown syndrome surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen operating for Brown syndrome, surgeons may take steps to reduce the risk of causing a symptomatic superior oblique weakness afterward. Which option is not considered a preventive strategy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Complete tenectomy of the posterior portion of the superior oblique tendon.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe concern in Brown syndrome surgery is \u201Cover-weakening\u201D the superior oblique tendon, which can convert a mechanical elevation limitation into a true symptomatic superior oblique palsy (with new vertical deviation, torsional symptoms, or diplopia).\u003C/strong\u003E Because of that, techniques that \u003Cstrong\u003Econtrol\u003C/strong\u003E how much the tendon is weakened are preferred.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA key surgical principle is that a partial posterior tenectomy (often described as ~80% of the posterior fibers) can relieve the restrictive component while still preserving enough tendon function to reduce the chance of a clinically significant superior oblique weakness.\u003C/strong\u003E In contrast, \u003Cstrong\u003Ea complete posterior tenectomy removes too much tendon effect and therefore is the option most likely to precipitate symptomatic superior oblique palsy rather than prevent it.\u003C/strong\u003E That is why it is the \u201CEXCEPT\u201D choice.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other interventions can help reduce postoperative symptomatic superior oblique palsy:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECareful handling of the intermuscular septum during tenotomy\u003C/strong\u003E can reduce scarring or unintended traction effects that may worsen motility outcomes or destabilize tendon function after surgery.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESimultaneous ipsilateral inferior oblique weakening\u003C/strong\u003E can be used in selected cases to balance vertical/torsional forces and reduce the likelihood that a surgically weakened superior oblique will become clinically symptomatic.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESewing an inert spacer between the cut ends of the superior oblique tendon\u003C/strong\u003E is a \u201Ccontrolled weakening\u201D approach: \u003Cstrong\u003Eit lengthens the tendon rather than fully disrupting it, providing a more titratable effect and lowering the risk of an abrupt, excessive loss of superior oblique function.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1676,
    "Name": "Clinical significance thresholds for A- and V-pattern strabismus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFor pattern strabismus, what minimum difference between measurements in upgaze and downgaze is generally used to label an A-pattern as clinically meaningful?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: 10 prism diopters.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EAn A-pattern describes a horizontal deviation that changes with vertical gaze\u2014classically the deviation differs between upgaze and downgaze in a way that forms an \u201CA\u201D when plotted.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EIn routine clinical practice, an A-pattern is typically considered significant when the upgaze\u2013downgaze difference reaches about 10 prism diopters or more.\u003C/strong\u003E This cutoff helps distinguish small measurement variability from a true pattern that may affect symptoms, head posture, or surgical planning.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA helpful comparison is the V-pattern threshold: V-pattern strabismus is usually considered clinically significant at a larger difference\u2014around 15 prism diopters between upgaze and downgaze.\u003C/strong\u003E The higher cutoff reflects how these patterns are commonly categorized for decision-making.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1677,
    "Name": "Pediatric superotemporal eyelid mass with adnexal elements on histology",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 4-year-old is brought in with a firm, palpable lump near the lateral aspect of the upper eyelid. The caregiver noticed it incidentally during bathing and cannot say when it first appeared. The lesion is removed, and the accompanying histology images are provided. What is the most likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-12-15048d5a-2534-4086-8a65-efac5046436b.png\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-12-a11b010d-dcf1-49a5-bc7b-a844b59a6e67.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-12-b493366d-f922-496b-986b-36cd78614d1c.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Dermoid cyst.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe location and pathology together strongly support a dermoid cyst.\u003C/strong\u003E \u003Cstrong\u003EClinically, dermoid cysts in children often present as a painless, slowly noticed mass near the superotemporal orbital rim, classically around the frontozygomatic suture.\u003C/strong\u003E \u003Cstrong\u003EOn histology, the defining feature is a cyst lined by keratinizing stratified squamous epithelium with keratin debris in the lumen, plus skin adnexal structures in the cyst wall (such as hair follicles and sebaceous/sweat glands).\u003C/strong\u003E \u003Cstrong\u003EThose adnexal elements are what separate a dermoid cyst from an epidermoid cyst.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EKey concept (high yield)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EDermoid cyst =adnexal structures present.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EEpidermoid cyst =adnexal structures absent.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not the diagnosis\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EEpidermoid cyst:\u003C/strong\u003E \u003Cstrong\u003ECan look similar clinically, but histology lacks adnexal structures.\u003C/strong\u003E \u003Cstrong\u003EIf the specimen shows hair follicles or sebaceous glands within the cyst wall, that points away from epidermoid and toward dermoid.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAdenoid cystic carcinoma:\u003C/strong\u003E \u003Cstrong\u003EThis is typically a painful lacrimal gland malignancy and would be very unusual as a painless incidental eyelid-margin mass in a young child.\u003C/strong\u003E \u003Cstrong\u003EPathology classically shows a cribriform (\u201CSwiss-cheese\u201D) pattern rather than a keratin-filled cyst with adnexal elements.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EPyogenic granuloma:\u003C/strong\u003E \u003Cstrong\u003EUsually appears as a bright red, friable, vascular lesion (often after surgery, trauma, or chronic irritation).\u003C/strong\u003E \u003Cstrong\u003EIt does not present as a well-encapsulated cystic lesion with keratin and adnexal structures on histology.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical relevance/complication:\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EDermoid cysts can rupture spontaneously or during manipulation.\u003C/strong\u003E \u003Cstrong\u003EWhen the cyst contents (keratin) spill into surrounding tissues, an intense inflammatory reaction can occur and may mimic preseptal/orbital cellulitis.\u003C/strong\u003E \u003Cstrong\u003EDuring excision, careful removal without violating the cyst wall helps reduce postoperative inflammation.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1678,
    "Name": "Newborn retinal hemorrhages found incidentally on exam",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-day-old newborn is evaluated for suspected neonatal conjunctivitis. During a full eye examination with dilation, you notice a small amount of intraretinal hemorrhage in both eyes. The newborn otherwise looks well, interactive, and medically stable. What is the most appropriate next step in management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Observation only.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ESmall, intraretinal hemorrhages detected in the first days of life are commonly related to the mechanical stresses of delivery (especially vaginal delivery) and are usually self-limited.\u003C/strong\u003E \u003Cstrong\u003EIn an otherwise well-appearing newborn with no neurologic symptoms and only mild hemorrhages, the safest and most appropriate approach is reassurance with follow-up rather than urgent systemic investigations.\u003C/strong\u003E\u003Cbr\u003E\u003Cstrong\u003EBirth-related retinal hemorrhages typically fade over days to weeks and usually resolve within about the first month.\u003C/strong\u003E \u003Cstrong\u003EBecause the finding is common and transient, immediate escalation (imaging, hematologic testing, or mandatory reporting) is not the default when the infant is clinically well and the hemorrhages are mild.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not appropriate in this specific vignette\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EHematologic workup for a bleeding disorder\u003C/strong\u003E\u003Cbr\u003E\nA coagulation evaluation becomes more relevant when hemorrhages are unusually extensive, recurrent, occur without an obvious perinatal explanation, or are accompanied by systemic bleeding signs (bruising, bleeding from venipuncture sites, mucosal bleeding) or a concerning family history.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EImaging for non-accidental trauma\u003C/strong\u003E\u003Cbr\u003E\nRetinal hemorrhages from abusive head trauma are typically more severe and have a different \u201Cpattern \u002B context.\u201D They are often numerous, multilayered (intra-, pre-, and subretinal), can extend to the retinal periphery, and may be associated with retinal structural injury such as perimacular folds or traumatic retinoschisis. Importantly, affected infants are frequently clinically unwell (altered consciousness, seizures, vomiting, irritability, poor feeding) and may have evidence of intracranial injury.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EImmediate reporting to child protective services\u003C/strong\u003E\u003Cbr\u003E\nReporting is appropriate when there is reasonable suspicion of abuse based on the overall clinical picture (history inconsistencies, systemic/neurologic findings, or a hemorrhage pattern strongly suggestive of trauma).\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhat \u201Cobservation\u201D should include (practical documentation)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EDocument the hemorrhage type and extent (intraretinal, mild, bilateral), overall infant wellness, and arrange follow-up to confirm resolution.\u003C/strong\u003E \u003Cstrong\u003EEscalate evaluation if hemorrhages are extensive, multilayered, associated with retinal splitting/folds, persist beyond the expected resolution window, or if any systemic/neurologic concerns emerge.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1679,
    "Name": "Iris coloboma: \u201Ctypical\u201D location, laterality, and posterior association",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ERegarding to the lesion showed in the picture, If the defect is the typical type, which statement is correct regarding which eye is shown and whether deeper (posterior) ocular structures may also be involved?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-12-d064ad31-87f2-4c0b-ae5a-125b071d6543.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Typical coloboma \u2192 right eye, and posterior involvement may occur.\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhat the photo represents\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThe abnormality is an iris coloboma, which results from incomplete closure of the embryonic (choroidal) fissure during early gestation (classically around the 5th week).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ETypical vs atypical: the key distinction\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EA \u201Ctypical\u201D coloboma lies in the inferonasal quadrant because that is where the embryonic fissure closes.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EBecause the same fissure relates to multiple ocular layers, a typical iris coloboma can be accompanied by colobomas of deeper structures such as the ciliary body, choroid, retina, and even the optic nerve.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy this is the right eye (when typical)\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EIn standard anterior segment photos, the inferonasal defect appears in the inferonasal part of the iris. The orientation in the pictured eye is consistent with a right eye when you assume a typical inferonasal defect.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ETherefore, \u201Cright eye \u002B may involve posterior structures\u201D is the correct combined statement.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1680,
    "Name": "Estimating visual acuity in a preverbal child",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA preverbal child needs an estimate of visual acuity. Which method is appropriate for measuring visual acuity in a child who cannot yet name letters or match symbols?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Teller card\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ETeller preferential-looking cards are designed specifically for infants and other preverbal children.\u003C/strong\u003E \u003Cstrong\u003EThey rely on the principle that babies naturally look toward a patterned target (high-contrast stripes) rather than a blank field.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EEach card has one blank side and one side with black-and-white gratings; the examiner watches the child\u2019s gaze through a small central viewing hole.\u003C/strong\u003E \u003Cstrong\u003EBy presenting progressively finer stripe widths, the examiner identifies the smallest grating that still attracts consistent looking\u2014this \u201Cthreshold\u201D provides an estimate of visual acuity.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EOther ways to estimate vision in preverbal children include objective/behavioral methods such as visual evoked potentials (VEP) and optokinetic nystagmus (OKN), but among the listed choices, Teller cards are the classic option for preverbal acuity estimation.\u003C/strong\u003E\u003C/p\u003E\n\u003Ch3\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EWhy the other options are not the best fit here\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAllen cards\u003C/strong\u003E use picture optotypes and generally require a level of recognition/communication that many young infants do not have.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHOTV\u003C/strong\u003E is typically used once a child can match letters (often with a matching card), so it is better suited to slightly older, cooperative children.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESnellen\u003C/strong\u003E requires letter identification and is intended for literate/verbal patients, not preverbal infants.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1681,
    "Name": "Mild eyelid cellulitis in a child: next step",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child presents with redness and swelling of the left upper eyelid. Examination shows eyelid erythema and edema, but there is full, painless extraocular motility, no proptosis, no chemosis or conjunctival injection, normal visual acuity, and the child is afebrile and otherwise well-appearing. What is the most appropriate management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Treat as an outpatient with oral amoxicillin\u2013clavulanate and close follow-up.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe findings described fit preseptal (periorbital) cellulitis rather than orbital cellulitis.\u003C/strong\u003E Preseptal cellulitis is limited to tissues \u003Cstrong\u003Eanterior to the orbital septum\u003C/strong\u003E, so it typically causes \u003Cstrong\u003Eeyelid erythema and edema\u003C/strong\u003E but \u003Cstrong\u003Edoes not\u003C/strong\u003E cause the \u201Cpostseptal red flags\u201D seen in orbital cellulitis. The most important features that argue against orbital involvement here are: \u003Cstrong\u003Efull, painless extraocular movements (no restriction or pain with eye movement), absence of proptosis, absence of conjunctival chemosis/injection suggestive of orbital congestion, and an afebrile, non-toxic overall appearance.\u003C/strong\u003E In a stable child with these reassuring features, \u003Cstrong\u003Eoutpatient therapy is appropriate\u003C/strong\u003E provided reliable follow-up is arranged.\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EOral broad-spectrum coverage is standard for uncomplicated preseptal cellulitis\u003C/strong\u003E, and \u003Cstrong\u003Eamoxicillin\u2013clavulanate\u003C/strong\u003E provides coverage for common pathogens associated with skin/soft tissue and upper respiratory sources. \u003Cstrong\u003EClose follow-up is essential\u003C/strong\u003E to confirm improvement and to ensure that orbital signs do not develop.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other management approaches are less appropriate in this scenario:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EInpatient admission for IV antibiotics\u003C/strong\u003E is generally reserved for children who appear ill, have significant fever, cannot tolerate oral medication, are very young with unreliable observation, or show any signs concerning for orbital disease.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EUrgent orbital imaging\u003C/strong\u003E is most useful when the exam suggests orbital cellulitis or when the exam is unreliable (e.g., severe swelling preventing assessment) or when there is poor response to appropriate therapy.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDoxycycline or ciprofloxacin are not preferred routine choices in a young child for this indication.\u003C/strong\u003E \u003Cstrong\u003ETetracyclines (like doxycycline) are generally avoided in developing children due to tooth discoloration concerns\u003C/strong\u003E, and \u003Cstrong\u003Efluoroquinolones (like ciprofloxacin) are used selectively because of musculoskeletal adverse-effect concerns\u003C/strong\u003E; neither is a typical first-line outpatient option for straightforward preseptal cellulitis when safer, effective alternatives exist.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EPractical safety-net (what should be documented and advised):\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EProvide strict return precautions\u003C/strong\u003E for any development of \u003Cstrong\u003Efever, worsening swelling, decreased vision, new diplopia, proptosis, pain with eye movements, or restricted eye movements\u003C/strong\u003E, and reassess promptly if symptoms fail to improve within \u003Cstrong\u003E24\u201348 hours\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1682,
    "Name": "Ophthalmia neonatorum with heavy purulent discharge at day 5",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-day-old infant has copious pus-like discharge from both eyes consistent with neonatal conjunctivitis. What is the most likely way the infection was acquired?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Exposure during delivery while passing through the maternal genital tract (birth canal).\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EConjunctivitis appearing within the first month of life is termed ophthalmia neonatorum, and the timing after birth is a practical clue to the underlying cause.\u003C/strong\u003E \u003Cstrong\u003EWhen an infant presents very early with profuse purulent discharge, a birth-acquired bacterial infection is most likely, because organisms in the maternal genital tract can directly inoculate the conjunctiva during delivery.\u003C/strong\u003E This is why \u003Cstrong\u003Ethe most typical route for infectious neonatal conjunctivitis is acquisition during passage through the birth canal.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe clinical timing pattern that supports this reasoning is:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EChemical conjunctivitis\u003C/strong\u003E tends to occur \u003Cstrong\u003Ewithin the first 24 hours\u003C/strong\u003E and usually improves quickly (often by \u003Cstrong\u003Eday 2\u003C/strong\u003E), so it would be less consistent with new, heavy purulence on day 5.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EGonococcal conjunctivitis\u003C/strong\u003E classically presents around \u003Cstrong\u003Edays 3\u20135\u003C/strong\u003E and is often \u003Cstrong\u003Ethe most dramatically purulent\u003C/strong\u003E and can be severe\u2014so day 5 with abundant discharge strongly fits a birth-acquired mechanism.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EChlamydial conjunctivitis\u003C/strong\u003E more often presents around \u003Cstrong\u003Edays 5\u201314\u003C/strong\u003E (commonly near \u003Cstrong\u003E1 week\u003C/strong\u003E), though it can appear earlier in certain circumstances; it is still typically \u003Cstrong\u003Eacquired intrapartum\u003C/strong\u003E, which again points to birth-canal exposure as the mechanism.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHSV conjunctivitis\u003C/strong\u003E is uncommon and more typical around \u003Cstrong\u003E~2 weeks\u003C/strong\u003E, making it less likely in this specific day\u20115 scenario.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other mechanisms are less appropriate here:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETransplacental spread\u003C/strong\u003E is not the usual mechanism for neonatal conjunctivitis; it is more relevant for congenital infections that affect multiple systems rather than presenting primarily as isolated purulent conjunctivitis.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHospital personnel/environment contamination\u003C/strong\u003E can cause neonatal eye infection, but the classic, high-yield etiologies of ophthalmia neonatorum (especially gonorrhea and chlamydia) are most strongly linked to \u003Cstrong\u003Eintrapartum exposure\u003C/strong\u003E rather than postnatal hospital contact.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHematogenous spread from another infection site\u003C/strong\u003E would typically imply a systemically ill infant or signs of sepsis; the common neonatal conjunctivitis pathogens usually reach the eyes by \u003Cstrong\u003Edirect contact\u003C/strong\u003E, not via the bloodstream.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1683,
    "Name": "Mean normal intraocular pressure (IOP) in a newborn",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the mean NORMAL intraocular pressure (IOP) of a newborn child?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: 10 to 12 mmHg.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ENewborns have a lower average IOP than older children and adults.\u003C/strong\u003E The commonly quoted mean normal IOP range in a newborn is \u003Cstrong\u003Eabout 10\u201312 mmHg\u003C/strong\u003E, and \u003Cstrong\u003EIOP gradually increases with age\u003C/strong\u003E, reaching roughly \u003Cstrong\u003E~14 mmHg by around school age (about 8 years)\u003C/strong\u003E. This age-related rise reflects maturation of ocular rigidity and aqueous dynamics.\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003ECongenital glaucoma is not a subtle elevation.\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E When primary congenital glaucoma is present, IOP is often \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Emarkedly high (commonly in the 30\u201340 mmHg range)\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E. Also, \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EIOP measurements taken under general anesthesia may read lower than awake measurements\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, yet affected infants can still show elevated pressures (often remaining in the \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003E20s\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E), so exam context is important.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1684,
    "Name": "Eye movements that are typically not fully present at birth",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn newborns, which type of eye movement is commonly not yet fully developed?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Conjugate vertical gaze.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EAt birth, many ocular motor functions are present, especially basic horizontal conjugate movements and vestibular-driven eye movements (the vestibulo-ocular reflex), because these pathways are relatively mature early and are critical for stabilizing gaze.\u003C/strong\u003E In contrast, \u003Cstrong\u003Ecoordinated vertical gaze is often immature in newborns and may not appear fully developed until several months of age (commonly cited around ~6 months).\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1685,
    "Name": "Stargardt disease (fundus flavimaculatus)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 17-year-old candidate for military aviation is found to have reduced best-corrected vision (20/40 in one eye and 20/70 in the other). His dilated fundus exam is seen below. Which feature is most characteristic of this condition?\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-16-d07200c3-9fe6-474e-8182-8c2e160217a1.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: \u201CDark choroid\u201D sign on fluorescein angiography.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\nThe fundus appearance described (juvenile onset decreased central acuity with macular changes and yellow pisciform flecks) is most consistent with Stargardt disease, often discussed together with fundus flavimaculatus. This is a juvenile macular dystrophy in which lipofuscin accumulates within the retinal pigment epithelium (RPE), producing flecks and progressive macular dysfunction.\u003C/p\u003E\n\u003Cp\u003EThe hallmark fluorescein angiography clue is the \u201Cdark choroid\u201D sign. In early phases of FA, the choroid appears unusually hypofluorescent because excess lipofuscin in the RPE blocks normal background choroidal fluorescence (a masking effect). As a result, the retinal vessels can look relatively prominent against a darker-than-expected choroidal background.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EWhy the other statements are wrong:\u003C/strong\u003E\u003Cbr\u003E\nA congenital color deficiency without progressive loss of acuity describes inherited color vision deficiency (such as protan/deutan defects). Those patients typically have a normal fundus and do not develop a bull\u2019s-eye maculopathy with flecks or progressive central retinal changes.\u003C/p\u003E\n\u003Cp\u003EProgressive color vision loss with \u201Chemeralopia\u201D (day-blindness) is more typical of cone dystrophies. Cone dystrophy can also produce a bull\u2019s-eye pattern, but it usually causes more prominent photophobia, dyschromatopsia, and often worse eventual acuity than typical Stargardt presentations, and the FA signature tested here is not \u201Cdark choroid\u201D as a defining feature.\u003C/p\u003E\n\u003Cp\u003E\u201CQuenching\u201D on fluorescein angiography is classically linked to certain white-dot chorioretinopathies (such as birdshot chorioretinopathy), not Stargardt disease. That phenomenon refers to characteristic angiographic behavior in those inflammatory choroidopathies rather than lipofuscin-related masking.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1686,
    "Name": "Quantifying a manifest deviation (heterotropia) in strabismus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has strabismus with a manifest deviation. Which clinical test is used to measure the size of the manifest deviation (heterotropia)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Simultaneous prism-and-cover test.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe key concept is the difference between measuring only the manifest deviation (heterotropia) versus measuring the full deviation (heterotropia plus any latent component, heterophoria).\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe simultaneous prism-and-cover test is designed to quantify the manifest component only.\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E It does this by \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eplacing a prism in front of the deviating eye while the fixing eye is covered at the same time\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, preventing fusion but \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Enot \u201Cdissociating\u201D the eyes enough to bring out the latent phoria.\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EYou increase prism strength until the deviating eye no longer makes a refixation movement\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, which gives the magnitude of the heterotropia.\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ECover\u2013uncover test: This detects the presence of a tropia by observing a refixation movement when the cover is removed, but it does not provide a prism-neutralized measurement of the deviation by itself. It is primarily a detection test for manifest deviation.\u003C/li\u003E\n\u003Cli\u003EAlternate cover test with prism (prism alternate cover): This fully dissociates the eyes, so it measures the total deviation\u2014tropia plus phoria\u2014rather than isolating the heterotropia alone.\u003C/li\u003E\n\u003Cli\u003EHirschberg test: This uses the corneal light reflex position to estimate alignment, but it is only a rough, qualitative (or at best very approximate) estimate and is not the standard way to precisely quantify a manifest deviation in prism diopters.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1687,
    "Name": "Angle of the oblique muscles relative to the visual axis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EHow many degrees do the superior oblique and inferior oblique muscles typically make with the eye\u2019s visual axis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: 51 degrees.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe oblique extraocular muscles have a characteristic course such that their line of pull is angled significantly relative to the visual axis.\u003C/strong\u003E The commonly cited value is that \u003Cstrong\u003Eboth the superior oblique and inferior oblique form an angle of about 51\u00B0 with the visual axis.\u003C/strong\u003E This relationship is clinically useful because \u003Cstrong\u003Ethe actions of the obliques (torsion plus vertical components) are highly position-dependent\u003C/strong\u003E, and understanding their geometry helps explain why their vertical actions are most evident in adduction.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA high-yield contrast is the vertical rectus muscles.\u003C/strong\u003E \u003Cstrong\u003EThe superior and inferior rectus are oriented about 23\u00B0 from the visual axis\u003C/strong\u003E, which is why their actions include a combination of \u003Cstrong\u003Evertical movement and torsion\u003C/strong\u003E, with the torsional component depending on gaze position.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1688,
    "Name": "CPEO with pigmentary retinopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 25-year-old has gradually worsening droopy eyelids and difficulty tracking moving objects, beginning in adolescence. Examination suggests a chronic progressive external ophthalmoplegia picture, and the fundus shows mild \u201Csalt-and-pepper\u201D pigmentary changes in both eyes. There is no delayed relaxation on handshake. Which additional test is most important to obtain as part of the workup?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Electrocardiogram (EKG).\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis presentation is most consistent with a mitochondrial ophthalmic syndrome in the chronic progressive external ophthalmoplegia spectrum, and the added finding of pigmentary retinopathy strongly points toward Kearns\u2013Sayre syndrome.\u003C/strong\u003E Kearns\u2013Sayre classically combines progressive ptosis/ophthalmoplegia with pigmentary retinopathy and can be associated with serious cardiac conduction abnormalities, including heart block. Because conduction disease can be silent until it becomes dangerous, an EKG is a key screening test and is the most urgent ancillary study among the listed options.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ETensilon (edrophonium) test:\u003C/strong\u003E \u003Cstrong\u003EThis is used to support a diagnosis of myasthenia gravis.\u003C/strong\u003E Myasthenia typically causes fluctuating fatigable ptosis/ophthalmoparesis and does not explain a pigmentary retinopathy pattern; additionally, the vignette leans toward a slowly progressive mitochondrial process rather than fatigability.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESingle-fiber EMG:\u003C/strong\u003E \u003Cstrong\u003EThis is most helpful for neuromuscular junction disorders (especially myasthenia) and may also be used in certain myopathic conditions, but the scenario specifically notes no handshake abnormality (arguing against myotonic dystrophy) and highlights pigmentary retinopathy, which pushes the diagnosis toward Kearns\u2013Sayre where cardiac screening is the priority.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EElectroretinography (ERG):\u003C/strong\u003E \u003Cstrong\u003EERG can help characterize retinal dystrophies, and it may be informative if the diagnosis is uncertain, but it does not address the major potentially life-threatening association of Kearns\u2013Sayre\u2014cardiac conduction block.\u003C/strong\u003E\u0026nbsp;\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1689,
    "Name": "Pediatric open-globe injury with \u201Cfluffy\u201D anterior chamber material",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 7-year-old sustains a knife injury to the eye. Slit-lamp exam reveals a 3 mm peripheral corneal laceration and a shallow anterior chamber. Wispy \u201Cfluffy\u201D material is seen floating in the anterior chamber, and the anterior lens capsule is difficult to assess through it. Orbital CT shows no intraocular foreign body. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Globe exploration and repair in the operating room only.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis presentation should be managed as a penetrating/open-globe injury, so the priority is urgent surgical exploration and watertight globe repair.\u003C/strong\u003E \u003Cstrong\u003EIn children, inflammatory fibrin can form rapidly after penetration and may look like \u201Clens material\u201D in the anterior chamber.\u003C/strong\u003E Because this appearance can be misleading, \u003Cstrong\u003Eperforming a lens removal at the time of primary repair is not recommended unless there is clear, definite evidence that the anterior lens capsule is violated (for example, obvious capsular rupture, lens matter extruding, or a traumatic cataract with unmistakable capsular disruption).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EEven if capsular injury is suspected, it is often safer to stabilize the globe first and address the lens in a planned second stage once the eye is quieter and less inflamed.\u003C/strong\u003E \u003Cstrong\u003EImmediate lensectomy during the primary open-globe repair can increase surgical complexity and may worsen inflammation or compromise outcomes if the diagnosis is uncertain.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy conservative measures alone are not enough:\u003C/strong\u003E \u003Cstrong\u003EUsing glue or a bandage contact lens is appropriate for selected non-penetrating corneal problems or very small self-sealing injuries, but a knife-induced corneal laceration with a shallow anterior chamber raises strong concern for an open globe and needs operative repair rather than office-based temporizing measures.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1690,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ENeonatal conjunctivitis in the first month is termed ophthalmia neonatorum. At what time after birth does chemical conjunctivitis most commonly appear?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Within the first 24 hours.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EChemical conjunctivitis is the earliest form of ophthalmia neonatorum and typically shows up in the first day after birth.\u003C/strong\u003E \u003Cstrong\u003EIt most often follows exposure to prophylactic eye medications (classically older silver nitrate preparations), leading to a transient irritative reaction rather than an active infection.\u003C/strong\u003E \u003Cstrong\u003EBecause it is an irritant response, it usually improves quickly\u2014often resolving by about the second day of life.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other time points are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003E3\u20134 days\u003C/strong\u003E is more typical of \u003Cstrong\u003Egonococcal conjunctivitis\u003C/strong\u003E, which often produces \u003Cstrong\u003Every copious purulent discharge\u003C/strong\u003E and is a more urgent infection to recognize.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E~7 days\u003C/strong\u003E is a common timing for \u003Cstrong\u003Echlamydial conjunctivitis\u003C/strong\u003E (though it can present earlier in certain situations such as prolonged rupture of membranes).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E~14 days\u003C/strong\u003E fits better with \u003Cstrong\u003EHSV-related conjunctivitis\u003C/strong\u003E, which is uncommon but classically later than chemical causes.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1691,
    "Name": "Acute comitant esotropia after short-term patching",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 5-year-old develops a new inward eye deviation over one week. One week earlier, the child sustained blunt trauma to the left eye with a hyphema, and the family has kept that eye patched continuously for protection. There was no prior strabismus history. Alignment measures a 25 prism-diopter comitant esotropia at distance and near. Eye movements are full. Visual acuity is 20/20 in the right eye and 20/30 in the left eye. Cycloplegic refraction is \u002B0.50 D in both eyes. What is the most likely explanation for this esotropia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Acquired nonaccommodative esotropia.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis is most consistent with a basic acquired nonaccommodative esotropia triggered by temporary disruption of binocularity.\u003C/strong\u003E The key clues are \u003Cstrong\u003E(1) the deviation began after a week of occluding one eye\u003C/strong\u003E, \u003Cstrong\u003E(2) the esotropia is comitant (same size in all gaze positions)\u003C/strong\u003E, and \u003Cstrong\u003E(3) there is minimal hyperopia (\u002B0.50 D), so accommodation is not driving the deviation.\u003C/strong\u003E Short-term patching can \u003Cstrong\u003Eremove fusional control\u003C/strong\u003E, allowing a previously compensated tendency to become manifest as a comitant esotropia.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy refractive accommodative esotropia is unlikely:\u003C/strong\u003E \u003Cstrong\u003ERefractive accommodative esotropia typically requires meaningful hyperopia and improves substantially with full hyperopic correction.\u003C/strong\u003E With \u003Cstrong\u003Eonly \u002B0.50 D OU\u003C/strong\u003E, there is \u003Cstrong\u003Enot enough accommodative demand\u003C/strong\u003E to explain a 25\u0394 esotropia.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy sensory esotropia is unlikely:\u003C/strong\u003E \u003Cstrong\u003ESensory esotropia occurs when there is significant unilateral visual impairment that disrupts fusion.\u003C/strong\u003E Here, the left eye is \u003Cstrong\u003Eonly mildly reduced (20/30)\u003C/strong\u003E and the vision loss is \u003Cstrong\u003Enot severe enough\u003C/strong\u003E to be the usual driver of a sensory deviation\u2014especially over such a short timeline.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy CN VI palsy is unlikely:\u003C/strong\u003E \u003Cstrong\u003EAn abducens palsy causes an incomitant esotropia with limited abduction\u003C/strong\u003E (often worse in the direction of action of the weak lateral rectus). This child has \u003Cstrong\u003Efull ductions\u003C/strong\u003E and a \u003Cstrong\u003Ecomitant\u003C/strong\u003E deviation, which argues strongly against CN VI palsy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1692,
    "Name": "Iris stromal cyst in an infant obstructing the visual axis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-year-old is evaluated for an apparent iris mass. Examination under anesthesia with ultrasound biomicroscopy confirms a primary iris stromal cyst, and the lesion fully blocks the visual axis. What is the preferred management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Surgical excision.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EA primary iris stromal cyst in infancy behaves differently from many benign iris pigment epithelial cysts.\u003C/strong\u003E \u003Cstrong\u003EStromal cysts can enlarge quickly and may cause clinically important complications, especially when the cyst blocks the pupil/visual axis.\u003C/strong\u003E These complications include \u003Cstrong\u003Edeprivation amblyopia from occluding the visual axis\u003C/strong\u003E, as well as \u003Cstrong\u003Ecorneal damage from intermittent or sustained corneal touch, secondary glaucoma, and anterior uveitis if cyst contents leak.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBecause the visual axis is completely obstructed in this child, observation is not appropriate.\u003C/strong\u003E \u003Cstrong\u003ELeaving the axis blocked during the amblyogenic period can lead to permanent reduction in visual potential\u003C/strong\u003E, even if the cyst later regresses or is treated.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAmong active treatment options, surgical excision is preferred because it offers the best chance of definitive control with lower recurrence compared with less definitive approaches.\u003C/strong\u003E \u003Cstrong\u003ESimple aspiration or laser-based methods often have higher recurrence\u003C/strong\u003E, since the cyst wall/lining may remain and can reaccumulate fluid.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1693,
    "Name": "Spasm of the near reflex",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 21-year-old develops sudden diplopia and an inward deviation during a stressful exam period. Distance acuity is reduced, but near acuity is excellent in both eyes. Alignment shows a comitant esotropia of about 15 prism diopters at both distance and near. Monocular ductions are full, yet on binocular versions both eyes appear to have limited abduction. Pupils are small and respond poorly to light. Non-cycloplegic refraction shows moderate myopia, and the patient declines cycloplegia. Which diagnosis best explains this presentation?\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Spasm of the near reflex.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis presentation is classic for spasm of the near reflex (also called convergence spasm or ciliary spasm), which is characterized by an inappropriate, excessive activation of the near triad: convergence, accommodation, and miosis.\u003C/strong\u003E \u003Cstrong\u003EThe stress trigger, acute onset diplopia, small pupils, and a myopic-looking manifest refraction all strongly support this.\u003C/strong\u003E The apparent \u201Cabduction deficit\u201D on versions occurs because \u003Cstrong\u003Ewhen both eyes are open, excessive convergence makes the eyes look like they cannot abduct\u003C/strong\u003E, but \u003Cstrong\u003Etrue lateral rectus function is intact\u2014proved by full monocular ductions.\u003C/strong\u003E That \u201Cversions look limited, ductions are full\u201D pattern is a major clue that this is functional/convergence-driven rather than a cranial nerve palsy.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe visual acuity pattern also fits.\u003C/strong\u003E \u003Cstrong\u003ENear vision is excellent while distance acuity is reduced, which can happen when accommodation is inappropriately engaged at distance, producing pseudomyopia.\u003C/strong\u003E \u003Cstrong\u003EWithout cycloplegia, the refraction may look more myopic than the true baseline because accommodative spasm adds extra minus power.\u003C/strong\u003E Cycloplegic refraction often reveals much less myopia (or even minimal refractive error), and it can temporarily \u201Cbreak\u201D the spasm.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other diagnoses are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAccommodative insufficiency:\u003C/strong\u003E \u003Cstrong\u003EThis primarily causes near blur, asthenopia, and difficulty sustaining near work.\u003C/strong\u003E It does not typically cause \u003Cstrong\u003Emiosis with acute comitant esotropia\u003C/strong\u003E or a binocular-only abduction limitation that disappears on monocular ductions.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHorner syndrome:\u003C/strong\u003E \u003Cstrong\u003EHorner syndrome causes a small pupil with poor dilation in dim light (often with mild ptosis and dilation lag), but it does not cause episodic excessive convergence, pseudomyopia, or a binocular-only abduction limitation.\u003C/strong\u003E In addition, Horner pupils usually have a relatively preserved light reaction; the key issue is sympathetic denervation and impaired dilation rather than a near-triad spasm picture.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDivergence insufficiency:\u003C/strong\u003E \u003Cstrong\u003EThis produces distance esotropia that is greater at distance than near\u003C/strong\u003E, typically in older patients, and it does not explain \u003Cstrong\u003Emiosis, pseudomyopia, or the mismatch of full ductions with limited abduction only on versions.\u003C/strong\u003E Here the deviation is the same at distance and near, which argues against divergence insufficiency.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical pearl (high-yield):\u003C/strong\u003E \u003Cstrong\u003ESpasm of the near reflex is often functional and associated with stress/anxiety.\u003C/strong\u003E \u003Cstrong\u003ETreatment focuses on breaking the accommodative component (cycloplegic drops such as atropine or cyclopentolate), reducing triggers, and sometimes using plus lenses/bifocals for near comfort.\u003C/strong\u003E Persistent cases may need orthoptic support; invasive treatments are rarely required.\u003C/p\u003E\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1694,
    "Name": "Shortest overall extraocular muscle",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen you consider both the muscle belly and its tendon together, which extraocular muscle has the smallest total length?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: inferior oblique.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis is an anatomy \u201Ctotal length\u201D question\u2014muscle belly length plus tendon length\u2014not simply which muscle has the shortest contractile portion.\u003C/strong\u003E Several rectus muscles have \u003Cstrong\u003Esimilar active (contractile) lengths\u003C/strong\u003E, so the \u003Cstrong\u003Etendon length\u003C/strong\u003E becomes the deciding factor.\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe medial rectus, lateral rectus, and inferior rectus (and also the superior rectus) have active muscle bellies that are roughly similar in size (commonly cited around 40 mm).\u003C/strong\u003E The inferior oblique\u2019s active belly is \u003Cstrong\u003Eslightly shorter (around the high 30s mm)\u003C/strong\u003E, but what really matters is that \u003Cstrong\u003Ethe inferior oblique has an extremely short tendon\u2014often described as about 1 mm.\u003C/strong\u003E Because the tendon contributes very little additional length, \u003Cstrong\u003Ethe inferior oblique ends up being the shortest extraocular muscle overall when \u201Cmuscle \u002B tendon\u201D are added together.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe superior oblique is often the longest overall because it has a long tendon (classically around the mid\u201120s mm),\u003C/strong\u003E so even if its contractile portion is not the longest, the tendon substantially increases its total length. This \u201Clong tendon vs very short tendon\u201D contrast explains why \u003Cstrong\u003Esuperior oblique tends toward the longest overall\u003C/strong\u003E, while \u003Cstrong\u003Einferior oblique tends toward the shortest overall.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1695,
    "Name": "Lisch nodules \u002B multiple caf\u00E9-au-lait macules",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has multiple small, well-defined raised spots on the anterior iris consistent with the appearance in the photo. The patient also has numerous discrete hyperpigmented patches on the trunk. Which chromosome contains the gene locus most classically associated with this systemic diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-17-04bee7d9-1bfc-4fb4-a755-257f3788c690.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Chromosome 17.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThe iris findings shown are most consistent with Lisch nodules, which are melanocytic iris hamartomas.\u003C/strong\u003E \u003Cstrong\u003EWhen Lisch nodules occur together with multiple caf\u00E9-au-lait macules, the unifying diagnosis is neurofibromatosis type 1 (NF1).\u003C/strong\u003E \u003Cstrong\u003ENF1 is caused by pathogenic variants in the NF1 gene, which is located on chromosome 17.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\nLisch nodules are highly characteristic of NF1 and become increasingly common with age, often appearing in childhood and being very common in adults. The presence of multiple caf\u00E9-au-lait macules strengthens the diagnosis because pigmentary skin findings are among the most frequent early clues to NF1. NF1 is a \u201Cphakomatosis\u201D (neurocutaneous syndrome), so ocular signs plus skin findings are a classic board-style pairing.\u003C/p\u003E\u003Cp\u003E\nNF1 is diagnosed clinically using a criteria-based approach, and meeting at least two of the standard features supports the diagnosis. Typical features include multiple caf\u00E9-au-lait macules, axillary/inguinal freckling, neurofibromas (including plexiform types), optic pathway glioma, characteristic bony lesions (such as sphenoid dysplasia), and Lisch nodules.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other chromosomes are not the best match:\u003C/strong\u003E\u003Cbr\u003E\nChromosome 22 is associated with neurofibromatosis type 2 (NF2), which is classically linked to bilateral vestibular schwannomas and different ocular findings (for example certain cataracts and retinal hamartomas), rather than Lisch nodules as the hallmark.\u003Cbr\u003E\nChromosomes 9 and 16 are commonly tested in tuberous sclerosis (TSC1 on 9 and TSC2 on 16), which has a different neurocutaneous pattern (e.g., facial angiofibromas, cortical tubers) and different ophthalmic associations than NF1.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1696,
    "Name": "Treatment of isoametropic (bilateral refractive) amblyopia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the standard first-line treatment for isoametropic amblyopia (amblyopia from high, symmetric refractive error in both eyes)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Optimal refractive correction alone.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EIsoametropic amblyopia happens when both eyes are blurred during early visual development because of high, relatively equal refractive error (such as large hyperopia, myopia, significant astigmatism, or a combination) in both eyes.\u003C/strong\u003E Since the problem is \u003Cstrong\u003Ebilateral and symmetric\u003C/strong\u003E, the main issue is \u003Cstrong\u003Eglobal deprivation of a clear retinal image\u003C/strong\u003E, not one eye \u201Cwinning\u201D over the other.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ETherefore, the primary treatment is simply to provide the best optical clarity with full, appropriate refractive correction (usually glasses).\u003C/strong\u003E \u003Cstrong\u003EMany children improve substantially with spectacles alone over weeks to months as the visual system receives a consistently focused image in both eyes.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy patching or atropine is usually not needed at the start:\u003C/strong\u003E\u003Cbr\u003E\nPenalization therapies (patching or atropine) are designed to force use of a weaker eye when there is competition between the eyes (most commonly anisometropic or strabismic amblyopia). In isoametropic amblyopia, both eyes are under-stimulated, so penalizing one eye does not address the root cause and can even be counterproductive if it reduces binocular input unnecessarily.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhen you would add penalization:\u003C/strong\u003E\u003Cbr\u003E\nIf vision does not improve adequately with consistent spectacle wear, or if an additional amblyogenic factor is present (like anisometropia or strabismus), then patching or other amblyopia therapy may be considered. But the best initial step remains glasses alone.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1697,
    "Name": "First follow-up after starting full-time patching",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAfter prescribing full-time occlusion therapy for amblyopia in a 4-year-old, what is the usual timing for the first review visit?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: 4 weeks.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EFull-time patching carries a real risk of \u201Creverse amblyopia\u201D (new reduction of vision in the patched, previously better eye), so the first follow-up is scheduled relatively early.\u003C/strong\u003E \u003Cstrong\u003EA practical, commonly taught approach is to review children on full-time occlusion at an interval roughly tied to age (about \u201Cone month\u201D for a 4-year-old), which balances early safety monitoring with allowing enough time to see a treatment response.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other timeframes are less appropriate:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003E2 weeks\u003C/strong\u003E is often used for \u003Cem\u003Eyounger\u003C/em\u003E children or when there is heightened concern about compliance or reverse amblyopia risk, but it is not the \u201Ctypical\u201D first interval for an otherwise stable 4-year-old starting full-time patching.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E8 weeks\u003C/strong\u003E is usually too long for an initial check on \u003Cem\u003Efull-time\u003C/em\u003E occlusion because you could miss early reverse amblyopia or over-treatment.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E12 weeks\u003C/strong\u003E is even longer and generally inappropriate as a first review interval for full-time patching.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1698,
    "Name": "V-pattern strabismus: clinically significant cutoff",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn pattern strabismus, what minimum difference between the measured horizontal deviation in upgaze versus downgaze is generally used to call a V-pattern clinically meaningful?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: 15 prism diopters.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EA V-pattern is defined by a significant change in the horizontal deviation between upgaze and downgaze, and it becomes clinically relevant when that change is large enough to influence symptoms, abnormal head posture, or surgical planning.\u003C/strong\u003E The commonly used threshold is \u003Cstrong\u003Ea difference of at least 15 prism diopters\u003C/strong\u003E between measurements taken in upgaze and downgaze.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA useful comparison is the A-pattern cutoff.\u003C/strong\u003E \u003Cstrong\u003EAn A-pattern is typically labeled clinically significant at a smaller change\u2014about 10 prism diopters or more between upgaze and downgaze\u2014whereas the V-pattern requires a larger difference to meet significance criteria.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1699,
    "Name": "Upper eyelid change after a large superior rectus recession",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a 30\u2011prism\u2011diopter right hypertropia. You plan a single\u2011muscle operation consisting of a right superior rectus recession. Which postoperative eyelid change is most likely?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Widening of the palpebral fissure.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EVertical rectus surgery often affects eyelid position because the vertical recti have anatomic/fascial relationships with the eyelid retractors.\u003C/strong\u003E This effect is usually more noticeable with inferior rectus surgery, but it can also occur with the superior rectus because of its association with the levator complex.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA useful rule of thumb is that vertical rectus recession tends to produce lid retraction (a \u201Chigher\u201D lid position) and therefore widens the palpebral fissure, whereas vertical rectus resection tends to produce the opposite effect (relative lid lowering and narrowing).\u003C/strong\u003E In this vignette, the hypertropia is large (30 PD), so the superior rectus recession would also be relatively large; with larger recessions, the eyelid effect becomes more clinically apparent, making \u003Cstrong\u003Eupper lid retraction with fissure widening\u003C/strong\u003E the most expected change.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EUpper lid lowering: This is more consistent with an effect seen after a superior rectus resection (tightening/advancing) rather than recession, or with postoperative swelling mimicking ptosis\u2014not the typical direction of change for a large recession.\u003C/li\u003E\n\u003Cli\u003EPseudoptosis: Pseudoptosis usually reflects a smaller palpebral fissure because the eye is hypotropic (or the fellow eye is hypertropic) and the lid \u201Cappears\u201D lower; it is not the classic lid effect expected specifically from a superior rectus recession.\u003C/li\u003E\n\u003Cli\u003ENo changes in the upper lid: Eyelid changes are common enough with vertical rectus procedures that \u201Cno change\u201D is not the best answer\u2014especially when the recession is large, which increases the likelihood of a noticeable lid position shift.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1700,
    "Name": "Vernal keratoconjunctivitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 12-year-old has severe bilateral ocular itching that tends to recur seasonally and is worse this year. Slit-lamp exam of the upper tarsal conjunctiva shows the lesion showed in the picture. Which additional ocular finding would most likely be seen with the underlying diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-20-3dd98d68-df11-4b9c-b4e2-e92f521f51ce.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: epithelial defect of the superior cornea\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis presentation most strongly points to vernal keratoconjunctivitis (VKC).\u003C/strong\u003E \u003Cstrong\u003EThe key clues are intense itching, seasonal recurrence (often spring/fall), and the tarsal conjunctival appearance consistent with giant papillary conjunctivitis.\u003C/strong\u003E \u003Cstrong\u003EVKC is a chronic, allergic inflammation seen mainly in children and adolescents and is characterized by prominent tarsal papillae and/or limbal disease.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA classic corneal complication of VKC is a \u201Cshield ulcer,\u201D which is essentially an epithelial defect that typically involves the superior cornea.\u003C/strong\u003E \u003Cstrong\u003EIt occurs because large papillae and inflammatory mediators (including eosinophil-derived proteins) mechanically and chemically injure the corneal epithelium.\u003C/strong\u003E \u003Cstrong\u003ESo a superior corneal epithelial defect fits perfectly with VKC.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other findings are wrong (and what they actually suggest):\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMultiple circular subepithelial infiltrates\u003C/strong\u003E are more typical of \u003Cstrong\u003Eadenoviral epidemic keratoconjunctivitis\u003C/strong\u003E, where immune-mediated subepithelial infiltrates appear after the acute conjunctivitis (EKC pattern).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESmall gaps in pannus from healed limbal follicles\u003C/strong\u003E describes \u003Cstrong\u003EHerbert pits\u003C/strong\u003E, which are characteristic of \u003Cstrong\u003Etrachoma\u003C/strong\u003E (healed limbal follicles leaving depressed scars).\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELinear subconjunctival scarring of the everted upper lid\u003C/strong\u003E describes \u003Cstrong\u003EArlt line\u003C/strong\u003E, also a classic scarring sign of \u003Cstrong\u003Etrachoma\u003C/strong\u003E.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1701,
    "Name": "Craniosynostosis syndrome most strongly linked to syndactyly",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following craniosynostosis is most commonly associated with syndactyly?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Apert syndrome.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003ESyndactyly is the key discriminator here.\u003C/strong\u003E \u003Cstrong\u003EApert syndrome is the craniosynostosis syndrome that classically includes marked syndactyly\u2014often severe \u201Cmitten-hand\u201D and \u201Csock-foot\u201D fusion\u2014alongside craniosynostosis and midface hypoplasia.\u003C/strong\u003E Because the question asks for the craniosynostosis condition most commonly linked to syndactyly, \u003Cstrong\u003EApert syndrome is the best match.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are wrong:\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ECrouzon syndrome is a common craniosynostosis syndrome but typically does not have syndactyly.\u003C/strong\u003E The phenotype centers on craniofacial findings (e.g., proptosis/midface hypoplasia) rather than limb fusion.\u003Cbr\u003E\n\u003Cstrong\u003ESaethre\u2013Chotzen syndrome is usually milder and may show subtle limb changes (like brachydactyly or partial soft-tissue syndactyly), but it does not characteristically produce the dramatic, extensive syndactyly seen in Apert syndrome.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EPierre Robin sequence is not a craniosynostosis syndrome and is not defined by syndactyly.\u003C/strong\u003E It is a sequence involving mandibular hypoplasia with airway/tongue position issues and is often discussed with connective tissue disorders (for example, Stickler syndrome), not craniosynostosis with limb fusion.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1702,
    "Name": "Megalocornea: key associated feature",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA question asks which clinical association is most characteristic of megalocornea. Which statement is most likely to be true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: Female carriers may have mildly enlarged corneal diameters.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EMegalocornea is classically an X-linked disorder, so it is seen predominantly in males, while heterozygous carriers (often mothers) can show subtle manifestations such as slightly larger-than-average corneal diameters.\u003C/strong\u003E \u003Cstrong\u003EThis inheritance pattern is the key reason the \u201Ccarrier mother with mild enlargement\u201D association is a high-yield clue.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EClinically, megalocornea is typically a non-progressive enlargement of the cornea with a deep anterior chamber, and it is usually not accompanied by elevated intraocular pressure. That distinction matters because enlarged corneas in infancy can also be caused by primary congenital glaucoma, which \u003Cem style=\u0022\u0022\u003Edoes\u003C/em\u003E feature high IOP, corneal edema, Haab striae, and progressive globe enlargement. So, when you see large corneas without the glaucoma picture, megalocornea becomes a leading consideration.\u003C/p\u003E\n\u003Cp\u003EMegalocornea can coexist with lens and iris abnormalities (such as lens subluxation, iris hypoplasia, radial transillumination defects, or an ectopic pupil). Because the cornea is large and the anterior chamber is often deep, the angle structures may be visible without gonioscopy in some patients.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other statements are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMegalocornea is generally stable rather than progressively enlarging.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EThe deep chamber can allow direct visualization in many cases.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIris hyperplasia is not a classic association\u003C/strong\u003E; \u003Cstrong\u003Eif anything, iris underdevelopment or transillumination-type changes are more typical in the megalocornea spectrum.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1703,
    "Name": "Spiral of Tillaux",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring scleral buckle surgery, you plan to hook the rectus muscles. Based on their normal insertion distances from the limbus, which rectus muscle ranks as the third closest insertion?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: lateral rectus.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis is a \u201CSpiral of Tillaux\u201D anatomy question.\u003C/strong\u003E \u003Cstrong\u003EThe four rectus muscles do not insert at the same distance from the limbus; instead, they form a spiral where insertions become progressively farther posterior.\u003C/strong\u003E A high-yield order is: \u003Cstrong\u003Emedial rectus (closest) \u2192 inferior rectus \u2192 lateral rectus \u2192 superior rectus (farthest).\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ETypical insertion distances (approximate) help lock in the ranking:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMedial rectus ~5.5 mm\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior rectus ~6.5 mm\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ELateral rectus ~6.9\u20137.0 mm\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior rectus ~7.5\u20137.7 mm\u003C/strong\u003E\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003ETherefore, the third closest rectus insertion is the lateral rectus.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EExtra surgical pearl:\u003C/strong\u003E \u003Cstrong\u003EThe vertical recti insert slightly obliquely, with the temporal edge sitting a bit more posterior than the nasal edge\u003C/strong\u003E, which can matter when judging the insertion during exposure.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1704,
    "Name": "Thyroid eye disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with thyroid eye disease has prominent proptosis, eyelid retraction, and binocular diplopia. When surgery is required, which sequence best reflects the standard staging of surgical management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer:\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eorbital decompression, strabismus surgery, lid surgery.\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/strong\u003E\u003C/span\u003E\u003C/div\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe surgical plan in thyroid eye disease is staged because each operation can change measurements needed for the next step.\u003C/strong\u003E The goal is to correct \u003Cstrong\u003Eorbital volume/globe position first\u003C/strong\u003E, then \u003Cstrong\u003Eocular alignment\u003C/strong\u003E, and finally \u003Cstrong\u003Eeyelid position\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EOrbital decompression is performed first\u003C/strong\u003E because \u003Cstrong\u003Eit can significantly alter ocular motility and alignment\u003C/strong\u003E by changing orbital anatomy and extraocular muscle mechanics. If alignment surgery is done before decompression, the deviation may shift afterward, creating a new or different diplopia problem.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EStrabismus surgery is performed after decompression\u003C/strong\u003E once motility has stabilized, allowing the surgeon to correct diplopia based on a more reliable deviation measurement.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EEyelid surgery is performed last\u003C/strong\u003E because \u003Cstrong\u003Elid position can change after strabismus surgery\u003C/strong\u003E, and it is also influenced by globe position and vertical alignment. Doing lid surgery earlier risks over- or under-correcting lid retraction once the alignment is later adjusted.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1705,
    "Name": " unilateral congenital cataract",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003EA newborn has a dense, centrally located nuclear cataract in one eye, with the rest of the eye exam normal. What is the accepted timing window for cataract extraction to reduce the risk of deprivation amblyopia?\u003C/p\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ebefore 6 weeks of age\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-weight: normal; font-size: small;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EA \u201Crelatively-dense\u201D and \u201Ccentral\u201D congenital cataract is very likely to be amblyogenic because it blocks the visual axis during the most sensitive period of visual development.\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EUnilateral visual deprivation is especially damaging because the brain strongly favors the clear fellow eye, accelerating deprivation amblyopia in the affected eye.\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E For that reason, \u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Ea visually significant unilateral congenital cataract is treated urgently, with surgery typically targeted within the first several weeks of life\u2014classically by about 4\u20136 weeks, and certainly before 6 weeks.\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: normal; font-size: small;\u0022\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/span\u003E\u003C/div\u003E\n\u003Cp\u003E\u003Cstrong style=\u0022text-decoration-line: underline;\u0022\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003Ecataract surgery is not indicated at this time\u003C/span\u003E\u003Cbr\u003E\nThis is incorrect because a dense central cataract in a newborn obstructs the visual axis and is not something you \u201Cwatch\u201D if it is visually significant. Delaying intervention risks irreversible deprivation amblyopia.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003Ebefore 4 weeks of age\u003C/span\u003E\u003Cbr\u003E\nThis can be \u201Ctoo aggressive\u201D as a universal rule. While some cases are operated very early, the commonly taught accepted window for unilateral visually significant congenital cataract is around 4\u20136 weeks to balance amblyopia prevention against perioperative considerations.\u0026nbsp;\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003Ebefore 10 weeks of age\u003C/span\u003E\u003Cbr\u003E\nThis timing is more consistent with bilateral congenital cataracts rather than unilateral disease. Bilateral cataracts can sometimes be removed slightly later (often before ~10 weeks) because both eyes are similarly deprived and there is less interocular competition, whereas unilateral cataracts must be addressed earlier.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1706,
    "Name": "Infantile (congenital) esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-month-old has had constant inward deviation noted since 3 months of age. Examination shows a comitant esotropia measuring 50 prism diopters. Cycloplegic refraction reveals \u002B1.00 sphere in each eye, and fixation alternates without evidence of amblyopia. What is the next best management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Surgery to correct the large angle esotropia\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis presentation is most consistent with infantile esotropia: an early-onset, large-angle, comitant esodeviation that begins within the first months of life and is not driven by significant hyperopia.\u003C/strong\u003E \u003Cstrong\u003EThe refractive error here is mild (\u002B1.00 OU), which makes a refractive accommodative mechanism very unlikely, so glasses alone will not meaningfully reduce a 50 prism-diopter deviation.\u003C/strong\u003E \u003Cstrong\u003EBecause large-angle infantile esotropia rarely resolves on its own once established, the definitive management is surgical alignment of the eyes.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe main reason to intervene early is sensory development.\u003C/strong\u003E \u003Cstrong\u003EBinocular pathways are most plastic in infancy, and aligning the eyes closer to orthotropia during this early period gives the best chance for developing some level of binocular function and stereopsis.\u003C/strong\u003E \u003Cstrong\u003EMany pediatric strabismus practices aim for early alignment in infancy (often within the first year, and sometimes as early as several months) when the deviation is large and stable, especially in otherwise healthy infants.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EObservation until 2 years of age\u003C/span\u003E; since this condition may spontaneously improve by age 2.\u003Cbr\u003E\nA large, constant esotropia beginning in early infancy is unlikely to spontaneously \u201Cgrow out of it.\u201D Waiting risks missing the window for binocular development and increases the chance of persistent suppression and poor stereopsis, even if amblyopia is not yet evident.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAlternate patching of both eyes\u003C/span\u003E\u003Cbr\u003E\nAlternating occlusion can be used to treat or prevent fixation preference and amblyopia, but it does not correct a large, stable infantile esotropia. This child already alternates fixation (no clear amblyopia), so patching does not address the primary problem: the large constant misalignment requiring mechanical correction.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA prescription for the \u002B1.00 with a prism ground into the glasses to correct for the deviation\u003C/span\u003E\u003Cbr\u003E\nPrism is not a practical primary solution for a 50 prism-diopter deviation. The amount of prism required would be optically and physically impractical (thick, heavy, distortion) and would not reliably restore stable binocular alignment in a large-angle infantile deviation. Mild hyperopia correction also will not collapse a deviation of this magnitude when accommodation is not the driver.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1707,
    "Name": "Estimated visual acuity at birth",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA question asks for the approximate Snellen-equivalent visual acuity expected in a healthy newborn immediately after birth. Which value best matches typical newborn vision?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: 20/400\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENewborn visual acuity is poor compared with older infants and adults because the central retina is structurally and functionally immature at birth.\u003C/strong\u003E \u003Cstrong\u003EThe fovea has not yet achieved adult-like cone packing and foveal specialization, and visual pathways (including myelination and cortical processing) are still developing.\u003C/strong\u003E \u003Cstrong\u003EAs a result, a typical estimate for term newborn acuity is around 20/400.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EFoveal maturation continues through infancy, with major improvements over the first year as cone density and foveal architecture become more adult-like.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1708,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003ENeonatal conjunctivitis occurs during the first month of life. At what postnatal age does herpes simplex virus conjunctivitis most commonly present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: 14 days\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EHSV-related ophthalmia neonatorum most commonly appears around 2 weeks of life, so the best answer is 14 days.\u003C/strong\u003E \u003Cstrong\u003EThe timing is clinically useful because different etiologies cluster at different postnatal ages, reflecting incubation periods and exposure patterns.\u003C/strong\u003E HSV infection in newborns is \u003Cstrong\u003Euncommon but important\u003C/strong\u003E because it can be associated with keratitis and systemic neonatal HSV disease.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003Ewithin the first day\u003C/strong\u003E is most consistent with \u003Cstrong\u003Echemical conjunctivitis\u003C/strong\u003E (an irritative reaction to prophylaxis) and usually improves quickly.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E3-4 days\u003C/strong\u003E is the classic timeframe for \u003Cstrong\u003ENeisseria gonorrhoeae\u003C/strong\u003E conjunctivitis, often with very copious purulent discharge.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E7 days\u003C/strong\u003E aligns best with \u003Cstrong\u003EChlamydia trachomatis\u003C/strong\u003E conjunctivitis (often around 5\u201314 days, commonly near one week).\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1709,
    "Name": "Shortest overall extraocular muscle (muscle belly \u002B tendon)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIncluding both the active muscle belly and the tendon, which extraocular muscle is the shortest overall?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cp\u003E\u003Cstrong\u003EAnswer: inferior oblique.\u003C/strong\u003E\u003C/p\u003E\u003Cp\u003E\n\u003Cstrong\u003EThis question is asking about total length, meaning the active (contractile) muscle belly plus the tendon, not just the muscle belly alone.\u003C/strong\u003E Several extraocular muscles have similar belly lengths, so \u003Cstrong\u003Etendon length becomes the deciding factor\u003C/strong\u003E when comparing \u201Coverall\u201D size.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EKey anatomy numbers:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ERectus muscles (medial rectus, lateral rectus, superior rectus, inferior rectus)\u003C/strong\u003E have \u003Cstrong\u003Eactive muscular portions of about 40 mm\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESuperior oblique\u003C/strong\u003E has a \u003Cstrong\u003Eshorter muscle belly (~32 mm)\u003C/strong\u003E but a \u003Cstrong\u003Every long tendon (~26 mm)\u003C/strong\u003E, making it \u003Cstrong\u003Ethe longest overall\u003C/strong\u003E when belly \u002B tendon are combined.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior oblique\u003C/strong\u003E has an \u003Cstrong\u003Eactive muscle belly of ~37 mm\u003C/strong\u003E, and crucially it has an \u003Cstrong\u003Eextremely short tendon (~1 mm)\u003C/strong\u003E. \u003Cstrong\u003EThat tiny tendon adds almost nothing to its total length\u003C/strong\u003E, which is why the \u003Cstrong\u003Einferior oblique ends up being the shortest overall extraocular muscle\u003C/strong\u003E.\u003C/li\u003E\u003C/ul\u003E\u003Cul\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EMemory anchor:\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ELongest overall = superior oblique (long tendon).\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EShortest overall = inferior oblique (almost no tendon).\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1710,
    "Name": "Brushfield spots",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child is noted to have multiple pale, speckled iris lesions consistent with Brushfield spots. Which statement correctly describes the most likely clinical association of this iris finding?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-21-a913de63-9a72-4dfd-86a8-d7a57420c828.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EIt is associated with trisomy 21\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe described iris finding is most consistent with Brushfield spots, which are small, pale stromal iris speckles that are especially noticeable in lighter irides.\u003C/strong\u003E \u003Cstrong\u003EThese spots represent focal areas of iris stromal hyperplasia surrounded by relatively thinner stroma, creating a \u201Cspeckled\u201D appearance.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBrushfield spots are strongly associated with Down syndrome (trisomy 21), occurring in a large proportion of affected individuals.\u003C/strong\u003E \u003Cstrong\u003EImportantly, Brushfield spots themselves do not typically affect vision and are usually an incidental finding.\u003C/strong\u003E A similar-appearing benign variant, \u003Cstrong\u003EW\u00F6lfflin nodules\u003C/strong\u003E, can also be seen in individuals without systemic disease.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other statements are incorrect (and what they refer to):\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EIt can result in secondary glaucoma and corectopia\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThis describes the iris nodules and iris changes seen in ICE syndrome (especially Cogan\u2013Reese), which can lead to corectopia and secondary angle-closure glaucoma.\u003C/strong\u003E\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIt is associated with optic gliomas and hyperpigmented macules of the skin\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThis points to neurofibromatosis type 1\u003C/strong\u003E, where \u003Cstrong\u003ELisch nodules\u003C/strong\u003E (iris hamartomas) are associated with caf\u00E9-au-lait macules and optic pathway gliomas\u2014different from Brushfield spots.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIt can be associated with oculodermal melanocytosis\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EThis is more consistent with iris mammillations\u003C/strong\u003E, which can be seen with oculodermal melanocytosis, not Brushfield spots.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1711,
    "Name": "Acute Brown syndrome presentation",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 34-year-old develops recent diplopia that is worse in right gaze. Examination shows limited elevation of the left eye when the patient looks to the right, and forced ductions confirm a mechanical restriction in that position. Elevation is less restricted when the patient looks to the left. The patient recently had an upper respiratory-type illness. What should be done next?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003ECT of the orbits and paranasal sinuses\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThis motility pattern is classic for Brown syndrome: a mechanical limitation of elevation in adduction.\u003C/strong\u003E The key supportive clues are \u003Cstrong\u003E(1) elevation restriction that is position-dependent (worst when the affected eye is adducted), and (2) a positive forced duction test\u003C/strong\u003E, which indicates a restrictive (mechanical) process rather than a neurogenic palsy.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe history of upper respiratory tract infection raises concern for inflammatory or infectious involvement near the trochlea/superior oblique tendon-trochlear complex (for example, sinus-related inflammation).\u003C/strong\u003E In an acute presentation like this, the appropriate next step is \u003Cstrong\u003Eorbital and paranasal sinus imaging\u003C/strong\u003E to identify or exclude an adjacent inflammatory process, structural abnormality, or other secondary cause that would change treatment.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe other options are not the best next step because treatment should be directed only after identifying the underlying cause.\u003C/strong\u003E A \u003Cstrong\u003Esuperior oblique spacer\u003C/strong\u003E is a surgical option for selected cases, but it is not the initial step in a new-onset, potentially secondary Brown syndrome. \u003Cstrong\u003ELocal steroid injection\u003C/strong\u003E can be considered in some inflammatory trochleitis/tendon-related cases, but imaging is a key next step first when sinus involvement is suspected. \u003Cstrong\u003EBotulinum toxin injection into the superior rectus\u003C/strong\u003E does not address the primary restrictive mechanism at the superior oblique tendon-trochlea interface.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical pearl:\u003C/strong\u003E \u003Cstrong\u003EBrown syndrome is often associated with a V-pattern\u003C/strong\u003E, whereas \u003Cstrong\u003Einferior oblique palsy tends to produce an A-pattern\u003C/strong\u003E, which can help with pattern recognition in complex motility cases.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1712,
    "Name": "Yoke muscles for up-and-right gaze",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen assessing cardinal gazes, you ask a patient to look up and to the right. Which pair of yoke muscles (one from each eye) produces this movement?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: right superior rectus and left inferior oblique\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EYoke muscles are the paired muscles\u2014one in each eye\u2014that contract together to move both eyes into the same direction of gaze (Hering\u2019s law of equal innervation).\u003C/strong\u003E For \u003Cstrong\u003Eup-and-right gaze\u003C/strong\u003E, the \u003Cstrong\u003Eright eye is abducted\u003C/strong\u003E, so its primary elevator in abduction is the \u003Cstrong\u003Eright superior rectus\u003C/strong\u003E. At the same time, the \u003Cstrong\u003Eleft eye is adducted\u003C/strong\u003E, and its primary elevator in adduction is the \u003Cstrong\u003Eleft inferior oblique\u003C/strong\u003E. \u003Cstrong\u003EThat is why the correct yoke pair is right superior rectus with left inferior oblique.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-03-21-f0b187fb-1f99-42ff-993e-983785d13f63.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1713,
    "Name": "Periodic alternating nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old has had abnormal eye and head movements since infancy. Examination shows a horizontal jerk nystagmus beating to one side that stays horizontal even when looking up or down. After a brief absence, the nystagmus is now beating in the opposite direction. Based on the most likely diagnosis, about how much time passed?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: 60-120 seconds\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003EThis pattern is most consistent with periodic alternating nystagmus (PAN), in which the direction of horizontal jerk nystagmus reverses in a regular cycle. In PAN, the nystagmus typically beats in one direction for about 60\u201390 seconds, then there is often a brief \u201Cquiet\u201D interval (commonly ~10\u201320 seconds) with minimal or no nystagmus, followed by nystagmus beating in the opposite direction for a similar duration. So a full \u201Cdirection-to-direction\u201D change generally occurs over roughly 1\u20132 minutes, making 60-120 seconds the best estimate for the time you were away.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EClinical pearl:\u003C/strong\u003E \u003Cstrong\u003EChildren with PAN may show alternating head turns to follow the shifting null zone as the fast phase changes direction, which can make the head posture seem inconsistent over short periods.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1714,
    "Name": "Primary action of inferior oblique and secondary action of superior rectus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich option correctly pairs the primary action of the inferior oblique with the secondary action of the superior rectus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: extorsion and intorsion\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe key is remembering what \u201Cprimary\u201D and \u201Csecondary\u201D actions mean and using a few high-yield rules.\u003C/strong\u003E \u003Cstrong\u003EPrimary action\u003C/strong\u003E refers to the main effect of a muscle when the eye is in primary position. \u003Cstrong\u003ESecondary\u003C/strong\u003E (and tertiary) actions are the additional rotational effects that occur because the muscle\u2019s pull is not perfectly aligned with a single axis of rotation.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EInferior oblique (IO): primary action = torsion, specifically extorsion.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003EOblique muscles primarily produce torsion.\u003C/strong\u003E The inferior oblique\u2019s torsional effect is \u003Cstrong\u003Eextorsion\u003C/strong\u003E (top of the eye rotates away from the nose). Its other actions are \u003Cstrong\u003Eelevation\u003C/strong\u003E (secondary; opposite of \u201Cinferior\u201D) and \u003Cstrong\u003Eabduction\u003C/strong\u003E (tertiary).\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ESuperior rectus (SR): primary action = elevation; secondary action = intorsion.\u003C/strong\u003E\u003Cbr\u003E\nThe superior rectus is a \u003Cstrong\u003Erectus muscle\u003C/strong\u003E, so in addition to its main vertical action (elevation), it also contributes to torsion and horizontal movement due to its angled insertion. A useful mnemonic is \u003Cstrong\u003E\u201CSIN\u2013RAD\u201D\u003C/strong\u003E:\u003Cbr\u003E\n\u003Cstrong\u003ESuperior muscles INtort\u003C/strong\u003E, and \u003Cstrong\u003ERecti ADduct\u003C/strong\u003E.\u003Cbr\u003E\nSo for the superior rectus, \u003Cstrong\u003Ethe secondary torsional action is intorsion\u003C/strong\u003E, and the horizontal (tertiary) action is \u003Cstrong\u003Eadduction\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1715,
    "Name": "Congenital glaucoma suspicion in an infant",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-month-old has persistent tearing and frequent squeezing/shutting of both eyes since early infancy. The ocular appearance is consistent with corneal edema, raising concern for a pressure-related disorder. Which ancillary test is most useful for tracking treatment response over time?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px;\u0022\u003EA-scan ultrasound\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe symptom cluster of tearing with frequent squeezing/shutting of the eyes in an infant is highly suggestive of primary congenital glaucoma, especially when the cornea appears edematous.\u003C/strong\u003E \u003Cstrong\u003EIn congenital glaucoma, elevated intraocular pressure can enlarge the eye (buphthalmos) and stretch the cornea, leading to edema and an abnormal light reflex.\u003C/strong\u003E Because the key threat is \u003Cstrong\u003Eongoing globe enlargement and optic nerve damage\u003C/strong\u003E, monitoring should focus on objective measures of disease control and progression.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EA-scan ultrasound is the best choice here because it allows reliable measurement of axial length over time, which is a practical way to monitor whether the eye is continuing to enlarge.\u003C/strong\u003E \u003Cstrong\u003EIf axial length is increasing faster than expected for age, that strongly suggests inadequate intraocular pressure control\u003C/strong\u003E, even if single IOP readings are variable (especially when measured under anesthesia). This makes A-scan ultrasound a high-yield tool for following response after treatment (most often surgical in primary congenital glaucoma).\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EMagnetic resonance imaging\u003Cbr\u003E\n\u003Cstrong\u003EMRI does not monitor glaucoma control and is not the routine way to track progression in suspected primary congenital glaucoma.\u003C/strong\u003E\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003ECorneal pachymetry\u003Cbr\u003E\n\u003Cstrong\u003ECorneal thickness can be altered by edema and may affect interpretation of measured IOP, but pachymetry does not directly track progression or response as well as axial length monitoring does in infantile glaucoma.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003EVisual evoked potentials\u003Cbr\u003E\n\u003Cstrong\u003EVEP may estimate visual pathway function, but it is not the preferred method to monitor congenital glaucoma treatment response\u003C/strong\u003E, because it does not directly reflect pressure control or globe enlargement.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1716,
    "Name": "Posterior lenticonus in children",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following statements is TRUE regarding cataracts associated with posterior lenticonus in children?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: These cataracts are not present at birth\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPosterior lenticonus is a localized, cone-like protrusion of the central posterior lens capsule due to thinning/weakness of that capsule.\u003C/strong\u003E \u003Cstrong\u003EOn retroillumination it can create an \u201Coil droplet\u201D appearance.\u003C/strong\u003E Over time, \u003Cstrong\u003Ethe abnormal posterior bulge tends to induce progressive lens changes\u003C/strong\u003E, and \u003Cstrong\u003Eopacification may develop as the capsule continues to stretch and the overlying cortex becomes affected\u003C/strong\u003E. This clinical behavior is why posterior lenticonus\u2013associated cataract is commonly described as \u003Cstrong\u003Eacquired/diagnosed after birth rather than clearly present at birth\u003C/strong\u003E, making \u201CThese cataracts are not present at birth\u201D the correct statement.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other statements are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EPosterior lenticonus cataracts are classically more often unilateral in children.\u003C/strong\u003E \u003Cstrong\u003EBilateral involvement can occur, but it is not the typical presentation\u003C/strong\u003E.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EAlport syndrome is classically associated with anterior lenticonus (and dot-and-fleck retinopathy), not posterior lenticonus.\u003C/strong\u003E \u003Cstrong\u003EPosterior lenticonus in Alport is rare and mainly reported as isolated case reports\u003C/strong\u003E.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EPosterior lenticonus is not characteristically linked to microphthalmos or a consistent inter-eye size discrepancy.\u003C/strong\u003E When microphthalmos is present, it usually points to other developmental lens/anterior segment disorders rather than posterior lenticonus as the typical association.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1717,
    "Name": "Congenital motor nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 3-year-old has congenital motor nystagmus with a left jerk pattern. Which abnormal head posture would most likely be adopted to reduce the nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Eleft head turn\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA \u201Cleft jerk nystagmus\u201D is defined by a fast phase that beats to the left.\u003C/strong\u003E \u003Cstrong\u003EBy Alexander\u2019s law, jerk nystagmus typically becomes stronger when the eyes look toward the direction of the fast phase, and it becomes quieter when the eyes look away from that direction.\u003C/strong\u003E\u003Cbr\u003E\n\u003Cstrong\u003ESo, a left-beating (left jerk) nystagmus tends to worsen in left gaze and dampen in right gaze.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EChildren with congenital motor nystagmus often adopt a compensatory head posture to place their eyes in the gaze position where the nystagmus is minimal (the null zone).\u003C/strong\u003E \u003Cstrong\u003EIf the null zone is in right gaze, the child can keep the eyes in right gaze while still looking straight ahead by turning the face to the left.\u003C/strong\u003E That is why the expected posture is \u003Cstrong\u003Ea left head turn\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1718,
    "Name": "Congenital motor nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA young child has had a horizontal nystagmus since early infancy and has relatively good visual function on age-appropriate testing. You are trying to distinguish congenital motor nystagmus from other congenital nystagmus entities. Which ancillary finding is considered specific for congenital motor nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: paradoxical inversion of the OKN response\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA horizontal nystagmus beginning in early infancy with relatively preserved vision most commonly fits congenital motor nystagmus (CMN).\u003C/strong\u003E CMN is a diagnosis of an ocular motor \u201Ccontrol\u201D problem rather than a primary retinal/optic nerve sensory deficit, so many children maintain better-than-expected visual behavior compared with sensory nystagmus causes.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAlthough CMN is often described as uniplanar (remaining horizontal even in upgaze and downgaze), that feature is supportive but not mandatory.\u003C/strong\u003E The absence of strict uniplanar behavior does not rule CMN out, because congenital nystagmus phenotypes can vary and some overlap exists with other early-onset nystagmus categories.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ECMN also does not have to be a classic jerk waveform.\u003C/strong\u003E CMN can present with jerk, pendular, or more complex oscillation patterns (including circular or elliptical-appearing movements). So waveform shape alone is not the best \u201Csingle discriminator.\u201D\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe key high-yield feature that occurs only in CMN is paradoxical inversion of the optokinetic nystagmus (OKN) response.\u003C/strong\u003E In typical jerk nystagmus, an OKN stimulus that drives pursuit in one direction tends to \u003Cstrong\u003Eincrease\u003C/strong\u003E the nystagmus in that same direction. In CMN, the opposite can happen: an OKN drum moving in a direction that would normally reinforce the existing jerk can instead \u003Cstrong\u003Edampen\u003C/strong\u003E the jerk nystagmus or even \u003Cstrong\u003Eflip\u003C/strong\u003E the beating direction. That counterintuitive (\u201Cparadoxical\u201D) behavior is the classic specific clue.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003Emarkedly reduced ERG responses in both eyes\u003C/strong\u003E points toward a retinal dystrophy/sensory cause of nystagmus (for example, inherited retinal disease), not CMN.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Enystagmus that becomes vertical in upgaze and downgaze\u003C/strong\u003E is not a defining or specific feature for CMN and would push you to consider other ocular motor or central causes depending on the full pattern.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Ea relative afferent pupillary defect in one eye\u003C/strong\u003E suggests asymmetric optic nerve or severe retinal disease and is not expected in isolated CMN.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1719,
    "Name": "Congenital iris ectropion with pediatric glaucoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-year-old has a unilateral iris abnormality on slit-lamp exam, and the affected eye has markedly elevated intraocular pressure compared with the fellow eye. Based on the most likely ocular diagnosis suggested by the iris appearance and unilateral glaucoma, which additional finding could be present?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-03-22-ec86b4db-f37b-4114-878d-1cb25789b0c1.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px;\u0022\u003Ecaf\u00E9 au lait spot\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe iris photo is most consistent with ectropion uveae (also called iris ectropion), where the posterior iris pigment epithelium extends onto the anterior surface at the pupillary margin.\u003C/strong\u003E \u003Cstrong\u003EWhen this is congenital and unilateral and is accompanied by high iris insertion/cryptless iris and glaucoma (as suggested by the markedly elevated unilateral IOP), the picture fits congenital ectropion uveae syndrome.\u003C/strong\u003E \u003Cstrong\u003EThis syndrome is classically associated with neurofibromatosis type 1 (NF1), and caf\u00E9 au lait macules are a common cutaneous feature of NF1\u2014so caf\u00E9 au lait spot is the best associated abnormality.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003Eadenoma sebaceum\u003C/strong\u003E \u003Cstrong\u003Eis a misnomer for facial angiofibromas, which are associated with tuberous sclerosis, not congenital ectropion uveae syndrome.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENevus of Ota\u003C/strong\u003E \u003Cstrong\u003Eis associated with oculodermal melanocytosis and can be linked to ipsilateral ocular hyperpigmentation and glaucoma, but it does not match the characteristic ectropion uveae syndrome association being tested here.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Edilated cardiomyopathy\u003C/strong\u003E \u003Cstrong\u003Eis a systemic association classically discussed with Alstr\u00F6m syndrome (which features a cone-rod dystrophy), not with congenital ectropion uveae syndrome.\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1720,
    "Name": "Pediatric intermediate uveitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 7-year-old has difficult-to-control intermediate uveitis, and you are considering systemic immunosuppression. Which of the listed agents is usually avoided in children unless disease is extremely severe?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px;\u0022\u003Ecyclophosphamide\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECyclophosphamide is an alkylating agent, and alkylating immunosuppressives are generally discouraged in children because of high long-term toxicity.\u003C/strong\u003E \u003Cstrong\u003EThe major concerns include profound bone marrow suppression, serious infection risk, future infertility (gonadotoxicity), and an increased risk of secondary malignancy.\u003C/strong\u003E \u003Cstrong\u003EA classic board-relevant adverse effect specific to cyclophosphamide is hemorrhagic cystitis\u003C/strong\u003E, which reflects toxic metabolites affecting the bladder.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBecause of these risks, cyclophosphamide is typically reserved for only the most severe, vision-threatening, refractory uveitis scenarios when safer steroid-sparing agents have failed or are contraindicated.\u003C/strong\u003E In most pediatric uveitis management pathways, clinicians prefer agents with a more favorable long-term risk profile.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other options are not the best answer:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003Emethotrexate\u003C/strong\u003E is commonly used as a first-line steroid-sparing immunomodulatory therapy in children with uveitis (including JIA-associated disease). \u003Cstrong\u003ECommon issues include gastrointestinal upset\u003C/strong\u003E, and more serious toxicities include \u003Cstrong\u003Ehepatotoxicity, mucositis, and rarely pneumonitis\u003C/strong\u003E, but it remains a standard pediatric option with appropriate monitoring.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Ecyclosporine\u003C/strong\u003E is also used in selected pediatric uveitis cases; its major limitation is \u003Cstrong\u003Enephrotoxicity\u003C/strong\u003E, and other notable adverse effects include \u003Cstrong\u003Egingival hyperplasia and gastrointestinal symptoms\u003C/strong\u003E, but it is not broadly \u201Cdiscouraged\u201D in children in the same way alkylators are.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Einfliximab\u003C/strong\u003E (a TNF-\u03B1 inhibitor) is frequently used for refractory noninfectious uveitis in children, especially when there is associated systemic inflammatory disease. \u003Cstrong\u003EThe risks center on infection/reactivation and infusion reactions\u003C/strong\u003E, but it is a commonly accepted steroid-sparing option under specialist supervision.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1721,
    "Name": "Neurofibromatosis type 2",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA teenager with bilateral sensorineural hearing loss and a suspected intracranial meningioma is being evaluated for ocular signs of an underlying phakomatosis. Which set of eye findings is most likely to be present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: posterior subcapsular cataracts, wedge cortical cataracts, and retinal hamartomas\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe history strongly points to neurofibromatosis type 2 (NF2).\u003C/strong\u003E \u003Cstrong\u003EBilateral sensorineural hearing loss is classically due to bilateral vestibular schwannomas, and intracranial meningiomas are also a common tumor type in NF2.\u003C/strong\u003E When a question pairs hearing loss with meningioma in an adolescent, NF2 is the unifying diagnosis.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIn NF2, the most common ocular abnormality is cataract, particularly posterior subcapsular cataracts.\u003C/strong\u003E \u003Cstrong\u003EWedge-shaped cortical cataracts are also commonly described in NF2\u003C/strong\u003E, and \u003Cstrong\u003Eretinal hamartomas (including combined retinal\u2013RPE hamartomas) can occur as additional ocular findings.\u003C/strong\u003E Therefore, the combination that best matches NF2 is the one that includes \u003Cstrong\u003Eposterior subcapsular cataracts\u003C/strong\u003E, \u003Cstrong\u003Ewedge cortical cataracts\u003C/strong\u003E, and \u003Cstrong\u003Eretinal hamartomas\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003Eposterior subcapsular cataracts, optic nerve melanocytoma, and iris hamartomas\u003Cbr\u003E\n\u003Cstrong\u003EIris hamartomas (Lisch nodules) are much more characteristic of neurofibromatosis type 1 (NF1), not NF2.\u003C/strong\u003E \u003Cstrong\u003EOptic nerve melanocytoma is not a classic hallmark of NF2\u003C/strong\u003E and does not fit the \u201Chearing loss \u002B meningioma\u201D syndrome pattern being tested.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003Eposterior subcapsular cataracts, neuroblastomas, and combined hamartomas of the retina and RPE\u003Cbr\u003E\n\u003Cstrong\u003ENeuroblastoma is not part of the NF2 tumor spectrum.\u003C/strong\u003E It is classically linked to opsoclonus\u2013myoclonus syndrome rather than NF2. Even though \u003Cstrong\u003Ecombined hamartomas can be seen in NF2\u003C/strong\u003E, the inclusion of \u003Cstrong\u003Eneuroblastomas\u003C/strong\u003E makes this combination inconsistent with the vignette.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003Eposterior subcapsular cataracts, retinal hamartomas, and optic nerve melanocytoma\u003Cbr\u003E\n\u003Cstrong\u003EPosterior subcapsular cataracts and retinal hamartomas can fit NF2\u003C/strong\u003E, but \u003Cstrong\u003Eoptic nerve melanocytoma is not a typical NF2 association\u003C/strong\u003E, so this set is less appropriate than the option that includes the better-known NF2 lens finding of \u003Cstrong\u003Ewedge cortical cataracts\u003C/strong\u003E.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1722,
    "Name": "Quantifying cyclodeviation in an acquired 4th nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has an acquired trochlear nerve palsy and you want to measure the amount of torsional misalignment. Which test is used to quantify cyclodeviation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer:\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003Edouble Maddox rod test\u003C/span\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECyclodeviation is a torsional misalignment (incyclotorsion or excyclotorsion), and the classic bedside method to \u003Cem\u003Emeasure\u003C/em\u003E its magnitude is the double Maddox rod test.\u003C/strong\u003E \u003Cstrong\u003EThe test converts each eye\u2019s perceived image into a line, allowing torsion to be quantified by the amount of rotation needed to make the two lines appear parallel.\u003C/strong\u003E In practice, a Maddox rod is placed in front of each eye (usually in a trial frame), the patient views a single light, and the rods are rotated until the patient reports the two lines are aligned/parallel; \u003Cstrong\u003Ethe degree of rotation required corresponds to the amount of subjective torsion.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EMaddox rod test\u003C/strong\u003E (single Maddox rod) is mainly used to \u003Cstrong\u003Emeasure horizontal or vertical deviations\u003C/strong\u003E, not torsion. It creates a line for one eye and a light for the other, helping quantify the separation in prism diopters rather than cyclotorsion.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Ered glass test\u003C/strong\u003E helps \u003Cstrong\u003Edetect diplopia patterns\u003C/strong\u003E and can support sensory evaluation (including suppression/ARC in some contexts), but it is \u003Cstrong\u003Enot the standard test to quantify torsion in degrees\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EParks-Bielchowsky 3-step test\u003C/strong\u003E is a diagnostic framework to \u003Cstrong\u003Eidentify the paretic muscle in vertical strabismus (classically 4th nerve palsy)\u003C/strong\u003E, but it does \u003Cstrong\u003Enot quantify cyclodeviation\u003C/strong\u003E.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1723,
    "Name": "Chronic tearing in a 6\u2011month\u2011old with normal corneas",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6\u2011month\u2011old has had persistent tearing in both eyes since early infancy. Exam shows copious clear tearing, clear corneas, normal corneal diameter for age (10.0 mm in both eyes), no photophobia, and otherwise normal ocular findings. What is the best next management?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: Crigler massage\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe presentation is most consistent with congenital nasolacrimal duct obstruction (NLDO).\u003C/strong\u003E \u003Cstrong\u003EChronic, clear tearing beginning in early infancy with a normal ocular exam strongly favors NLDO.\u003C/strong\u003E \u003Cstrong\u003EA key first-step clinical consideration is ruling out primary congenital glaucoma, because glaucoma can also present with tearing in infants; however, congenital glaucoma typically comes with additional red flags such as photophobia, blepharospasm, corneal edema/clouding, and enlarged corneal diameter (buphthalmos).\u003C/strong\u003E \u003Cstrong\u003EHere, the corneas are clear, the corneal diameter is not enlarged, and there is no photophobia, which makes congenital glaucoma unlikely in this vignette.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EFor uncomplicated NLDO at 6 months, the preferred initial treatment is conservative therapy with digital lacrimal sac massage (Crigler massage).\u003C/strong\u003E \u003Cstrong\u003EThis technique increases hydrostatic pressure within the lacrimal sac and can help open the membranous obstruction at the distal nasolacrimal duct (classically at the valve of Hasner).\u003C/strong\u003E \u003Cstrong\u003EMany cases resolve spontaneously during the first year of life, and massage is the standard first-line step while waiting for that natural resolution.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other choices are wrong:\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003Eexamination under anesthesia\u003Cbr\u003E\n\u003Cstrong\u003EThis is not the best next step in a stable infant whose exam is otherwise normal and whose findings fit NLDO without glaucoma signs.\u003C/strong\u003E \u003Cstrong\u003EAnesthesia-based evaluation is generally reserved for cases where the diagnosis is uncertain, the examination cannot be adequately performed in clinic, or there is strong concern for glaucoma/other serious pathology requiring detailed assessment.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003Egoniotomy\u003Cbr\u003E\n\u003Cstrong\u003EGoniotomy is a surgical procedure used to treat primary congenital glaucoma.\u003C/strong\u003E \u003Cstrong\u003EBecause this child lacks the typical glaucoma features (photophobia, corneal haze/edema, enlarged cornea), goniotomy is not indicated.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003Etopical antibiotics for 1-2 weeks\u003Cbr\u003E\n\u003Cstrong\u003ETopical antibiotics can be helpful if there is secondary bacterial conjunctivitis or mucopurulent discharge, but they do not correct the underlying drainage obstruction.\u003C/strong\u003E \u003Cstrong\u003EIn this case, the tearing is described as clear and the remainder of the exam is normal, so antibiotics are not the primary management.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1724,
    "Name": "Delayed visual maturation in a healthy 3\u2011month\u2011old",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA healthy full-term 3\u2011month\u2011old does not fixate or track, and this is confirmed on exam. The rest of the eye exam is normal. What is the best next step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer: observe closely\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA normal ocular examination in a young infant who is not yet reliably fixing and following most strongly suggests delayed visual maturation (DVM).\u003C/strong\u003E \u003Cstrong\u003EDVM is a developmental delay in visual attention and visual behaviors rather than a primary structural eye disease.\u003C/strong\u003E \u003Cstrong\u003EImportantly, DVM can be seen in children with neurologic/developmental issues, but it can also occur in otherwise healthy infants and often improves with time.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EAt 3 months of age, careful observation is an appropriate next step because visual behaviors are still maturing and many infants show rapid improvement over the next several weeks.\u003C/strong\u003E \u003Cstrong\u003EJumping immediately to advanced testing (VEP/ERG) is usually reserved for cases with concerning exam findings, systemic red flags, or failure to show improvement as the infant approaches the age when fixation and tracking should be more consistent.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EWhy the other answer choices are not the best next step right now\u003C/strong\u003E\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003Eperform a visual evoked potential (VEP)\u003Cbr\u003E\n\u003Cstrong\u003EVEP can be useful to assess the integrity of the visual pathway when the diagnosis is uncertain, but it is not the first move in a healthy 3\u2011month\u2011old with a completely normal eye exam.\u003C/strong\u003E \u003Cstrong\u003EIt becomes more appropriate if visual behavior does not improve as the infant gets closer to ~6 months or if additional concerns arise.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003Eorder a MRI of the brain\u003Cbr\u003E\n\u003Cstrong\u003ENeuroimaging is not the routine next step when the eye exam is normal and the infant is otherwise healthy.\u003C/strong\u003E \u003Cstrong\u003EMRI is typically considered when there are neurologic signs, abnormal head growth, seizures, abnormal tone, developmental regression, or other features that raise suspicion for central pathology.\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003Eperform an electroretinogram (ERG)\u003Cbr\u003E\n\u003Cstrong\u003EERG helps evaluate retinal function and can be important when a retinal dystrophy is suspected, but a normal ocular exam without other suggestive clues makes immediate ERG less appropriate than observation.\u003C/strong\u003E \u003Cstrong\u003ELike VEP, it becomes reasonable if vision does not begin to emerge as expected or if the clinical picture changes.\u003C/strong\u003E\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003EPractical follow-up point:\u003C/strong\u003E \u003Cstrong\u003EClose observation means arranging a timely re-check and documenting objective visual behaviors (response to faces/lights, fixation, tracking), and escalating to VEP/ERG and/or neurologic evaluation if the infant fails to improve by the expected developmental window or if any systemic red flags appear.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1725,
    "Name": "Retinal detachment",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhich of the following is a risk factor that may justify \u003Cspan class=\u0022s1\u0022 style=\u0022\u0022\u003Eprophylactic laser treatment\u003C/span\u003E for lattice degeneration?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhich of the following is a risk factor that may justify \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eprophylactic laser treatment\u003C/b\u003E\u003C/span\u003E for lattice degeneration?\u003C/p\u003E\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELattice degeneration \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edoes not routinely require prophylactic laser\u003C/b\u003E\u003C/span\u003E in the absence of additional risk factors.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ELong-term natural history data (Byer) shows a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Every low risk of retinal detachment (~1% over 10 years)\u003C/b\u003E\u003C/span\u003E in uncomplicated lattice.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ETherefore, routine treatment of lattice (with or without atrophic holes) in low-risk eyes is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot recommended\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ERisk factors that justify prophylactic laser include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHistory of retinal detachment in the fellow eye\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E \u2190 strongest indication\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EHigh myopia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EFlap (tractional) tears within lattice\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAphakia\u003C/b\u003E\u003C/span\u003E (not pseudophakia)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAtrophic holes alone\u003C/b\u003E\u003C/span\u003E\u0026nbsp;are typically low risk and do not require treatment.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPseudophakia\u003C/b\u003E\u003C/span\u003E\u0026nbsp; is not a strong standalone indication (aphakia carries higher risk).\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntraocular inflammation\u003C/b\u003E\u003C/span\u003E\u0026nbsp;is not a recognised indication for prophylactic lattice treatment.\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1726,
    "Name": "Cancer associated retinopathy CAR",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 45-year-old Caucasian man presents with progressive bilateral visual loss over several months. He says the vision loss started peripherally and is now affecting central vision. He also reports intermittent photopsia. Intraocular pressures are normal. Goldmann perimetry shows dense ring scotomas in both eyes. Fundus examination is as shown. His vision was normal before this year. Which protein is most likely involved in this condition?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-04-12-0facb98d-ce5c-4503-be8b-a0594d9441f8.jpg\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThis presentation is most consistent with \u003C/span\u003E\u003Cb\u003Ecancer-associated retinopathy (CAR)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E, a form of \u003C/span\u003E\u003Cb\u003Eparaneoplastic autoimmune retinopathy\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EKey clues are:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ERapidly progressive bilateral visual loss\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EInitial \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral field loss\u003C/b\u003E\u003C/span\u003E progressing to central involvement\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EPhotopsia\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EDense ring scotomas\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPreviously normal vision, arguing against inherited retinal dystrophy\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\u003Cp class=\u0022p1\u0022\u003EFundus appears normal initially.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cli style=\u0022margin-bottom: 0.1em; border-radius: 0px !important;\u0022\u003EWith progression, clinically apparent retinal degenerations can be seen (RPE thinning and mottling, attenuation of the arterioles, optic nerve pallor). Other fundus findings such as macular edema, vitreous cells, vascular sheathing, and periphlebitis have been documented.\u003C/li\u003E\u003Cp\u003E\u003C/p\u003E\n\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ECAR is classically associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautoantibodies against recoverin\u003C/b\u003E\u003C/span\u003E, a 23-kDa calcium-binding retinal photoreceptor protein.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThe autoimmune response leads to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephotoreceptor degeneration\u003C/b\u003E\u003C/span\u003E, producing symptoms that can mimic retinitis pigmentosa but with a much more rapid onset.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERhodopsin\u003C/b\u003E\u003C/span\u003E is associated with some forms of inherited \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinitis pigmentosa\u003C/b\u003E\u003C/span\u003E, which is usually gradual and longstanding rather than rapidly acquired in midlife.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptineurin\u003C/b\u003E\u003C/span\u003E is associated with some forms of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enormal tension glaucoma\u003C/b\u003E\u003C/span\u003E.\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ELOXL1\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E is strongly associated with \u003C/span\u003E\u003Cb\u003Epseudoexfoliation syndrome/glaucoma\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003ERemember:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold; text-decoration-line: underline;\u0022\u003EDifferential diagnoses to be considered and ruled out:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EOther causes of retinal degeneration such as any hereditary or toxic retinal degeneration.\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EOptic nerve diseases such as retrobulbar optic neuropathy, optic neuropathy related to smoking/nutritional deficiency, and hereditary optic neuropathy\u0026nbsp;\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EDrug-related damage to the optic nerve or retina.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold;\u0022\u003EFurther reading and source of image:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://eyewiki.org/Cancer_Associated_Retinopathy\u0022 target=\u0022_blank\u0022\u003ECAR - eyewiki\u003C/a\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal; font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/div\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1727,
    "Name": "Retinitis Pigmentosa",
    "Body": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 34-year-old man is referred with a bilateral retinal abnormality confined to a sector of the fundus, symmetrical bilaterally. He reports mild difficulty with night vision. What is the most appropriate management?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-04-12-cad5b262-69e1-4bad-94fa-ec8ba0520120.jpg\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003EThe image shows \u003C/span\u003E\u003Cb\u003Esector retinitis pigmentosa (RP)\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E with:\u003C/span\u003E\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESharp demarcation\u003C/b\u003E\u003C/span\u003E between affected and normal retina\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003EBilateral involvement\u003C/b\u003E\u003Cspan class=\u0022s1\u0022\u003E confined to a sector\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThis distinguishes it from:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EGeneralised RP (diffuse involvement)\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESecondary pigmentation (e.g. trauma, inflammation), which is usually \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eunilateral\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ESymptoms are mild and include:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cb\u003ENyctalopia (night vision difficulty)\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften preserved central vision\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EPathophysiology:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOften associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erhodopsin mutations\u003C/b\u003E\u003Cb\u003E\u003C/b\u003E\u003C/span\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EThought to involve \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elight-induced retinal toxicity\u003C/b\u003E\u003C/span\u003E in susceptible individuals\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EManagement:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003ENo definitive treatment\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUV protection and antioxidants\u003C/b\u003E\u003C/span\u003E are commonly advised to potentially slow progression (although evidence is limited)\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003EOther options:\u003C/p\u003E\n\u003Cp class=\u0022p2\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003C/span\u003E\u003C/p\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EValproic acid\u003C/b\u003E\u003C/span\u003E: no established role and controversial\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECataract surgery\u003C/b\u003E\u003C/span\u003E: not indicated unless visually significant cataract\u003C/p\u003E\n\u003C/li\u003E\u003Cli\u003E\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcetazolamide\u003C/b\u003E\u003C/span\u003E: used for cystoid macular edema, not primary disease\u003C/p\u003E\n\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/sectoral-RP/index.htm#gsc.tab=0\u0022 target=\u0022_blank\u0022\u003ESectoral RP - WebEye\u003C/a\u003E\u003C/div\u003E\u003Cul\u003E\u003Cp\u003E\u003C/p\u003E\n\u003C/ul\u003E\u003Cp\u003E\u003C/p\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1728,
    "Name": "Sclerocornea: identifying the incorrect statement",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is incorrect when describing the typical features of sclerocornea?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer:\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Ethe cornea is generally steeper than normal eyes.\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESclerocornea is a congenital anterior segment dysgenesis in which the cornea takes on scleral\u2011like characteristics, including opacity and loss of the normal limbal architecture.\u003C/strong\u003E \u003Cstrong\u003EA key anatomic feature is that the cornea is typically flatter than normal, not steeper.\u0026nbsp;\u003C/strong\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe opacity pattern helps distinguish sclerocornea from other causes of congenital corneal opacity.\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EIn sclerocornea, the peripheral cornea is usually more opaque than the central cornea\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E, whereas \u003C/span\u003E\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EPeter\u2019s anomaly classically has more central corneal opacity due to a posterior corneal defect.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ESclerocornea is also clinically important because it is frequently associated with systemic abnormalities\u003C/strong\u003E, especially when bilateral or severe. \u003Cstrong\u003EAdditionally, the normal scleral sulcus and limbal demarcation are often absent\u003C/strong\u003E, reflecting abnormal differentiation between cornea and sclera.\u003C/p\u003E\n\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003ESclerocornea classically included as the \u201CS\u201D in the mnemonic \u003Cstrong\u003ESTUMPED\u003C/strong\u003E, which stands for \u003Cstrong\u003ESclerocornea\u003C/strong\u003E, \u003Cstrong\u003ETrauma/tears in Descemet\u2019s membrane\u003C/strong\u003E, \u003Cstrong\u003EUlcer\u003C/strong\u003E (e.g. bacterial), \u003Cstrong\u003EMetabolic disorders\u003C/strong\u003E (such as mucopolysaccharidoses including Hurler syndrome), \u003Cstrong\u003EPosterior corneal defect\u003C/strong\u003E (e.g. Peters anomaly), \u003Cstrong\u003EEndothelial defect\u003C/strong\u003E (e.g. CHED), and \u003Cstrong\u003EDermoid\u003C/strong\u003E.\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1729,
    "Name": "Sherrington\u2019s law",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with esotropia is noted to have narrowing of the palpebral fissure and retraction of the globe when attempting to adduct the eye. Which fundamental ocular motor principle is violated in this condition?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003ESherrington\u2019s law\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\n\u003Cp\u003EThe findings of lid fissure narrowing and globe retraction on adduction are classic for Duane syndrome, a congenital ocular motility disorder characterized by anomalous innervation of the lateral rectus muscle. In Duane syndrome, the medial rectus and lateral rectus muscles abnormally contract at the same time during attempted adduction, producing globe retraction and narrowing of the palpebral fissure. This directly violates \u003Cspan style=\u0022font-weight: bold;\u0022\u003ESherrington\u2019s law\u003C/span\u003E of reciprocal innervation, which states that when an agonist muscle contracts, its antagonist should simultaneously relax. Because both antagonist muscles are contracting instead of one relaxing, Sherrington\u2019s law is broken.\u003Cspan style=\u0022font-weight: bold;\u0022\u003E Hering\u2019s law\u003C/span\u003E of equal innervation applies to yoked muscles in the two eyes and is classically violated in dissociated vertical deviation, while \u003Cspan style=\u0022font-weight: bold;\u0022\u003EDonder\u2019s and Listing\u2019s laws\u003C/span\u003E relate to ocular torsion and eye position in space rather than muscle innervation. Therefore, the violated principle in this scenario is Sherrington\u2019s law.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1730,
    "Name": "Primary congenital glaucoma (PCG)",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement correctly describes a common clinical or epidemiologic characteristic of patients with primary congenital glaucoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003EPCG is bilateral in approximately two\u2011thirds of case.\u003C/strong\u003E\u003C/span\u003E\u003C/h2\u003E\u003Cp\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EPrimary congenital glaucoma most often presents during the first year of life rather than immediately at birth and shows a clear male predominance, making statements about equal sex distribution and routine diagnosis at birth incorrect; although PCG is a potentially vision\u2011threatening condition, advances in surgical management have significantly reduced poor visual outcomes, with permanent blindness occurring in only about 5\u201315% of affected individuals rather than the much higher percentages suggested, and a well\u2011established epidemiologic feature of PCG is that both eyes are involved in roughly two\u2011thirds of patients, which makes bilateral involvement the true statement.\u003C/span\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1731,
    "Name": "Inferior rectus resection",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient undergoing inferior rectus resection surgery for a hypertropia, which postoperative change in lower eyelid position may be seen?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Elower lid elevation\u003C/strong\u003E\u003C/span\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, because the inferior rectus muscle is anatomically and functionally linked to the lower eyelid retractors through\u0026nbsp; the capsulopalpebral fascia, which is continuous with Lockwood\u2019s ligament and the inferior tarsal attachments; inferior rectus resection shortens and tightens this muscle\u2013fascial complex, increasing tension transmitted to the lower lid retractors and their ligamentous insertions on the tarsus, thereby pulling the lower eyelid upward, whereas inferior rectus recession lengthens and relaxes this system, leading instead to lower lid retraction and widening of the palpebral fissure.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1732,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAt what postnatal age does neonatal conjunctivitis caused by \u003Cem\u003ENeisseria gonorrhoeae\u003C/em\u003E most commonly present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer :\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003E3\u20134 days of life\u003C/strong\u003E\u003C/span\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, because the timing of ophthalmia neonatorum is a key diagnostic clue and gonococcal conjunctivitis classically presents early, typically between the third and fourth day after birth, reflecting rapid bacterial proliferation after acquisition during passage through the birth canal; this form is notable for producing the most profuse purulent discharge among neonatal conjunctivitides and must be recognized promptly, whereas chemical conjunctivitis usually occurs within the first 24 hours, chlamydial conjunctivitis most often presents around 7 days of life, and HSV conjunctivitis is rare and typically presents later, around 2 weeks of age.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1733,
    "Name": "Normal cup\u2011to\u2011disc ratio in newborns",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen examining a newborn for suspected primary congenital glaucoma, what cup\u2011to\u2011disc ratio is considered normal for an infant optic nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer :\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Eless than 0.3\u003C/strong\u003E\u003C/span\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, because most normal newborns have small physiologic cups with cup\u2011to\u2011disc ratios below 0.3, and there is typically minimal asymmetry between the two eyes (generally less than 0.2 difference), making larger cups or significant asymmetry concerning for glaucoma in this age group; importantly, unlike adult glaucoma, optic nerve cupping in congenital glaucoma can partially reverse after successful lowering of intraocular pressure, which is why recognizing abnormal cupping relative to expected newborn norms is critical during early evaluation.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1734,
    "Name": "Botulinum toxin in strabismus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich strabismus scenario is the poorest fit for treatment with botulinum toxin chemodenervation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px; font-size: 14px;\u0022\u003Edissociated vertical deviation\u003C/strong\u003E\u003Cspan style=\u0022font-weight: 400; letter-spacing: 0.14994px; font-size: 14px;\u0022\u003E, because dissociated vertical deviation is not fundamentally a \u201Csingle-muscle overaction\u201D problem that can be predictably neutralized by temporarily weakening one extraocular muscle, but rather a supranuclear, dissociated binocular control disorder in which one eye drifts upward (often with extorsion/abduction components) when fusion is disrupted and the magnitude is variable, latent/intermittent, frequently bilateral (even if asymmetric), and tightly linked to early-onset sensory adaptations (latent nystagmus, suppression, inferior oblique overaction), so weakening a rectus with botulinum toxin tends to give inconsistent, non-durable alignment effects and may simply trade a dissociated drift for iatrogenic incomitance, ptosis, or an unwanted hypotropia in primary position; by contrast, botulinum toxin is mechanistically well suited to situations where a clear agonist\u2013antagonist imbalance is driving diplopia or a small/moderate comitant deviation\u2014such as small angle esotropia (temporary MR weakening can reduce the manifest angle and sometimes \u201Creset\u201D fusion in selected cases), acute paralytic strabismus during recovery (weakening the antagonist can reduce diplopia and prevent secondary contracture while nerve function returns), and selected active thyroid eye disease cases when surgery is deferred because measurements are unstable (temporary weakening can palliate diplopia without committing to a definitive recession pattern), making dissociated vertical deviation the least useful indication among the options.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1735,
    "Name": "Crouzon syndrome (craniosynostosis) presenting with proptosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with proptosis has an external appearance shows in the picture below; which gene mutation is classically responsible?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-04-21-15703e72-c9bf-42e6-966c-866452e81474.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFGFR2\u003C/strong\u003E, because the clinical context is most consistent with Crouzon syndrome, a common autosomal dominant craniosynostosis syndrome in which premature fusion of cranial sutures leads to midface hypoplasia and shallow orbits with resultant proptosis/exposure risk, and the best-established genetic association for Crouzon is activating mutations in \u003Cstrong\u003EFGFR2\u003C/strong\u003E (classically on chromosome 10); this also fits the key differentiator from Apert syndrome\u2014Crouzon typically lacks syndactyly\u2014while the other listed genes point to different entities (TWIST is associated with Saethre\u2013Chotzen syndrome, MYOC is associated with juvenile open-angle glaucoma and some primary open-angle glaucoma cases, and OPTN is associated with normal tension glaucoma).\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1736,
    "Name": "RPE function",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of the following is a physiological function of the retinal pigment epithelium (RPE)?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe retinal pigment epithelium (RPE) is a single layer of pigmented cells located between:\u003Cul\u003E\u003Cli\u003EThe neurosensory retina\u003C/li\u003E\u003Cli\u003EBruch\u2019s membrane\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAdjacent RPE cells are connected by tight junctions near their apices.\u003C/li\u003E\u003Cli\u003EThese tight junctions form the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eouter blood-retinal (blood-ocular) barrier\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EMajor functions of the RPE include:\u003Cul\u003E\u003Cli\u003EFormation of the outer blood-retinal barrier\u003C/li\u003E\u003Cli\u003EMaintenance of the subretinal space\u003C/li\u003E\u003Cli\u003EAbsorption (not reflection) of light\u003C/li\u003E\u003Cli\u003EPhagocytosis of photoreceptor \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eouter segments\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EParticipation in vitamin A metabolism and the visual cycle\u003C/li\u003E\u003Cli\u003EScar formation and healing responses\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThe RPE generates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E11-cis-retinaldehyde\u003C/b\u003E\u003C/span\u003E, not all-trans-retinaldehyde, during the visual cycle.\u003C/li\u003E\u003Cli\u003EPhotoreceptor \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eouter segments\u003C/b\u003E\u003C/span\u003E are phagocytosed, not inner segments.\u003C/li\u003E\u003Cli\u003EMelanin within the RPE absorbs stray light to improve image quality.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1737,
    "Name": "    Rod monochromatism",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 5-year-old child presents with \u003Cspan class=\u0022s1\u0022\u003E0.6 LogMAR visual acuity OU\u003C/span\u003E, nystagmus, and lightly pigmented fundi. There is no obvious maculopathy or retinal degeneration. ERG shows \u003Cspan class=\u0022s1\u0022\u003Ecomplete absence of cone responses\u003C/span\u003E. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003ERod monochromatism is a form of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecomplete achromatopsia\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EIt presents in early childhood with:\u003Cul\u003E\u003Cli\u003EReduced vision\u003C/li\u003E\u003Cli\u003ENystagmus\u003C/li\u003E\u003Cli\u003EPhotophobia\u003C/li\u003E\u003Cli\u003EAbsent colour discrimination\u003C/li\u003E\u003Cli\u003EAbsent cone responses on ERG\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EIt can be confused with albinism because patients may have \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elightly pigmented fundi\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EIn albinism, cone function and colour vision are usually preserved, so a complete absence of cone ERG responses argues against albinism.\u003C/li\u003E\u003Cli\u003ECone dystrophy can show reduced cone responses, but it usually causes progressive macular dysfunction or retinal degeneration, which is absent here.\u003C/li\u003E\u003Cli\u003ECongenital colour vision defects, including achromatopsia, do not show retinal degeneration, unlike cone dystrophy.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003EFurther reading:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://eyewiki.org/Achromatopsia\u0022 target=\u0022_blank\u0022\u003EAchromatopsia - Eyewiki\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1738,
    "Name": "Verteporfin photodynamic therapy (PDT)",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA patient undergoing verteporfin photodynamic therapy (PDT) for a progressive subfoveal occult choroidal neovascular membrane develops acute back, side, and chest pain during the infusion. What is the most appropriate explanation to give the patient regarding this adverse effect?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EAcute back, chest, and flank pain is a recognised adverse effect of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Everteporfin infusion during PDT\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EThis complication occurs in approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2.5% of patients\u003C/b\u003E\u003C/span\u003E in major PDT trials.\u003C/li\u003E\u003Cli\u003EThe pain is specifically related to the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einfusion phase\u003C/b\u003E\u003C/span\u003E of verteporfin administration.\u003C/li\u003E\u003Cli\u003ESymptoms characteristically:\u003Cul\u003E\u003Cli\u003EBegin during the infusion\u003C/li\u003E\u003Cli\u003EResolve completely shortly after the infusion ends\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThe mechanism is not fully understood but is thought to relate to transient infusion-related reactions rather than true cardiopulmonary pathology.\u003C/li\u003E\u003Cli\u003EPersistent symptoms lasting 24-48 hours or recurrent episodes are not typical.\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EThe most common side effect of PDT is verteporfin-induced photosensitivity\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EThe most frequently reported adverse events (10-30%) were injection site reactions such as pain, edema, inflammation, rashes, hemorrhage, and discoloration; rare cases of skin necrosis have been reported.\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003EFurther Reading:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://eyewiki.org/Photodynamic_Therapy_(PDT)\u0022 target=\u0022_blank\u0022\u003EPDT - Eyewiki\u003C/a\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; letter-spacing: normal;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1739,
    "Name": "Retinal vascularisation - development",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EAt what gestational ages is peripheral retinal vascularization normally completed on the nasal and temporal sides of the retina?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003ERetinal vascularization begins at approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E4\u20135 months of gestation\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EVascular development proceeds centrifugally from the optic disc toward the peripheral retina.\u003C/li\u003E\u003Cli\u003ECompletion of vascularization occurs earlier nasally because the nasal retina is anatomically shorter.\u003C/li\u003E\u003Cli\u003ENormal completion times:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENasal retina \u2192 36 weeks gestation\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETemporal retina \u2192 40 weeks gestation\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThese values are important in:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003ERetinopathy of prematurity (ROP) screening\u003C/li\u003E\u003Cli\u003EUnderstanding avascular peripheral retina in premature infants\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022/upload-2026-05-12-9f9e6805-bbc1-468b-a956-472d88088c47.png\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan class=\u0022label\u0022 style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0022Figure 1\u003C/span\u003E\u003Cspan style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E.\u0026nbsp;\u003C/span\u003E\u003Cspan style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003ETimeline of normal vascular development versus pathological vascular development (ROP phases) by weeks of gestational age. The development of the choriocapillaris starts between 5.5 and 8 weeks and is completed at 20\u201322 weeks. Retinal vascularization starts at around 16 weeks. Retinal blood vessels grow radially from the optic disc towards the ora serrata. Vascularization of the nasal retina is completed at around 36 weeks and that of the temporal retina at 40 weeks. The transition between phase 1 and phase 2 of ROP generally occurs around 32 weeks.\u0022\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.sciencedirect.com/science/article/pii/S0039625722001692\u0022 target=\u0022_blank\u0022\u003ERetinopathy of prematurity: A review of pathophysiology and signaling pathways\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1740,
    "Name": "Retinal phototoxicity",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich ophthalmic procedure carries the greatest risk of retinal phototoxicity?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EIndocyanine green (ICG) may act as a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ephotosensitizer\u003C/b\u003E\u003C/span\u003E, increasing susceptibility of the retina to light-induced toxicity.\u003C/li\u003E\u003Cli\u003EDuring membrane peeling surgery:\u003Cul\u003E\u003Cli\u003EThe endoillumination probe is often positioned \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Every close to the macula\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EThis significantly increases retinal light exposure\u003C/li\u003E\u003Cli\u003ECombined with ICG, this increases the risk of photochemical retinal injury\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThe macula is particularly vulnerable because:\u003Cul\u003E\u003Cli\u003ESurgical exposure times may be prolonged\u003C/li\u003E\u003Cli\u003EIllumination is concentrated over a small retinal area\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EReported manifestations of phototoxicity include:\u003Cul\u003E\u003Cli\u003ERPE changes\u003C/li\u003E\u003Cli\u003ECentral scotoma\u003C/li\u003E\u003Cli\u003EReduced visual acuity\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1741,
    "Name": "Peripheral exudative hemorrhagic chorioretinopathy (PEHCR)",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 55-year-old woman is noted incidentally after cataract surgery to have an asymptomatic peripheral fundus lesion in the left eye, as shown. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-05-12-b57ea08f-c477-42c4-835d-b57bcea5cc73.jpg\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EPEHCR represents a form of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral choroidal neovascular membrane (CNVM)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ETypical features:\u003Cul\u003E\u003Cli\u003EPeripheral (usually temporal) lesion\u003C/li\u003E\u003Cli\u003EHemorrhagic and exudative appearance\u003C/li\u003E\u003Cli\u003EOften asymptomatic\u003C/li\u003E\u003Cli\u003ECommonly detected incidentally\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EEpidemiology:\u003Cul\u003E\u003Cli\u003ETypically affects older patients\u003C/li\u003E\u003Cli\u003EMore common in women\u003C/li\u003E\u003Cli\u003EApproximately 25% may have bilateral lesions\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EPresence of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehard exudates\u003C/b\u003E\u003C/span\u003E adjacent to the lesion supports PEHCR rather than melanoma.\u003C/li\u003E\u003Cli\u003EChoroidal melanoma is less likely because melanomas rarely produce prominent lipid exudation.\u003C/li\u003E\u003Cli\u003ERhegmatogenous retinal detachment usually presents with:\u003Cul\u003E\u003Cli\u003EFlashes\u003C/li\u003E\u003Cli\u003EFloaters\u003C/li\u003E\u003Cli\u003EVisual field defect\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAcute retinal necrosis typically presents with:\u003Cul\u003E\u003Cli\u003EPain\u003C/li\u003E\u003Cli\u003EReduced vision\u003C/li\u003E\u003Cli\u003EVitritis\u003C/li\u003E\u003Cli\u003EPeripheral necrotizing retinitis\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EManagement:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EObservation is often appropriate\u003C/li\u003E\u003Cli\u003EAnti-VEGF may be considered if exudation threatens the macula\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://eyewiki-images.s3.us-east-va.perf.cloud.ovh.us/thumb/0/06/OCT_before_and_after_Avastin.jpg/573px-OCT_before_and_after_Avastin.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-size: 12.3704px; letter-spacing: normal; background-color: rgb(248, 249, 250);\u0022\u003EA: A widefield fundus showing infero-temporal quadrant lesion with subretinal fibrosis and hemorrhage. B: OCT at the time of presentation with subretinal fluid extending to the fovea. C: Fundus photo showing partially regressing hemorrhagic lesion. D: On OCT, the previously-seen sunretinal fluid is resolved one week after an injection of\u0026nbsp;\u003C/span\u003E\u003Ca href=\u0022https://eyewiki.org/Bevacizumab\u0022 title=\u0022Bevacizumab\u0022 style=\u0022color: rgb(62, 135, 203); background: none rgb(248, 249, 250); width: 100%; font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-size: 12.3704px; letter-spacing: normal; border-radius: 0px !important;\u0022\u003Ebevacizumab\u003C/a\u003E\u003Cspan style=\u0022color: rgb(33, 37, 41); font-family: Lato, \u0026quot;Helvetica Neue\u0026quot;, Helvetica, Arial, sans-serif; font-size: 12.3704px; letter-spacing: normal; background-color: rgb(248, 249, 250);\u0022\u003E, a type of anti-VEGF.\u0026nbsp;\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://eyewiki.org/Peripheral_Exudative_Hemorrhagic_Chorioretinopathy\u0022 target=\u0022_blank\u0022\u003EEyewiki - peripheral exudative hemorrhagic chorioretinopathy (PEHCR)\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1742,
    "Name": "Toxoplasma chorioretinitis",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 28-year-old man presents with 3 weeks of progressive visual loss in the left eye, associated with floaters, photophobia, and redness. Visual acuity is \u003Cspan class=\u0022s1\u0022\u003E0.0 LogMAR\u003C/span\u003E in the right eye and \u003Cspan class=\u0022s1\u0022\u003E1.1 LogMAR\u003C/span\u003E in the left eye. Fundus examination shows an active chorioretinal inflammatory lesion adjacent to an old scar. If standard therapy is unavailable, which alternative treatment is appropriate?\u003C/span\u003E\u003C/p\u003E\u003Cp class=\u0022p1\u0022\u003E\u003Cimg src=\u0022/upload-2026-05-12-4b45bf6d-29de-47e6-bfbb-919f1f721744.jpg\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe fundus photograph shows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eactive retinochoroiditis adjacent to an old chorioretinal scar\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EThis is typical of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etoxoplasma chorioretinitis\u003C/b\u003E\u003C/span\u003E, the most common cause of posterior uveitis worldwide.\u003C/li\u003E\u003Cli\u003EClassic treatment is \u201Ctriple therapy\u201D:\u003Cul\u003E\u003Cli\u003EPyrimethamine\u003C/li\u003E\u003Cli\u003ESulfadiazine\u003C/li\u003E\u003Cli\u003ECorticosteroids\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EHowever, pyrimethamine may be difficult to obtain or poorly tolerated.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESulfamethoxazole/trimethoprim\u003C/b\u003E\u003C/span\u003E is a recognised alternative oral regimen.\u003C/li\u003E\u003Cli\u003EIt may be used with or without \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eclindamycin\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EAnother alternative oral option is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eazithromycin\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EDoxycycline is more relevant for infections such as Lyme disease or Bartonella.\u003C/li\u003E\u003Cli\u003EOral moxifloxacin is not standard therapy for ocular toxoplasmosis.\u003C/li\u003E\u003Cli\u003EFluconazole is antifungal and would not treat toxoplasma retinochoroiditis.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EImage source:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.aao.org/education/current-insight/retinal-choroidal-manifestations-of-toxoplasmosis\u0022 target=\u0022_blank\u0022\u003ERetinal and Choroidal Manifestations of Toxoplasmosis\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1743,
    "Name": "Peroxisome biogenesis disorders (PBDs)",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EA 3-month-old infant presents with seizures, developmental delay, hypotonia, hepatomegaly, and severe bilateral retinal degeneration. The child dies at 5 months of age. What is the most likely diagnosis?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EZellweger syndrome is the most severe disorder within the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EZellweger spectrum disorders\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EThe Zellweger spectrum consists of:\u003Cul\u003E\u003Cli\u003EInfantile Refsum disease (least severe)\u003C/li\u003E\u003Cli\u003ENeonatal adrenoleukodystrophy\u003C/li\u003E\u003Cli\u003EZellweger syndrome (most severe)\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThese disorders are classified as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperoxisome biogenesis disorders (PBDs)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ETypical clinical features of Zellweger syndrome include:\u003Cul\u003E\u003Cli\u003ESevere hypotonia\u003C/li\u003E\u003Cli\u003ESeizures\u003C/li\u003E\u003Cli\u003EDevelopmental delay\u003C/li\u003E\u003Cli\u003EHepatomegaly\u003C/li\u003E\u003Cli\u003ERetinal degeneration\u003C/li\u003E\u003Cli\u003EEarly infant death\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EOcular manifestations may include:\u003Cul\u003E\u003Cli\u003EPigmentary retinopathy\u003C/li\u003E\u003Cli\u003EOptic atrophy\u003C/li\u003E\u003Cli\u003ERetinal degeneration\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EMost affected infants do not survive beyond the first 6 months of life.\u003C/li\u003E\u003Cli\u003EBatten disease is a neuronal ceroid lipofuscinosis that usually presents later in childhood rather than early infancy.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1744,
    "Name": "Ophthalmodynamometry",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich of these investigation is can differentiate between central retinal vein occlusion (CRVO) and carotid occlusive disease?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EOphthalmodynamometry measures \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eretinal arterial pressure\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EFindings:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECRVO\u003C/b\u003E\u003C/span\u003E \u2192 retinal arterial pressure is usually normal\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECarotid occlusive disease\u003C/b\u003E\u003C/span\u003E \u2192 retinal arterial pressure is reduced\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ETherefore, it can help distinguish venous occlusive disease from ocular ischemia secondary to carotid stenosis.\u003C/li\u003E\u003Cli\u003EOCT evaluates retinal structure and macular edema but does not assess retinal arterial perfusion pressure.\u003C/li\u003E\u003Cli\u003EVEP assesses optic pathway conduction and is not specific for differentiating these vascular disorders.\u003C/li\u003E\u003Cli\u003EFluorophotometry measures aqueous humor formation by tracking fluorescein concentration decline in the anterior chamber and is unrelated to retinal vascular perfusion assessment.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1745,
    "Name": "Central Serous Chorioretinopathy CSCR",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich medication has been investigated for treatment of chronic central serous chorioretinopathy (CSCR) because of its antagonistic effect on mineralocorticoid receptors in the choroid?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EChronic CSCR is thought to involve:\u003Cul\u003E\u003Cli\u003EChoroidal vascular hyperpermeability\u003C/li\u003E\u003Cli\u003EIncreased choroidal hydrostatic pressure\u003C/li\u003E\u003Cli\u003EDysfunction of the retinal pigment epithelium (RPE)\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EExperimental evidence suggests overactivation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emineralocorticoid receptors\u003C/b\u003E\u003C/span\u003E in the choroid contributes to disease pathogenesis.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEplerenone\u003C/b\u003E\u003C/span\u003E is a selective mineralocorticoid receptor antagonist.\u003C/li\u003E\u003Cli\u003EIt has been investigated as a medical treatment for chronic CSCR with the aim of:\u003Cul\u003E\u003Cli\u003EReducing subretinal fluid\u003C/li\u003E\u003Cli\u003EReducing choroidal thickness\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022Yjhzub\u0022 jsaction=\u0022\u0022 jscontroller=\u0022zYmgkd\u0022 data-sfc-root=\u0022c\u0022 jsuid=\u0022u1Urld_10\u0022 data-sfc-cb=\u0022\u0022 data-processed=\u0022true\u0022 data-copy-service-computed-style=\u0022font-family: \u0026quot;Google Sans\u0026quot;, Arial, sans-serif; font-size: 16px; font-weight: 600; margin: 0px; text-decoration: none; border-bottom: 0px rgb(10, 10, 10);\u0022 style=\u0022font-family: \u0026quot;Google Sans\u0026quot;, Arial, sans-serif; font-size: 16px; font-weight: 600; border-bottom: 0px rgb(10, 10, 10);\u0022\u003EThe VICI Trial Evidence:\u003C!--TgQPHd|[]--\u003E\u003C/span\u003E The major \u003Cspan jsuid=\u0022u1Urld_11\u0022 data-sfc-cp=\u0022\u0022 jsaction=\u0022mouseenter:\u0026amp;u1Urld_11|WOQqYb;mouseleave:\u0026amp;u1Urld_11|Tx5Rb;focusin:\u0026amp;u1Urld_11|mrwrPd;focusout:\u0026amp;u1Urld_11|mFndSc;\u0022 jscontroller=\u0022KMhGd\u0022 data-sfc-root=\u0022c\u0022 data-sfc-cb=\u0022\u0022 data-processed=\u0022true\u0022 data-copy-service-computed-style=\u0022font-family: \u0026quot;Google Sans\u0026quot;, Arial, sans-serif; font-size: 16px; font-weight: 400; margin: 0px; text-decoration: none; border-bottom: 0px rgb(10, 10, 10);\u0022 style=\u0022font-family: \u0026quot;Google Sans\u0026quot;, Arial, sans-serif; font-size: 16px; border-bottom: 0px rgb(10, 10, 10);\u0022\u003E\u003Ca class=\u0022H23r4e\u0022 target=\u0022_blank\u0022 rel=\u0022noopener\u0022 data-hveid=\u0022CAIIAAgACBAQAg\u0022 href=\u0022https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)32981-2/fulltext\u0022 ping=\u0022/url?sa=t\u0026amp;source=web\u0026amp;rct=j\u0026amp;url=https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)32981-2/fulltext\u0026amp;ved=2ahUKEwjasIn8wrOUAxW12AIHHYOTAwUQy_kOegoIAggACAAIEBAC\u0026amp;opi=89978449\u0022 data-processed=\u0022true\u0022 data-copy-service-computed-style=\u0022font-family: \u0026quot;Google Sans\u0026quot;, Arial, sans-serif; font-size: 16px; font-weight: 500; margin: 0px; text-decoration: underline 1px rgb(26, 13, 171); border-bottom: 0px rgb(26, 13, 171);\u0022 style=\u0022text-decoration: underline 1px rgb(26, 13, 171); border-bottom: 0px rgb(26, 13, 171);\u0022\u003EVICI trial\u003C/a\u003E\u003C!--TgQPHd|[[\u0026quot;https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)32981-2/fulltext\u0026quot;,null,null,[null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,[{\u0026quot;1218\u0026quot;:[16]}]],16,null,\u0026quot;Eplerenone for chronic central serous chorioretinopathy in patients ...\u0026quot;,\u0026quot;Eplerenone was not superior to placebo for improving BCVA in people with chronic CSCR after 12 months of treatment. Ophthalmologists who currently prescribe eplerenone for CSCR should discontinue this practice.\u0026quot;,\u0026quot;https://encrypted-tbn3.gstatic.com/images?q\\u003dtbn:ANd9GcTbcGulvG5oELrTeAOrqzb9JN-JAsnz0fZKSoOJCePacGnCpYm_3wI4fBLp2OKkOv5MtzYHZPcaVn9jsZA5wg\u0026quot;,\u0026quot;The Lancet\u0026quot;,\u0026quot;https://encrypted-tbn3.gstatic.com/faviconV2?url\\u003dhttps://www.thelancet.com\\u0026client\\u003dAIM\\u0026size\\u003d64\\u0026type\\u003dFAVICON\\u0026enable_upscaled\\u003dtrue\\u0026fallback_opts\\u003dTYPE,SIZE,URL\u0026quot;,[[1778581114083418,117627061,84120451],null,null,null,null,[[2,0,0,12,127]]]]]--\u003E\u003C/span\u003E concluded that eplerenone was not superior to a placebo in improving visual acuity (BCVA) at 12 months in chronic CSCR patients.\u003C/li\u003E\u003Cli\u003ESpironolactone has also been studied for similar reasons.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003E\u003Cspan style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;M\u003C/span\u003E\u003Ca href=\u0022https://www.sciencedirect.com/topics/medicine-and-dentistry/mineralocorticoid-receptor\u0022 class=\u0022topic-link\u0022 style=\u0022background-color: rgba(0, 0, 0, 0); word-break: break-word; text-decoration: underline 1px rgb(31, 31, 31); color: rgb(31, 31, 31); text-underline-offset: 1px; font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003Eineralocorticoid receptor\u003C/a\u003E\u003Cspan style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003E\u0026nbsp;antagonists (\u003C/span\u003E\u003Cspan style=\u0022color: rgb(31, 31, 31); font-family: ElsevierGulliver, Georgia, \u0026quot;Times New Roman\u0026quot;, Times, STIXGeneral, \u0026quot;Cambria Math\u0026quot;, \u0026quot;Lucida Sans Unicode\u0026quot;, \u0026quot;Microsoft Sans Serif\u0026quot;, \u0026quot;Segoe UI Symbol\u0026quot;, \u0026quot;Arial Unicode MS\u0026quot;, serif, sans-serif; font-size: 16px; letter-spacing: normal;\u0022\u003EMRAs) offer short-term benefits in reducing SRF but may have limited long-term durability based on current evidence, highlighting the need for further studies.\u0026nbsp;\u003C/span\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EBevacizumab is an anti-VEGF agent and has limited benefit in typical CSCR unless secondary CNV is present.\u003C/li\u003E\u003Cli\u003EHydrochlorothiazide is a thiazide diuretic and has no established role in CSCR.\u003C/li\u003E\u003Cli\u003EAldosterone activates mineralocorticoid receptors and would theoretically worsen rather than treat CSCR.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003EFurther reading:\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.sciencedirect.com/science/article/pii/S0002939425003010\u0022 target=\u0022_blank\u0022\u003EEplerenone and Spironolactone for Chronic Central Serous Chorioretinopathy: A Systematic Review and Meta-Analysis\u003C/a\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1746,
    "Name": "Stickler Syndrome",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhat is the most common hereditary hyaloideoretinopathy?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EHereditary hyaloideoretinopathies are a group of disorders characterized by:\u003Cul\u003E\u003Cli\u003EPremature vitreous degeneration\u003C/li\u003E\u003Cli\u003EAn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Coptically empty vitreous\u201D\u003C/b\u003E\u003C/span\u003E appearance on examination\u003C/li\u003E\u003Cli\u003EIncreased risk of retinal tears and retinal detachment\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ERetinal detachment is thought to result from:\u003Cul\u003E\u003Cli\u003EExtensive lattice degeneration\u003C/li\u003E\u003Cli\u003EPeripheral retinal thinning\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAssociated ocular findings may include:\u003Cul\u003E\u003Cli\u003EHigh myopia\u003C/li\u003E\u003Cli\u003ECataract\u003C/li\u003E\u003Cli\u003EGlaucoma\u003C/li\u003E\u003Cli\u003EStrabismus\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EStickler syndrome is the most common hereditary hyaloideoretinopathy.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EIt is inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E manner.\u003C/li\u003E\u003Cli\u003EMost commonly caused by mutations affecting \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Etype II collagen (COL2A1)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EOcular features include:\u003Cul\u003E\u003Cli\u003EHigh myopia\u003C/li\u003E\u003Cli\u003EPremature vitreous liquefaction\u003C/li\u003E\u003Cli\u003ERetinal tears\u003C/li\u003E\u003Cli\u003ERetinal detachment (up to 60%)\u003C/li\u003E\u003Cli\u003EOptically empty vitreous\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ESystemic features include:\u003Cul\u003E\u003Cli\u003EPierre Robin sequence:\u003Cul\u003E\u003Cli\u003EMicrognathia\u003C/li\u003E\u003Cli\u003ECleft palate\u003C/li\u003E\u003Cli\u003EGlossoptosis\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EHypermobile joints\u003C/li\u003E\u003Cli\u003EEarly osteoarthritis\u003C/li\u003E\u003Cli\u003ESensorineural hearing loss\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWagner disease\u003C/b\u003E\u003C/span\u003E and \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EJansen disease\u003C/b\u003E\u003C/span\u003E are hereditary hyaloideoretinopathies but generally lack the systemic manifestations seen in Stickler syndrome.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMarfan syndrome\u003C/b\u003E\u003C/span\u003E is not classified as a hereditary hyaloideoretinopathy.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1747,
    "Name": "Branch retinal vein occlusion",
    "Body": "\u003Cdiv\u003E\u003Cimg src=\u0022https://upload.wikimedia.org/wikipedia/commons/7/78/Branch_retinal_vein_occlusion.jpg\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhich factor is the most important predictor of visual recovery for the condition shown in this fundus photo?\u003C/p\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe image demonstrates a \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ebranch retinal vein occlusion (BRVO)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EVisual loss in BRVO may result from:\u003Cul\u003E\u003Cli\u003EMacular edema\u003C/li\u003E\u003Cli\u003EMacular ischemia\u003C/li\u003E\u003Cli\u003EEpiretinal membrane formation\u003C/li\u003E\u003Cli\u003EMacular exudation\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAmong these factors, the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eextent of retinal capillary non-perfusion (retinal ischemia)\u003C/b\u003E\u003C/span\u003E is the most important determinant of visual prognosis.\u003C/li\u003E\u003Cli\u003EGreater retinal ischemia is associated with:\u003Cul\u003E\u003Cli\u003EPoorer visual recovery\u003C/li\u003E\u003Cli\u003EHigher risk of retinal neovascularization\u003C/li\u003E\u003Cli\u003EIncreased likelihood of vitreous hemorrhage\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EFluorescein angiography is particularly useful in BRVO because it:\u003Cul\u003E\u003Cli\u003EIdentifies areas of capillary non-perfusion\u003C/li\u003E\u003Cli\u003EAssesses the degree of macular ischemia\u003C/li\u003E\u003Cli\u003EHelps estimate visual prognosis\u003C/li\u003E\u003Cli\u003EAssists in predicting the risk of future neovascular complications\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAlthough macular edema is a major cause of visual loss and a target for treatment, the degree of ischemia remains the strongest prognostic factor.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 2,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1748,
    "Name": "Marfan Syndrome",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA tall patient is found to have \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperotemporal ectopia lentis\u003C/b\u003E\u003C/span\u003E. Which specialist referral is most appropriate?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESuperotemporal lens subluxation\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E is classically associated with \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMarfan syndrome\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EMarfan syndrome is an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant connective tissue disorder\u003C/b\u003E\u003C/span\u003E caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFBN1 (fibrillin-1)\u003C/b\u003E\u003C/span\u003E gene.\u003C/li\u003E\u003Cli\u003EKey ocular features:\u003Cul\u003E\u003Cli\u003ESuperotemporal ectopia lentis\u003C/li\u003E\u003Cli\u003EHigh myopia\u003C/li\u003E\u003Cli\u003ERetinal detachment\u003C/li\u003E\u003Cli\u003EEarly cataract\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThe most serious systemic complications are cardiovascular:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAortic root dilatation\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAortic aneurysm\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAortic dissection\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMitral valve prolapse\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ETherefore, all patients with suspected Marfan syndrome require:\u003Cul\u003E\u003Cli\u003ECardiology assessment\u003C/li\u003E\u003Cli\u003EEchocardiography\u003C/li\u003E\u003Cli\u003EOngoing cardiovascular surveillance\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThis contrasts with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehomocystinuria\u003C/b\u003E\u003C/span\u003E, where lens subluxation is typically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einferonasal\u003C/b\u003E\u003C/span\u003E, rather than superotemporal.\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearl\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMarfan syndrome \u2192 lens up (superotemporal)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHomocystinuria \u2192 lens down (inferonasal)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 1,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1749,
    "Name": "Herpes Simplex Keratitis",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhy is oral acyclovir commonly used as part of the treatment of disciform keratitis?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDisciform keratitis\u003C/b\u003E\u003C/span\u003E is primarily an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eimmune-mediated endotheliitis\u003C/b\u003E\u003C/span\u003E associated with HSV or VZV infection.\u003C/li\u003E\u003Cli\u003EThe characteristic stromal edema occurs secondary to endothelial dysfunction.\u003C/li\u003E\u003Cli\u003EOral acyclovir is thought to reach the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edeeper corneal layers\u003C/b\u003E\u003C/span\u003E, particularly the endothelium, more effectively via diffusion from the aqueous humor.\u003C/li\u003E\u003Cli\u003EFor this reason, many corneal specialists use oral antiviral therapy in addition to topical treatment.\u003C/li\u003E\u003Cli\u003EClinical features of disciform keratitis:\u003Cul\u003E\u003Cli\u003ECentral or paracentral disc-shaped stromal edema\u003C/li\u003E\u003Cli\u003EEndothelial inflammation (endotheliitis)\u003C/li\u003E\u003Cli\u003EKeratic precipitates may be present\u003C/li\u003E\u003Cli\u003EAssociated stromal and epithelial edema\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EAntiviral treatment options:\u003Cul\u003E\u003Cli\u003EOral acyclovir\u003C/li\u003E\u003Cli\u003ETopical ganciclovir gel\u003C/li\u003E\u003Cli\u003ETopical trifluridine\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ESome corneal specialists use \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eoral acyclovir alone\u003C/b\u003E\u003C/span\u003E (e.g., 400 mg five times daily) for herpetic epithelial disease.\u003C/li\u003E\u003Cli\u003EOral therapy is preferred in some centres because it avoids the epithelial toxicity associated with topical antivirals.\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearl\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpithelial HSV keratitis \u2192 epithelial disease\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDisciform keratitis \u2192 endothelial disease (endotheliitis)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003ETherefore, oral antivirals are particularly useful because of their ability to reach the deeper corneal tissues.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1750,
    "Name": "Acanthamoeba",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA contact lens wearer presents with severe ocular pain and a linear epitheliopathy. Gram stain and confocal microscopy demonstrate cysts within the corneal stroma. What is the most appropriate initial treatment?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe clinical picture is typical of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAcanthamoeba keratitis\u003C/b\u003E\u003C/span\u003E:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EContact lens wear\u003C/li\u003E\u003Cli\u003ESevere pain out of proportion to clinical signs\u003C/li\u003E\u003Cli\u003ELinear epitheliopathy or pseudodendrites\u003C/li\u003E\u003Cli\u003ECorneal stromal cysts on confocal microscopy\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EEarly disease typically presents with:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EEpitheliopathy\u003C/li\u003E\u003Cli\u003EPerineural infiltrates (radial keratoneuritis)\u003C/li\u003E\u003Cli\u003ESevere pain\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPerineural infiltrates are virtually pathognomonic\u003C/b\u003E\u003C/span\u003E for Acanthamoeba keratitis.\u003C/li\u003E\u003Cli\u003EThe classic \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ering infiltrate\u003C/b\u003E\u003C/span\u003E is a relatively \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elate manifestation\u003C/b\u003E\u003C/span\u003E and is often overemphasized in examinations.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EAcanthamoeba exists in two forms:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETrophozoite\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E (active form)\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECyst\u003C/b\u003E\u003C/span\u003E (highly resistant form)\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EEffective treatment requires agents with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecysticidal activity\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EThe most effective anti-amoebic agents are:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBiguanides\u003C/b\u003E\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EPHMB 0.02%\u003C/li\u003E\u003Cli\u003EChlorhexidine 0.02%\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDiamidines\u003C/b\u003E\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EPropamidine isethionate 0.1%\u003C/li\u003E\u003Cli\u003EHexamidine 0.1%\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPHMB 0.02%\u003C/b\u003E\u003C/span\u003E is the most commonly used first-line treatment and is effective against both trophozoites and cysts.\u003C/li\u003E\u003Cli\u003ESome corneal specialists prefer \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPHMB monotherapy\u003C/b\u003E\u003C/span\u003E, as combination therapy has not consistently shown superiority and may increase corneal toxicity.\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EWhy the other options are incorrect\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChlorhexidine 0.01%\u003C/b\u003E\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EThe therapeutic concentration used for Acanthamoeba keratitis is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.02%\u003C/b\u003E\u003C/span\u003E, not 0.01%.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPropamidine isethionate 0.01%\u003C/b\u003E\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EThe effective concentration is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E0.1%\u003C/b\u003E\u003C/span\u003E, not 0.01%.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EParomomycin 0.5%\u003C/b\u003E\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EActive against trophozoites but \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eineffective against cysts\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ETherefore, it should not be used as primary therapy.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearl\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPain out of proportion to signs \u002B contact lens wearer = think Acanthamoeba.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPerineural infiltrates = virtually pathognomonic.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPHMB 0.02% and chlorhexidine 0.02% are the key cysticidal agents.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1751,
    "Name": "Toxoplasma chorioretinitis",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhat is the most common mode of acquiring \u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EToxoplasma gondii\u003C/i\u003E\u003C/span\u003E infection?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EToxoplasma gondii\u003C/i\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E is a protozoan parasite and is the \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common cause of posterior uveitis worldwide\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EIt is estimated to infect up to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eone-third of the world\u2019s population\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EThe most common route of acquisition (~50% of cases) is:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIngestion of raw or undercooked meat\u003C/b\u003E\u003C/span\u003E containing tissue cysts.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EOther recognised routes of transmission include:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EIngestion of oocysts from cat faeces\u003C/li\u003E\u003Cli\u003EContaminated soil\u003C/li\u003E\u003Cli\u003EUnwashed fruits and vegetables\u003C/li\u003E\u003Cli\u003ETransplacental transmission during pregnancy\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003ECongenital toxoplasmosis may cause:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EChorioretinitis\u003C/li\u003E\u003Cli\u003ESeizures\u003C/li\u003E\u003Cli\u003EIntellectual disability\u003C/li\u003E\u003Cli\u003EVisual impairment\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EPregnant women should avoid:\u003Cul\u003E\u003Cli\u003EHandling cat litter\u003C/li\u003E\u003Cli\u003EConsuming raw or undercooked meat\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u003Cbr\u003E\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearl\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMost common cause of posterior uveitis worldwide \u2192 Toxoplasmosis\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMost common route of acquisition \u2192 Ingestion of undercooked meat\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EClassic ocular lesion \u2192 Focal retinochoroiditis adjacent to a pigmented scar (\u201Cheadlight in the fog\u201D)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 12,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1752,
    "Name": "Hyphaema",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA patient sustained blunt trauma to the eye 2 months ago and was diagnosed with a large traumatic hyphaema. Examination now demonstrates corneal blood staining. In which direction does the corneal opacity typically clear?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe clinical finding is \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal blood staining\u003C/b\u003E\u003C/span\u003E, a recognised complication of a large or prolonged hyphaema.\u003C/li\u003E\u003Cli\u003EResolution typically begins in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eperipheral cornea\u003C/b\u003E\u003C/span\u003E and progresses towards the centre; therefore, clearance occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecentripetally\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ECorneal blood staining develops when haemoglobin and its breakdown products pass through a compromised endothelium into the posterior corneal stroma.\u003C/li\u003E\u003Cli\u003EKeratocytes take up haemoglobin and convert it to \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehaemosiderin\u003C/b\u003E\u003C/span\u003E, which may cause keratocyte injury and prolonged loss of corneal transparency.\u003C/li\u003E\u003Cli\u003EImportant risk factors include:\u003Cul\u003E\u003Cli\u003ETotal or prolonged hyphaema\u003C/li\u003E\u003Cli\u003ERebleeding\u003C/li\u003E\u003Cli\u003ESustained raised intraocular pressure\u003C/li\u003E\u003Cli\u003EEndothelial dysfunction\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003ESecondary haemorrhage most commonly occurs \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E2-5 days after the initial injury\u003C/b\u003E\u003C/span\u003E and increases the likelihood of raised IOP and corneal blood staining.\u003C/li\u003E\u003Cli\u003EClearance may take months or years. In young children, prolonged corneal opacity may cause \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edeprivation amblyopia\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 13,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1753,
    "Name": "Corneal dystrophies - Lattice",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA patient presents to your clinic with\u0026nbsp;\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elattice corneal dystrophy\u003C/b\u003E\u003C/span\u003E. What is its pattern of inheritance?\u003C/p\u003E",
    "Explanation": "\u003Cdiv\u003E\u003Cimg src=\u0022https://upload.wikimedia.org/wikipedia/commons/b/bc/Lattice_corneal_dystrophy_type_1.JPEG\u0022\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe image demonstrates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elattice corneal dystrophy (LCD)\u003C/b\u003E\u003C/span\u003E, characterised by:\u003Cul\u003E\u003Cli\u003EGlass-like branching refractile lines\u003C/li\u003E\u003Cli\u003EStromal amyloid deposition\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EMost cases represent \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELattice Corneal Dystrophy Type I (LCD1)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ELCD1 is inherited in an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E manner.\u003C/li\u003E\u003Cli\u003EIt is caused by mutations in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETGFBI\u003C/b\u003E\u003C/span\u003E gene on chromosome \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5q31\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EMutant TGFBI protein undergoes abnormal folding, resulting in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eamyloid deposition\u003C/b\u003E\u003C/span\u003E within the corneal stroma.\u003C/li\u003E\u003Cli\u003EModern classification includes:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELCD Type I (classic form)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVariants (Types IIIA, IIIA, IV and polymorphic amyloidosis)\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThese variants are also caused by \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETGFBI mutations\u003C/b\u003E\u003C/span\u003E and are inherited as \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eautosomal dominant\u003C/b\u003E\u003C/span\u003E disorders, but typically present later in life than classic LCD1.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMeretoja syndrome\u003C/b\u003E\u003C/span\u003E\u0026nbsp;represents \u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Efamilial amyloidosis, Finnish type (gelsolin amyloidosis)\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E caused by mutations in the \u003C/span\u003E\u003Cspan class=\u0022s1\u0022 style=\u0022letter-spacing: 0.14994px;\u0022\u003E\u003Cb\u003Egelsolin (GSN) gene on chromosome 9q32\u201334\u003C/b\u003E\u003C/span\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EPatients develop lattice-like corneal changes together with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esystemic amyloidosis\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EClinical features of lattice corneal dystrophy:\u003Cul\u003E\u003Cli\u003EAmyloid deposits begin in the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esubepithelial region and anterior stroma\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EProgress posteriorly with time\u003C/li\u003E\u003Cli\u003EBegin centrally and spread \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecentrifugally\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003ERecurrent corneal erosions are common (particularly in LCD1 and type IIIA)\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EHistopathology:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECongo red positive\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EDemonstrates \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eapple-green birefringence\u003C/b\u003E\u003C/span\u003E under polarized light\u003C/li\u003E\u003Cli\u003EShows \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emetachromasia\u003C/b\u003E\u003C/span\u003E with crystal violet\u003C/li\u003E\u003Cli\u003EExhibits \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edichroism\u003C/b\u003E\u003C/span\u003E, alternating from red to green with a rotating polarizing filter\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EHigh-yield FRCOphth facts:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHighest recurrence after corneal transplantation among stromal dystrophies:\u003C/b\u003E\u003C/span\u003E Lattice \u0026gt; Granular \u0026gt; Macular\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EYoungest age at presentation among stromal dystrophies:\u003C/b\u003E\u003C/span\u003E Macular \u2192 Lattice \u2192 Granular\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1754,
    "Name": "Keratoconus",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhich of the following is the most common indication for penetrating keratoplasty (PKP)?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoconus\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E has traditionally been the \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Emost common indication for penetrating keratoplasty (PKP)\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EPatients with advanced keratoconus may require PKP when:\u003Cul\u003E\u003Cli\u003EContact lenses no longer provide adequate vision\u003C/li\u003E\u003Cli\u003ECorneal scarring develops\u003C/li\u003E\u003Cli\u003ECorneal thinning is too advanced for other treatments\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EKeratoconus has an excellent prognosis following PKP because:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EIt is a non-inflammatory disorder\u003C/li\u003E\u003Cli\u003ECorneal endothelium is typically healthy\u003C/li\u003E\u003Cli\u003EGraft survival rates are high\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EOther common indications for PKP include:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EFuchs endothelial dystrophy\u003C/li\u003E\u003Cli\u003EPseudophakic bullous keratopathy\u003C/li\u003E\u003Cli\u003ERepeat corneal transplantation\u003C/li\u003E\u003Cli\u003ECorneal scarring\u003C/li\u003E\u003Cli\u003EInfectious keratitis\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EFRCOphth Pearl:\u003C/b\u003E\u003C/span\u003E Modern practice has shifted toward \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Elamellar keratoplasty\u003C/b\u003E\u003C/span\u003E (especially DALK for keratoconus and endothelial keratoplasty [DMEK/DSAEK] for endothelial disease), reducing the frequency of PKP for many indications. However, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ehistorically and in FRCOphth examinations, keratoconus remains the classic answer as the most common indication for PKP.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1755,
    "Name": "Culture medium",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhich culture medium is most appropriate for isolation of fungi?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESabouraud\u2019s dextrose agar\u003C/b\u003E\u003C/span\u003E is the standard culture medium for the isolation of \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Efungi\u003C/b\u003E\u003C/span\u003E, including yeasts and filamentous fungi.\u003C/li\u003E\u003Cli\u003EIt has an acidic pH that inhibits bacterial growth and promotes fungal growth.\u003C/li\u003E\u003Cli\u003EOther commonly used microbiological media:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELowenstein\u2013Jensen medium\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EMycobacterium tuberculosis\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMiddlebrook agar\u003C/b\u003E\u003C/span\u003E \u2192 Non-tuberculous mycobacteria (e.g. post-LASIK keratitis)\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChocolate agar\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 Fastidious aerobic bacteria (e.g. \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EHaemophilus\u003C/i\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E, \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003ENeisseria\u003C/i\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E)\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlood agar\u003C/b\u003E\u003C/span\u003E \u2192 General-purpose medium for most aerobic bacteria\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThioglycollate broth\u003C/b\u003E\u003C/span\u003E \u2192 Enrichment medium, particularly useful for \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eanaerobic bacteria\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThayer\u2013Martin agar\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003ENeisseria\u003C/i\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E species\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENon-nutrient agar with an Escherichia coli overlay\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EAcanthamoeba\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Microbiology Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESabouraud\u2019s agar\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 Fungi\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBlood agar\u003C/b\u003E\u003C/span\u003E \u2192 Most aerobic bacteria\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChocolate agar\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EHaemophilus\u003C/i\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E and \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003ENeisseria\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThioglycollate broth\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 Anaerobes\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ELowenstein\u2013Jensen\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EMycobacterium tuberculosis\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EMiddlebrook agar\u003C/b\u003E\u003C/span\u003E \u2192 Non-tuberculous mycobacteria\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThayer\u2013Martin\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003ENeisseria gonorrhoeae\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENon-nutrient agar \u002B E. coli overlay\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Ci\u003EAcanthamoeba\u003C/i\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1756,
    "Name": "Keratoplasty",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EIn which clinical situation is \u003Cspan class=\u0022s1\u0022\u003Epenetrating keratoplasty (PKP) using a continuous (running) suture\u003C/span\u003E most appropriate?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe choice between \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Erunning and interrupted sutures\u003C/b\u003E\u003C/span\u003E depends on the underlying corneal pathology and the anticipated risk of postoperative complications.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERunning sutures\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E are most suitable for \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ekeratoconus\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E because:\u003C/span\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003EThe cornea is typically avascular and non-inflamed.\u003C/li\u003E\u003Cli\u003EWound healing is generally predictable.\u003C/li\u003E\u003Cli\u003EGraft survival is excellent.\u003C/li\u003E\u003Cli\u003EAstigmatism can be managed by selective adjustment or removal of the running suture.\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInterrupted sutures\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E are preferred in:\u003C/span\u003E\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EChildren\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EVascularized corneas\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInflamed corneas\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EThin or high-risk grafts\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EInterrupted sutures allow selective removal of individual sutures if:\u003Cul\u003E\u003Cli\u003ELocalized vascularization develops\u003C/li\u003E\u003Cli\u003EInfection occurs\u003C/li\u003E\u003Cli\u003EWound loosening is confined to one area\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EIf a running suture is used in a vascularized or inflamed graft, localized complications cannot be managed by removing only the affected portion of the suture.\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ERunning suture \u2192 Keratoconus (low-risk graft).\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInterrupted sutures \u2192 Children, vascularized corneas, inflamed corneas, high-risk grafts.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoconus has one of the longest graft survival rates following PKP.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1757,
    "Name": "Dry eye",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003E\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich tear production test measures \u003Cspan class=\u0022s1\u0022\u003Eonly basal tear secretion\u003C/span\u003E?\u003C/span\u003E\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ebasic secretion test\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E measures \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ebasal tear secretion only\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003ETechnique:\u003Cul\u003E\u003Cli\u003EInstil topical anaesthetic.\u003C/li\u003E\u003Cli\u003EBlot excess tears from the tear meniscus.\u003C/li\u003E\u003Cli\u003EPlace a standard Schirmer strip at the junction of the middle and lateral third of the lower eyelid.\u003C/li\u003E\u003Cli\u003EMeasure wetting after \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E5 minutes\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EInterpretation:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026lt;3 mm\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E = abnormal\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E3\u201310 mm\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E = equivocal\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EReduced values suggest \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eaqueous tear deficiency (ATD)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchirmer I test\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EPerformed \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ewithout topical anaesthesia\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EMeasures \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Eboth basal and reflex tear secretion\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026lt;5.5 mm at 5 minutes\u003C/b\u003E\u003C/span\u003E is considered abnormal.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchirmer II test\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EPerformed \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ewith topical anaesthesia\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EThe nasal mucosa is stimulated with a cotton-tipped applicator.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EMeasures \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ereflex tear secretion only\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026lt;15 mm at 2 minutes\u003C/b\u003E\u003C/span\u003E is considered abnormal.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPhenol red thread test\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EA newer alternative for assessing tear production.\u003C/li\u003E\u003Cli\u003EA phenol red-impregnated cotton thread is placed in the lower fornix.\u003C/li\u003E\u003Cli\u003EMeasures tear production over a short period by the length of colour change.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u0026lt;10 mm\u003C/b\u003E\u003C/span\u003E is considered abnormal and suggests dry eye.\u003C/li\u003E\u003Cli\u003EIt has not been directly compared with Schirmer testing in clinical trials.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBasic secretion test\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBasal tears only\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E (topical anaesthetic).\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchirmer I\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EBasal \u002B reflex tears\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E (no anaesthetic).\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESchirmer II\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E \u2192 \u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EReflex tears only\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E (anaesthetic \u002B nasal stimulation).\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1758,
    "Name": "Pentacam",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EDuring preoperative assessment for LASIK, which device is most suitable for identifying the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ethinnest point of the cornea\u003C/b\u003E\u003C/span\u003E?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EPentacam\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E is a \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EScheimpflug imaging system\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E that provides \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ethree-dimensional corneal tomography\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EIt scans the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eentire cornea\u003C/b\u003E\u003C/span\u003E, allowing accurate identification of:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ethinnest corneal point\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EAnterior and posterior corneal elevation\u003C/li\u003E\u003Cli\u003EPachymetry map\u003C/li\u003E\u003Cli\u003EAnterior chamber measurements\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EBecause it evaluates the entire corneal surface, it is superior to single-point pachymetry for pre-LASIK assessment.\u003C/li\u003E\u003Cli\u003EPentacam is particularly valuable for:\u003Cul\u003E\u003Cli\u003EDetecting early keratoconus\u003C/li\u003E\u003Cli\u003EIdentifying forme fruste keratoconus\u003C/li\u003E\u003Cli\u003EScreening for ectasia risk before refractive surgery\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EOptical pachymetry\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EMeasures corneal thickness at a limited location.\u003C/li\u003E\u003Cli\u003EIs largely obsolete in modern refractive practice.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EUltrasound pachymetry\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003EProvides accurate central corneal thickness measurements.\u003C/li\u003E\u003Cli\u003EHowever, it measures only the point where the probe is placed.\u003C/li\u003E\u003Cli\u003EMeasurements may be falsely high if the probe is not exactly perpendicular to the corneal surface.\u003C/li\u003E\u003Cli\u003EIt cannot reliably identify the thinnest point of the cornea.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorneal topography\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E:\u003C/span\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EMaps \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Ecorneal curvature\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E only.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EDoes \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot\u003C/b\u003E\u003C/span\u003E provide full pachymetric or posterior elevation data.\u003C/li\u003E\u003Cli\u003ETomography (Pentacam) is superior for refractive surgery screening.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETopography = curvature map.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ETomography (Pentacam) = curvature \u002B pachymetry \u002B anterior/posterior elevation \u002B thinnest point.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPentacam is the preferred imaging modality for pre-LASIK ectasia screening.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1759,
    "Name": "Cornea physiology",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhat is the normal water content of the cornea?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003EThe normal cornea contains approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E78% water\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EMaintaining this level of hydration is essential for preserving \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ecorneal transparency\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003ECorneal hydration is regulated by:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntact epithelial barrier\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EIntact endothelial barrier\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEndothelial Na\u207A/K\u207A-ATPase pump\u003C/b\u003E\u003C/span\u003E, which actively pumps fluid out of the corneal stroma into the anterior chamber\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EFailure of the endothelial pump or endothelial cell loss leads to:\u003Cul\u003E\u003Cli\u003EIncreased stromal hydration\u003C/li\u003E\u003Cli\u003ECorneal edema\u003C/li\u003E\u003Cli\u003ELoss of transparency\u003C/li\u003E\u003Cli\u003EReduced visual acuity\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ENormal corneal water content = 78%.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorneal transparency depends on relative stromal deturgescence.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EThe corneal endothelium does not regenerate\u003C/b\u003E\u003C/span\u003E; endothelial cell loss is compensated by enlargement and spreading of adjacent cells.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECritical endothelial cell density:\u003C/b\u003E\u003C/span\u003E approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E400\u2013700 cells/mm\u00B2\u003C/b\u003E\u003C/span\u003E, below which corneal decompensation is likely.\u003C/li\u003E\u003Cli\u003EThe \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eepithelium acts as a barrier to tear fluid\u003C/b\u003E\u003C/span\u003E, while the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eendothelium provides the metabolic pump\u003C/b\u003E\u003C/span\u003E responsible for maintaining corneal dehydration.\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1760,
    "Name": "Pellucid marginal degeneration",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EWhat is the classic corneal topography pattern seen in \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Epellucid marginal degeneration (PMD)\u003C/b\u003E\u003C/span\u003E?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPellucid marginal degeneration (PMD)\u003C/b\u003E\u003C/span\u003E is a bilateral ectatic corneal disorder.\u003C/li\u003E\u003Cli\u003EIt is characterised by:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EA \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003E1\u20132 mm band of inferior peripheral corneal thinning\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003ETypically extending from approximately \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E4 o\u2019clock to 8 o\u2019clock\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EUnlike keratoconus:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003EThe \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003Emaximal corneal protrusion occurs above the area of thinning\u003C/b\u003E\u003C/span\u003E\u003Cspan class=\u0022s1\u0022\u003E.\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EIn \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Ekeratoconus\u003C/b\u003E\u003C/span\u003E, the area of maximal protrusion corresponds to the area of maximal thinning.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThe classic topographic appearance of PMD is the \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003E\u201Ccrab-claw\u201D (or kissing doves) pattern\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EThis reflects the transition from:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAgainst-the-rule astigmatism superiorly\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003ETo \u003C/span\u003E\u003Cspan class=\u0022s2\u0022\u003E\u003Cb\u003EWith-the-rule astigmatism inferiorly\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EDifferentiating PMD from keratoconus may be difficult clinically.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ECorneal tomography (e.g. Pentacam)\u003C/b\u003E\u003C/span\u003E is particularly useful because it provides:\u003C/li\u003E\u003Cul\u003E\u003Cli\u003ECorneal topography\u003C/li\u003E\u003Cli\u003EPachymetry\u003C/li\u003E\u003Cli\u003ECorrelation between the location of thinning and maximal protrusion\u003C/li\u003E\u003C/ul\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003ECompared with keratoconus, PMD has:\u003Cul\u003E\u003Cli\u003ELess frequent corneal scarring\u003C/li\u003E\u003Cli\u003ELess frequent acute hydrops\u003C/li\u003E\u003Cli\u003ELess frequent Fleischer (iron) lines\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPMD \u2192 Crab-claw (kissing doves) topography.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoconus \u2192 Inferior steepening / asymmetric bow-tie pattern.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EPMD: protrusion above the thinning.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKeratoconus: protrusion at the site of thinning.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 6,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1761,
    "Name": "Dermoid - corneal",
    "Body": "\n\n\n\n\u003Cp class=\u0022p1\u0022\u003EA 3-year-old child has a congenital limbal lesion that has remained largely unchanged since birth. What is the correct statement regarding the most likely diagnosis?\u003C/p\u003E",
    "Explanation": "\n\n\n\n\u003Cdiv\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cimg src=\u0022https://www.pathologyoutlines.com/imgau/eyedermoidtumorCortes01.jpg\u0022\u003E\u003C/div\u003E\u003Cul\u003E\u003Cli\u003EThe lesion is an \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eepibulbar dermoid\u003C/b\u003E\u003C/span\u003E, a congenital choristoma.\u003C/li\u003E\u003Cli\u003ETypical features include:\u003Cul\u003E\u003Cli\u003EPresent at birth\u003C/li\u003E\u003Cli\u003ESlow-growing or stable over time\u003C/li\u003E\u003Cli\u003EUsually located at the limbus\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EEpibulbar dermoids are associated with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EGoldenhar syndrome (oculo-auriculo-vertebral spectrum)\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003EAssociated systemic abnormalities include:\u003Cul\u003E\u003Cli\u003EPreauricular skin tags\u003C/li\u003E\u003Cli\u003EDental abnormalities\u003C/li\u003E\u003Cli\u003ESkeletal abnormalities\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EVertebral anomalies include:\u003Cul\u003E\u003Cli\u003EButterfly vertebrae\u003C/li\u003E\u003Cli\u003EHemivertebrae\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThese vertebral abnormalities may result in:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EKyphosis\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003EScoliosis\u003C/li\u003E\u003Cli\u003ERib anomalies\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EEpibulbar dermoids most commonly occur \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Einferotemporally\u003C/b\u003E\u003C/span\u003E, \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Enot superotemporally\u003C/b\u003E\u003C/span\u003E.\u003C/li\u003E\u003Cli\u003E(Do not confuse them with \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Edermoid cysts\u003C/b\u003E\u003C/span\u003E, which are classically \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Esuperotemporal\u003C/b\u003E\u003C/span\u003E.)\u003C/li\u003E\u003Cli\u003EEpibulbar dermoids typically induce \u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003Eplus-cylinder astigmatism with the axis 90\u00B0 away from the lesion\u003C/b\u003E\u003C/span\u003E, which should be corrected early to reduce the risk of amblyopia.\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EComplete excision is generally not recommended\u003C/b\u003E\u003C/span\u003E, as the lesion may extend deeply into the cornea.\u003C/li\u003E\u003Cli\u003EIf visually significant or cosmetically concerning, management may include:\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EShave biopsy\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003ESuperficial lamellar keratectomy/dissection\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003EThese procedures may also reduce induced astigmatism.\u003C/li\u003E\u003C/ul\u003E\n\u003Ch3\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EHigh-Yield FRCOphth Pearls\u003C/b\u003E\u003C/span\u003E\u003C/h3\u003E\n\u003Cul\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EEpibulbar dermoid \u2192 Inferotemporal limbus.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EDermoid cyst \u2192 Superotemporal orbit.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAssociated syndrome \u2192 Goldenhar syndrome.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EInduces plus-cylinder astigmatism with axis 90\u00B0 away from the lesion.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003Cli\u003E\u003Cspan class=\u0022s1\u0022\u003E\u003Cb\u003EAvoid complete excision if deep corneal involvement is present.\u003C/b\u003E\u003C/span\u003E\u003C/li\u003E\u003C/ul\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003Cbr\u003E\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003EFurther Reading:\u003C/span\u003E\u003C/div\u003E\u003Cdiv\u003E\u003Ca href=\u0022https://www.pathologyoutlines.com/topic/eyedermoidtumor.html\u0022 target=\u0022_blank\u0022\u003EOcular dermoid\u003C/a\u003E\u003Cspan style=\u0022font-weight: 700;\u0022\u003E\u003C/span\u003E\u003C/div\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1762,
    "Name": "Megalocornea",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical feature is most characteristically associated with megalocornea?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EAnswer: carrier mothers have slightly enlarged corneal diameters\u003C/strong\u003E, because congenital megalocornea is classically an X-linked condition, so most affected individuals are male, while carrier mothers may show a milder phenotype with slightly enlarged corneal diameters; the condition is usually non-progressive, typically not associated with elevated intraocular pressure, and must be differentiated from primary congenital glaucoma, which presents with progressive corneal enlargement, corneal edema, photophobia, tearing, and high IOP. Megalocornea may be associated with anterior segment abnormalities such as lens subluxation, iris hypoplasia, radial iris transillumination defects, and ectopic pupil, but not iris hyperplasia; additionally, the anterior chamber is often very deep and the angle may sometimes be visible directly without gonioscopy, making the carrier-mother association the most accurate feature.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1763,
    "Name": "Spiral of Tillaux",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring scleral buckle surgery, which rectus muscle has the third closest insertion to the limbus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer:\u0026nbsp;\u003Cstrong style=\u0022letter-spacing: 0.14994px;\u0022\u003Elateral rectus\u003C/strong\u003E\u003C/span\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, because the rectus muscle insertions follow the \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003ESpiral of Tillaux\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, in which the insertions become progressively farther from the limbus in the order \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003Emedial rectus \u2192 inferior rectus \u2192 lateral rectus \u2192 superior rectus\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E; the commonly remembered distances are approximately \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E5.5 mm\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E for the medial rectus, \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E6.5 mm\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E for the inferior rectus, \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E6.9\u20137.0 mm\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E for the lateral rectus, and \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003E7.7 mm\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E for the superior rectus, so the lateral rectus is the third closest rectus insertion from the limbus. A useful mnemonic is \u003C/span\u003E\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003EM-I-L-S\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, and it is also important surgically to remember that the temporal ends of the vertical rectus insertions lie slightly more posterior than their nasal ends, which matters when isolating muscles during procedures such as scleral buckle placement.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1764,
    "Name": "Thyroid eye disease",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with thyroid eye disease who has proptosis, eyelid retraction, and diplopia, what is the proper sequence of surgery if multiple procedures are needed?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003E\u003Cspan style=\u0022font-size: medium;\u0022\u003EAnswer:\u003C/span\u003E\u0026nbsp;\u003Cstrong style=\u0022font-size: 14px; letter-spacing: 0.14994px;\u0022\u003Eorbital decompression, strabismus surgery, lid surgery\u003C/strong\u003E\u003Cspan style=\u0022font-size: 14px; font-weight: 400; letter-spacing: 0.14994px;\u0022\u003E, because thyroid eye disease surgery is performed in a staged sequence from posterior/deep orbital correction to anterior eyelid refinement: orbital decompression is done first because it changes globe position, orbital volume, extraocular muscle paths, and restriction patterns, so it can significantly alter the measured strabismus and diplopia; strabismus surgery is therefore delayed until after decompression and until the deviation has stabilized, because operating on the muscles before decompression may lead to an inaccurate or unstable alignment result; eyelid surgery is performed last because lid position is influenced by both globe position and ocular alignment, and upper eyelid retraction may improve, worsen, or become more asymmetric after decompression or vertical muscle surgery, so definitive lid recession/repair should wait until the orbit and strabismus have already been addressed.\u003C/span\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 9,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1765,
    "Name": "Unilateral congenital cataract",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA newborn is found to have a dense central congenital cataract in one eye, while the rest of the ocular examination is normal. By what age should surgery generally be performed to reduce the risk of deprivation amblyopia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ebefore 6 weeks of age\u003C/strong\u003E, because a dense central unilateral congenital cataract blocks the visual axis during the most critical period of visual development and produces severe deprivation amblyopia if not removed promptly; unilateral cataracts are especially urgent because the clear fellow eye creates strong interocular competition, causing the brain to suppress the blurred cataractous eye rapidly, so visually significant unilateral congenital cataracts are generally removed before 6 weeks of age. Bilateral visually significant congenital cataracts can usually be managed slightly later, often before 10 weeks of age, because both eyes are similarly deprived and there is less asymmetric competition, but in this case the cataract is unilateral, central, and relatively dense, making early surgery before 6 weeks the accepted timeframe.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1766,
    "Name": "Infantile esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-month-old infant has had a constant large-angle esotropia since early infancy, measures 50 prism diopters, has only mild hyperopia of \u002B1.00 OU, and alternates fixation without evidence of amblyopia. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESurgery to correct the large angle esotropia\u003C/strong\u003E, because this presentation is typical of infantile esotropia: onset within the first 6 months of life, a large comitant esodeviation, minimal hyperopia, and no primary neurologic or restrictive cause suggested by the vignette; the \u002B1.00 hyperopia is too small to explain a 50 prism-diopter deviation, so refractive accommodative esotropia is unlikely and spectacles will not correct the alignment, while prism correction is impractical for such a large angle and does not address the underlying motor misalignment. Alternate patching is only useful if there is fixation preference or amblyopia risk, but this child uses both eyes equally, so patching would not correct the esotropia. Observation until 2 years of age is inappropriate because large-angle infantile esotropia appearing between 2\u20136 months is unlikely to resolve spontaneously, and delaying alignment reduces the chance of developing binocular function. Early surgical alignment, often performed in infancy once the angle is stable, aims to bring the eyes as close to orthotropia as possible and maximize the possibility of sensory fusion and stereopsis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1767,
    "Name": "Estimated visual acuity of a newborn at birth",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the approximate Snellen-equivalent visual acuity expected in a healthy newborn immediately after birth?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E20/400\u003C/strong\u003E, because newborn visual acuity is limited by immaturity of both the retina and the visual pathways; at birth, the fovea is not fully developed, cone packing is much lower than in the adult fovea, the outer segments are immature, and cortical visual processing is still developing, so central visual resolution is poor despite an otherwise normal eye. Over the first months of life, visual acuity improves rapidly as the fovea elongates and specializes, cone density increases, photoreceptor alignment improves, and the retinocortical pathways mature; adult-like foveal cone density is approached around the end of the first year, which explains why newborn acuity is estimated around \u003Cstrong\u003E20/400\u003C/strong\u003E rather than better values such as \u003Cstrong\u003E20/100\u003C/strong\u003E or \u003Cstrong\u003E20/60\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1768,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAt what age does neonatal conjunctivitis caused by herpes simplex virus most typically present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E14 days\u003C/strong\u003E, because the timing of ophthalmia neonatorum helps narrow the likely cause: chemical conjunctivitis appears earliest, usually within the first 24 hours after prophylactic drops and resolves quickly; gonococcal conjunctivitis typically presents at 3\u20134 days of life with very heavy purulent discharge and is the most hyperacute bacterial form; chlamydial conjunctivitis usually appears around 7 days of life, although it may occur earlier if there was prolonged rupture of membranes; and HSV conjunctivitis is uncommon but classically presents later, around 2 weeks of life.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1769,
    "Name": "Brushfield spots",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child is found to have multiple pale hypopigmented iris spots on examination. Which statement correctly describes the systemic association of this iris finding?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-20-478dce03-4d74-468e-b563-2827425a3156.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EIt is associated with trisomy 21\u003C/strong\u003E, because the described multiple hypopigmented iris spots are \u003Cstrong\u003EBrushfield spots\u003C/strong\u003E, which are focal areas of iris stromal hyperplasia surrounded by relative stromal thinning or hypoplasia, giving a pale speckled appearance that is most easily appreciated in lightly pigmented irides; these lesions are benign and do not themselves impair vision, but they are a classic ocular sign of \u003Cstrong\u003EDown syndrome (trisomy 21)\u003C/strong\u003E and are found in a high proportion of affected individuals. The important distinction is that Brushfield spots are not Lisch nodules: Lisch nodules are melanocytic iris hamartomas associated with neurofibromatosis type 1, caf\u00E9-au-lait macules, and optic pathway gliomas; Brushfield spots also do not behave like the iris changes of Cogan\u2013Reese/ICE syndrome, which can cause corectopia and secondary glaucoma, and they are not the same as iris mammillations, which may be seen with oculodermal melanocytosis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1770,
    "Name": "Acute acquired Brown syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient develops acute diplopia with a limitation of elevation of the left eye in adduction, confirmed by positive forced ductions, and has a recent history suggestive of an upper respiratory or sinus illness. What is the most appropriate next step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECT of the orbits and paranasal sinuses\u003C/strong\u003E, because the motility pattern is highly suggestive of \u003Cstrong\u003Eacquired Brown syndrome\u003C/strong\u003E, in which elevation is mechanically restricted when the affected eye is adducted due to impaired passage or function of the superior oblique tendon through the trochlea; the positive forced duction test is crucial because it confirms a restrictive process rather than a neurogenic inferior oblique weakness. In this case, the acute onset raise concern for inflammatory or infectious involvement of the superior oblique tendon\u2013trochlear complex, particularly from adjacent sinus disease, so orbital and paranasal sinus CT is the appropriate next step to look for sinusitis, trochlear inflammation, orbital inflammatory disease, or another structural cause before committing to treatment. Local steroid injection may be useful in selected inflammatory trochleitis or acquired inflammatory Brown syndrome, but imaging should first define the anatomy and exclude sinus or orbital pathology; a superior oblique spacer is a surgical option for persistent or congenital/refractory Brown syndrome, not the immediate step in a new acute presentation; and botulinum toxin injection into the superior rectus does not address the primary mechanical restriction at the superior oblique tendon\u2013trochlea interface. A useful motility distinction is that Brown syndrome commonly produces a \u003Cstrong\u003EV-pattern\u003C/strong\u003E because elevation in adduction is restricted, whereas inferior oblique palsy is classically associated with an \u003Cstrong\u003EA-pattern\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1771,
    "Name": "Yoke muscles",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen a patient is asked to look upward and to the right during testing of cardinal gaze positions, which paired extraocular muscles act together as the yoke muscles for that direction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eright superior rectus and left inferior oblique\u003C/strong\u003E, because yoke muscles are the paired muscles, one in each eye, that receive equal innervational drive under \u003Cstrong\u003EHering\u2019s law\u003C/strong\u003E to move the eyes conjugately into a particular field of gaze. In up-and-right gaze, the \u003Cstrong\u003Eright eye is abducted and elevated\u003C/strong\u003E, and the superior rectus is the main elevator of an abducted eye, so the right superior rectus is the principal muscle in the right eye; at the same time, the \u003Cstrong\u003Eleft eye is adducted and elevated\u003C/strong\u003E, and the inferior oblique is the main elevator of an adducted eye, so the left inferior oblique is the paired yoke muscle. This distinction is clinically important in strabismus and palsy assessment because vertical recti act most strongly as elevators/depressors in abduction, whereas obliques act most strongly as elevators/depressors in adduction.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1772,
    "Name": "Periodic alternating nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with long-standing horizontal jerk nystagmus is observed to have the fast phase beating in one direction, but shortly afterward the fast phase has reversed to the opposite direction. In the likely diagnosis, what is the approximate time interval for this reversal?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E60-120 seconds\u003C/strong\u003E, because this vignette describes \u003Cstrong\u003Eperiodic alternating nystagmus (PAN)\u003C/strong\u003E, a horizontal jerk nystagmus in which the fast phase periodically reverses direction in a stereotyped cycle; classically, the nystagmus beats in one horizontal direction for roughly \u003Cstrong\u003E60\u201390 seconds\u003C/strong\u003E, then passes through a brief neutral or \u201Cnull\u201D interval of about \u003Cstrong\u003E10\u201320 seconds\u003C/strong\u003E, followed by resumption of jerk nystagmus in the opposite direction, so the observed switch from right-beating to left-beating nystagmus would most plausibly occur over about \u003Cstrong\u003E1\u20132 minutes\u003C/strong\u003E rather than many minutes. congenital PAN may be idiopathic or associated with sensory disorders such as oculocutaneous albinism, while acquired PAN should prompt consideration of lesions around the cervicomedullary junction or cerebellum, including Chiari malformation, demyelination, cerebellar degeneration, or posterior fossa pathology. The child may also show alternating head turns because the null point shifts as the fast phase reverses, so the abnormal head posture can appear to change over short observation periods.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1773,
    "Name": "Primary and secondary actions",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich paired actions correctly describe the main action of the inferior oblique muscle and the secondary action of the superior rectus muscle?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eextorsion and intorsion\u003C/strong\u003E, because the primary action of the oblique muscles in primary position is torsion, and the inferior oblique is an \u003Cstrong\u003Eextorter\u003C/strong\u003E of the globe, rotating the superior pole of the eye temporally; its secondary action is elevation, which is most effective when the eye is adducted, and its tertiary action is abduction. The superior rectus, by contrast, is primarily an elevator because it is a vertical rectus muscle, but because the rectus muscles run at an angle of approximately 23\u00B0 to the visual axis, the superior rectus also has torsional and horizontal components: its secondary action is \u003Cstrong\u003Eintorsion\u003C/strong\u003E, rotating the superior pole of the eye nasally, and its tertiary action is adduction.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1774,
    "Name": "Primary congenital glaucoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-month-old infant has chronic epiphora and blepharospasm with ocular findings suggestive of congenital glaucoma. Which ancillary investigation is most useful for following disease progression and response after treatment?\u0026nbsp;\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA-scan ultrasound\u003C/strong\u003E\u0026nbsp;is particularly valuable because it objectively measures axial length over time, and failure of axial length growth to stabilize after treatment suggests inadequate pressure control even when single IOP readings are affected by anesthesia, corneal thickness, or measurement variability. Corneal pachymetry can help interpret IOP because corneal edema or abnormal corneal thickness may distort tonometry, but pachymetry does not directly monitor globe enlargement or treatment success; magnetic resonance imaging is not the routine test for primary congenital glaucoma unless an alternative orbital or neurologic diagnosis is suspected; and visual evoked potentials assess visual pathway function rather than the structural pressure-related enlargement that defines progression in infantile glaucoma.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1775,
    "Name": "Posterior lenticonus cataract in children",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement accurately describes the typical clinical behavior of cataracts that develop in children with posterior lenticonus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThese cataracts are not present at birth\u003C/strong\u003E, because posterior lenticonus is a localized conical or globular outpouching of the posterior lens capsule caused by congenital thinning and weakness of the central posterior capsule, but the visually significant cataract usually develops \u003Cstrong\u003Eprogressively after birth\u003C/strong\u003E as the abnormal capsule stretches, the posterior cortex becomes increasingly disturbed, and the lenticonus may eventually opacify or even rupture; on retroillumination, posterior lenticonus may produce the classic \u003Cstrong\u003E\u201Coil droplet\u201D reflex\u003C/strong\u003E, and over time it may lead to a posterior polar/posterior subcapsular-type opacity with progressive visual loss and amblyopia risk. These cataracts are usually \u003Cstrong\u003Eunilateral\u003C/strong\u003E rather than bilateral and are not characteristically associated with microphthalmos or interocular size discrepancy. \u003Cstrong\u003EAlport syndrome is classically associated with anterior lenticonus\u003C/strong\u003E, not posterior lenticonus; anterior lenticonus occurs due to abnormal type IV collagen in the lens capsule and is associated with systemic features such as hereditary nephritis, hematuria, sensorineural hearing loss, and dot-and-fleck retinopathy.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1776,
    "Name": "Congenital motor nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with congenital motor nystagmus has a left-beating jerk nystagmus and adopts an abnormal head posture. What head position would be expected to reduce the nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eleft head turn\u003C/strong\u003E, because the direction of a jerk nystagmus is defined by its \u003Cstrong\u003Efast phase\u003C/strong\u003E, so a \u201Cleft jerk nystagmus\u201D means that the fast phase beats to the left; according to \u003Cstrong\u003EAlexander\u2019s law\u003C/strong\u003E, jerk nystagmus usually increases when gaze is directed toward the fast phase and decreases when gaze is directed away from the fast phase, so a left-beating nystagmus becomes more intense in left gaze and is dampened in right gaze. In congenital motor nystagmus, the child adopts an abnormal head posture to place the eyes in the \u003Cstrong\u003Enull zone\u003C/strong\u003E, the gaze position where nystagmus intensity is lowest and visual acuity is best; because this child\u2019s nystagmus dampens in \u003Cstrong\u003Eright gaze\u003C/strong\u003E, the child must turn the face/head to the \u003Cstrong\u003Eleft\u003C/strong\u003E to keep the eyes positioned to the right while still looking straight ahead at the target. This is why a left head turn is expected: the head turns opposite the preferred eye position, allowing the eyes to rest in the right-gaze null point, reducing foveation instability and improving functional vision.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1777,
    "Name": "Congenital iris ectropion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has a unilateral iris abnormality associated with markedly elevated intraocular pressure in the same eye. Which systemic feature may be associated with this ocular diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-21-6a4644f9-4f5d-4d9b-8dd3-5d9b172838af.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ecaf\u00E9 au lait spot\u003C/strong\u003E, because the described unilateral iris finding with ipsilateral glaucoma is most consistent with \u003Cstrong\u003Econgenital iris ectropion syndrome\u003C/strong\u003E, also called \u003Cstrong\u003Econgenital ectropion uveae\u003C/strong\u003E, although \u201Cuveae\u201D is technically a misnomer because the abnormal tissue visible on the anterior iris surface is posterior iris pigment epithelium rather than true uveal stroma. This condition is characterized by anterior extension of the iris pigment epithelium over the pupillary margin onto the anterior iris surface, often with a smooth cryptless iris, high iris insertion/anterior chamber angle dysgenesis, and secondary childhood glaucoma, as reflected by the high intraocular pressure in the affected eye. The key association is with \u003Cstrong\u003Eneurofibromatosis type 1\u003C/strong\u003E, in which cutaneous \u003Cstrong\u003Ecaf\u00E9 au lait spots\u003C/strong\u003E are common; congenital iris ectropion may occur as an isolated developmental anomaly but can also be seen with systemic associations such as NF1, facial hemihypertrophy, Rieger anomaly/anterior segment dysgenesis, and rarely other syndromic conditions. The other options point to different entities: \u003Cstrong\u003Eadenoma sebaceum\u003C/strong\u003E refers to facial angiofibromas of tuberous sclerosis, \u003Cstrong\u003ENevus of Ota\u003C/strong\u003E is linked to oculodermal melanocytosis and may be associated with iris mammillations and glaucoma but not this classic congenital iris ectropion pattern, and \u003Cstrong\u003Edilated cardiomyopathy\u003C/strong\u003E is associated with Alstr\u00F6m syndrome, which has cone-rod dystrophy as its major ocular manifestation rather than unilateral iris ectropion with childhood glaucoma.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1778,
    "Name": "Pediatric intermediate uveitis: systemic immunosuppressive",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a child with difficult-to-control intermediate uveitis requiring escalation to systemic immunosuppression, which listed drug is generally avoided because of its toxicity profile in children?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ecyclophosphamide\u003C/strong\u003E, because cyclophosphamide is an \u003Cstrong\u003Ealkylating cytotoxic immunosuppressive\u003C/strong\u003E that cross-links DNA and suppresses rapidly dividing immune cells, but in children its toxicity profile makes it generally discouraged except in exceptionally severe, sight-threatening, refractory uveitis where safer steroid-sparing agents have failed; the major concerns are \u003Cstrong\u003Ebone marrow suppression with infection risk, gonadal toxicity with future infertility, secondary malignancy risk, and hemorrhagic cystitis\u003C/strong\u003E due to the toxic metabolite acrolein. In pediatric noninfectious uveitis, treatment escalation usually favors agents with better long-term safety and monitoring profiles: \u003Cstrong\u003Emethotrexate\u003C/strong\u003E is commonly used as a first-line antimetabolite steroid-sparing agent, especially in JIA-associated uveitis, with adverse effects such as gastrointestinal upset, stomatitis, hepatotoxicity, and rarely pneumonitis; \u003Cstrong\u003Ecyclosporine\u003C/strong\u003E can be used in selected cases but is limited mainly by nephrotoxicity, hypertension, gingival hyperplasia, and gastrointestinal intolerance; and \u003Cstrong\u003Einfliximab\u003C/strong\u003E, an anti\u2013TNF-\u03B1 biologic, is an accepted option for refractory pediatric inflammatory eye disease, with infection/reactivation and infusion reactions being the key concerns. Therefore, among the listed drugs, the alkylating agent \u003Cstrong\u003Ecyclophosphamide\u003C/strong\u003E is the one generally avoided in children because the long-term systemic risks are disproportionate unless the ocular inflammatory disease is extraordinarily severe.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1779,
    "Name": "Neurofibromatosis type 2",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA teenager with bilateral sensorineural hearing loss and an intracranial meningioma is being evaluated for ocular manifestations of the underlying neurocutaneous syndrome. Which ocular findings are most likely?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eposterior subcapsular cataracts, wedge cortical cataracts, and retinal hamartomas\u003C/strong\u003E, because the combination of \u003Cstrong\u003Ebilateral sensorineural hearing loss\u003C/strong\u003E and \u003Cstrong\u003Eintracranial meningioma\u003C/strong\u003E strongly indicates \u003Cstrong\u003Eneurofibromatosis type 2\u003C/strong\u003E, an autosomal dominant tumor-predisposition syndrome caused by pathogenic variants in the \u003Cstrong\u003ENF2 gene on chromosome 22\u003C/strong\u003E, which encodes \u003Cstrong\u003Emerlin/schwannomin\u003C/strong\u003E, a tumor-suppressor protein. The hallmark systemic lesion is bilateral vestibular schwannoma, explaining the hearing loss and tinnitus, and affected patients may also develop meningiomas, ependymomas, and schwannomas of other cranial or spinal nerves. Ocularly, the most common manifestation of NF2 is \u003Cstrong\u003Eearly-onset cataract\u003C/strong\u003E, especially \u003Cstrong\u003Eposterior subcapsular cataract\u003C/strong\u003E, and \u003Cstrong\u003Ewedge-shaped cortical cataracts\u003C/strong\u003E are also classically described; these lens opacities may be subtle but are highly relevant because they can precede or accompany neurologic diagnosis. Retinal findings are less common but important and include \u003Cstrong\u003Eretinal hamartomas\u003C/strong\u003E, particularly combined hamartomas of the retina and retinal pigment epithelium, as well as epiretinal membranes and optic nerve sheath meningiomas. This differs from neurofibromatosis type 1, where the classic ocular signs are \u003Cstrong\u003ELisch nodules\u003C/strong\u003E and optic pathway gliomas with caf\u00E9-au-lait macules; optic nerve melanocytoma is not a typical NF2 hallmark, and neuroblastoma belongs to a different pediatric oncology context rather than the NF2 tumor spectrum.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1780,
    "Name": "Acquired fourth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a child with an acquired trochlear nerve palsy, which clinical test is used to measure the degree of torsional deviation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Edouble Maddox rod test\u003C/strong\u003E, because an acquired fourth nerve palsy commonly produces symptomatic \u003Cstrong\u003Eexcyclotorsion\u003C/strong\u003E from superior oblique weakness, and the double Maddox rod test is specifically designed to quantify subjective cyclodeviation in degrees by placing a Maddox rod before each eye, usually in a trial frame, so that the patient sees two streaks of light; the rods are then rotated until the two perceived lines become parallel, and the amount of rotation required reflects the magnitude and direction of torsion. This is particularly useful in acquired superior oblique palsy because patients have not had time to develop sensory adaptation and therefore often perceive torsional diplopia clearly, unlike many congenital fourth nerve palsies where long-standing adaptation may make subjective torsion less prominent despite objective fundus torsion. A single Maddox rod is mainly used to quantify horizontal or vertical deviations depending on rod orientation, but it does not accurately measure cyclodeviation; the red glass test helps assess diplopia, suppression, and sensory correspondence but is not the standard method for measuring torsion; and the Parks-Bielchowsky 3-step test is a diagnostic localization tool for identifying the paretic cyclovertical muscle in vertical strabismus, especially superior oblique palsy, but it does not quantify the amount of cyclotorsion.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1781,
    "Name": "Congenital nasolacrimal duct obstruction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 6-month-old infant has bilateral chronic clear tearing since early infancy, with\u0026nbsp;\u003Cspan style=\u0022color: rgb(66, 66, 66); letter-spacing: 0.14994px;\u0022\u003Ecorneal diameter of \u003C/span\u003E\u003Cspan style=\u0022font-weight: 700; color: rgb(66, 66, 66); letter-spacing: 0.14994px;\u0022\u003E10.0 mm\u003C/span\u003E, clear corneas, no photophobia, and an otherwise normal eye examination. What is the most appropriate initial treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECrigler massage\u003C/strong\u003E, because the presentation is most consistent with \u003Cstrong\u003Econgenital nasolacrimal duct obstruction (CNLDO)\u003C/strong\u003E rather than primary congenital glaucoma: the infant has chronic clear epiphora beginning in early infancy, but lacks the glaucoma warning signs of photophobia, blepharospasm severe enough to suggest corneal irritation, corneal edema, Haab striae, buphthalmos, or enlarged horizontal corneal diameter; a corneal diameter of \u003Cstrong\u003E10.0 mm\u003C/strong\u003E at 6 months is within the expected range, and clear corneas further argue against raised IOP as the cause of tearing. In CNLDO, the obstruction is most commonly a persistent membranous blockage at the distal nasolacrimal duct near the \u003Cstrong\u003Evalve of Hasner\u003C/strong\u003E, so first-line management in a 6-month-old is conservative treatment with \u003Cstrong\u003ECrigler massage\u003C/strong\u003E, in which firm downward pressure over the lacrimal sac increases hydrostatic pressure within the duct and may rupture the distal membrane while spontaneous maturation continues. A full ophthalmic examination is still essential in any tearing infant to exclude glaucoma and keratitis, and refraction is useful because some children with CNLDO may have associated anisometropia/amblyopia risk, but examination under anesthesia is not indicated when the office examination is reassuring; goniotomy is a treatment for primary congenital glaucoma, not uncomplicated CNLDO; and topical antibiotics may temporarily reduce secondary mucopurulent discharge if infection occurs but do not relieve the underlying mechanical obstruction, making \u003Cstrong\u003ECrigler massage\u003C/strong\u003E the best management here.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1782,
    "Name": "Delayed visual maturation in a healthy infant",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA healthy full-term 3-month-old infant has poor visual attention and does not fix or follow, but the ocular examination is otherwise normal. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eobserve closely\u003C/strong\u003E, because the combination of absent or poor fixation/tracking at around 3 months with an otherwise normal ocular examination is most consistent with \u003Cstrong\u003Edelayed visual maturation\u003C/strong\u003E, a diagnosis in which visual behavior is delayed despite no detectable structural ocular abnormality, normal media clarity, and no obvious retinal or optic nerve pathology; at this age, visual attention, fixation stability, pursuit, foveal function, and cortical visual processing are still maturing, and some otherwise healthy infants show a transient delay before developing normal visual responsiveness over the following weeks to months. Delayed visual maturation is a clinical diagnosis of exclusion: the examiner must first exclude important causes of poor visual behavior such as congenital cataract or media opacity, optic nerve hypoplasia, retinal dystrophy, severe refractive error, nystagmus-related sensory disease, and cerebral visual impairment; however, when the infant is healthy, full term, neurologically well, and the ocular examination is completely normal, immediate VEP, ERG, or MRI is not mandatory at 3 months. \u003Cstrong\u003EVEP\u003C/strong\u003E becomes useful if visual pathway dysfunction or cortical visual impairment remains a concern, \u003Cstrong\u003EERG\u003C/strong\u003E is appropriate if retinal dysfunction such as Leber congenital amaurosis, achromatopsia, or cone-rod disease is suspected, and \u003Cstrong\u003EMRI\u003C/strong\u003E is indicated when there are neurological abnormalities, developmental delay, seizures, abnormal head growth, optic nerve abnormalities, or persistent failure of visual development, but in this vignette the appropriate step is careful observation with close follow-up to ensure that fixation and tracking emerge as expected, especially as the infant approaches 6 months of age.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1783,
    "Name": "Sclerocornea",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is incorrect regarding the usual clinical and anatomic features of sclerocornea?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethe cornea is generally steeper than normal eyes\u003C/strong\u003E, because sclerocornea is a congenital anterior segment dysgenesis in which the cornea shows scleralization, loss of the normal limbal transition, and often absence of an obvious scleral sulcus, but the cornea is typically \u003Cstrong\u003Eflatter\u003C/strong\u003E than normal rather than steeper. The opacity in sclerocornea is classically more marked \u003Cstrong\u003Eperipherally\u003C/strong\u003E with relatively greater central clarity, which helps distinguish it from \u003Cstrong\u003EPeters anomaly\u003C/strong\u003E, where the opacity is usually central and associated with a posterior corneal defect, iridocorneal adhesions, or lenticulocorneal adhesions depending on severity. Sclerocornea may occur in isolation but is often associated with other ocular or systemic abnormalities, especially when bilateral or severe. It is also remembered as the \u003Cstrong\u003E\u201CS\u201D in STUMPED\u003C/strong\u003E, a mnemonic for congenital corneal opacity: \u003Cstrong\u003ESclerocornea\u003C/strong\u003E, \u003Cstrong\u003ETrauma/tears in Descemet\u2019s membrane\u003C/strong\u003E, \u003Cstrong\u003EUlcer\u003C/strong\u003E, \u003Cstrong\u003EMetabolic disorders\u003C/strong\u003E such as mucopolysaccharidoses including Hurler syndrome, \u003Cstrong\u003EPosterior corneal defect\u003C/strong\u003E such as Peters anomaly, \u003Cstrong\u003EEndothelial defect\u003C/strong\u003E such as congenital hereditary endothelial dystrophy, and \u003Cstrong\u003EDermoid\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1784,
    "Name": "violation of Sherrington\u2019s law",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with esotropia shows globe retraction and narrowing of the palpebral fissure when attempting adduction. Which ocular motor law is disrupted by this pattern of abnormal muscle activation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESherrington\u0027s law\u003C/strong\u003E, because the findings are classic for \u003Cstrong\u003EDuane retraction syndrome\u003C/strong\u003E, in which anomalous innervation of the lateral rectus, most commonly due to abnormal development of the abducens nucleus/nerve with aberrant oculomotor innervation, causes inappropriate \u003Cstrong\u003Eco-contraction of the medial rectus and lateral rectus\u003C/strong\u003E during attempted adduction; normally, under \u003Cstrong\u003ESherrington\u2019s law of reciprocal innervation\u003C/strong\u003E, contraction of an agonist muscle should be accompanied by relaxation of its antagonist, so when the medial rectus contracts to adduct the eye, the lateral rectus should relax, but in Duane syndrome both horizontal recti contract simultaneously, pulling the globe posteriorly into the orbit and producing \u003Cstrong\u003Eglobe retraction with palpebral fissure narrowing\u003C/strong\u003E. This is different from \u003Cstrong\u003EHering\u2019s law\u003C/strong\u003E, which concerns equal innervation to yoke muscles in the two eyes and is classically discussed in dissociated vertical deviation; \u003Cstrong\u003EDonder\u2019s law\u003C/strong\u003E and \u003Cstrong\u003EListing\u2019s law\u003C/strong\u003E relate to ocular orientation and torsion in different gaze positions rather than reciprocal agonist\u2013antagonist innervation.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1785,
    "Name": "Primary congenital glaucoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement accurately describes a typical epidemiologic or clinical feature of primary congenital glaucoma?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPCG is bilateral in approximately two-thirds of cases\u003C/strong\u003E, because primary congenital glaucoma is usually caused by developmental abnormality of the trabecular meshwork/anterior chamber angle leading to impaired aqueous outflow, raised intraocular pressure, and pressure-related enlargement of the infant eye; since the infantile sclera and cornea are distensible, affected children may develop epiphora, photophobia, blepharospasm, corneal edema, Haab striae, enlarged corneal diameter, buphthalmos, progressive myopia, and optic nerve cupping that may partially reverse after successful IOP control. Epidemiologically, PCG is more common in males than females, so equal sex distribution is incorrect; it is usually diagnosed during the first year of life rather than necessarily at birth, and cases diagnosed after early childhood are generally classified differently, often as juvenile open-angle glaucoma. Although PCG is potentially blinding if untreated, modern angle surgery such as goniotomy, trabeculotomy, or combined trabeculotomy-trabeculectomy has markedly improved prognosis, so blindness occurs in a much smaller proportion than 40-75%. A classic clinical fact is that PCG is \u003Cstrong\u003Ebilateral in about two-thirds of affected children\u003C/strong\u003E, although the severity may be asymmetric.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1786,
    "Name": "Inferior rectus resection",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAfter resecting the right inferior rectus muscle to treat a hypertropia, which postoperative lower eyelid position change may occur?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Elower lid elevation\u003C/strong\u003E, because the inferior rectus is intimately connected to the lower eyelid retractor system through fascial expansions, particularly the \u003Cstrong\u003Ecapsulopalpebral fascia\u003C/strong\u003E, which is the lower lid analogue of the levator aponeurosis and contributes to lower eyelid depression in downgaze; the inferior rectus muscle is also linked anatomically to \u003Cstrong\u003ELockwood\u2019s ligament\u003C/strong\u003E, the inferior conjunctival fornix suspensory system, and the lower eyelid retractors that insert into the inferior tarsal plate. When the inferior rectus is \u003Cstrong\u003Eresected\u003C/strong\u003E, the muscle is shortened and strengthened, increasing tension through this inferior rectus\u2013capsulopalpebral fascia\u2013lower lid retractor complex, so the lower lid can be pulled upward, producing \u003Cstrong\u003Elower lid elevation\u003C/strong\u003E and relative narrowing of the palpebral fissure. This is the opposite of what is seen after \u003Cstrong\u003Einferior rectus recession\u003C/strong\u003E, where posterior displacement and weakening of the inferior rectus can reduce retractor support and transmit downward/posterior traction that causes \u003Cstrong\u003Elower lid retraction\u003C/strong\u003E, scleral show, and widening of the palpebral fissure.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1787,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAt what postnatal age does neonatal conjunctivitis caused by Neisseria gonorrhoeae most typically present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E3-4 days of life\u003C/strong\u003E, because gonococcal ophthalmia neonatorum has a short incubation period after exposure to infected maternal genital secretions during delivery, so symptoms usually appear very early, classically around the third to fourth day of life; this timing helps distinguish it from chemical conjunctivitis, which begins within the first 24 hours after prophylactic drops and usually resolves quickly, chlamydial conjunctivitis, which more often presents around 5\u201314 days and is commonly remembered near 7 days, and HSV conjunctivitis, which is rare and tends to present later around 2 weeks. Neisseria gonorrhoeae is particularly important because it is a hyperacute, pyogenic, Gram-negative diplococcal infection capable of penetrating intact corneal epithelium, producing marked lid edema, chemosis, and copious purulent discharge, with risk of keratitis, corneal ulceration, perforation, endophthalmitis, and systemic dissemination if not treated urgently; therefore, suspected gonococcal neonatal conjunctivitis requires immediate conjunctival sampling/Gram stain and culture or NAAT where available, systemic third-generation cephalosporin therapy rather than topical treatment alone, saline irrigation to clear purulent debris, and evaluation/treatment of the mother and contacts.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1788,
    "Name": "Normal cup-to-disc ratio in newborns",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring evaluation of an infant suspected of having primary congenital glaucoma, what cup-to-disc ratio is generally expected in a normal newborn optic nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eless than 0.3\u003C/strong\u003E, because normal newborn optic discs usually have small physiologic cups, and a cup-to-disc ratio below approximately \u003Cstrong\u003E0.3\u003C/strong\u003E is considered the expected range in most normal infant eyes; in addition, interocular asymmetry is usually small, commonly less than about \u003Cstrong\u003E0.2\u003C/strong\u003E, so either a clearly enlarged cup or significant asymmetry between the two optic nerves should raise suspicion for pediatric glaucoma, especially when accompanied by corneal enlargement, Haab striae, corneal edema, photophobia, epiphora, or buphthalmos. The optic nerve in primary congenital glaucoma behaves differently from adult glaucomatous optic neuropathy because the infant sclera, lamina cribrosa, and optic nerve head tissues are more elastic; raised intraocular pressure can produce rapid cupping from posterior bowing and stretching of the lamina rather than purely irreversible neuroretinal rim loss, which is why \u003Cstrong\u003Ereversal of cupping\u003C/strong\u003E may occur after successful surgical IOP lowering.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1789,
    "Name": "Botulinum toxin in strabismus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed strabismus condition is least likely to benefit from botulinum toxin chemodenervation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Edissociated vertical deviation\u003C/strong\u003E, because botulinum toxin is most useful when a deviation is produced by an identifiable muscle imbalance that can be improved by temporarily weakening a specific extraocular muscle, whereas dissociated vertical deviation is a complex supranuclear dissociated ocular motor phenomenon rather than a simple paretic, restrictive, or single-muscle overaction problem. In dissociated vertical deviation, one eye drifts upward when fusion is interrupted, often with associated excyclotorsion and abduction, and the deviation is characteristically variable, latent/intermittent, frequently bilateral but asymmetric, and commonly associated with early-onset strabismus, latent nystagmus, suppression, and abnormal binocular development; because the mechanism is disordered binocular control rather than tonic overaction of one predictable muscle, chemodenervation gives unreliable and often transient results and may create unwanted hypotropia, incomitance, ptosis, or vertical imbalance without treating the underlying dissociated drive. By contrast, botulinum toxin can be useful in selected cases of \u003Cstrong\u003Esmall angle esotropia\u003C/strong\u003E by weakening the medial rectus and reducing the manifest deviation, in \u003Cstrong\u003Eacute paralytic strabismus\u003C/strong\u003E by weakening the antagonist muscle while nerve recovery occurs and helping prevent secondary contracture, and in \u003Cstrong\u003Eactive thyroid eye disease\u003C/strong\u003E when measurements are unstable and definitive surgery should be deferred but temporary reduction of diplopia or deviation is desired.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1790,
    "Name": "Crouzon syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with proptosis and craniofacial features suggestive of a craniosynostosis syndrome is being evaluated. Which gene is classically mutated in the most likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-23-d017b572-cce1-4927-bf86-d00db7812e6a.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFGFR2\u003C/strong\u003E, because the clinical appearance with marked proptosis in the setting of a craniosynostosis phenotype is most consistent with \u003Cstrong\u003ECrouzon syndrome\u003C/strong\u003E, an autosomal dominant craniosynostosis disorder caused by pathogenic variants in \u003Cstrong\u003EFGFR2\u003C/strong\u003E, the fibroblast growth factor receptor 2 gene on chromosome 10; abnormal FGFR signaling promotes premature fusion of cranial sutures, producing cranial vault restriction, midface hypoplasia, shallow orbits, relative exorbitism/proptosis, exposure keratopathy risk, and sometimes optic nerve compromise from raised intracranial pressure or optic canal crowding. The key differentiating point is that \u003Cstrong\u003ECrouzon syndrome typically lacks syndactyly or brachydactyly\u003C/strong\u003E, whereas Apert syndrome shares FGFR2 involvement but is distinguished by severe syndactyly of the hands and feet. \u003Cstrong\u003ETWIST\u003C/strong\u003E is associated with Saethre\u2013Chotzen syndrome, another craniosynostosis syndrome that is usually milder and may include ptosis, facial asymmetry, low frontal hairline, and limb anomalies; \u003Cstrong\u003EMYOC\u003C/strong\u003E is associated with juvenile-onset open-angle glaucoma and some primary open-angle glaucoma cases; and \u003Cstrong\u003EOPTN\u003C/strong\u003E is associated with normal-tension glaucoma.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1791,
    "Name": "CHED versus CHSD",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a child with bilateral congenital corneal opacity, which clinical finding most strongly supports congenital hereditary endothelial dystrophy rather than congenital hereditary stromal dystrophy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Epresence of epithelial edema\u003C/strong\u003E, because the key pathophysiologic distinction is that \u003Cstrong\u003ECHED is an endothelial pump failure disorder\u003C/strong\u003E, whereas \u003Cstrong\u003ECHSD is a stromal structural dystrophy without true corneal edema\u003C/strong\u003E; in CHED, dysfunctional corneal endothelium cannot adequately maintain stromal deturgescence, so fluid accumulates first in the stroma and, when sufficiently severe, extends anteriorly to produce \u003Cstrong\u003Eepithelial edema\u003C/strong\u003E, giving diffuse \u201Cground-glass\u201D corneal haze that may cause photophobia, tearing, amblyopia risk, and sometimes nystagmus if vision is significantly degraded early. In contrast, CHSD causes bilateral, flaky or feathery stromal opacities due to abnormal stromal collagen/keratocyte-related changes, but the epithelium is not edematous because endothelial pump function is preserved.\u003C/p\u003E\u003Cp\u003EIncreased horizontal corneal diameters and increased intraocular pressure would instead raise concern for \u003Cstrong\u003Eprimary congenital glaucoma\u003C/strong\u003E, not CHED or CHSD, because both CHED and CHSD typically have normal IOP and normal corneal diameter; absence of nystagmus is not a reliable differentiator, since nystagmus depends on severity and timing of visual deprivation rather than being specific to either diagnosis. This question also sits within the broader differential of congenital corneal opacity remembered by \u003Cstrong\u003ESTUMPED\u003C/strong\u003E: \u003Cstrong\u003ESclerocornea\u003C/strong\u003E, \u003Cstrong\u003ETrauma/tears in Descemet\u2019s membrane\u003C/strong\u003E, \u003Cstrong\u003EUlcer\u003C/strong\u003E, \u003Cstrong\u003EMetabolic disorders\u003C/strong\u003E such as mucopolysaccharidoses, \u003Cstrong\u003EPeters anomaly/posterior corneal defect\u003C/strong\u003E, \u003Cstrong\u003EEndothelial defect\u003C/strong\u003E such as CHED, and \u003Cstrong\u003EDermoid\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1792,
    "Name": "Thyroid eye disease with new diplopia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with new-onset binocular diplopia, upper eyelid retraction, right hypotropia, and marked restriction of elevation of the right eye is likely to have thyroid eye disease. What is the most appropriate management at this stage?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eobservation\u003C/strong\u003E, because the motility pattern are most consistent with \u003Cstrong\u003Ethyroid eye disease causing restrictive strabismus\u003C/strong\u003E, especially involvement of the \u003Cstrong\u003Einferior rectus\u003C/strong\u003E, which is the most commonly affected extraocular muscle and produces hypotropia with limited elevation of the affected eye; however, the diplopia is new and has been present for only a few weeks, so this is likely the \u003Cstrong\u003Eactive/inflammatory phase\u003C/strong\u003E, during which extraocular muscle enlargement, edema, glycosaminoglycan deposition, and evolving fibrosis can cause rapidly changing ocular alignment. Definitive strabismus surgery should not be performed until the disease is inactive and the deviation has been stable, classically for at least \u003Cstrong\u003E6 months\u003C/strong\u003E, because operating during active thyroid eye disease risks an unpredictable result as muscle restriction and globe position may continue to change.  The staged surgical order is also important: \u003Cstrong\u003Eorbital decompression first\u003C/strong\u003E if significant proptosis or optic neuropathy requires it, then \u003Cstrong\u003Estrabismus surgery\u003C/strong\u003E for persistent diplopia after stabilization, and finally \u003Cstrong\u003Eeyelid surgery\u003C/strong\u003E, because decompression can change motility and strabismus surgery can alter eyelid position.  A large right inferior rectus recession may eventually be appropriate if a stable restrictive right hypotropia persists, but not at this acute time point; superior rectus resection would be inappropriate because the limitation is restrictive rather than due to isolated superior rectus weakness, and strengthening the superior rectus against a tight inferior rectus can worsen restriction or induce poor motility; a Knapp procedure is used for double elevator palsy/supranuclear or monocular elevation deficiency patterns, not typical thyroid-related inferior rectus restriction, making \u003Cstrong\u003Eobservation\u003C/strong\u003E with medical/endocrine assessment, symptomatic diplopia management, and follow-up until stability the best answer now.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1793,
    "Name": "Alport syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich inheritance pattern accounts for the majority of Alport syndrome cases?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EX-linked recessive\u003C/strong\u003E, because Alport syndrome is a hereditary type IV collagen disorder affecting basement membranes in the \u003Cstrong\u003Eglomerulus, cochlea, lens capsule, cornea, and retina\u003C/strong\u003E, producing the classic systemic triad of progressive nephropathy with persistent hematuria, sensorineural hearing loss, and ocular abnormalities; the most common form is \u003Cstrong\u003EX-linked Alport syndrome\u003C/strong\u003E, caused by pathogenic variants in \u003Cstrong\u003ECOL4A5\u003C/strong\u003E on the X chromosome, and it accounts for the great majority of cases, classically around \u003Cstrong\u003E80\u201385%\u003C/strong\u003E, while autosomal recessive and autosomal dominant forms are due to \u003Cstrong\u003ECOL4A3\u003C/strong\u003E or \u003Cstrong\u003ECOL4A4\u003C/strong\u003E variants and are less common. The ocular phenotype reflects abnormal type IV collagen in ocular basement membranes: the lens is usually normal at birth, but affected patients\u2014especially males with X-linked disease\u2014may later develop anterior lenticonus with an \u201Coil droplet\u201D reflex, anterior polar/subcapsular lens opacities, recurrent corneal erosions, posterior polymorphous corneal dystrophy, and the characteristic dot-and-fleck retinopathy, which is often asymptomatic visually but is diagnostically helpful; anterior lenticonus is particularly high-yield because it is strongly associated with Alport syndrome and is usually acquired rather than congenital.  The inheritance matters clinically because males with X-linked disease are typically more severely affected, with earlier renal disease and higher penetrance of hearing loss, whereas heterozygous females may have milder or more variable manifestations due to X-inactivation; autosomal recessive disease can also be severe in both sexes, while autosomal dominant Alport spectrum disease is generally rarer and often milder.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1794,
    "Name": "Visual acuity assessment in a 1-year-old infant",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed method is not appropriate for estimating visual acuity in a 1-year-old preverbal infant?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAllen cards\u003C/strong\u003E, because a 1-year-old infant is usually preverbal and cannot reliably name or identify picture optotypes, so Allen picture cards are generally more appropriate for older toddlers and preschool children who can recognize, match, or verbalize familiar pictures; in a 1-year-old, visual acuity assessment relies on developmentally appropriate behavioral or objective methods, including \u003Cstrong\u003Efixation behavior\u003C/strong\u003E (central, steady, maintained fixation; fixation preference; ability to fix and follow), \u003Cstrong\u003Epreferential looking\u003C/strong\u003E techniques such as Teller acuity cards/Cardiff cards that exploit an infant\u2019s tendency to look toward a patterned grating or picture target rather than a blank field, and \u003Cstrong\u003EVEP\u003C/strong\u003E, especially sweep VEP, which estimates visual pathway resolution by recording cortical responses to alternating or progressively changing visual stimuli. The key distinction is between \u003Cstrong\u003Erecognition acuity\u003C/strong\u003E and \u003Cstrong\u003Eresolution/behavioral acuity\u003C/strong\u003E: Allen cards require recognition and cooperation, so they are not suitable for most 1-year-olds, whereas preferential looking and VEP estimate acuity without requiring verbal identification; fixation behavior is less quantitative but remains clinically useful for detecting gross asymmetry, severe visual impairment, or amblyopia risk in preverbal children.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1795,
    "Name": "Marcus Gunn jaw-winking syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has eyelid movement (up and down) that occurs synchronously with chewing or jaw movement. Which cranial nerves are involved in this synkinetic syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECN III and CN V\u003C/strong\u003E, because the described phenomenon is \u003Cstrong\u003EMarcus Gunn jaw-winking syndrome\u003C/strong\u003E, also known as \u003Cstrong\u003Econgenital trigemino-oculomotor synkinesis\u003C/strong\u003E, in which abnormal congenital neural connections link the motor division of the trigeminal nerve to the oculomotor innervation of the upper eyelid. The eyelid elevation occurs because the \u003Cstrong\u003Elevator palpebrae superioris\u003C/strong\u003E, normally supplied by the superior division of \u003Cstrong\u003ECN III\u003C/strong\u003E, receives aberrant activation during jaw movements mediated by the mandibular division of \u003Cstrong\u003ECN V\u003C/strong\u003E, especially movements involving the pterygoid muscles during chewing, mouth opening, jaw protrusion, or lateral jaw movement. The key concept is that this is not a facial nerve disorder and not a primary orbicularis phenomenon; the abnormal movement is due to synkinetic activation of the \u003Cstrong\u003Elevator\u003C/strong\u003E, producing elevation of a usually ptotic upper lid during trigeminal motor activity. The exact jaw movement that triggers the wink can vary depending on which trigeminal motor branch is aberrantly linked: eyelid elevation with mouth opening, jaw protrusion, or contralateral jaw movement is classically attributed to aberrant connections involving the \u003Cstrong\u003Eexternal/lateral pterygoid\u003C/strong\u003E, whereas eyelid elevation with mouth closure may reflect linkage involving the \u003Cstrong\u003Einternal/medial pterygoid\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1796,
    "Name": "Strabismus surgery after scleral buckle",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA high myopic patient develops restrictive diplopia after scleral buckle surgery, and recession of the restricted right medial rectus is planned. What is the safest and most appropriate surgical approach?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Emedial rectus recession via \u0022hang back\u0022 technique\u003C/strong\u003E, because strabismus surgery after scleral buckle repair is technically challenging: the buckle may distort normal anatomy, produce scarring around the rectus muscles, restrict muscle excursion, and make posterior scleral passes hazardous, especially in a \u003Cstrong\u003Ehigh myope\u003C/strong\u003E whose sclera is already thin and more prone to perforation. A standard recession requiring posterior scleral fixation at the new insertion site may be difficult or dangerous because the buckle and surrounding scar tissue can obstruct access, and a deep posterior needle pass risks scleral perforation, retinal injury, or damage near the previous retinal detachment repair. In a \u003Cstrong\u003Ehang-back recession\u003C/strong\u003E, the medial rectus is disinserted and reattached using sutures placed at or near the original insertion, allowing the muscle to \u201Chang back\u201D to the intended recessed position without requiring a posterior scleral pass; this makes the technique particularly useful when the sclera is thin, when posterior exposure is limited, or when a scleral buckle lies near the desired reattachment site. Removing the scleral buckle is generally avoided unless absolutely necessary because it may risk recurrent retinal detachment; displacing the medial rectus superiorly could create unwanted vertical/torsional incomitance and does not address the main safety issue; and attaching the muscle directly to the buckle is not physiologic and may worsen restriction or produce unpredictable alignment.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1797,
    "Name": "Weill-Marchesani syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 13-year-old child presents to your clinic for a routine eye exam. On exam, you note somewhat small crystalline lenses and a cycloplegic refraction of -9.00 OU. His intraocular pressures (IOPs) are 15 mmHg OU. His pediatrician notes states that he is at the 2nd percentile for height and that he has \u0022stubby fingers and toes.\u0022 Besides dispensing glasses, which of the following is generally recommended for patients with this disorder?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Elaser peripheral iridotomies\u003C/strong\u003E, because the constellation of \u003Cstrong\u003Eshort stature\u003C/strong\u003E, \u003Cstrong\u003Ebrachydactyly/stubby fingers and toes\u003C/strong\u003E, \u003Cstrong\u003Ehigh myopia\u003C/strong\u003E, and \u003Cstrong\u003Esmall spherical crystalline lenses\u003C/strong\u003E is classic for \u003Cstrong\u003EWeill-Marchesani syndrome\u003C/strong\u003E, a connective tissue disorder associated with \u003Cstrong\u003Emicrospherophakia\u003C/strong\u003E, ectopia lentis, joint stiffness, and sometimes cardiac abnormalities; the key ophthalmic danger is that the small, thick, round lens can move anteriorly and crowd the anterior chamber angle, predisposing to \u003Cstrong\u003Epupillary block angle-closure glaucoma\u003C/strong\u003E even when the intraocular pressure is normal at presentation. In microspherophakia, the lens equator is reduced and the anteroposterior lens diameter is increased, so the lens-iris diaphragm may sit more anteriorly, blocking aqueous flow from posterior to anterior chamber and causing iris bombe with acute or intermittent angle closure; therefore, \u003Cstrong\u003Eprophylactic laser peripheral iridotomy\u003C/strong\u003E is generally recommended to create an alternative pathway for aqueous flow and reduce the risk of pupillary block. \u003Cstrong\u003EIntermittent cycloplegic use\u003C/strong\u003E may be useful during an actual pupillary block attack because cycloplegia can relax the ciliary body-zonular configuration and allow the lens to move posteriorly, but it is not the main prophylactic recommendation; \u003Cstrong\u003Epilocarpine\u003C/strong\u003E may worsen the situation by moving the lens-iris diaphragm forward and increasing pupillary block risk in microspherophakia; and \u003Cstrong\u003Elensectomy\u003C/strong\u003E may be required if there is uncontrolled glaucoma, severe lens subluxation, cataract, or persistent angle closure despite iridotomy, but it is not the routine first preventive step in an asymptomatic child with normal IOP.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1798,
    "Name": "Pediatric sarcoidosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA young child has granulomatous anterior uveitis with mutton-fat keratic precipitates and a markedly elevated ACE level, suggesting pediatric sarcoidosis. Compared with adult sarcoidosis, which clinical feature is true in young children?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethe incidence of lung involvement is much less frequent as compared to adults\u003C/strong\u003E, because the large greasy \u003Cstrong\u003Emutton-fat keratic precipitates\u003C/strong\u003E, indicating granulomatous uveitis, and the very elevated ACE level supports sarcoidosis, although ACE must be interpreted cautiously in children because baseline ACE levels can be higher than in adults; pediatric sarcoidosis has an age-dependent phenotype, and in \u003Cstrong\u003Eearly-onset disease under about 5 years\u003C/strong\u003E, the typical presentation is not the adult pattern of bilateral hilar lymphadenopathy and pulmonary parenchymal disease, but rather the triad of \u003Cstrong\u003Euveitis, arthritis, and skin rash\u003C/strong\u003E, corresponding to the same clinicogenetic spectrum as early-onset sarcoidosis/Blau syndrome, whereas older children more closely resemble adults with pulmonary and lymph node involvement.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1799,
    "Name": "Iris mammillations",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has unilateral, diffuse, smooth iris surface nodules that are the same color as the surrounding iris, with no corneal abnormality. Which associated condition should be considered?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-24-4b8ca8ce-ba31-4989-811e-51db088774b8.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eoculodermal melanocytosis\u003C/strong\u003E, because the slit-lamp finding is most consistent with \u003Cstrong\u003Eiris mammillations\u003C/strong\u003E, which are numerous, smooth, regularly distributed, dome-shaped elevations of the anterior iris surface that usually have the \u003Cstrong\u003Esame pigmentation as the surrounding iris\u003C/strong\u003E, unlike Lisch nodules, which are typically lighter or darker than the background iris and more discrete. Iris mammillations are often unilateral, are more noticeable in darker irides, and may be associated with \u003Cstrong\u003Eoculodermal melanocytosis / nevus of Ota\u003C/strong\u003E, a congenital melanocytic condition involving increased melanocytes in ocular and periocular tissues; this association matters clinically because oculodermal melanocytosis can increase the risk of \u003Cstrong\u003Euveal melanoma\u003C/strong\u003E and secondary glaucoma, so careful lifelong surveillance of the iris, angle, choroid, and intraocular pressure is appropriate. \u003Cstrong\u003ESpontaneous hyphema\u003C/strong\u003E is classically associated with juvenile xanthogranuloma, where fragile iris lesions may bleed; \u003Cstrong\u003Ecorectopia\u003C/strong\u003E points toward Cogan-Reese syndrome within the ICE spectrum, but ICE usually occurs in adults and is associated with abnormal corneal endothelium, which this question specifically excludes; and \u003Cstrong\u003Esphenoid dysplasia\u003C/strong\u003E is a diagnostic feature of neurofibromatosis type 1, where the characteristic iris lesions are Lisch nodules rather than same-colored diffuse mammillations.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1800,
    "Name": "Blau syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child has granulomatous anterior uveitis with band keratopathy, multifocal choroiditis, polyarthritis, recurrent rash, and a family history of a similar blinding inflammatory disorder. What is the most accurate diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-24-8639013f-f437-48cf-bad9-a89b42436a4e.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBlau syndrome\u003C/strong\u003E, because the combination of \u003Cstrong\u003Egranulomatous uveitis\u003C/strong\u003E with mutton-fat keratic precipitates, \u003Cstrong\u003Eband keratopathy\u003C/strong\u003E, \u003Cstrong\u003Emultifocal choroiditis\u003C/strong\u003E, \u003Cstrong\u003Epolyarthritis\u003C/strong\u003E, recurrent rash, and an apparent familial pattern is highly characteristic of \u003Cstrong\u003EBlau syndrome\u003C/strong\u003E, also called \u003Cstrong\u003Efamilial juvenile systemic granulomatosis\u003C/strong\u003E or \u003Cstrong\u003EJabs syndrome\u003C/strong\u003E; Blau syndrome is a rare monogenic autoinflammatory disease that classically presents in childhood with the triad of \u003Cstrong\u003Egranulomatous dermatitis, arthritis, and uveitis\u003C/strong\u003E, and it is usually inherited in an \u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E pattern due to gain-of-function mutations in \u003Cstrong\u003ENOD2/CARD15 on chromosome 16q12\u003C/strong\u003E, leading to dysregulated innate immune activation and granulomatous inflammation. The retinal photographs showing multifocal chorioretinal inflammatory lesions are a major clue against ordinary JIA: JIA-associated uveitis is typically a chronic \u003Cstrong\u003Enongranulomatous anterior uveitis\u003C/strong\u003E, often ANA-positive and usually without multifocal choroiditis, whereas Blau syndrome can cause severe granulomatous panuveitis/posterior segment disease with choroiditis, cystoid macular edema, optic nerve involvement, neovascular complications, cataract, glaucoma, and poor visual prognosis despite aggressive immunosuppression.  Psoriatic arthritis may be associated with uveitis but does not explain this familial granulomatous arthritis-dermatitis-uveitis syndrome with multifocal choroiditis, and Heerfordt-Waldenstr\u00F6m syndrome is a sarcoid variant characterized by uveitis, parotid enlargement, fever, and facial nerve palsy rather than childhood familial granulomatous rash, arthritis, and sight-threatening chorioretinal disease.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1801,
    "Name": "Prism stacking in strabismus measurement",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen measuring a large strabismic deviation with prisms, which prism placement method gives an inaccurate measurement and should not be used?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eplacing two base-down prisms together in front of the same eye\u003C/strong\u003E, because stacking two prisms of the \u003Cstrong\u003Esame orientation and same meridian\u003C/strong\u003E in front of one eye does not produce a simple arithmetic addition of prism power and can introduce significant optical error due to prism nonlinearity, induced image distortion, and altered effective prism power when light passes through sequential prisms; therefore, two vertical prisms such as two base-down prisms should not be stacked over the same eye to measure a vertical deviation. It is acceptable to combine \u003Cstrong\u003Eone horizontal prism and one vertical prism\u003C/strong\u003E in front of the same eye, such as base-out with base-up or base-out with base-down, because the prisms are acting in different meridians and are being used to neutralize horizontal and vertical components separately. For very large deviations, the better approach is to \u003Cstrong\u003Esplit prisms between the two eyes\u003C/strong\u003E in the same corrective direction relative to the deviation, such as using base-out prism before both eyes for a large esotropia, because this reduces optical distortion and avoids the error created by stacking same-axis prisms in front of one eye.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1802,
    "Name": "Dissociated vertical deviation",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child treated surgically for infantile esotropia later shows slow upward and outward drift of the covered eye, without a matching downward movement of the fellow eye. What ocular motor disorder does this represent, and which law does it violate?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Edissociated vertical deviation, which disobeys Hering\u0027s law\u003C/strong\u003E, because the child shows the classic behavior of \u003Cstrong\u003Edissociated vertical deviation (DVD)\u003C/strong\u003E: when one eye is occluded, that eye slowly drifts upward, often with an extorsional and abducting component, and when the occluder is removed the eye slowly moves back down to refixate; the key diagnostic point is that this vertical movement is \u003Cstrong\u003Edissociated\u003C/strong\u003E, meaning it is not obeying the normal yoked movement pattern expected between the two eyes. Under \u003Cstrong\u003EHering\u2019s law of equal innervation\u003C/strong\u003E, paired yoke muscles in the two eyes should receive equal and simultaneous neural drive, so if one eye truly moved downward as part of a conjugate vertical movement, the fellow eye should show an equal corresponding upward or downward movement depending on the direction of gaze; in DVD, however, the covered eye drifts upward without the fellow eye making the expected conjugate downward movement, so the phenomenon violates \u003Cstrong\u003EHering\u2019s law\u003C/strong\u003E, not Sherrington\u2019s law. Sherrington\u2019s law refers to reciprocal innervation between agonist and antagonist muscles within the same eye, such as medial rectus contraction with lateral rectus relaxation, and is classically violated in Duane syndrome because of medial and lateral rectus co-contraction. DVD is strongly associated with early-onset strabismus, especially \u003Cstrong\u003Einfantile/congenital esotropia\u003C/strong\u003E, and may become apparent after horizontal alignment surgery because the horizontal deviation has been corrected and the dissociated vertical component becomes more obvious; it is not a true hypertropia or skew deviation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1803,
    "Name": "Myelinated retinal nerve fiber layer",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA fundus photograph shows a feathery white retinal lesion following the nerve fiber layer distribution, consistent with myelinated retinal nerve fibers. Which source of reduced vision may be associated with this finding?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-25-9aca2144-7f74-498a-a56e-b7782c66595d.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eamblyopia\u003C/strong\u003E, because the photograph shows \u003Cstrong\u003Emyelinated retinal nerve fibers\u003C/strong\u003E, seen as a white, feathery, striated retinal patch following the normal distribution of the retinal nerve fiber layer; physiologically, optic nerve axons are myelinated posterior to the lamina cribrosa, while the intraocular retinal nerve fiber layer is normally unmyelinated, but in this congenital anomaly myelination extends anteriorly into the retina. Most cases are incidental and visually asymptomatic when the macula is spared, but reduced vision may occur if the myelination is extensive, involves the macula, or is associated with significant refractive error and abnormal visual development. The classic high-yield association is \u003Cstrong\u003EStraatsma syndrome\u003C/strong\u003E, which refers to the triad of \u003Cstrong\u003Emyelinated retinal nerve fibers, ipsilateral high myopia, and amblyopia\u003C/strong\u003E, often with possible associated strabismus; the amblyopia is usually driven by anisometropia from high myopia, macular involvement by the myelinated fibers, or both, and can be difficult to treat if dense or diagnosed late. \u003Cstrong\u003EHigh hyperopia\u003C/strong\u003E is therefore incorrect because the typical refractive association is high \u003Cstrong\u003Emyopia\u003C/strong\u003E, not hyperopia; \u003Cstrong\u003Etractional retinal detachment\u003C/strong\u003E is not a usual consequence of myelinated nerve fibers; and saying the condition is never associated with vision loss is too absolute, because \u003Cstrong\u003EStraatsma syndrome\u003C/strong\u003E is a recognized mechanism by which myelinated retinal nerve fibers may be associated with reduced vision through amblyopia.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1804,
    "Name": "Hereditary cataracts",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich inheritance pattern is most commonly seen in hereditary congenital or childhood cataracts?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eautosomal dominant\u003C/strong\u003E, because most isolated hereditary congenital or developmental cataracts follow an autosomal dominant inheritance pattern, often showing vertical transmission through successive generations with variable expressivity in cataract morphology, density, age of onset, and visual significance; the affected lens opacity is typically bilateral, although asymmetry in severity can occur, and many genes may be involved, including crystallin genes, connexin genes such as \u003Cstrong\u003EGJA3/GJA8\u003C/strong\u003E, membrane protein genes such as \u003Cstrong\u003EMIP\u003C/strong\u003E, and transcription factor genes involved in lens development. It is important to separate \u003Cstrong\u003Eisolated hereditary cataract\u003C/strong\u003E from cataract associated with systemic/metabolic disease: inherited isolated cataracts are most commonly autosomal dominant, whereas metabolic or syndromic cataracts may show autosomal recessive, X-linked, mitochondrial, or sporadic patterns depending on the disorder. Another key clinical principle is that \u003Cstrong\u003Ehereditary cataracts are usually bilateral\u003C/strong\u003E, and congenital cataracts associated with systemic disease are also generally bilateral; however, bilaterality alone does \u003Cstrong\u003Enot\u003C/strong\u003E prove a systemic disorder, because many isolated familial cataracts are bilateral without systemic disease.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1805,
    "Name": "V-pattern esotropia without oblique overaction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has V-pattern esotropia but no clinical evidence of inferior oblique overaction. What is the most appropriate surgical approach?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ebilateral medial rectus recessions, inferior displacement of the insertions\u003C/strong\u003E, because this is a \u003Cstrong\u003EV-pattern esotropia without over-elevation in adduction\u003C/strong\u003E, so the pattern is not being driven by clinically significant inferior oblique overaction and therefore does not require inferior oblique weakening. In pattern strabismus, the surgical plan depends first on whether there is associated oblique dysfunction: if a V-pattern is associated with inferior oblique overaction, bilateral inferior oblique weakening is appropriate, but when the obliques are normal, the pattern is corrected by \u003Cstrong\u003Evertical transposition of the horizontal rectus insertions\u003C/strong\u003E at the time of horizontal muscle surgery. The rule is remembered as \u003Cstrong\u003EMALE: Medial recti to the Apex, Lateral recti to the Empty space\u003C/strong\u003E; in a \u003Cstrong\u003EV pattern\u003C/strong\u003E, the \u201Capex\u201D is inferior and the \u201Copen/empty\u201D part is superior, so the \u003Cstrong\u003Emedial recti are displaced inferiorly\u003C/strong\u003E, whereas lateral recti would be displaced superiorly if lateral rectus surgery were being performed. Since this patient has esotropia, the horizontal correction is bilateral medial rectus recession, and because the V pattern needs collapse without oblique weakening, the medial rectus insertions should be shifted \u003Cstrong\u003Einferiorly\u003C/strong\u003E. The vertical transposition direction does not depend on whether the horizontal rectus is recessed or resected; it depends on whether the involved muscle is a medial rectus or lateral rectus and whether the pattern is A or V, making \u003Cstrong\u003Ebilateral medial rectus recessions, inferior displacement of the insertions\u003C/strong\u003E the most appropriate plan.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1806,
    "Name": "Topical glaucoma medication",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA child with poorly controlled juvenile open-angle glaucoma is already taking systemic methazolamide. Which additional topical glaucoma drop would be expected to provide the least extra IOP-lowering effect?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ebrinzolamide\u003C/strong\u003E, because this child is already taking \u003Cstrong\u003Emethazolamide\u003C/strong\u003E, a systemic carbonic anhydrase inhibitor, so adding \u003Cstrong\u003Ebrinzolamide\u003C/strong\u003E, a topical carbonic anhydrase inhibitor, is unlikely to provide meaningful additional intraocular pressure reduction because the same aqueous-suppression pathway is already pharmacologically inhibited at a systemic level. Carbonic anhydrase inhibitors reduce aqueous production by inhibiting carbonic anhydrase in the ciliary processes, decreasing bicarbonate formation and thereby reducing sodium and fluid transport into the posterior chamber; once this mechanism is already substantially suppressed by systemic methazolamide, topical brinzolamide has limited incremental value and is therefore the least effective choice in this context. By contrast, \u003Cstrong\u003Elatanoprost\u003C/strong\u003E works through a different mechanism by increasing uveoscleral outflow, and \u003Cstrong\u003Etimolol\u003C/strong\u003E and \u003Cstrong\u003Elevobunolol\u003C/strong\u003E are topical beta-blockers that reduce aqueous production through beta-adrenergic blockade rather than carbonic anhydrase inhibition, so these may still provide additive pressure lowering. The practical principle is to avoid duplicating drug classes when escalation is needed: in a child already on oral acetazolamide or methazolamide, adding topical dorzolamide or brinzolamide is usually low-yield compared with adding a prostaglandin analogue or beta-blocker if not contraindicated. Also, although not listed here, \u003Cstrong\u003Ebrimonidine\u003C/strong\u003E deserves special pediatric caution because alpha-2 agonists can cause central nervous system depression, lethargy, hypotonia, apnea, and somnolence in young children, and are especially avoided in children under 2 years.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1807,
    "Name": "ectopia lentis with neonatal seizures",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 2-month-old infant has neonatal-onset seizures, hypertonia, deep-set eyes, and a severe form of ectopia lentis/lens luxation on ocular examination. Which metabolic defect best explains the systemic and ocular findings?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\u003Ch2\u003E\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-size: 14px; font-weight: 400; line-height: 20px;\u0022\u003E\n\u003Cp\u003E\u003Cstrong\u003Edeficiency of molybdenum cofactor\u003C/strong\u003E, because a severely displaced/luxated crystalline lens, representing an extreme form of \u003Cstrong\u003Eectopia lentis\u003C/strong\u003E, and the systemic picture of seizures beginning in the first days of life, hypertonia, severe neurologic disease, and deep-set eyes is classic for \u003Cstrong\u003Emolybdenum cofactor deficiency\u003C/strong\u003E, which causes functional deficiency of molybdenum-dependent enzymes, especially \u003Cstrong\u003Esulfite oxidase\u003C/strong\u003E; sulfite oxidase normally converts toxic sulfite to sulfate during sulfur amino acid metabolism, and failure of this pathway leads to sulfite accumulation with neonatal encephalopathy, refractory seizures, abnormal tone, feeding/respiratory difficulty, progressive neurodegeneration, and poor survival. Ectopia lentis has a broad differential and should not automatically be attributed to Marfan syndrome: important causes include \u003Cstrong\u003EMarfan syndrome\u003C/strong\u003E from defective fibrillin, classically with superotemporal lens subluxation; \u003Cstrong\u003Ehomocystinuria\u003C/strong\u003E, often with inferonasal lens subluxation and thromboembolic risk; \u003Cstrong\u003EWeill-Marchesani syndrome\u003C/strong\u003E, with microspherophakia, short stature, brachydactyly, and risk of pupillary block glaucoma; \u003Cstrong\u003Esulfite oxidase deficiency / molybdenum cofactor deficiency\u003C/strong\u003E, with neonatal seizures and severe neurodevelopmental disease; \u003Cstrong\u003Econgenital syphilis\u003C/strong\u003E from maternal transmission of \u003Cem\u003ETreponema pallidum\u003C/em\u003E; \u003Cstrong\u003EEhlers-Danlos syndrome\u003C/strong\u003E due to connective tissue fragility; \u003Cstrong\u003Etrauma\u003C/strong\u003E; \u003Cstrong\u003Eaniridia\u003C/strong\u003E; \u003Cstrong\u003Eiris coloboma\u003C/strong\u003E; \u003Cstrong\u003Eprimary congenital glaucoma\u003C/strong\u003E with globe enlargement and zonular stretching; \u003Cstrong\u003Ehereditary isolated ectopia lentis\u003C/strong\u003E; \u003Cstrong\u003Eectopia lentis et pupillae\u003C/strong\u003E, where the pupil and lens are typically displaced in opposite directions; and \u003Cstrong\u003Ehyperlysinemia\u003C/strong\u003E due to alpha-aminoadipic semialdehyde synthase pathway defects. In this infant, however, the neonatal-onset seizures, hypertonia, deep-set eyes, and lens luxation specifically favor \u003Cstrong\u003Edeficiency of molybdenum cofactor\u003C/strong\u003E rather than defective fibrillin protein, hyperlysinemia, or congenital syphilis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E\u003C/h2\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1808,
    "Name": "Normal newborn eye dimensions",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat are the typical average axial length and horizontal corneal diameter measurements expected in a normal newborn eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eaxial length: 15-17 mm; corneal horizontal diameter: 9.5-10.5 mm\u003C/strong\u003E, because the newborn eye is substantially smaller than the adult eye: the average newborn axial length is approximately \u003Cstrong\u003E16\u201317 mm\u003C/strong\u003E, compared with roughly \u003Cstrong\u003E23\u201324 mm\u003C/strong\u003E in adults, and the normal newborn horizontal corneal diameter is approximately \u003Cstrong\u003E9.5\u201310.5 mm\u003C/strong\u003E, increasing gradually during infancy and early childhood. These baseline dimensions are clinically important in pediatric ophthalmology because abnormal enlargement of either parameter can indicate pressure-related ocular expansion, especially \u003Cstrong\u003Eprimary congenital glaucoma\u003C/strong\u003E, where elevated intraocular pressure stretches the infantile sclera and cornea, causing increased axial length, enlarged corneal diameter, buphthalmos, corneal edema, Haab striae, progressive myopic shift, and optic nerve cupping. In practical terms, a corneal diameter above about \u003Cstrong\u003E13 mm\u003C/strong\u003E in an infant is highly suspicious for congenital glaucoma, whereas a newborn cornea below about \u003Cstrong\u003E9 mm\u003C/strong\u003E suggests microcornea; therefore, knowing that the normal newborn eye is approximately \u003Cstrong\u003E15\u201317 mm\u003C/strong\u003E axially with a \u003Cstrong\u003E9.5\u201310.5 mm\u003C/strong\u003E horizontal corneal diameter helps distinguish normal developmental anatomy from congenital glaucoma, microcornea, megalocornea, or other anterior segment disorders.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1809,
    "Name": "Pediatric ocular trauma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 3-month-old child presents to your clinic after an injury to his right eye. Your examination reveals periorbital ecchymosis, a large temporal subconjunctival hemorrhage, and a 25% hyphema. The child\u0027s dilated fundus exam is normal. The mother is visibly agitated and says the injury occurred when the child climbed out of a high chair. Which of the following is the most appropriate management for this child?\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Erestrict activities for this child and report this incident to child protective services\u003C/strong\u003E, because a 4-month-old infant is not developmentally capable of independently climbing out of a high chair in the way described, so the history is inconsistent with the child\u2019s motor abilities and with the severity of the ocular injury; this discrepancy is a major red flag for \u003Cstrong\u003Enon-accidental trauma\u003C/strong\u003E. A hyphema in an infant indicates significant blunt anterior segment trauma, and when accompanied by periorbital ecchymosis and a large subconjunctival hemorrhage, the clinician must manage the eye medically while also safeguarding the child. Activity restriction is appropriate for hyphema management because it reduces the risk of rebleeding, which typically occurs within the first several days and can worsen intraocular pressure, corneal blood staining, and optic nerve risk; the child also needs close ophthalmic follow-up for intraocular pressure monitoring, anterior chamber blood clearance, corneal status, and later complications such as angle recession glaucoma. However, the key medicolegal point is that clinicians are \u003Cstrong\u003Emandated reporters\u003C/strong\u003E when child abuse is suspected; the threshold is reasonable suspicion, not proof. Reporting to a hospital board or simply warning the caregiver is inadequate and potentially dangerous because it does not activate the child-protection pathway. Therefore, the correct management combines appropriate ocular precautions for hyphema with immediate reporting to \u003Cstrong\u003Echild protective services\u003C/strong\u003E because the mechanism of injury is not credible for a 4-month-old infant.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1810,
    "Name": "Ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAt what age does neonatal conjunctivitis caused by \u003Cem\u003EChlamydia trachomatis\u003C/em\u003E most typically present?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E7 days\u003C/strong\u003E, because chlamydial ophthalmia neonatorum typically presents after an incubation period of several days following exposure to infected maternal genital secretions during delivery, and for examination purposes it is classically remembered as appearing around \u003Cstrong\u003E1 week of life\u003C/strong\u003E; clinically, \u003Cem\u003EChlamydia trachomatis\u003C/em\u003E may cause watery, mucopurulent, or sometimes bloody discharge with eyelid swelling and a papillary conjunctivitis, and because neonates do not yet form conjunctival follicles, the typical follicular response seen in older children and adults is absent. The timing pattern is important because it helps separate the major causes of ophthalmia neonatorum: chemical conjunctivitis occurs earliest, within the first 24 hours after prophylactic drops and resolves rapidly; gonococcal conjunctivitis presents earlier than chlamydia, usually around \u003Cstrong\u003E3-4 days\u003C/strong\u003E, with hyperacute purulence, chemosis, and risk of corneal ulceration/perforation because \u003Cem\u003ENeisseria gonorrhoeae\u003C/em\u003E can invade intact corneal epithelium; chlamydial conjunctivitis most commonly presents around \u003Cstrong\u003E7 days\u003C/strong\u003E, although the broader clinical window is often \u003Cstrong\u003E5-14 days\u003C/strong\u003E and may be earlier with prolonged rupture of membranes; HSV conjunctivitis is uncommon and is classically later, around \u003Cstrong\u003E10-14 days\u003C/strong\u003E or roughly 2 weeks. Chlamydial neonatal conjunctivitis is also important systemically because infection may involve the nasopharynx and lungs, causing afebrile pneumonia weeks later, so treatment requires systemic macrolide therapy rather than topical therapy alone, with maternal/partner evaluation and treatment to prevent reinfection.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1811,
    "Name": "CSM visual acuity assessment in infants",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn an infant or preverbal child recorded as having \u201CCSM\u201D fixation, which parts of the fixation assessment are tested with one eye occluded and which part requires both eyes open?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe \u0022C\u0022 and \u0022S\u0022 are done monocularly the \u0022M\u0022 is done binocularly\u003C/strong\u003E, because \u003Cstrong\u003ECSM\u003C/strong\u003E is a qualitative fixation assessment used mainly in infants and preverbal children, where formal optotype acuity is not possible; \u003Cstrong\u003EC\u003C/strong\u003E means \u003Cstrong\u003Ecentral\u003C/strong\u003E, referring to whether the tested eye fixates with the fovea so that the corneal light reflex is centered while the fellow eye is occluded, making centrality a \u003Cstrong\u003Emonocular\u003C/strong\u003E assessment; \u003Cstrong\u003ES\u003C/strong\u003E means \u003Cstrong\u003Esteady\u003C/strong\u003E, referring to whether fixation remains stable as the target is held still and then moved slightly, again while the fellow eye is occluded, so steadiness is also assessed \u003Cstrong\u003Emonocularly\u003C/strong\u003E and may be disrupted by nystagmus, poor foveation, macular disease, or severe amblyopia; \u003Cstrong\u003EM\u003C/strong\u003E means \u003Cstrong\u003Emaintained\u003C/strong\u003E, and this is the binocular component because after the tested eye is shown to fix centrally and steadily under monocular conditions, the examiner uncovers the fellow eye and observes whether the tested eye continues to hold fixation or whether fixation immediately shifts to the fellow eye.\u0026nbsp; This distinction is clinically important because \u003Cstrong\u003Ecentral and steady fixation assess the quality of monocular fixation\u003C/strong\u003E, while \u003Cstrong\u003Emaintained fixation assesses fixation preference and interocular competition\u003C/strong\u003E, helping detect amblyopia or fixation dominance in preverbal children; an eye that is central and steady but \u003Cstrong\u003Enot maintained\u003C/strong\u003E may still have reduced visual function relative to the fellow eye, especially in strabismus or anisometropia. Therefore, \u003Cstrong\u003EC and S are tested monocularly\u003C/strong\u003E, while \u003Cstrong\u003EM is tested binocularly\u003C/strong\u003E after the occluder is removed from the fellow eye.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1812,
    "Name": "Fusional amplitudes",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a typical person, how do convergence, divergence, and vertical fusional amplitudes compare in relative size?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Econvergence fusional amplitudes \u0026gt; divergence fusional amplitudes \u0026gt; vertical fusional amplitudes\u003C/strong\u003E, because normal fusional reserves are not equal in all directions: humans generally have the greatest capacity for \u003Cstrong\u003Epositive fusional vergence/convergence\u003C/strong\u003E, a smaller capacity for \u003Cstrong\u003Enegative fusional vergence/divergence\u003C/strong\u003E, and only a very limited ability to compensate for \u003Cstrong\u003Evertical misalignment\u003C/strong\u003E. For distance fixation, the usual approximate values are around \u003Cstrong\u003E14 prism diopters\u003C/strong\u003E for convergence fusional amplitude, around \u003Cstrong\u003E6 prism diopters\u003C/strong\u003E for divergence fusional amplitude, and only about \u003Cstrong\u003E2\u20133 prism diopters\u003C/strong\u003E for vertical fusional amplitude. This reflects the physiology of binocular single vision: horizontal vergence mechanisms are strongly developed because near viewing normally requires convergence and distance/near adaptation requires horizontal vergence flexibility, whereas vertical vergence is mainly a fine compensatory mechanism for small vertical phorias or minor anatomic asymmetries and therefore has a much smaller reserve. This is clinically important because even a small vertical deviation may become symptomatic with diplopia or asthenopia, while larger horizontal deviations may be compensated if fusional reserves are adequate.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1813,
    "Name": "Primary congenital glaucoma after failed first angle surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn infant with primary congenital glaucoma still has markedly elevated intraocular pressure (around 30 mmHg) after one previous goniotomy. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Egoniotomy\u003C/strong\u003E, because in primary congenital glaucoma the initial surgical approach is usually directed at the abnormal anterior chamber angle, where developmental trabeculodysgenesis causes impaired aqueous outflow; if one goniotomy has not adequately controlled the IOP, it is common and appropriate to attempt a \u003Cstrong\u003Esecond angle procedure\u003C/strong\u003E, such as repeat goniotomy or trabeculotomy, before escalating to more invasive filtration surgery or a glaucoma drainage implant.\u0026nbsp; The success of angle surgery depends on age at presentation, corneal clarity, extent of the angle treated, severity of trabecular dysgenesis, and whether the disease is primary or associated with anterior segment anomalies; many infants presenting between approximately 3 months and 1 year of age still have a good chance of IOP control after one or two angle surgeries, with success rates often quoted around \u003Cstrong\u003E80%\u003C/strong\u003E in favorable cases. Observation is inappropriate because IOP in the 30 mmHg range in an infant risks progressive corneal enlargement, Haab striae, axial length increase, myopic shift, optic nerve cupping, and amblyopia; trabeculectomy with mitomycin C and glaucoma drainage implantation are generally reserved for refractory cases after angle surgery failure, complex secondary pediatric glaucomas, or eyes with poor angle-surgery prognosis, because these procedures carry greater long-term risks in children, including bleb-related infection, scarring/failure, hypotony, tube complications, motility problems, and need for revision. Therefore, after a single failed goniotomy in an infant with PCG, the next best step is another \u003Cstrong\u003Egoniotomy\u003C/strong\u003E rather than immediate drainage implant surgery.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1814,
    "Name": " postoperative lower eyelid elevation",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAfter vertical rectus surgery, a patient develops elevation of the right lower eyelid. Which operation most likely caused this eyelid position change?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eright inferior rectus resection\u003C/strong\u003E, because vertical rectus surgery can alter eyelid position through the fascial connections between the extraocular muscles and the eyelid retractor systems, and this effect is especially important with the \u003Cstrong\u003Einferior rectus\u003C/strong\u003E because it is anatomically linked to the lower eyelid retractors through the \u003Cstrong\u003Ecapsulopalpebral fascia\u003C/strong\u003E, the lower lid analogue of the levator aponeurosis. The capsulopalpebral fascia arises from the region of the inferior rectus sheath, passes anteriorly through the lower eyelid, and inserts into the inferior tarsal plate, with additional support from the inferior fornix suspensory system and \u003Cstrong\u003ELockwood\u2019s ligament\u003C/strong\u003E; therefore, changing the tension or position of the inferior rectus can transmit force directly to the lower lid. In \u003Cstrong\u003Einferior rectus resection\u003C/strong\u003E, the muscle is shortened and strengthened, increasing traction through the inferior rectus\u2013capsulopalpebral fascia\u2013lower lid retractor complex, which tends to pull the lower eyelid \u003Cstrong\u003Eupward\u003C/strong\u003E, producing lower lid elevation and relative narrowing of the palpebral fissure. This is the opposite of \u003Cstrong\u003Einferior rectus recession\u003C/strong\u003E, which weakens and posteriorly displaces the inferior rectus and can produce lower lid retraction, inferior scleral show, and widening of the palpebral fissure. Superior rectus surgery more commonly affects the upper eyelid through its relationship with the levator complex rather than directly advancing the lower eyelid, so the operation most consistent with upward advancement of the right lower lid is \u003Cstrong\u003Eright inferior rectus resection\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1815,
    "Name": "Infant aphakia after cataract surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 1-month-old infant is left aphakic after bilateral lensectomy for congenital cataracts, and cycloplegic refraction shows \u002B12.00 OU. What spectacle correction should be prescribed to provide the most appropriate visual focus for this infant\u2019s functional viewing distance?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Esingle vision glasses with power of \u002B14.00 sphere OU\u003C/strong\u003E, because a 1-month-old aphakic infant does not use vision primarily at adult distance fixation and cannot effectively use bifocals; instead, the infant\u2019s visual world is mainly at near/arm\u2019s-length distances, roughly \u003Cstrong\u003E50 cm\u003C/strong\u003E, which optically corresponds to about \u003Cstrong\u003E2 diopters\u003C/strong\u003E of accommodative demand. Because an aphakic infant has no crystalline lens and therefore essentially no accommodation, prescribing only the measured distance aphakic correction of \u003Cstrong\u003E\u002B12.00 OU\u003C/strong\u003E would focus the infant for distance but leave near targets blurred, increasing deprivation/amblyopia risk during the critical period of visual development. For bilateral aphakia in a very young infant, the spectacle correction is therefore intentionally \u003Cstrong\u003Eover-plussed\u003C/strong\u003E relative to the cycloplegic distance refraction to leave the infant functionally focused for near; adding approximately \u003Cstrong\u003E\u002B2.00 D\u003C/strong\u003E to the measured \u002B12.00 correction gives \u003Cstrong\u003E\u002B14.00 sphere OU\u003C/strong\u003E, effectively creating the desired near focus for a 50 cm working distance. Bifocals are not the best choice at 1 month because an infant cannot reliably direct gaze through the near segment, and bifocals become more relevant later when the child is older and has more purposeful distance/near viewing behavior. This is different from intraocular lens planning in infants, where surgeons often aim for postoperative hyperopia because the eye will grow and myopic shift will occur over time; with aphakic spectacles in a tiny infant, the priority is immediate near visual stimulation, so \u003Cstrong\u003Esingle vision glasses with power of \u002B14.00 sphere OU\u003C/strong\u003E are most appropriate.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1816,
    "Name": "Myelinated optic nerve fibers",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed disorder is classically associated with myelinated retinal nerve fiber layer involving the optic nerve region?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBasal Cell Nevus Syndrome\u003C/strong\u003E, because myelinated retinal nerve fibers are congenital white, feathery, striated patches that follow the retinal nerve fiber layer distribution, reflecting extension of myelination anterior to the lamina cribrosa into the retina; while most cases are isolated and incidental, they have recognized associations, including \u003Cstrong\u003EBasal Cell Nevus Syndrome\u003C/strong\u003E (Gorlin-Goltz syndrome), a multisystem autosomal dominant disorder characterized by multiple basal cell carcinomas, odontogenic keratocysts, skeletal abnormalities, falx cerebri/intracranial calcification, and various ocular findings. The important differential point is that myelinated nerve fibers are also classically associated with \u003Cstrong\u003EStraatsma syndrome\u003C/strong\u003E, which consists of \u003Cstrong\u003Emyelinated retinal nerve fibers, ipsilateral high myopia, and amblyopia\u003C/strong\u003E, sometimes with strabismus; therefore, \u003Cstrong\u003EUnilateral high hyperopia\u003C/strong\u003E is incorrect because the refractive association is high \u003Cstrong\u003Emyopia\u003C/strong\u003E, not hyperopia. \u003Cstrong\u003ENeurofibromatosis Type 2\u003C/strong\u003E is instead associated with posterior subcapsular cataracts, wedge cortical cataracts, retinal hamartomas/combined retinal-RPE hamartomas, and optic nerve sheath meningioma, not myelinated nerve fibers as the classic association. \u003Cstrong\u003ETuberous Sclerosis\u003C/strong\u003E is associated with retinal astrocytic hamartomas, facial angiofibromas, cortical tubers, and systemic hamartomas, rather than myelinated retinal nerve fibers.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1817,
    "Name": "Dorsal midbrain syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with Parinaud/dorsal midbrain syndrome, which maneuver best brings out convergence-retraction nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ehave the patient track a downward-rotating OKN drum\u003C/strong\u003E, because convergence-retraction \u201Cnystagmus\u201D in dorsal midbrain syndrome is not a true rhythmic vestibular nystagmus but a \u003Cstrong\u003Edisjunctive saccadic oscillation\u003C/strong\u003E that is best elicited by provoking attempted \u003Cstrong\u003Eupward saccades\u003C/strong\u003E; a downward-moving or downward-rotating OKN stimulus normally induces upward quick phases, but in dorsal midbrain syndrome the vertical saccadic burst pathways in the rostral midbrain/pretectal region are impaired, so attempted upgaze produces inappropriate co-contraction of extraocular muscles, especially simultaneous activation of the medial recti, causing the eyes to jerk inward and retract into the orbit. This is why a \u003Cstrong\u003Edownward-rotating OKN drum\u003C/strong\u003E is the classic bedside test: the patient attempts upward refixation movements, and instead of normal up saccades, the examiner sees convergence with globe retraction. The broader dorsal midbrain syndrome pattern includes \u003Cstrong\u003Eupgaze palsy\u003C/strong\u003E, \u003Cstrong\u003Elight-near dissociation of the pupils\u003C/strong\u003E, \u003Cstrong\u003Elid retraction (Collier sign)\u003C/strong\u003E, convergence-retraction nystagmus, and impaired convergence or accommodation depending on lesion extent. The lesion localizes to the dorsal rostral midbrain/pretectal area affecting vertical gaze centers, including pathways around the posterior commissure, riMLF, and interstitial nucleus of Cajal; causes vary by age, with pineal region tumors and aqueductal stenosis important in children, demyelination in young adults, and midbrain infarction more typical in older patients. Moving a target toward or away from the patient tests voluntary convergence/divergence and does not reliably elicit this sign, while an upward-rotating OKN drum would preferentially drive downward quick phases rather than the attempted upward saccades needed to demonstrate convergence-retraction nystagmus.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1818,
    "Name": "Alagille syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EYou are examining a 1-year-old child in the hospital who was admitted for jaundice. Your examination is notable for the anterior segment finding seen in the photograph below. The child\u0027s past medical history is also significant for pulmonary stenosis and developmental delay. Which of the following is the most likely diagnosis for this infant?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAlagille syndrome\u003C/strong\u003E, because the anterior segment photo shows \u003Cstrong\u003Eposterior embryotoxon\u003C/strong\u003E, which is an anteriorly displaced and prominent Schwalbe line visible at the peripheral cornea, and although posterior embryotoxon can be seen in normal individuals and in anterior segment dysgenesis syndromes such as Axenfeld-Rieger syndrome, the systemic context here is much more specific for \u003Cstrong\u003EAlagille syndrome\u003C/strong\u003E: chronic jaundice from cholestatic liver disease due to paucity of intrahepatic bile ducts, \u003Cstrong\u003Epulmonary stenosis\u003C/strong\u003E or other congenital cardiac defects, developmental delay, characteristic craniofacial and skeletal findings such as broad forehead, pointed chin, and butterfly vertebrae, and ocular findings including posterior embryotoxon. Alagille syndrome is usually an autosomal dominant disorder most commonly caused by mutations in \u003Cstrong\u003EJAG1\u003C/strong\u003E on chromosome 20p12, less commonly \u003Cstrong\u003ENOTCH2\u003C/strong\u003E, affecting Notch signaling during embryologic development of the liver, heart, skeleton, and eye; the ocular finding is typically not visually threatening but is diagnostically useful when paired with cholestasis and cardiac disease. \u003Cstrong\u003EAxenfeld-Rieger syndrome\u003C/strong\u003E can also show posterior embryotoxon, but it is more strongly associated with iris strands to Schwalbe line, corectopia, polycoria, anterior segment dysgenesis, and glaucoma rather than neonatal cholestasis and pulmonary stenosis. \u003Cstrong\u003EWilson\u0027s disease\u003C/strong\u003E causes a \u003Cstrong\u003EKayser-Fleischer ring\u003C/strong\u003E from copper deposition in Descemet membrane, not posterior embryotoxon, and would not typically present with this congenital pulmonary stenosis pattern. \u003Cstrong\u003Evelocardiofacial syndrome\u003C/strong\u003E is associated with conotruncal cardiac defects, palatal abnormalities, and developmental issues, but posterior embryotoxon with jaundice and pulmonary stenosis most strongly supports \u003Cstrong\u003EAlagille syndrome\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1819,
    "Name": "Bilateral fourth nerve palsy with marked excyclotorsion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 30-year-old man presents to your clinic 8 months after head trauma from motor vehicle accident. He has seen several eye doctors since the accident but unfortunately he continues to suffer from persistent diplopia. On examination in primary gaze you note a subtle right hypertropia measuring 4 prism diopters. The right hypertropia increases in left gaze and right head tilt. You also observe a left hypertropia in right gaze and left head tilt. On double maddox rod testing, you measure 30 degrees of excyclotorsion. Which of the following represents the most appropriate initial management for this patient\u0027s condition?\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ebilateral splitting and displacement of superior oblique fibers\u003C/strong\u003E, because this presentation is most consistent with \u003Cstrong\u003Ebilateral acquired fourth nerve palsy\u003C/strong\u003E after head trauma: the patient has alternating hypertropia patterns depending on gaze and head tilt, with a right hypertropia that worsens in left gaze and right head tilt and a left hypertropia that worsens in right gaze and left head tilt, reflecting bilateral superior oblique weakness. The most important management clue is the very large \u003Cstrong\u003E30 degrees of excyclotorsion\u003C/strong\u003E on double Maddox rod testing, which indicates that the patient\u2019s dominant symptomatic problem is torsional diplopia rather than a large vertical deviation; prism may help small vertical deviations, but it cannot adequately correct large torsional diplopia, and the primary position hypertropia is only subtle at 4 prism diopters. In this setting, the appropriate operation is a \u003Cstrong\u003Ebilateral Harada-Ito procedure\u003C/strong\u003E, described here as \u003Cstrong\u003Ebilateral splitting and displacement of superior oblique fibers\u003C/strong\u003E, in which the anterior fibers of the superior oblique tendon\u2014those most responsible for intorsion\u2014are separated and advanced/displaced anteriorly and laterally to increase the intorsional effect without producing a large vertical correction. Bilateral inferior oblique recessions may be useful in bilateral superior oblique palsy when the main finding is inferior oblique overaction with significant hypertropia and little symptomatic torsion, but inferior oblique weakening usually reduces excyclotorsion only modestly and is not the best choice for severe torsional diplopia; bilateral inferior rectus recessions do not address the underlying superior oblique torsional deficit and could create problematic vertical imbalance; and prism-only management is inadequate when the patient has large symptomatic excyclotorsion. Therefore, in traumatic bilateral fourth nerve palsy with marked excyclotorsion and minimal vertical deviation, the best initial management is \u003Cstrong\u003Ebilateral splitting and displacement of superior oblique fibers\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1820,
    "Name": "High AC/A accommodative esotropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA mother brings in her 5-year old child with complaints of intermittent inward crossing of both eyes. You write down in your chart: \u002235 PD ET and 50 PD ET\u0027.\u0022 The cycloplegic refraction shows \u002B2.00 D sphere OD and \u002B2.75 D OS. You initially prescribe the full cycloplegic refraction in a single distance lens which results in orthotropia at distance. However, you still measure 15 PD ET\u0027 when the child wears these new glasses. Which of the following pictures shows the correct glasses that should be prescribed for this child?\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-28-c7344a83-8889-4b4c-a5a5-18375a624f50.png\u0022\u003E\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EB\u003C/strong\u003E, because this child has \u003Cstrong\u003Enon-refractive accommodative esotropia with a high AC/A ratio\u003C/strong\u003E, shown by a near deviation that is larger than the distance deviation and by persistent near esotropia despite full cycloplegic hyperopic correction; the full hyperopic prescription removes the accommodative drive enough to straighten the eyes at distance, but near viewing still triggers excessive accommodative convergence, leaving residual near esotropia. The correct management is to prescribe the \u003Cstrong\u003Efull cycloplegic distance correction\u003C/strong\u003E with a near add, typically \u003Cstrong\u003E\u002B2.50 to \u002B3.00 D\u003C/strong\u003E, in a bifocal design that the child will actually use. In young children, the bifocal segment must be set \u003Cstrong\u003Every high\u003C/strong\u003E, classically with the \u003Cstrong\u003Eexecutive-style bifocal line bisecting the pupil\u003C/strong\u003E, because toddlers often look downward through the distance portion of standard low bifocals and therefore fail to use the near add during near fixation. The diagram marked by a straight horizontal bifocal segment passing across the pupil represents the correct design: it forces near fixation through the plus add and reduces accommodative demand, thereby reducing accommodative convergence and controlling the residual near esotropia. A low flat-top or low segment design is ineffective in this age group because the child can look over the add; single-vision lenses are insufficient because the near deviation persists despite full hyperopic correction; and the bifocal height should be high enough to ensure use of the add but not so excessive that it leaves too little distance viewing area.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1821,
    "Name": "Congenital fibrosis syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn adult has had a constant elevated eye position since birth, and a sibling has a similar congenital ocular motility problem. What is the most likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Econgenital fibrosis syndrome\u003C/strong\u003E, because the key clues are \u003Cstrong\u003Eonset since birth\u003C/strong\u003E, a constant abnormal vertical eye position, and a similar problem in the twin sibling, all of which point toward a congenital inherited restrictive ocular motility disorder rather than an acquired thyroid or traumatic process. Congenital fibrosis syndromes, including the congenital cranial dysinnervation disorders such as \u003Cstrong\u003Econgenital fibrosis of the extraocular muscles (CFEOM)\u003C/strong\u003E, are characterized by congenital non-progressive ophthalmoplegia with restrictive strabismus due to abnormal development/innervation of extraocular muscles and secondary fibrotic replacement; depending on the subtype, patients may have severe limitation of elevation, depression, or horizontal movements, ptosis, abnormal head posture, and eyes fixed in an abnormal position. One variant described as \u003Cstrong\u003Evertical retraction syndrome\u003C/strong\u003E can involve a fibrotic or abnormally innervated \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E, causing a hypertropic or elevated eye that cannot depress normally, which fits the description of a constantly elevated left eye since birth. The familial clue is important because congenital fibrosis syndromes may be inherited, often autosomal dominant in some CFEOM forms, whereas \u003Cstrong\u003Ethyroid eye disease\u003C/strong\u003E is typically acquired in adulthood and often shows inflammatory/restrictive changes rather than a lifelong sibling-associated presentation; \u003Cstrong\u003Eforceps injury during delivery\u003C/strong\u003E could cause an isolated traumatic cranial nerve palsy but would not explain a similar problem in the sibling; and \u003Cstrong\u003EMobius syndrome\u003C/strong\u003E classically involves congenital facial weakness with abduction deficits from sixth and seventh nerve involvement rather than an isolated congenital elevated eye from vertical extraocular muscle fibrosis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1822,
    "Name": "Ocular hypertelorism",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EHow is ocular hypertelorism properly defined on clinical examination?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eexcessive interpupillary distance\u003C/strong\u003E, because \u003Cstrong\u003Eocular hypertelorism\u003C/strong\u003E refers clinically to an abnormally increased distance between the pupils compared with age-appropriate normative values, meaning the eyes appear widely spaced because the interpupillary distance is excessive; this implies underlying \u003Cstrong\u003Eorbital hypertelorism\u003C/strong\u003E, but the strict terms are different. \u003Cstrong\u003EOrbital hypertelorism\u003C/strong\u003E is a radiologic/anatomic diagnosis defined by increased distance between the \u003Cstrong\u003Emedial orbital walls\u003C/strong\u003E due to lateral displacement of the orbits, whereas \u003Cstrong\u003Etelecanthus\u003C/strong\u003E means increased distance between the \u003Cstrong\u003Einner canthi\u003C/strong\u003E with a normal interpupillary distance, often due to medial canthal tendon displacement or epicanthal configuration.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1823,
    "Name": "Saethre-Chotzen syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the listed craniosynostosis syndromes, which one usually produces the least severe cranial/skull deformity?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESaethre-Chotzen syndrome\u003C/strong\u003E, because this craniosynostosis syndrome is generally considered one of the milder syndromic craniosynostoses and may be underdiagnosed when the skull deformity is subtle; the typical phenotype includes unilateral or bilateral coronal synostosis with \u003Cstrong\u003Eplagiocephaly\u003C/strong\u003E, facial asymmetry, \u003Cstrong\u003Eptosis\u003C/strong\u003E, low frontal hairline, small or posteriorly rotated ears, and mild limb findings such as \u003Cstrong\u003Ebrachydactyly\u003C/strong\u003E or partial soft-tissue syndactyly, while intelligence is often normal or only mildly affected. Saethre-Chotzen syndrome is classically caused by pathogenic variants in \u003Cstrong\u003ETWIST1\u003C/strong\u003E on chromosome 7, affecting cranial suture development through abnormal osteoblast differentiation and premature suture fusion; the orbital findings may include hypertelorism, shallow orbits, strabismus, amblyopia risk, and exposure problems depending on severity, but the cranial deformity is usually less dramatic than in Apert, Crouzon, or Pfeiffer syndromes. \u003Cstrong\u003ECrouzon syndrome\u003C/strong\u003E is a more prominent autosomal dominant craniosynostosis syndrome, commonly related to \u003Cstrong\u003EFGFR2\u003C/strong\u003E, with craniosynostosis, midface hypoplasia, shallow orbits, and proptosis but typically no syndactyly; \u003Cstrong\u003EApert syndrome\u003C/strong\u003E is also usually FGFR2-related and is more severe, with craniosynostosis plus marked syndactyly of the hands and feet; \u003Cstrong\u003EPfeiffer syndrome\u003C/strong\u003E is another FGFR-related craniosynostosis syndrome associated with broad thumbs and great toes and variable severity. Therefore, among the listed options, the mildest craniosynostosis syndrome in terms of skull deformity is \u003Cstrong\u003ESaethre-Chotzen syndrome\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1824,
    "Name": "Gonococcal ophthalmia neonatorum",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA newborn develops severe bilateral purulent conjunctivitis with marked chemosis, conjunctival injection, and photophobia on day 4 of life. What is the most appropriate treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Esystemic ceftriaxone\u003C/strong\u003E, because a neonate with \u003Cstrong\u003Eprofuse purulent discharge\u003C/strong\u003E, severe chemosis, marked conjunctival injection, eyelid matting, and photophobia at \u003Cstrong\u003E3\u20134 days of life\u003C/strong\u003E should be presumed to have \u003Cstrong\u003Egonococcal ophthalmia neonatorum until proven otherwise\u003C/strong\u003E; \u003Cem\u003ENeisseria gonorrhoeae\u003C/em\u003E classically presents within the first \u003Cstrong\u003E2\u20135 days after birth\u003C/strong\u003E and is uniquely dangerous because it can penetrate intact corneal epithelium, causing keratitis, corneal ulceration, corneal melting, perforation, endophthalmitis, and permanent blindness if treatment is delayed. The management must be \u003Cstrong\u003Esystemic\u003C/strong\u003E, not topical alone, because neonatal gonococcal infection can also disseminate and cause sepsis, arthritis, or meningitis, so the mainstay is systemic third-generation cephalosporin therapy, classically \u003Cstrong\u003Eceftriaxone\u003C/strong\u003E, with urgent ophthalmology involvement, conjunctival Gram stain/culture or NAAT testing, copious saline irrigation to remove purulent material, and assessment for corneal involvement and disseminated disease. \u003Cstrong\u003Esystemic erythromycin\u003C/strong\u003E is used for chlamydial neonatal conjunctivitis rather than hyperacute gonococcal disease; \u003Cstrong\u003Etopical erythromycin eyedrops and ointment at night\u003C/strong\u003E is insufficient because prophylactic/topical therapy does not treat invasive gonococcal ophthalmia; and \u003Cstrong\u003Efortified cefazolin eyedrops\u003C/strong\u003E may be used for selected bacterial keratitis but does not address the systemic and rapidly destructive nature of neonatal gonococcal infection, making \u003Cstrong\u003Esystemic ceftriaxone\u003C/strong\u003E the correct treatment.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 14,
    "Category": null,
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  },
  {
    "Id": 1825,
    "Name": "Heavy eye syndrome in high myopia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a highly myopic patient with diplopia from myopia-related restrictive strabismus, which extraocular muscle is not usually part of the typical pathogenic displacement pattern?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Einferior rectus\u003C/strong\u003E, because symptomatic strabismus in high myopia is classically related to \u003Cstrong\u003Eheavy eye syndrome / myopic strabismus fixus\u003C/strong\u003E, where progressive axial elongation of the globe causes the posterior superotemporal globe to prolapse or herniate between the \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E and \u003Cstrong\u003Elateral rectus\u003C/strong\u003E, with degeneration or dehiscence of the superotemporal band/intermuscular septum that normally stabilizes the relationship between these muscles. This changes the vector forces of the horizontal and vertical recti: the \u003Cstrong\u003Elateral rectus\u003C/strong\u003E typically slips inferiorly, reducing its abducting efficiency and adding a depressor component, while the \u003Cstrong\u003Esuperior rectus\u003C/strong\u003E may be displaced medially, reducing elevation and altering vertical balance; the result is usually progressive \u003Cstrong\u003Eesotropia and hypotropia\u003C/strong\u003E with limitation of abduction and elevation. The \u003Cstrong\u003Emedial rectus\u003C/strong\u003E may also become secondarily tight or contracted from long-standing esotropia, so medial rectus recession may sometimes be added surgically. The \u003Cstrong\u003Einferior rectus\u003C/strong\u003E, however, is not typically involved in the characteristic displacement complex of high-myopic strabismus; the primary anatomic problem is the abnormal relationship between the superior rectus, lateral rectus, and elongated globe. Management may include prism for small deviations, but significant cases often require surgery aimed at restoring the globe\u2013muscle relationship, such as \u003Cstrong\u003Eloop myopexy/Yokoyama procedure\u003C/strong\u003E joining the superior rectus and lateral rectus to reposition the globe, with medial rectus recession added if there is contracture, making \u003Cstrong\u003Einferior rectus\u003C/strong\u003E the muscle not typically involved.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1826,
    "Name": "Traumatic sixth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has persistent diplopia 3 months after traumatic left abducens nerve palsy, with partial residual lateral rectus function and a moderate esotropia in primary position. What is the most appropriate management at this stage?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eobservation / prisms\u003C/strong\u003E, because traumatic sixth nerve palsy can continue to recover spontaneously for several months, and definitive strabismus surgery is generally deferred until the deviation and duction deficit have been stable for at least about \u003Cstrong\u003E6 months\u003C/strong\u003E; the priority is symptomatic control while waiting for further neurologic recovery. Temporary measures include Fresnel prism if the deviation is reasonably comitant in primary/reading gaze, occlusion if prism is not tolerated or diplopia is too incomitant, and close follow-up to document recovery, secondary medial rectus contracture, and stability of measurements. Botulinum toxin can sometimes be used in acute sixth nerve palsy to weaken the \u003Cstrong\u003Eipsilateral medial rectus\u003C/strong\u003E and reduce contracture while the lateral rectus recovers, but the listed option incorrectly names the \u003Cstrong\u003Eright medial rectus\u003C/strong\u003E; in a \u003Cstrong\u003Eleft\u003C/strong\u003E sixth nerve palsy, the antagonist to the weak left lateral rectus is the \u003Cstrong\u003Eleft medial rectus\u003C/strong\u003E, not the right medial rectus. Large recession\u2013resection surgery would be considered later only if there is adequate residual lateral rectus function and a stable residual esotropia, while vertical rectus transposition procedures are generally reserved for complete or near-complete sixth nerve palsy with poor lateral rectus function after the recovery period. Therefore, at 3 months after traumatic CN VI palsy, the most appropriate management is \u003Cstrong\u003Eobservation / prisms\u003C/strong\u003E rather than definitive surgery.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1827,
    "Name": "Tobacco-alcohol optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn older patient with a long history of tobacco and alcohol exposure has slowly progressive bilateral visual loss and a Goldmann visual field in the image below. Which optic nerve appearance best matches this presentation?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-28-4addab14-3887-4188-88b5-16b0c17618e0.png\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-28-3abac655-e6f8-439f-ba3e-859638d2308e.png\u0022 style=\u0022color: rgb(66, 66, 66); font-family: Roboto, Helvetica, Arial, \u0026quot;sans-serif\u0026quot;; letter-spacing: 0.14994px;\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EImage D\u003C/strong\u003E, because the visual field demonstrates a \u003Cstrong\u003Ecentral scotoma\u003C/strong\u003E, and in the clinical setting of chronic progressive bilateral visual loss with heavy tobacco and alcohol exposure, the most likely process is a \u003Cstrong\u003Etoxic/nutritional optic neuropathy\u003C/strong\u003E, classically affecting the \u003Cstrong\u003Epapillomacular bundle\u003C/strong\u003E; damage to these small-caliber fibers produces reduced central vision, dyschromatopsia, and central or cecocentral scotomas, and the corresponding optic nerve finding is usually \u003Cstrong\u003Etemporal pallor\u003C/strong\u003E, because the papillomacular bundle enters the temporal aspect of the optic disc. Image D shows mild-to-moderate temporal optic disc pallor, which best fits this bilateral central field loss pattern. Image A shows a small crowded disc or \u201Cdisc at risk,\u201D which may predispose to non-arteritic anterior ischemic optic neuropathy but would not explain a chronic bilateral central scotoma in this context. Image B shows marked disc edema, most consistent with papilledema or severe optic nerve swelling, where early field loss is typically enlargement of the blind spot rather than isolated central scotoma, with central acuity often preserved until later. Image C shows glaucomatous cupping with neuroretinal rim loss/notching, which usually produces nerve fiber bundle defects such as nasal step, arcuate scotoma, or paracentral defects rather than a classic symmetric central/cecocentral scotoma from papillomacular bundle toxicity. Therefore, the optic nerve appearance expected in this patient is \u003Cstrong\u003EImage D\u003C/strong\u003E, reflecting temporal pallor from papillomacular bundle injury in toxic/nutritional optic neuropathy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1828,
    "Name": "Oculopalatal myoclonus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich ocular motor disorder is classically associated with disruption of the central tegmental tract?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOculopalatal myoclonus\u003C/strong\u003E, because oculopalatal myoclonus is a distinctive delayed ocular motor syndrome caused by disruption of the \u003Cstrong\u003Edentato-rubro-olivary pathway\u003C/strong\u003E, also known as the \u003Cstrong\u003Etriangle of Guillain-Mollaret\u003C/strong\u003E, which links the \u003Cstrong\u003Edentate nucleus of the cerebellum\u003C/strong\u003E, the \u003Cstrong\u003Ered nucleus in the midbrain\u003C/strong\u003E, and the \u003Cstrong\u003Einferior olivary nucleus in the medulla\u003C/strong\u003E; the \u003Cstrong\u003Ecentral tegmental tract\u003C/strong\u003E carries fibers from the red nucleus down to the inferior olivary nucleus, so a lesion in this tract\u2014often from brainstem stroke, hemorrhage, demyelination, trauma, or tumor\u2014can cause trans-synaptic degeneration and subsequent \u003Cstrong\u003Ehypertrophic olivary degeneration\u003C/strong\u003E. Clinically, this produces acquired, usually bilateral, vertical or pendular nystagmus together with rhythmic palatal movements, and the myorhythmia may also involve the pharynx, larynx, tongue, face, diaphragm, or limbs, sometimes causing audible clicking or involuntary throat/laryngeal sounds. A key point is the \u003Cstrong\u003Edelay\u003C/strong\u003E: the abnormal eye movements often appear \u003Cstrong\u003Emonths to years after\u003C/strong\u003E the original brainstem/cerebellar lesion, and MRI may show the highly suggestive finding of \u003Cstrong\u003Einferior olivary hypertrophy\u003C/strong\u003E rather than simple atrophy. By contrast, periodic alternating nystagmus is linked to instability of the vestibular velocity-storage mechanism involving the cerebellar nodulus/uvula and cervicomedullary pathways; upbeat nystagmus localizes to lesions involving the medulla, midbrain, or cerebellar vermis; and see-saw nystagmus is typically associated with parasellar or midbrain lesions, such as craniopharyngioma in children.\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-07-28-7533c8b2-a789-4800-a1ed-776b2585c220.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1829,
    "Name": "Oculomasticatory myorhythmia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with chronic diarrhea develops non-volitional rhythmic convergent eye oscillations associated with rhythmic jaw muscle contractions. What is the appropriate treatment?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAntibiotics\u003C/strong\u003E, because the combination of rhythmic convergent ocular oscillations with synchronous rhythmic contraction of the masticatory muscles is \u003Cstrong\u003Eoculomasticatory myorhythmia\u003C/strong\u003E, a highly characteristic and essentially pathognomonic sign of \u003Cstrong\u003Ecentral nervous system Whipple disease\u003C/strong\u003E, caused by infection with \u003Cem\u003ETropheryma whipplei\u003C/em\u003E. This is not a functional or voluntary ocular movement disorder, and the associated chronic diarrhea supports systemic Whipple disease with gastrointestinal involvement; other systemic features may include weight loss, arthralgia or arthritis, fever, lymphadenopathy, and malabsorption, while neurologic disease may cause supranuclear gaze palsy, cognitive change, sleep disturbance, ataxia, or myorhythmia. The key diagnostic point is that oculomasticatory myorhythmia consists of slow, rhythmic, often convergent-divergent pendular eye movements occurring with rhythmic contraction of jaw muscles, and is considered a major localizing clue to CNS Whipple disease rather than ordinary nystagmus; diagnosis is supported by duodenal/jejunal biopsy showing PAS-positive macrophages and/or PCR for \u003Cem\u003ETropheryma whipplei\u003C/em\u003E in tissue or CSF. Treatment must be \u003Cstrong\u003Eantibiotic therapy\u003C/strong\u003E, using agents that penetrate the CNS when neurologic involvement is suspected; commonly described regimens include initial IV ceftriaxone or penicillin-based therapy followed by prolonged oral therapy such as trimethoprim-sulfamethoxazole for 1\u20132 years, although doxycycline-based regimens may also be used depending on specialist protocols. Whipple disease was historically fatal before effective antibiotics, and CNS involvement is potentially life-threatening but treatable, so reassurance, gabapentin, or IV steroids would not address the infectious cause and could delay definitive treatment.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1830,
    "Name": "Physiologic miosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed condition is most commonly associated with bilaterally smaller-than-average pupils?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOlder age\u003C/strong\u003E, because normal pupil size decreases with aging due to progressive senile miosis, which reflects age-related changes in the iris dilator muscle, sympathetic tone, and the balance between sympathetic dilation and parasympathetic constriction; therefore, older individuals commonly have smaller resting pupils and reduced dilation in dim illumination. Bilateral miosis can also be seen with opioid/narcotic ingestion, pontine hemorrhage, sleep, parasympathomimetic agents such as pilocarpine, and chronic tonic pupils that may become smaller over time, but among the listed options \u003Cstrong\u003EOlder age\u003C/strong\u003E is the best association. \u003Cstrong\u003EGrand mal seizures\u003C/strong\u003E are more typically associated with sympathetic activation and larger pupils during or after the event, \u003Cstrong\u003EAnoxic brain injury\u003C/strong\u003E can cause bilateral larger pupils when there is midbrain dysfunction or severe autonomic disturbance, and \u003Cstrong\u003EParasympathetic blocking agents\u003C/strong\u003E such as atropine or cyclopentolate cause mydriasis rather than miosis by blocking the sphincter pupillae response.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1831,
    "Name": "Idiopathic intracranial hypertension",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with confirmed IIH has preserved central vision, only mild papilledema with enlarged blind spots, but disabling chronic headaches refractory to extensive medical therapy and transiently improved after lumbar puncture. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eneurosurgical referral for possible lumboperitoneal shunt\u003C/strong\u003E, because the main uncontrolled problem in this patient is \u003Cstrong\u003Emedically refractory raised-pressure headache\u003C/strong\u003E, not progressive visual failure: central acuity is 20/20, papilledema is mild, and repeated 24-2 fields show only blind spot enlargement, which is an early papilledema-related field change rather than sight-threatening progressive optic neuropathy. In IIH, surgery is considered when there is either \u003Cstrong\u003Eprogressive visual loss despite maximal medical therapy\u003C/strong\u003E or \u003Cstrong\u003Eintractable headache despite appropriate medical management\u003C/strong\u003E; when visual function is threatened, \u003Cstrong\u003Eoptic nerve sheath fenestration\u003C/strong\u003E is often favored because it directly decompresses the perioptic subarachnoid space and protects the optic nerve, but it is less reliable for chronic headache control because intracranial pressure may remain elevated outside the optic nerve sheath. By contrast, CSF diversion procedures such as \u003Cstrong\u003Elumboperitoneal or ventriculoperitoneal shunting\u003C/strong\u003E lower CSF pressure more globally and are therefore the more appropriate surgical consideration when disabling headache is the dominant refractory symptom; the fact that the headaches improved for 12\u201324 hours after diagnostic lumbar punctures supports a pressure-responsive component. Published discussions of IIH surgery emphasize that operative treatment is generally reserved for worsening vision despite maximal medication or rapid visual decline, and CSF shunting can improve both vision and headache but carries substantial revision/failure risk, while ONSF is mainly a vision-protective procedure and often does not reliably treat headache.  Serial high-volume lumbar punctures are no longer a preferred long-term treatment because CSF is rapidly replenished, benefit is transient, and repeated procedures are burdensome and complication-prone; long-term prednisone is also inappropriate for chronic IIH headache because corticosteroids do not provide durable pressure control and add major adverse effects such as weight gain, which may worsen IIH risk. Therefore, with preserved vision but severe refractory pressure-responsive headaches, the next best step is \u003Cstrong\u003Eneurosurgical referral for possible lumboperitoneal shunt\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1832,
    "Name": "Optic nerve hypoplasia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is incorrect regarding the clinical associations and visual prognosis of optic nerve hypoplasia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethere is a strong correlation between optic disc size and visual acuity\u003C/strong\u003E, because optic nerve hypoplasia is a congenital, non-progressive reduction in the number of optic nerve axons, usually producing a small optic disc often surrounded by a peripapillary \u201Cdouble-ring\u201D sign, but the apparent disc size does \u003Cstrong\u003Enot\u003C/strong\u003E reliably predict visual function; some children with very small discs may retain surprisingly good acuity, while others with only mildly small or subtly hypoplastic discs may have severe visual impairment, nystagmus, visual field loss, or even no light perception, so the visual prognosis must be assessed clinically rather than inferred from disc size alone. The systemic evaluation is crucial because both unilateral and bilateral optic nerve hypoplasia can be associated with \u003Cstrong\u003Esepto-optic dysplasia / de Morsier syndrome\u003C/strong\u003E, including midline brain abnormalities such as absence or hypoplasia of the septum pellucidum or corpus callosum, pituitary hypoplasia, and hypothalamic-pituitary endocrine dysfunction; importantly, endocrine problems can occur even when MRI does not show obvious midline defects and even when ONH appears unilateral, so children with ONH require neuroimaging and endocrine assessment rather than reassurance based on laterality or visual acuity. The superior segmental optic nerve hypoplasia variant, often described as a \u201Ctopless disc,\u201D is classically associated with maternal diabetes during pregnancy and may produce corresponding inferior visual field defects.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1833,
    "Name": "MRI FLAIR sequence",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich MRI sequence suppresses the bright CSF signal and therefore best highlights periventricular white matter lesions, such as those seen in multiple sclerosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFLAIR\u003C/strong\u003E, because \u003Cstrong\u003Efluid-attenuated inversion recovery\u003C/strong\u003E is a modified T2-weighted MRI sequence that uses an inversion pulse to suppress the normally bright signal from free fluid, especially CSF, while preserving the high T2 signal from pathological tissue water; this makes periventricular and juxtacortical white matter lesions much easier to see because the bright CSF in the ventricles and sulci no longer obscures adjacent hyperintense plaques. At a neuro-ophthalmology level, this is particularly important in \u003Cstrong\u003Emultiple sclerosis\u003C/strong\u003E, where demyelinating plaques commonly occur in the periventricular white matter, often oriented perpendicular to the lateral ventricles along medullary veins, producing the classic \u201CDawson\u2019s fingers\u201D appearance; on standard T2 imaging, both CSF and demyelinating lesions are bright, reducing contrast near the ventricles, whereas FLAIR darkens the CSF and increases conspicuity of periventricular lesions. \u003Cstrong\u003ET1 weighted imaging\u003C/strong\u003E is best for anatomy and can show chronic \u201Cblack holes\u201D or gadolinium enhancement when contrast is used, but it is not the best sequence for detecting typical periventricular plaques; \u003Cstrong\u003EDWI\u003C/strong\u003E highlights restricted diffusion and is most useful for acute ischemia or some inflammatory/infective lesions rather than routine MS plaque detection; and \u003Cstrong\u003EStandard T2 weighted imaging\u003C/strong\u003E is sensitive to increased water content but leaves CSF bright, making periventricular lesions less clearly separated from adjacent ventricular fluid.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1834,
    "Name": "Internuclear ophthalmoplegia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical sign is the most sensitive indicator of internuclear ophthalmoplegia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESlowed adducting saccadic velocity\u003C/strong\u003E, because internuclear ophthalmoplegia results from a lesion of the \u003Cstrong\u003Emedial longitudinal fasciculus (MLF)\u003C/strong\u003E, which carries the internuclear signal from the abducens nucleus of one side to the contralateral medial rectus subnucleus of the oculomotor complex; when this pathway is damaged, the affected eye may still be able to adduct incompletely or even fully, especially in mild or partially recovered cases, but the \u003Cstrong\u003Espeed of the adducting saccade is characteristically slowed\u003C/strong\u003E, making it the most sensitive sign. The laterality of INO is named according to the eye with impaired or slowed adduction, so a right INO means the right eye has slowed adduction on attempted left gaze. \u003Cstrong\u003EAbducting nystagmus\u003C/strong\u003E of the fellow eye is common and reflects adaptive or dysmetric innervation during attempted conjugate gaze, but it is not as sensitive or as essential as slowed adducting saccadic velocity. \u003Cstrong\u003ELimited range of adduction\u003C/strong\u003E may occur in more obvious cases, but absence of a marked adduction deficit does not exclude INO if adducting saccades are slow. \u003Cstrong\u003EExotropia\u003C/strong\u003E is seen in wall-eyed bilateral INO and is therefore a more specific severe/bilateral pattern rather than the cardinal finding.\u0026nbsp;TThe key bedside distinction is that convergence is often relatively preserved in a classic INO because the medial rectus subnucleus and medial rectus muscle are intact, while horizontal conjugate gaze is impaired due to interruption of the internuclear MLF pathway; therefore, the most sensitive feature is \u003Cstrong\u003ESlowed adducting saccadic velocity\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
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    "Category": null,
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  },
  {
    "Id": 1835,
    "Name": "Oculopalatal myoclonus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich nystagmus syndrome characteristically appears after a delay of months to years following a brainstem lesion such as a stroke?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOculopalatal myoclonus\u003C/strong\u003E, because oculopalatal myoclonus is a distinctive delayed ocular motor syndrome that typically develops \u003Cstrong\u003Emonths to years after\u003C/strong\u003E an inciting lesion in the brainstem or cerebellar outflow pathways, especially a stroke affecting the \u003Cstrong\u003Ecentral tegmental tract\u003C/strong\u003E or related components of the \u003Cstrong\u003Edentato-rubro-olivary pathway\u003C/strong\u003E, also called the \u003Cstrong\u003Etriangle of Guillain-Mollaret\u003C/strong\u003E. This circuit links the \u003Cstrong\u003Edentate nucleus of the cerebellum\u003C/strong\u003E, the \u003Cstrong\u003Ered nucleus in the midbrain\u003C/strong\u003E, and the \u003Cstrong\u003Einferior olivary nucleus in the medulla\u003C/strong\u003E; disruption of this pathway causes trans-synaptic degeneration and the highly characteristic MRI finding of \u003Cstrong\u003Ehypertrophic olivary degeneration\u003C/strong\u003E, in which the inferior olive paradoxically enlarges rather than simply atrophies. Clinically, oculopalatal myoclonus produces acquired pendular, often vertical ocular oscillations together with rhythmic movements of the soft palate, and the rhythmic myorhythmia may also involve the face, pharynx, tongue, larynx, diaphragm, or limbs, sometimes causing audible clicking or involuntary throat/laryngeal sounds. \u003Cstrong\u003EPeriodic alternating nystagmus\u003C/strong\u003E instead reflects instability of the vestibular velocity-storage mechanism, often involving the cerebellar nodulus/uvula, and has a cyclical reversal pattern over minutes rather than delayed onset after olivary degeneration. \u003Cstrong\u003EUpbeat nystagmus\u003C/strong\u003E localizes to brainstem or cerebellar pathways, commonly medulla, midbrain, or anterior cerebellar vermis, but it is not defined by a delayed post-stroke onset. \u003Cstrong\u003ESee-saw nystagmus\u003C/strong\u003E localizes classically to parasellar or midbrain lesions and may be associated with bitemporal hemianopic field loss when the optic chiasm is involved.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1836,
    "Name": "Physiologic anisocoria",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich cause of unequal pupil size typically produces the same degree of anisocoria in both bright and dim illumination?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPhysiologic anisocoria\u003C/strong\u003E, because physiologic anisocoria is a benign, common cause of unequal pupil size in which the difference is usually small, typically around 1 mm or less, with normal light and near responses and no associated ptosis, ophthalmoplegia, pain, or neurologic signs; the key clinical feature is that the anisocoria remains approximately the same in bright light and in darkness, because neither the sympathetic dilator pathway nor the parasympathetic constrictor pathway is truly pathologically weak.  Anisocoria should be analyzed by asking whether the difference is greater in the dark or greater in the light: if anisocoria is greater in the dark, the smaller pupil is abnormal and a sympathetic lesion such as Horner syndrome should be considered; carotid dissection and cluster headache can both produce ipsilateral Horner syndrome, so the affected miotic pupil dilates poorly in darkness and anisocoria becomes more obvious in the dark.  If anisocoria is greater in bright light, the larger pupil is abnormal, indicating impaired parasympathetic constriction, as may occur with a pupil-involving third nerve palsy from a posterior communicating artery aneurysm, where compressive involvement of superficial parasympathetic fibers causes mydriasis that becomes more apparent in light.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1837,
    "Name": "Functional color vision loss",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 15-year-old otherwise healthy male comes in with a complaint of sudden loss of color vision in both eyes for the last 2 weeks. He had a head CT in the ER about a week ago which was normal. His neuro-ophthalmic examination shows 20/20 vision in both eyes with normal pupillary testing and no afferent pupillary defect. He identified 3/9 Ishihara color plates OU but in both eyes missed the color plates shown above. His confrontation visual fields were full. Motility and alignment were normal. Slit lamp examination and dilated fundus examination were normal with healthy appearing optic nerves in both eyes. Based on his history and examination, what is the next best step in management?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-07-31-912b2597-bfbc-4b9f-b271-197aee92e8f6.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EReassurance that his color vision will return\u003C/strong\u003E, because the examination provides a positive internal inconsistency supporting \u003Cstrong\u003Efunctional visual loss\u003C/strong\u003E rather than merely failing to identify an organic lesion: the patient reports profound acquired bilateral dyschromatopsia yet retains 20/20 acuity, full confrontation fields, normal pupils without a relative afferent pupillary defect, and normal macular and optic nerve examinations, while also failing a control/demonstration plate whose figure is distinguished predominantly by luminance contrast and should therefore remain visible even in severe congenital or acquired color deficiency. Ishihara control plates are designed so that people with normal color vision and those with color vision deficiency can identify the figure; inconsistent responses to control and diagnostic plates can provide objective evidence of non-organic visual dysfunction. Published reports describe using incompatible Ishihara responses as a positive sign of functional visual loss rather than treating the diagnosis as one of exclusion alone. Genuine acquired dyschromatopsia should prompt localization to the macula, optic nerve, chiasm, or retrochiasmal visual pathways, but clinically meaningful bilateral optic neuropathy would usually produce some combination of reduced acuity, contrast sensitivity loss, central or cecocentral field defects, impaired pupillary responses if asymmetric, or optic disc change over time; Leber hereditary optic neuropathy may initially have subtle disc findings, but mitochondrial testing is not justified by a physiologically incompatible color-plate response with otherwise entirely normal visual function. MRI is likewise unnecessary when positive functional signs are demonstrated and there are no localizing neurologic or neuro-ophthalmic abnormalities, while the Farnsworth-Munsell 100-hue test would only characterize the reported deficit further without resolving the fundamental inconsistency. Functional visual loss should be managed non-confrontationally by explaining that the visual pathways appear structurally healthy, offering confident reassurance that recovery is expected, arranging follow-up, and remaining alert for any subsequent objective abnormality rather than accusing the patient of deliberate fabrication; therefore, the best management is \u003Cstrong\u003EReassurance that his color vision will return\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1838,
    "Name": "Optic nerve pit",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement does not accurately describe the usual appearance, visual function, or associated retinal and visual field findings of optic nerve pits?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethey generally occur in eyes with poor visual acuity (e.g. visual acuity \u0026lt; 20/200)\u003C/strong\u003E, because a congenital optic nerve pit is usually a unilateral, solitary, oval excavation of the optic disc, most often situated inferotemporally and appearing gray, white, or yellow, but the pit itself generally does not reduce central visual acuity; vision is usually normal unless optic disc pit maculopathy develops, with intraretinal schisis-like fluid, serous macular detachment, cystoid change, or chronic retinal pigment epithelial disturbance involving the fovea. Optic disc pit maculopathy is reported in approximately 25\u201375% of affected eyes and may cause substantial central visual loss, metamorphopsia, and a central scotoma, but visual acuity below 20/200 is therefore a complication-dependent finding rather than the typical baseline state of an eye containing an optic nerve pit. The pit represents herniation of dysplastic retinal tissue through a defect in the lamina cribrosa, sometimes extending toward the subarachnoid space, although the source of macular fluid remains debated and may involve vitreous fluid, cerebrospinal fluid, or leakage from vessels within the pit; OCT typically demonstrates schisis-like separation within the inner retinal layers followed by outer retinal dehiscence and secondary subretinal fluid accumulation.  Optic nerve pits can also produce nerve fiber bundle visual field abnormalities, including paracentral or arcuate scotomas, an enlarged blind spot, localized peripheral constriction, or a nasal or temporal step, even when central acuity remains preserved.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1839,
    "Name": "Thyroid-associated orbitopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old patient with Graves disease and confirmed thyroid-associated orbitopathy reports binocular diplopia that is most pronounced in upgaze. Ocular motility examination demonstrates unequal limitation of elevation, graded -2 in the right eye and -1 in the left eye. How should the mechanism and comitance of this strabismus be classified?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERestrictive and incomitant\u003C/strong\u003E, because thyroid-associated orbitopathy produces a restrictive myopathy rather than a primary neurogenic paresis: autoimmune activation of orbital fibroblasts causes glycosaminoglycan accumulation, edema, enlargement, and ultimately fibrosis of the extraocular muscles and surrounding connective tissues, mechanically limiting rotation of the globe. The inferior rectus is most frequently affected, followed by the medial rectus, and fibrotic shortening of the inferior rectus restricts relaxation and elongation during attempted elevation, producing an upgaze deficit and a hypotropic tendency rather than true weakness of the superior rectus.  The deviation is \u003Cstrong\u003Eincomitant\u003C/strong\u003E because its magnitude varies with gaze direction: diplopia is greatest in upgaze, where the restricted inferior rectus is maximally stretched, and the unequal elevation deficits of -2 and -1 show asymmetric restriction between the two eyes. In comitant strabismus, by contrast, the angle remains approximately equal in all diagnostic positions of gaze, as is typical of many longstanding congenital deviations; both paretic and restrictive strabismus are usually incomitant because muscle force or excursion differs across gaze positions. Forced duction testing would be expected to show mechanical resistance to elevation, whereas force-generation testing may demonstrate preserved contractile ability of the superior rectus, helping distinguish restrictive thyroid myopathy from an elevator paresis.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1840,
    "Name": "Ishihara pseudoisochromatic plates",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich principal of color vision deficiency are Ishihara pseudoisochromatic plates specifically designed to detect during screening?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ered-green deficiency\u003C/strong\u003E, because Ishihara pseudoisochromatic plates are designed primarily to screen for congenital \u003Cstrong\u003Eprotan and deutan defects\u003C/strong\u003E, which arise from abnormalities of the long-wavelength-sensitive and medium-wavelength-sensitive cone systems, respectively; the plates contain figures formed by colored dots that are matched for luminance but differ along red-green chromatic confusion axes, preventing affected individuals from distinguishing the figure from its background reliably. Ishihara testing is rapid and highly useful for detecting red-green deficiency, but it is a screening rather than a comprehensive quantitative test: it does not reliably detect \u003Cstrong\u003Etritan or blue-yellow defects\u003C/strong\u003E, does not adequately grade severity, and cannot fully characterize acquired dyschromatopsia. More extensive assessment can be performed with the \u003Cstrong\u003EFarnsworth Panel D-15\u003C/strong\u003E, \u003Cstrong\u003ELanthony desaturated D-15\u003C/strong\u003E, or \u003Cstrong\u003EFarnsworth-Munsell 100-hue test\u003C/strong\u003E, which require the patient to arrange colored caps according to hue and can reveal protan, deutan, tritan, or nonspecific error axes; the Farnsworth-Munsell 100-hue test provides particularly detailed quantification but is time-consuming and therefore unsuitable for routine screening. Current comparisons confirm that Ishihara plates are intended for rapid red-green screening, while the D-15 and related arrangement tests can classify defects across red-green and blue-yellow axes.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1841,
    "Name": "Third nerve nuclear lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich clinical characteristic distinguishes a lesion involving the oculomotor nuclear complex from lesions affecting the oculomotor fascicles within the midbrain or the third cranial nerve after its emergence from the brainstem?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBilaterality\u003C/strong\u003E, because the oculomotor nuclear complex has a distinctive midline subnuclear organization that can produce bilateral findings even when the lesion is anatomically unilateral. The oculomotor nuclear complex lies in the rostral midbrain near the cerebral aqueduct at the level of the superior colliculus; the medial rectus, inferior rectus, and inferior oblique subnuclei principally innervate the ipsilateral muscles, but the superior rectus subnucleus innervates the \u003Cstrong\u003Econtralateral superior rectus\u003C/strong\u003E, with its axons decussating through or close to the opposite superior rectus subnucleus. In addition, both levator palpebrae superioris muscles receive innervation from a single unpaired midline \u003Cstrong\u003Ecentral caudal nucleus\u003C/strong\u003E. Consequently, a nuclear third nerve lesion classically produces an\u003Cspan style=\u0022font-weight: bold;\u0022\u003E ipsilateral third nerve palsy\u003C/span\u003E accompanied by \u003Cstrong\u003Econtralateral superior rectus weakness and bilateral, often incomplete, ptosis\u003C/strong\u003E, a pattern not expected from an isolated fascicular or peripheral third nerve lesion.  Fascicular lesions affect the exiting axons within the midbrain after leaving the nuclear complex and usually produce an ipsilateral third nerve palsy with accompanying crossed neurological signs determined by adjacent structure involvement, such as contralateral hemiparesis in Weber syndrome, tremor or ataxia in Benedikt syndrome, or cerebellar ataxia in Nothnagel syndrome, but do not intrinsically produce the characteristic bilateral nuclear pattern. Ptosis alone is not distinguishing because it can occur with nuclear, fascicular, subarachnoid, cavernous sinus, or orbital third nerve lesions, and pupillary involvement is likewise nonlocalizing because parasympathetic dysfunction may occur at several points along the oculomotor pathway.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1842,
    "Name": "Humphrey visual field reliability",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EDuring a 24-2 Humphrey visual field examination, a patient with limited attention repeatedly presses the response button when test stimuli are presented at the previously mapped physiologic blind spot. Which reliability index would be most directly elevated by these responses?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ehigh fixation losses\u003C/strong\u003E, because the Humphrey Field Analyzer traditionally monitors fixation using the \u003Cstrong\u003EHeijl-Krakau blind-spot method\u003C/strong\u003E: after mapping the physiologic blind spot, the perimeter intermittently presents suprathreshold stimuli at that location, where a correctly fixating patient should not perceive them because the optic disc contains no photoreceptors; a response to such a stimulus is recorded as a fixation loss, on the assumption that fixation has shifted and the stimulus has fallen onto seeing retina. The fixation-loss index is expressed as the number of responses to blind-spot checks divided by the total number of blind-spot stimuli presented, and a high rate therefore most directly reflects unstable fixation in this scenario. However,\u0026nbsp; an elevated fixation-loss rate must not be interpreted mechanically: responses at the presumed blind spot may also result from incorrect initial blind-spot mapping, head tilt, spectacle or trial-lens displacement, anatomic variation in blind-spot location, or a generally trigger-happy patient producing false-positive responses, so the gaze tracker, technician observations, raw field pattern, and other reliability indices must be reviewed together; if the blind spot was mapped incorrectly, the result may represent \u003Cstrong\u003Epseudofixation loss\u003C/strong\u003E rather than genuine fixation instability.  A \u003Cstrong\u003Ehigh false-positive response rate\u003C/strong\u003E is generated when the patient responds without a presented stimulus or responds implausibly quickly, often producing artificially high sensitivities and a \u201Cwhite scotoma\u201D appearance; a \u003Cstrong\u003Ehigh false-negative response rate\u003C/strong\u003E occurs when the patient fails to respond to a brighter stimulus at a location where a dimmer stimulus was previously seen, although this may also be elevated in genuine advanced field loss; and \u003Cstrong\u003Ehighly negative mean deviation\u003C/strong\u003E is a global index of generalized depression relative to age-matched normal sensitivity, not a reliability parameter.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1843,
    "Name": "Nystagmus terminology",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following descriptive terms of nystagmus is correctly defined below?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EDissociated nystagmus: the amplitude of oscillations differs in each eye\u003C/strong\u003E, because dissociated nystagmus describes a binocular oscillation in which the waveform is present in both eyes but its amplitude differs between the eyes, so the nystagmus may be substantially more prominent in one eye than in the fellow eye; the distinction is quantitative rather than directional. By contrast, \u003Cstrong\u003Edisconjugate nystagmus\u003C/strong\u003E, also termed \u003Cstrong\u003Edisjunctive nystagmus\u003C/strong\u003E, means that the two eyes oscillate differently in direction, phase, or plane, rather than indicating nystagmus confined to one eye; for example, the eyes may beat in opposite horizontal directions, as in convergence-retraction or convergent-divergent oscillations, or move in opposing vertical-torsional directions, as in see-saw nystagmus. A truly monocular oscillation should be described as \u003Cstrong\u003Emonocular nystagmus\u003C/strong\u003E, not merely disconjugate or disjunctive. The \u003Cstrong\u003Enull point\u003C/strong\u003E is also defined inaccurately in the listed statement: it is the gaze position in which nystagmus intensity is minimal and foveation and visual acuity are usually optimal, but the oscillation is generally dampened rather than completely absent; patients with infantile nystagmus may adopt a compensatory face turn, chin elevation or depression, or head tilt to place the eyes within this null zone.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1844,
    "Name": "Pituitary masses",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich visual field loss is classically produced when an enlarging pituitary mass compresses the optic chiasm?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBilateral mostly superotemporal deficits respecting the vertical midline but extending to a complete bitemporal hemianopia late in the disease course\u003C/strong\u003E, because an enlarging pituitary mass typically extends superiorly from the sella turcica and compresses the inferior central portion of the optic chiasm, where the decussating inferonasal retinal ganglion cell axons are particularly vulnerable; these fibers carry information from the \u003Cstrong\u003Esuperotemporal visual fields\u003C/strong\u003E, so early chiasmal compression commonly produces bilateral superotemporal defects that respect the vertical meridian. As compression progresses superiorly through the chiasm, additional crossing nasal retinal fibers become involved, expanding the defects into the remaining temporal fields and eventually producing a complete bitemporal hemianopia. Pituitary adenomas are the most common adult cause of optic chiasmal compression, and the classic field progression is from superior temporal loss to complete bitemporal hemianopia.  The defect may be asymmetric because the chiasm is not always positioned centrally over the pituitary gland and the mass itself may expand asymmetrically; a \u003Cstrong\u003Epostfixed chiasm\u003C/strong\u003E may expose the optic nerve\u2013chiasm junction and produce a junctional pattern consisting of central or cecocentral loss in one eye with a superotemporal defect in the fellow eye, whereas a \u003Cstrong\u003Eprefixed chiasm\u003C/strong\u003E may permit posterior extension toward the optic tracts and generate a homonymous defect. A defect limited to the central 5\u201310 degrees is uncommon and does not represent the classic pituitary pattern, while initial inferotemporal loss would imply preferential involvement of superior nasal retinal fibers and is more characteristic of compression directed from above rather than the usual inferior compression produced by a pituitary mass.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1845,
    "Name": "Convergence-retraction nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is actually a misnomer in that it does not meet the definition of a true nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EConvergence-retraction nystagmus\u003C/strong\u003E, because true nystagmus is a repetitive ocular oscillation initiated by an involuntary slow drift away from the fixation target, followed either by a corrective fast saccade in jerk nystagmus or by an oppositely directed slow phase in pendular nystagmus; convergence-retraction \u201Cnystagmus,\u201D however, is neither a rhythmic oscillation nor a sequence containing a pathologic slow phase. Instead, the eyes make repetitive, irregular convergence movements with globe retraction due to simultaneous co-contraction of the medial and lateral rectus muscles during attempted upward saccades. This phenomenon is a component of \u003Cstrong\u003Edorsal midbrain syndrome, or Parinaud syndrome\u003C/strong\u003E, caused by dysfunction of the rostral midbrain vertical gaze pathways, particularly structures around the posterior commissure and riMLF, and may accompany supranuclear upgaze palsy, light-near dissociation, eyelid retraction (Collier sign), and skew deviation. Convergence-retraction movements are best elicited by asking the patient to follow a downward-moving optokinetic target: the eyes follow the target downward and then attempt a rapid upward refixation, during which the abnormal convergence and retraction occur. Periodic alternating nystagmus, congenital nystagmus, and downbeat nystagmus all contain genuine oscillatory waveforms, whereas convergence-retraction nystagmus is more accurately described as \u003Cstrong\u003Econvergence-retraction saccades\u003C/strong\u003E, making \u003Cstrong\u003EConvergence-retraction nystagmus\u003C/strong\u003E the misnomer.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1846,
    "Name": "Drug-induced intracranial hypertension",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed medication has a recognized association with the development of secondary intracranial hypertension?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ecyclosporine\u003C/strong\u003E, because cyclosporine has been reported as a cause of drug-induced intracranial hypertension, although the strength of this association is weaker than that established for the principal high-risk medications. A systematic review classified \u003Cstrong\u003Evitamin A derivatives\u003C/strong\u003E, particularly isotretinoin and all-trans retinoic acid, \u003Cstrong\u003Etetracycline-class antibiotics\u003C/strong\u003E, recombinant growth hormone, and lithium among the drugs most strongly associated with intracranial hypertension; corticosteroid exposure or withdrawal has a moderate association, while cyclosporine belongs to a group with a weaker but documented association.  The syndrome may present with headache, pulse-synchronous tinnitus, transient visual obscurations, horizontal diplopia from sixth nerve palsy, and papilloedema, with the principal ophthalmic risk being permanent visual field loss from chronic pressure-related optic neuropathy; management requires withdrawal of the suspected medication where clinically feasible, exclusion of cerebral venous sinus thrombosis and other secondary causes, formal visual field monitoring, and intracranial pressure-lowering treatment when indicated. \u003Cstrong\u003Efurosemide (Lasix)\u003C/strong\u003E is not a typical cause and may instead be used as an adjunctive pressure-lowering agent when acetazolamide is inadequate or poorly tolerated; \u003Cstrong\u003Esildenafil (Viagra)\u003C/strong\u003E has been discussed mainly in relation to possible non-arteritic anterior ischaemic optic neuropathy rather than intracranial hypertension; and \u003Cstrong\u003Eescitalopram (Lexapro)\u003C/strong\u003E is not a classically established cause.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1847,
    "Name": "Right optic tract lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIf a lesion involves the right optic tract, which of the listed pupillary or visual field findings could be expected on clinical examination?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ean afferent pupillary defect (APD) in the left eye\u003C/strong\u003E, because the right optic tract carries visual and pupillomotor afferent fibers originating from the \u003Cstrong\u003Eright temporal retina\u003C/strong\u003E and \u003Cstrong\u003Eleft nasal retina\u003C/strong\u003E, and the nasal retinal contribution is quantitatively greater because more retinal fibers decussate at the optic chiasm than remain uncrossed; consequently, a right optic tract lesion disproportionately damages crossed fibers originating from the left eye, producing a relative afferent pupillary defect in the \u003Cstrong\u003Eleft eye\u003C/strong\u003E, contralateral to the tract lesion. Physiologic studies estimate that approximately 54\u201367% of human pupillomotor afferent fibers decussate, explaining the contralateral RAPD associated with a unilateral optic tract lesion.  The corresponding visual field defect would be a \u003Cstrong\u003Eleft homonymous hemianopia\u003C/strong\u003E, usually relatively incongruous because the lesion lies anteriorly in the retrochiasmal pathway, but that finding is not listed among the choices; a right homonymous hemianopia would instead indicate a lesion affecting the left retrochiasmal visual pathway, while a hemianopic defect confined to one eye would not be anatomically compatible with an optic tract lesion because each tract contains fibers from both eyes. Chronic optic tract disease may also produce a characteristic pattern of trans-synaptic optic atrophy, with \u003Cstrong\u003Eband or bow-tie atrophy in the contralateral optic disc\u003C/strong\u003E from loss of crossed nasal retinal fibers and \u003Cstrong\u003Ehourglass atrophy in the ipsilateral disc\u003C/strong\u003E from loss of uncrossed temporal retinal fibers. A recent optic tract lesion series found that homonymous defects were predominantly incongruous and that a contralateral RAPD was present in a subset of affected patients.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1848,
    "Name": "Benedikt syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich named brainstem syndrome is characterized by an oculomotor nerve palsy on the same side, together with tremor or other involuntary movements affecting the opposite side of the body?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBenedikt syndrome\u003C/strong\u003E, because this crossed midbrain syndrome results from a lesion involving the \u003Cstrong\u003Eoculomotor nerve fascicles\u003C/strong\u003E together with the \u003Cstrong\u003Ered nucleus and adjacent dentato-rubro-thalamic pathways\u003C/strong\u003E; involvement of the third nerve fascicles produces an ipsilateral oculomotor palsy with ptosis, impaired adduction, elevation and depression, a \u201Cdown-and-out\u201D eye position, and possible pupillary dilatation, while disruption of the red nucleus or nearby superior cerebellar peduncular fibers produces contralateral \u003Cstrong\u003EHolmes or rubral tremor\u003C/strong\u003E, ataxia, choreoathetosis, or other involuntary movements. Holmes tremor is characteristically slow and coarse, with resting, postural, and intention components, and it may emerge after a delay following the causative midbrain lesion. A useful mnemonic for distinguishing these crossed brainstem syndromes is \u003Cstrong\u003E\u201CWeak Weber, Bobbing Benedikt, Clumsy Claude\u201D\u003C/strong\u003E: \u003Cstrong\u003EWeber is weak\u003C/strong\u003E because cerebral peduncle involvement causes contralateral hemiparesis; \u003Cstrong\u003EBenedikt is bobbing\u003C/strong\u003E because red nucleus and cerebellothalamic pathway involvement causes contralateral tremor or involuntary movement; and \u003Cstrong\u003EClaude is clumsy\u003C/strong\u003E because superior cerebellar peduncle involvement produces contralateral cerebellar ataxia. \u003Cstrong\u003ERaymond syndrome\u003C/strong\u003E is a pontine syndrome involving the sixth nerve fascicle and corticospinal tract, producing an ipsilateral abducens palsy with contralateral hemiparesis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1849,
    "Name": "Jerk nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is NOT a defining characteristic of jerk nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENomenclature based on direction of the slow phase\u003C/strong\u003E, because jerk nystagmus consists of two unequal phases: a pathological \u003Cstrong\u003Eslow phase\u003C/strong\u003E, during which the eyes drift away from the desired fixation position, followed by a corrective \u003Cstrong\u003Efast phase\u003C/strong\u003E, representing a rapid saccade that returns the eyes toward the target; by convention, jerk nystagmus is named according to the direction of its \u003Cstrong\u003Efast phase\u003C/strong\u003E, not its slow phase, so a right-beating nystagmus has a rightward fast phase and a leftward slow drift. Jerk nystagmus is rhythmic and can be characterized quantitatively by its \u003Cstrong\u003Eamplitude\u003C/strong\u003E, \u003Cstrong\u003Efrequency\u003C/strong\u003E, and \u003Cstrong\u003Eslow-phase velocity\u003C/strong\u003E, with intensity conventionally expressed as amplitude multiplied by frequency; waveform analysis may also distinguish constant-velocity, decreasing-velocity, and increasing-velocity slow phases, which can assist clinical localization and differentiation of vestibular from infantile nystagmus. Pendular nystagmus differs because the oscillations occur in both directions with approximately similar velocity and no clearly identifiable corrective fast phase, although pendular nystagmus still qualifies as true nystagmus because it remains a repetitive rhythmic ocular oscillation. In contrast, nystagmoid movements such as square-wave jerks and superior oblique myokymia are not true nystagmus because they do not consist of a continuously rhythmic oscillation initiated by a pathological slow phase.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1850,
    "Name": "Gaze-evoked amaurosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EGaze-evoked amaurosis occurs when there is recurrent transient monocular vision loss when looking in a particular direction. What does the presence of gaze-evoked amaurosis suggest?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAn orbital mass\u003C/strong\u003E, because gaze-evoked amaurosis is a position-dependent, transient monocular visual loss classically caused by an orbital lesion that intermittently compresses or stretches the optic nerve, its pial vascular supply, or the retinal circulation when the eye rotates into a particular direction; vision typically recovers within seconds after the eye returns to primary position. Intraconal pathology is the classic association and accounts for most reported cases, including cavernous venous malformation, optic nerve sheath meningioma, optic glioma, and other orbital tumors, although inflammatory disease, foreign bodies, orbital fractures, thyroid orbitopathy, and sufficiently large extraconal lesions may occasionally produce the same phenomenon. The proposed mechanisms are transient interruption of axonal conduction from mechanical optic nerve deformation and reversible ischemia caused by gaze-dependent compromise of the optic nerve or retinal vasculature; examination during the provoking gaze position may reveal reduced acuity, color desaturation, a new or increased relative afferent pupillary defect, or optic disc vascular change, while associated orbital signs may include proptosis, globe displacement, restricted motility, optic disc edema, or optic atrophy.  The finding warrants dedicated contrast-enhanced orbital imaging, usually thin-section MRI of the orbits with fat suppression, because primary-position examination may be relatively normal and the compressive effect can be evident only in eccentric gaze. Multiple sclerosis may produce optic neuritis or internuclear ophthalmoplegia but does not classically cause reproducible gaze-position-dependent monocular blackout; giant cell arteritis can cause transient monocular ischemic loss but the episodes are not typically generated by a specific direction of gaze; and hypertensive retinopathy produces retinal vascular changes rather than this positional phenomenon.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1851,
    "Name": "Homonymous hemianopia in an adult",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old patient is found to have homonymous hemianopsia, while central visual acuity remains normal. Which of the listed conditions is the most frequent underlying cause of this field defect in adults?\u003Cbr\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eischemic stroke\u003C/strong\u003E, because homonymous hemianopia localizes to a lesion of the retrochiasmal visual pathway, including the optic tract, lateral geniculate nucleus, optic radiations, or occipital cortex, and vascular disease is the most frequent cause in adults, with cerebral infarction being more common than intracranial hemorrhage; lesions within the posterior cerebral artery territory are particularly important because the posterior cerebral artery supplies the occipital visual cortex, although middle cerebral artery infarction involving the temporal or parietal optic radiations can produce the same field pattern. Published clinical reviews report that vascular causes account for approximately 42% to 89% of adult homonymous hemianopia, followed by neoplasms, trauma, surgical injury, and other neurological conditions.  Normal visual acuity does not argue against a substantial homonymous field defect because bilateral central acuity can remain intact when macular representation is spared, particularly with occipital lesions, or when the lesion predominantly affects peripheral visual cortex; patients may incorrectly report that vision is blurred in one eye, although formal monocular testing demonstrates loss of the same side of the visual field in both eyes.  The congruity of the defect can assist localization, with more anterior retrochiasmal lesions tending to produce relatively incongruous defects and posterior occipital lesions producing more congruous defects, although this rule is not absolute. Any newly identified homonymous hemianopia requires urgent neuroimaging, preferably MRI of the brain with appropriate vascular evaluation when the onset is acute, even if visual acuity and the ocular examination are normal. In contrast, neoplasms and trauma are important causes but are less frequent than vascular events in adults, while neoplasms are proportionally more prominent among pediatric cases.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1852,
    "Name": "Demyelinating optic neuritis versus NAION",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAt initial presentation, demyelinating optic neuritis may need to be differentiated from non-arteritic anterior ischemic optic neuropathy. Which listed clinical feature is most characteristic of demyelinating optic neuritis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EEye pain\u003C/strong\u003E, because typical demyelinating optic neuritis usually produces acute or subacute monocular visual loss accompanied by periocular or retro-orbital pain, characteristically exacerbated by eye movement, whereas NAION usually causes sudden, painless monocular visual loss that is often noticed on awakening. The pain of optic neuritis is thought to reflect inflammation and mechanical traction at the orbital optic nerve sheath and adjacent extraocular muscle insertions during eye movement, and it may precede or accompany visual loss; associated findings commonly include dyschromatopsia, reduced contrast sensitivity, a central or cecocentral scotoma, and a relative afferent pupillary defect in unilateral or asymmetric disease.  \u003Cstrong\u003EOptic disc edema in the involved eye\u003C/strong\u003E favors NAION when it is segmental or diffuse and accompanied by peripapillary splinter hemorrhages and a small crowded fellow disc, but it is not an absolute discriminator because approximately one-third of typical demyelinating optic neuritis cases have anterior disc swelling, while the remainder have retrobulbar neuritis with a normal-appearing optic nerve at presentation.  \u003Cstrong\u003EAltitudinal visual field loss\u003C/strong\u003E is strongly suggestive of NAION, particularly an inferior altitudinal defect from superior disc involvement, but altitudinal defects may occasionally occur in optic neuritis and therefore are not completely specific; conversely, central defects are more typical of demyelinating optic neuritis. \u003Cstrong\u003EPoor visual acuity\u003C/strong\u003E can occur at presentation in either disorder, so the initial level of acuity alone is less useful than the age, tempo, pain pattern, disc appearance, field morphology, vascular risk factors, and subsequent recovery. When the clinical distinction remains uncertain, fat-suppressed, gadolinium-enhanced orbital MRI is particularly helpful because acute demyelinating optic neuritis generally shows optic nerve enhancement, whereas NAION usually does not demonstrate the same longitudinal intraneural enhancement pattern.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1853,
    "Name": "Right optic tract lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich right-sided lesion along the afferent visual pathway would be expected to produce a relative afferent pupillary defect in the left eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA right optic tract lesion\u003C/strong\u003E, because the right optic tract contains uncrossed fibers from the right temporal retina and crossed fibers from the left nasal retina, and there is a physiological preponderance of crossed pupillomotor fibers at the optic chiasm; a right optic tract lesion therefore interrupts afferent input from both eyes but causes a relatively greater reduction in input originating from the left eye, producing a \u003Cstrong\u003Eleft relative afferent pupillary defect\u003C/strong\u003E, contralateral to the side of the tract lesion. Pupillographic studies estimate that approximately 54%\u201367% of pupillomotor afferent fibers decussate, supporting this crossed-fiber asymmetry as the basis of the contralateral RAPD.  The accompanying field defect would be a \u003Cstrong\u003Eleft homonymous hemianopia\u003C/strong\u003E, often relatively incongruous because the optic tract is an anterior retrochiasmal structure. A right optic nerve lesion would instead produce a right RAPD and monocular right-eye dysfunction. Lesions of the right optic radiations or right primary visual cortex may also produce a left homonymous visual field defect, but they occur posterior to the point where retinal afferents leave the visual pathway for the pretectal pupillary nuclei and therefore do not ordinarily produce a clinically detectable RAPD. With chronic optic tract injury, trans-synaptic degeneration may additionally produce \u003Cstrong\u003Eband or bow-tie optic atrophy in the contralateral left eye\u003C/strong\u003E from loss of crossed nasal retinal fibers and \u003Cstrong\u003Ehourglass optic atrophy in the ipsilateral right eye\u003C/strong\u003E from loss of uncrossed temporal retinal fibers\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1854,
    "Name": "Isolated medial longitudinal fasciculus lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen a lesion is confined to the medial longitudinal fasciculus within the pons or midbrain, which additional ocular alignment abnormality frequently occurs?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESkew deviation\u003C/strong\u003E, because the medial longitudinal fasciculus is not limited to transmitting horizontal internuclear signals from the abducens nucleus to the contralateral medial rectus subnucleus; the MLF also carries ascending vestibular and cerebellar signals from the vestibular nuclei to the third and fourth nerve nuclear complexes, coordinating vertical alignment, ocular torsion, and the vestibulo-ocular reflex. Consequently, an MLF lesion classically produces an ipsilateral \u003Cstrong\u003Einternuclear ophthalmoplegia\u003C/strong\u003E, characterized by slowing or limitation of adduction during horizontal conjugate gaze with abducting nystagmus of the fellow eye, but interruption of the accompanying otolith-ocular pathways may also produce \u003Cstrong\u003Eskew deviation\u003C/strong\u003E, an acquired vertical misalignment that cannot be attributed to dysfunction of a single extraocular muscle or cranial nerve. The hypertropic eye may be ipsilateral to the MLF lesion, particularly in certain pontine or midbrain internuclear ophthalmoplegia patterns, although the laterality of skew depends on the level of the lesion and the crossing of graviceptive pathways; skew may also form part of the \u003Cstrong\u003Eocular tilt reaction\u003C/strong\u003E, together with conjugate ocular torsion and head tilt. Skew deviation is often comitant but may be incomitant, and the upright-supine test may support the diagnosis when the vertical deviation decreases significantly in the supine position.  \u003Cstrong\u003EA contralateral gaze palsy\u003C/strong\u003E is incorrect because a horizontal gaze palsy means that both eyes cannot look toward one side and usually requires involvement of the ipsilateral PPRF or abducens nucleus, whereas an isolated MLF lesion impairs adduction of one eye without preventing the fellow eye from abducting. \u003Cstrong\u003EDivergence insufficiency\u003C/strong\u003E produces distance esotropia greater than near esotropia and is not the characteristic consequence of an isolated MLF lesion, while \u003Cstrong\u003EAn up-gaze palsy\u003C/strong\u003E usually reflects rostral midbrain involvement of vertical gaze structures such as the riMLF or posterior commissure rather than the MLF alone.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1855,
    "Name": "Giant cell arteritis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with suspected giant cell arteritis who has already commenced corticosteroid therapy, for how long can temporal artery biopsy generally be deferred while retaining an acceptable histopathological diagnostic yield?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E1-2 weeks\u003C/strong\u003E, because suspected giant cell arteritis is an ophthalmic and medical emergency in which corticosteroid treatment must begin immediately to reduce the risk of irreversible visual loss in the fellow eye, and treatment should never be delayed while awaiting temporal artery biopsy; the characteristic histopathological abnormalities, including transmural granulomatous inflammation, multinucleated giant cells, fragmentation of the internal elastic lamina, and intimal hyperplasia, do not disappear immediately after corticosteroid initiation, so biopsy remains diagnostically useful during the first 1-2 weeks of treatment. The American College of Rheumatology guidance recommends obtaining the biopsy within 14 days of starting glucocorticoids, although positive histology may persist for several weeks or occasionally much longer. The biopsy should nevertheless be arranged as soon as practical and should include an adequately long arterial specimen because GCA produces discontinuous \u003Cstrong\u003Eskip lesions\u003C/strong\u003E; a negative biopsy therefore does not exclude the disease when clinical suspicion remains high, particularly if the specimen is short, treatment has been prolonged, or inflammation is confined to extracranial large vessels. Ultrasound behaves differently from biopsy because the arterial \u003Cstrong\u003Ehalo sign\u003C/strong\u003E may diminish rapidly after corticosteroids, so vascular imaging should be obtained promptly when used as part of the diagnostic pathway. The essential examination principle is \u003Cstrong\u003Etreat first and biopsy promptly afterward\u003C/strong\u003E: corticosteroids prevent further ischemic injury but rarely restore vision already lost from arteritic anterior ischemic optic neuropathy, central retinal artery occlusion, or posterior ischemic optic neuropathy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1856,
    "Name": "Recurrent bilateral visual blurring with vertigo and imbalance",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old has experienced recurrent episodes of simultaneous bilateral visual blurring for 6 months. Each episode lasts between 10 seconds and 10 minutes, is accompanied by vertigo and impaired balance, and resolves completely. There is no headache, although a sibling has migraine, and there are no symptoms of jaw claudication, diplopia, myalgia, fever, or unintentional weight loss. Carotid Doppler ultrasonography and brain MRI have been normal, and the clinical examination is unremarkable between episodes. What is the most appropriate next investigation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cstrong\u003EOrder a CT-angiogram (CTA) of the brain\u003C/strong\u003E, because recurrent simultaneous bilateral visual disturbance accompanied by transient vertigo and disequilibrium in a 70-year-old localizes to episodic dysfunction of the posterior circulation rather than to either eye individually; the occipital cortices, brainstem vestibular pathways, and cerebellum are supplied by the vertebrobasilar system, so transient hypoperfusion from vertebral or basilar atherosclerotic stenosis, embolism, or another vascular abnormality can produce binocular visual blurring together with vertigo, ataxia, imbalance, dysarthria, diplopia, or other brainstem symptoms. Vertebrobasilar insufficiency is particularly important in older patients with vascular risk because it represents a posterior-circulation transient ischemic syndrome and carries a subsequent stroke risk; a normal interictal examination and normal structural MRI do not exclude transient ischemia, and normal carotid Dopplers assess principally the anterior circulation without adequately evaluating the intracranial vertebral and basilar arteries. CTA is therefore appropriate to define the vertebral, basilar, and posterior cerebral arterial circulation and identify stenosis, occlusion, dissection, or other luminal pathology.  \u003Cstrong\u003EOrder an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)\u003C/strong\u003E would be appropriate if giant cell arteritis were suspected, but the absence of headache, jaw claudication, constitutional symptoms, and polymyalgic features, together with recurrent simultaneous bilateral blurring accompanied by vertigo and imbalance over 6 months, makes GCA less characteristic; GCA-related transient visual loss is usually monocular from ophthalmic or posterior ciliary arterial ischemia and may precede permanent visual loss. \u003Cstrong\u003EStart sumatriptan as necessary\u003C/strong\u003E is inappropriate because new-onset migraine aura at age 70 is a diagnosis of exclusion, the episodes are unusually brief for typical visual aura, there is no personal headache history, and associated imbalance raises concern for posterior-circulation ischemia; triptans also have vasoconstrictive properties and should not be started before cerebrovascular disease has been excluded. \u003Cstrong\u003EOrder an electroencephalography (EEG)\u003C/strong\u003E would be considered if occipital seizures were suspected, particularly with positive visual phenomena such as flashing lights, colored shapes, or formed hallucinations, but the negative visual blurring accompanied by vertigo and imbalance is more consistent with posterior-circulation hypoperfusion.\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1857,
    "Name": "Leber hereditary optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 22-year-old otherwise healthy patient develops profound, painless visual loss in one eye followed by the fellow eye over two weeks, reducing vision to hand movements. Fundus examination shows fine peripapillary telangiectatic vessels and subtle elevation of both optic nerve heads, while fluorescein angiography demonstrates no optic disc leakage. Which family history event would be most relevant to this pattern of visual loss?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea maternal uncle with sudden vision loss\u003C/strong\u003E, because the clinical pattern is characteristic of \u003Cstrong\u003ELeber hereditary optic neuropathy (LHON)\u003C/strong\u003E: a young adult with painless, severe, sequential central visual loss, pseudoedematous elevation of the retinal nerve fiber layer, peripapillary telangiectatic microangiopathy, and absence of fluorescein leakage from the optic discs, the latter helping distinguish LHON pseudoedema from true inflammatory or ischemic disc swelling. LHON is primarily caused by mitochondrial DNA point mutations affecting respiratory-chain complex I, with approximately 90% of cases associated with mutations in \u003Cstrong\u003EMT-ND4 m.11778G\u0026gt;A, MT-ND1 m.3460G\u0026gt;A, or MT-ND6 m.14484T\u0026gt;C\u003C/strong\u003E; impaired oxidative phosphorylation and increased oxidative stress selectively injure retinal ganglion cells, particularly the small-caliber fibers of the papillomacular bundle, resulting in dyschromatopsia and enlarging central or cecocentral scotomas before optic atrophy develops.  Mitochondrial DNA is transmitted through the ovum, so affected individuals inherit the mutation through the \u003Cstrong\u003Ematernal lineage\u003C/strong\u003E; all children of a carrier mother may inherit the mutation, but affected males do not transmit mitochondrial DNA to their children. Therefore, a maternal uncle shares the relevant maternal mitochondrial lineage with the patient and a similar episode of visual loss would strongly support LHON, whereas relatives on the paternal side do not provide relevant mitochondrial inheritance information. A maternal grandfather would not transmit mitochondrial DNA to the patient\u2019s mother, because fathers do not pass their mitochondria to offspring, making the maternal uncle the most informative listed relative. LHON shows incomplete penetrance with a marked predominance in males, and environmental factors such as smoking and excessive alcohol intake may increase conversion risk in genetically susceptible carriers; genetic confirmation and counselling should therefore be accompanied by advice to avoid mitochondrial toxins and by assessment of maternal relatives\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1858,
    "Name": "Microvascular sixth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with an isolated sixth cranial nerve palsy attributed to microvascular ischemia, which listed feature would not be expected?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EDiplopia worse at near\u003C/strong\u003E, because an isolated microvascular sixth nerve palsy weakens the lateral rectus, reducing abduction and producing an incomitant esotropia with \u003Cstrong\u003Ehorizontal binocular diplopia that is characteristically greater at distance\u003C/strong\u003E, where divergence and lateral rectus activity are required, and worse when the patient looks toward the affected side; at near, physiological convergence reduces the relative demand for abduction, so the esodeviation and diplopia are generally less marked rather than worse.  The typical clinical setting is an older patient, usually over 50 years, with vasculopathic risk factors such as diabetes mellitus, hypertension, hyperlipidemia, or smoking, presenting with an acute, isolated unilateral ocular motor palsy and no additional focal neurological deficit; ipsilateral periocular pain or headache may occur and does not exclude a microvascular mechanism. Most presumed microvascular sixth nerve palsies improve spontaneously over approximately \u003Cstrong\u003E8\u201312 weeks\u003C/strong\u003E, although complete resolution may take up to 2\u20134 months, making recovery by around 3 months characteristic.  MRI is expected to show no causative structural lesion when the diagnosis is genuinely microvascular, but the diagnosis should not be made solely because imaging is normal: neuroimaging is warranted when the patient is younger, the palsy is non-isolated, bilateral, progressive, recurrent, associated with papilloedema or other neurological signs, or fails to demonstrate expected improvement by about 3 months. During observation, diplopia may be managed with temporary Fresnel prism or monocular occlusion, while vascular risk factors should be identified and optimized.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1859,
    "Name": "Epiretinal membrane",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAssuming that no additional ocular abnormality is present, which listed finding is most likely to produce Binocular diplopia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EEpiretinal membrane\u003C/strong\u003E, because tangential traction from an epiretinal membrane can displace and distort the fovea, causing \u003Cstrong\u003Eretinal misregistration\u003C/strong\u003E between the two eyes and producing a sensory form of binocular diplopia known as \u003Cstrong\u003Edragged-fovea diplopia syndrome\u003C/strong\u003E, or central-peripheral rivalry-type diplopia; the peripheral retinal images remain sufficiently corresponding to maintain peripheral fusion, but the displaced fovea in the affected eye no longer corresponds spatially with the fovea of the fellow eye, so the two central images cannot be fused even when ocular motor alignment is clinically normal. The larger peripheral retinal fusion system generally dominates ocular alignment, leaving persistent central diplopia, metamorphopsia, and variable retinal aniseikonia; conventional prism is often ineffective because moving the entire retinal image to align the foveae simultaneously misaligns the peripheral retinal images, while aligning the peripheral images leaves the foveal images separated. The \u003Cstrong\u003Elights on-off test\u003C/strong\u003E, also called the small-field central fusion test, can demonstrate this central-peripheral conflict: reducing peripheral fusion in darkness may permit transient central fusion, whereas restoring room illumination re-establishes peripheral fusion and reproduces central diplopia.  OCT confirms the causative macular traction and foveal displacement; management may include partial monocular occlusion, selective filters, or epiretinal membrane peeling when anatomically appropriate, although diplopia may persist after successful surgery because the fovea may not return fully to its original location and cortical correspondence may remain abnormal.  \u003Cstrong\u003ECataract\u003C/strong\u003E, \u003Cstrong\u003EDry eye\u003C/strong\u003E, and \u003Cstrong\u003EUncorrected corneal astigmatism\u003C/strong\u003E more commonly cause monocular diplopia or image ghosting through optical degradation, meaning the duplicated image persists when the unaffected eye is covered but disappears when the affected eye is covered.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1860,
    "Name": "Brainstem syndromes",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following syndromes does not involve a palsy of the 3rd nerve nucleus or fasciculus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERaymond syndrome\u003C/strong\u003E, because Raymond syndrome localizes to the \u003Cstrong\u003Emedial ventral caudal pons\u003C/strong\u003E, not the midbrain, and involves the ipsilateral \u003Cstrong\u003Esixth nerve fascicle\u003C/strong\u003E together with the descending corticospinal tract, producing an ipsilateral abducens palsy and contralateral hemiparesis; the classic form may additionally involve corticofacial fibers and cause contralateral central facial weakness, whereas the common form may spare the face.  By contrast, Weber, Benedikt, and Claude syndromes are crossed \u003Cstrong\u003Emidbrain\u003C/strong\u003E syndromes involving the oculomotor fascicles: \u003Cstrong\u003EWeber syndrome\u003C/strong\u003E involves the cerebral peduncle, producing ipsilateral third nerve palsy with contralateral hemiparesis; \u003Cstrong\u003EBenedikt syndrome\u003C/strong\u003E involves the red nucleus and adjacent dentato-rubro-thalamic pathways, producing ipsilateral third nerve palsy with contralateral Holmes tremor, choreoathetosis, or ataxia; and \u003Cstrong\u003EClaude syndrome\u003C/strong\u003E involves the red nucleus or superior cerebellar peduncle, producing ipsilateral third nerve palsy with prominent contralateral cerebellar ataxia. Benedikt syndrome is particularly associated with contralateral tremor and ataxia following midbrain injury.  A useful mnemonic is\u003Cstrong\u003E\u201CRaymond looks sideways, Weak Weber, Bobbing Benedikt, Clumsy Claude\u201D\u003C/strong\u003E: Raymond affects the sixth nerve and therefore lateral gaze; Weber causes contralateral weakness; Benedikt causes contralateral tremor or \u201Cbobbing\u201D; and Claude causes contralateral cerebellar clumsiness.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1861,
    "Name": "Paradoxical pupillary reaction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed disorder is not recognized as a cause of the paradoxical pupillary response?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EDuane syndrome\u003C/strong\u003E, because paradoxical pupillary reaction, also called \u003Cstrong\u003Epupillary constriction to darkness\u003C/strong\u003E, is an unusual response in which the pupils transiently constrict immediately after the lights are extinguished instead of undergoing the expected sympathetic dilation; this sign is principally associated with congenital or early-onset retinal and optic nerve dysfunction and can be especially valuable when assessing a young child with unexplained poor vision, nystagmus, and an initially normal-appearing fundus. Documented associations include \u003Cstrong\u003Econgenital achromatopsia, congenital stationary night blindness, dominant optic atrophy, optic nerve hypoplasia, Leber congenital amaurosis, albinism, retinitis pigmentosa, and Best disease.\u0026nbsp;\u003C/strong\u003EThe precise mechanism remains incompletely defined, but the response is thought to reflect abnormal retinal adaptation and altered interaction between rod-driven and cone-driven afferent signals entering the pupillary light-reflex pathway, rather than a primary abnormality of the iris sphincter or sympathetic dilator pathway. \u003Cstrong\u003ECongenital achromatopsia\u003C/strong\u003E is particularly associated with this phenomenon and results from severe generalized cone dysfunction, typically producing poor visual acuity, photophobia, absent color discrimination, and infantile nystagmus.  \u003Cstrong\u003EDuane syndrome\u003C/strong\u003E, in contrast, is a congenital cranial dysinnervation disorder affecting horizontal ocular motility, with limited abduction and/or adduction, globe retraction, and palpebral fissure narrowing during attempted adduction due to anomalous lateral rectus innervation and medial-lateral rectus co-contraction; it is not a retinal or optic nerve disorder.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1862,
    "Name": "Internuclear ophthalmoplegia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat are the two most common causes for internuclear ophthalmoplegia (INO)?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EStroke and demyelination\u003C/strong\u003E, because internuclear ophthalmoplegia results from disruption of the \u003Cstrong\u003Emedial longitudinal fasciculus\u003C/strong\u003E, a heavily myelinated tract in the dorsomedial pons and midbrain that connects internuclear neurons from the abducens nucleus to the contralateral medial rectus subnucleus of the oculomotor complex, thereby coordinating abduction of one eye with adduction of the fellow eye during horizontal conjugate gaze.  \u003Cstrong\u003EDemyelination, particularly multiple sclerosis, is the leading cause in adolescents and younger adults\u003C/strong\u003E and commonly produces bilateral INO because the two medial longitudinal fasciculi run close together near the brainstem midline; \u003Cstrong\u003Eischemic stroke is the leading cause in older adults\u003C/strong\u003E and more often produces a unilateral INO, sometimes accompanied by other focal brainstem signs.  The cardinal ocular motor abnormality is slowed or limited adduction of the eye ipsilateral to the medial longitudinal fasciculus lesion during horizontal saccades, often with abducting nystagmus of the fellow eye; convergence may remain intact because the vergence pathway reaches the medial rectus subnucleus separately and does not depend on the horizontal gaze signal transmitted through the medial longitudinal fasciculus, although convergence can be impaired when the lesion lies rostrally near the oculomotor nucleus.  Neoplasms, sarcoidosis, trauma, infection, nutritional deficiency, and drug toxicity are recognized causes but are substantially less common than ischemia and demyelination. A useful mnemonic is\u003Cstrong\u003E\u201CYoung and bilateral, think MS; older and unilateral, think stroke.\u201D\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1863,
    "Name": "Posterior cortical atrophy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old patient reports progressively worsening vision in both eyes over several years. The patient frequently fails to notice objects directly ahead and has difficulty interpreting a clock face. Brain MRI has shown only mild generalized atrophy considered appropriate for age. Visual acuity measures 20/25 in each eye, and pupillary responses, ocular motility, alignment, intraocular pressures, anterior segments, fundi, and optic nerves are normal. The patient cannot identify any of nine Ishihara plate figures, including the displayed plates, yet can correctly name the individual colors when these are pointed out separately. Which diagnosis most accurately accounts for this pattern?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-01-c4f57a4b-49f5-4e95-9741-52cd8d1990a8.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003C!--StartFragment--\u003E\u003C!--EndFragment--\u003E\u003C/p\u003E\u003Cdiv style=\u0022font-family:\u0027Segoe UI\u0027;font-size:14px;font-style:normal;font-weight:400;line-height:20px\u0022\u003E\u003Cstrong\u003EPosterior cortical atrophy\u003C/strong\u003E, because the patient\u2019s visual acuity, pupils, ocular motility, anterior segments, fundi, and optic nerves are essentially normal, indicating that the progressive visual difficulty is not explained by primary ocular disease. The key finding is the discrepancy on Ishihara testing: the patient cannot recognize the numbers formed by the colored dots but can correctly identify the individual colors when they are pointed out. This demonstrates preserved color perception with impaired integration of multiple visual elements into a single meaningful image, a higher visual processing deficit known as \u003Cstrong\u003Esimultanagnosia\u003C/strong\u003E. Posterior cortical atrophy is a progressive neurodegenerative syndrome affecting the parieto-occipital and occipitotemporal association cortices, most commonly due to Alzheimer-type pathology, and often presents with vague visual complaints despite relatively preserved Snellen acuity and a normal ophthalmic examination. Simultanagnosia is the most frequent component of \u003Cstrong\u003EB\u00E1lint syndrome\u003C/strong\u003E, whose other components are \u003Cstrong\u003Eoptic ataxia\u003C/strong\u003E, meaning impaired visually guided reaching, and \u003Cstrong\u003Eocular motor apraxia\u003C/strong\u003E, meaning difficulty initiating purposeful saccades. The history of failing to notice objects directly ahead and difficulty interpreting a clock face further supports impaired visuospatial and visuoperceptual processing. Structural MRI may appear normal or show only subtle posterior cortical atrophy early in the disease, so age-appropriate generalized atrophy does not exclude the diagnosis. \u003Cstrong\u003ECone degeneration\u003C/strong\u003E would cause genuine dyschromatopsia, reduced central acuity, photophobia, and abnormal cone function rather than preserved identification of individual colors; \u003Cstrong\u003EOccipital lobe seizures\u003C/strong\u003E would usually produce brief, episodic visual phenomena rather than progressive deterioration over several years; and \u003Cstrong\u003EOccult giant cell arteritis\u003C/strong\u003E would cause ischemic visual dysfunction rather than selective failure to interpret complex visual images.\u003C/div\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1864,
    "Name": "Latent nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed feature would not be expected in latent nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EHighly associated with exotropia\u003C/strong\u003E, because latent nystagmus, now termed \u003Cstrong\u003Efusion maldevelopment nystagmus syndrome\u003C/strong\u003E, develops after disruption of normal binocular fusion during early infancy and is strongly associated with \u003Cstrong\u003Einfantile esotropia\u003C/strong\u003E, rather than exotropia; infantile esotropia may also be accompanied by dissociated vertical deviation, overelevation in adduction, and optokinetic asymmetry, reflecting abnormal binocular cortical development during the sensitive period.  The characteristic movement is a \u003Cstrong\u003Econjugate, bilateral, horizontal jerk nystagmus\u003C/strong\u003E that appears or increases when binocular viewing is interrupted, with the fast phase directed toward the \u003Cstrong\u003Efixing eye\u003C/strong\u003E, and therefore away from the occluded eye; covering the right eye produces left-beating nystagmus, while covering the left eye produces right-beating nystagmus. The slow phase has a decreasing-velocity waveform, distinguishing fusion maldevelopment nystagmus from the increasing-velocity waveform commonly seen in infantile nystagmus syndrome. In purely latent nystagmus, little or no oscillation is present with both eyes viewing, whereas in manifest-latent nystagmus a baseline oscillation persists binocularly but becomes more prominent when either eye is covered. The underlying mechanism involves loss or maldevelopment of binocular connections within the visual cortex during the first months of life, producing asymmetric monocular motion input to downstream gaze-stabilizing pathways rather than a primary lesion of the ocular motor nerves or extraocular muscles.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1865,
    "Name": "B\u00E1lint syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed visual-processing abnormality is not part of the classic clinical triad that defines B\u00E1lint syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EObject agnosia\u003C/strong\u003E, because the classic triad of B\u00E1lint syndrome comprises \u003Cstrong\u003Esimultagnosia, optic ataxia, and ocular apraxia\u003C/strong\u003E, usually resulting from bilateral parieto-occipital dysfunction. \u003Cstrong\u003ESimultagnosia\u003C/strong\u003E is the inability to perceive several objects or integrate the elements of a complex visual scene simultaneously, despite retaining the ability to recognize individual components; \u003Cstrong\u003Eoptic ataxia\u003C/strong\u003E is impaired visually guided reaching, in which the patient misdirects the hand toward a visible target despite preserved strength, sensation, and coordination for nonvisual tasks; and \u003Cstrong\u003Eocular apraxia\u003C/strong\u003E, more precisely oculomotor apraxia or psychic paralysis of gaze, is difficulty voluntarily disengaging fixation and directing the eyes toward a new visual target despite intact extraocular muscle function.  \u003Cstrong\u003EObject agnosia\u003C/strong\u003E is different: the patient can see an object but cannot identify or assign meaning to it visually, despite adequate acuity and no major language or intellectual deficit; this reflects dysfunction of the ventral occipitotemporal \u201Cwhat\u201D pathway and is not one of the three defining components of B\u00E1lint syndrome, although object-recognition difficulties may coexist when the underlying posterior cortical lesion is extensive. B\u00E1lint syndrome more characteristically reflects disruption of the dorsal occipitoparietal \u201Cwhere/how\u201D network and is most often caused by bilateral parieto-occipital infarction, particularly watershed injury, although posterior cortical atrophy, trauma, infection, tumors, and other neurodegenerative disorders can also produce it.  A useful mnemonic is\u003Cstrong\u003E\u201CSOS\u201D\u003C/strong\u003E: \u003Cstrong\u003ESimultagnosia, Optic ataxia, Saccadic or ocular apraxia\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1866,
    "Name": "Methanol ingestion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed substance can cause rapidly developing, profound visual loss in both eyes accompanied by acute optic disc edema following ingestion?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMethanol\u003C/strong\u003E, because methanol poisoning produces an acute, severe, bilateral toxic optic neuropathy, often after a latent interval while methanol is metabolized by alcohol dehydrogenase to formaldehyde and then to \u003Cstrong\u003Eformic acid or formate\u003C/strong\u003E, the principal toxic metabolite; formate inhibits mitochondrial cytochrome-c oxidase, impairing oxidative phosphorylation and producing histotoxic hypoxia, metabolic acidosis, and preferential injury to retinal ganglion cells and the retrolaminar optic nerve. Patients may initially develop headache, nausea, vomiting, abdominal discomfort, altered consciousness, or dyspnea from high-anion-gap metabolic acidosis, followed by blurred vision, photophobia, central or cecocentral scotomas, markedly reduced acuity, dyschromatopsia, and potentially complete blindness; fundus examination may demonstrate hyperemic optic disc edema and peripapillary retinal edema, later progressing to optic atrophy. The severity of ocular injury correlates more closely with the degree and duration of acidosis and formate accumulation than with the measured methanol concentration alone. Methanol toxicity is a medical emergency requiring immediate inhibition of alcohol dehydrogenase with \u003Cstrong\u003Efomepizole\u003C/strong\u003E, or ethanol when fomepizole is unavailable, correction of metabolic acidosis, folinic or folic acid to enhance formate metabolism, and hemodialysis in severe poisoning to remove methanol and formate.  \u003Cstrong\u003EEthambutol\u003C/strong\u003E and \u003Cstrong\u003EChloramphenicol\u003C/strong\u003E are associated more typically with subacute or chronic bilateral toxic optic neuropathy characterized by dyschromatopsia, central or cecocentral scotomas, selective papillomacular bundle injury, and eventual temporal optic disc pallor rather than dramatic acute disc edema; \u003Cstrong\u003EEthanol\u003C/strong\u003E itself is not the cause of this acute optic neuropathy and can competitively inhibit methanol metabolism by occupying alcohol dehydrogenase, although chronic excessive alcohol intake may contribute indirectly to nutritional optic neuropathy through folate, thiamine, or vitamin B12 deficiency.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1867,
    "Name": "Unexplained chin numbness",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old attending for a routine spectacle assessment mentions persistent numbness confined to the chin for one month. There is no history of trauma or another apparent explanation, and cranial nerve examination is otherwise normal. Which aspect of the medical history should be explored most urgently in view of this isolated sensory symptom?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EInquire about prior history of cancer\u003C/strong\u003E, because unexplained sensory loss involving the chin and lower lip corresponds to \u003Cstrong\u003Emental nerve neuropathy\u003C/strong\u003E, commonly termed \u003Cstrong\u003Enumb chin syndrome\u003C/strong\u003E, and in an older patient without recent dental treatment, mandibular trauma, or another local explanation, this is an important warning sign of occult, recurrent, or metastatic malignancy. The mental nerve is a terminal sensory branch of the inferior alveolar nerve, arising from the mandibular division of the trigeminal nerve, and supplies sensation to the chin, lower lip, and adjacent gingiva; malignant disease may affect this pathway through mandibular metastasis near the mental foramen, direct infiltration or compression of the inferior alveolar nerve, perineural spread, leptomeningeal disease, or skull-base involvement of the mandibular nerve. Numb chin syndrome may precede the diagnosis of a previously unsuspected cancer or indicate progression or recurrence of known disease, with breast carcinoma and hematological malignancies, particularly lymphoma and leukemia, among the most frequently reported associations; lung and prostate carcinoma, myeloma or plasmacytoma, osteosarcoma, and other metastatic tumors have also been described.  A careful history should therefore address previous cancer, unexplained weight loss, night sweats, lymphadenopathy, bone pain, and systemic symptoms, while also reviewing recent dental procedures, infection, mandibular trauma, and medication exposure; persistent unexplained symptoms warrant prompt dental and maxillofacial assessment with appropriate mandibular and skull-base imaging and systemic investigation rather than reassurance. Diabetes and alcohol misuse may cause peripheral neuropathy, but these usually produce a length-dependent, symmetrical polyneuropathy rather than an isolated mental nerve sensory deficit, while a family history of neurological disease is less immediately relevant to this focal acquired symptom.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1868,
    "Name": "Acute optic disc edema",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed structural or vascular finding would not be expected during the acute phase of true optic disc edema?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eloss of the capillary net on the optic disc surface\u003C/strong\u003E, because acute optic disc edema results from interruption of orthograde and retrograde axoplasmic transport within retinal ganglion cell axons at or immediately anterior to the lamina cribrosa, causing intracellular material and fluid to accumulate within the prelaminar nerve fiber layer; this produces elevation and hyperemia of the optic nerve head, blurred disc margins, obscuration of vessels crossing the swollen disc margin, venous congestion and tortuosity, peripapillary hemorrhages, cotton-wool spots, and exudation. True acute edema makes the superficial disc capillary network \u003Cstrong\u003Edilated and more prominent\u003C/strong\u003E, rather than causing loss of the capillary net; loss or attenuation of surface capillaries is instead associated with established optic atrophy after axonal loss and resolution of the acute swelling. Clinical descriptions of acute disc edema similarly emphasize prominent dilated surface capillaries and obscuration of overlying vessels by swollen retinal nerve fiber tissue.  \u003Cstrong\u003Eimpaired axoplasmic flow in ganglion cell axons\u003C/strong\u003E is central to the pathophysiology and may occur with raised intracranial pressure, ischemia, inflammation, infiltration, or optic nerve compression. \u003Cstrong\u003Echorioretinal folds\u003C/strong\u003E may develop when marked swelling and biomechanical stress at the optic nerve head deform the adjacent peripapillary choroid, Bruch membrane, and retina, particularly in papilledema or orbital compression. \u003Cstrong\u003Emacular edema\u003C/strong\u003E may accompany severe acute disc edema through leakage and extension of fluid or exudates from the swollen optic nerve toward the macula, sometimes producing a macular star in neuroretinitis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1869,
    "Name": "Visual evoked potential",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn which of the following clinical situations would recording a visual evoked potential provide clinically useful information?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea 10-year-old cognitively-delayed non-verbal boy is brought in by his parents for an eye check. His parents want to know how much he can see. A pattern reversal VEP is ordered to provide a rough estimate of the child\u0027s visual function.\u003C/strong\u003E, because a VEP records the electrical response generated over the occipital cortex after monocular visual stimulation and therefore provides an objective estimate of the functional integrity of the visual pathway from the retina through the optic nerves, chiasm, tracts, radiations, and visual cortex; pattern-reversal or sweep VEP can estimate visual resolution by presenting checkerboards of progressively smaller check size or increasing spatial frequency and identifying the threshold at which a reproducible cortical response is no longer obtained, making the test particularly useful in preverbal, non-verbal, or cognitively impaired patients who cannot perform conventional recognition acuity testing.  The result remains a \u003Cstrong\u003Erough estimate of visual function rather than a direct Snellen-equivalent measurement\u003C/strong\u003E, because VEP amplitude and latency are affected by fixation, attention, refractive blur, media clarity, macular function, check size, contrast, electrode placement, and cooperation; pattern-reversal VEP gives better spatial-resolution information but requires stable fixation and adequate optical correction, whereas flash VEP requires less cooperation but has greater interindividual variability and provides only a coarse assessment of pathway function.  A flash VEP cannot reliably distinguish whether reduced vision in a patient with both previous bilateral optic neuritis and bilateral occipital infarction arises from anterior or posterior visual pathway damage because a conventional single-channel VEP tests the integrated afferent pathway and has poor anatomical localization; OCT, visual fields, MRI, clinical optic nerve testing, and possibly multifocal or multichannel electrophysiology would be more informative. A pattern-reversal VEP should not be used in isolation to rule out multiple sclerosis when MRI and objective neurological findings do not support demyelination, because delayed P100 latency may indicate impaired conduction but is not specific for multiple sclerosis and can occur in other optic nerve or visual pathway disorders. A pattern-reversal VEP may contribute to the assessment of suspected functional visual loss when a robust response is incompatible with the claimed profound impairment, but the described patient is persistently blinking and refusing to open the eyes, so poor fixation and stimulus obstruction would falsely attenuate or abolish the response; moreover, VEP cannot by itself \u201Cprove\u201D functional visual loss, which requires positive clinical inconsistencies and exclusion of organic disease.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1870,
    "Name": "Leber hereditary optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 18-year-old male develops acute, painless visual loss in the right eye, reducing best-corrected visual acuity to 20/100, while the left eye remains 20/20. A right afferent pupillary defect is present, and fundus examination shows elevation and hyperemia of the right optic disc without fluorescein leakage. Which visual field defect is most commonly associated with the underlying disorder suggested by these findings?\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ececocentral\u003C/strong\u003E, because acute or subacute, painless central visual loss in a young adult, together with optic disc hyperemia, retinal nerve fiber layer elevation, and absence of fluorescein leakage, is characteristic of the acute stage of \u003Cstrong\u003ELeber hereditary optic neuropathy\u003C/strong\u003E; the elevated disc appearance represents \u003Cstrong\u003Epseudoedema\u003C/strong\u003E, not true inflammatory optic disc edema, because fluorescein angiography shows no leakage. Additional acute fundus findings may include circumpapillary telangiectatic microangiopathy, vascular tortuosity, and swelling of the peripapillary retinal nerve fiber layer.  LHON selectively injures retinal ganglion cells and their axons within the \u003Cstrong\u003Epapillomacular bundle\u003C/strong\u003E, which carries information from the macula to the temporal optic disc; this produces a central field defect that extends toward and incorporates the physiological blind spot, forming the characteristic \u003Cstrong\u003Ececocentral scotoma\u003C/strong\u003E. The scotoma usually enlarges and becomes denser as the disease progresses, accompanied by worsening dyschromatopsia and central visual acuity, while peripheral visual fields may remain relatively preserved.  LHON is caused by mitochondrial DNA mutations affecting complex I of the respiratory chain, most commonly \u003Cstrong\u003Em.11778G\u0026gt;A in MT-ND4\u003C/strong\u003E, with \u003Cstrong\u003Em.3460G\u0026gt;A in MT-ND1\u003C/strong\u003E and \u003Cstrong\u003Em.14484T\u0026gt;C in MT-ND6\u003C/strong\u003E accounting for most remaining cases; mitochondrial inheritance is exclusively maternal, although incomplete penetrance means that not every carrier develops visual loss. The fellow eye usually becomes clinically affected within weeks or months, and subtle color or visual field abnormalities may already be detectable before a subjective reduction in acuity.  \u003Cstrong\u003Ealtitudinal\u003C/strong\u003E field loss is more typical of anterior ischemic optic neuropathy, \u003Cstrong\u003Enasal step\u003C/strong\u003E and \u003Cstrong\u003Edouble arcuate\u003C/strong\u003E defects are characteristic retinal nerve fiber bundle defects associated mainly with glaucoma.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1871,
    "Name": "Brown syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed condition is not recognized as a congenital mechanism or acquired association of Brown syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMigraine disorder\u003C/strong\u003E, because Brown syndrome is a \u003Cstrong\u003Emechanical restrictive strabismus\u003C/strong\u003E characterized by limited elevation of the affected eye in adduction, with relatively preserved elevation in abduction and a positive forced-duction test when the globe is passively elevated in adduction; the underlying abnormality lies within the \u003Cstrong\u003Esuperior oblique tendon-trochlea complex\u003C/strong\u003E, where impaired tendon excursion through the trochlea prevents the superior oblique from lengthening normally as the eye attempts to elevate while adducted. Congenital cases are commonly attributed to a short, tight, or inelastic superior oblique tendon, although trochlear malformation, anomalous tendon development, fibrosis, and congenital cranial dysinnervation may also contribute.  Acquired Brown syndrome can result from inflammation or structural damage around the trochlea, including \u003Cstrong\u003EIdiopathic orbital inflammation\u003C/strong\u003E, trochleitis, rheumatoid arthritis-associated tenosynovitis, Sj\u00F6gren syndrome, sinusitis, orbital trauma, superior oblique or adjacent orbital surgery, tendon nodules, and rarely neoplasia.  The ocular motility pattern may include hypotropia in primary position, divergence in upgaze producing a V-pattern, downshoot in adduction, widening of the palpebral fissure on adduction, and a compensatory chin-up posture or contralateral face turn; severe unilateral disease may create secondary superior oblique overaction in the fellow eye through increased yoke-muscle innervation. \u003Cstrong\u003EMigraine disorder\u003C/strong\u003E may produce transient visual aura, headache-associated ocular symptoms, or occasionally cranial neuropathies, but it is not a recognized cause of mechanical restriction at the superior oblique tendon-trochlea complex.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 10,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1872,
    "Name": "Acute demyelinating optic neuritis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old presents with acute visual loss in the right eye, pain exacerbated by ocular movement, best-corrected visual acuity of 20/60 in the right eye and 20/20 in the left eye, a right relative afferent pupillary defect, and impaired color vision in the affected eye. Which investigation provides the most important information about the long-term probability of developing multiple sclerosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMRI of the brain to look for white matter lesions\u003C/strong\u003E, because the presentation is typical of acute demyelinating optic neuritis, and the most powerful established predictor of subsequent multiple sclerosis is the presence and burden of characteristic demyelinating lesions on the baseline brain MRI, rather than the severity of the initial visual loss or confirmation of optic nerve enhancement. In the final 15-year follow-up of the Optic Neuritis Treatment Trial, the cumulative probability of developing multiple sclerosis after an initial episode of optic neuritis was approximately 50%, but the risk differed markedly according to baseline brain MRI: approximately 25% of patients with no cerebral white matter lesions developed multiple sclerosis, compared with approximately 72% of patients with one or more lesions.  The prognostically relevant abnormalities are ovoid T2/FLAIR hyperintense lesions in locations typical of demyelination, particularly periventricular, juxtacortical or cortical, infratentorial, and callosal regions; lesion number, morphology, and distribution help establish dissemination in space, while new T2 lesions or gadolinium-enhancing lesions on follow-up imaging may demonstrate dissemination in time under contemporary diagnostic criteria. MRI of the orbits with fat-suppressed post-contrast sequences is useful to demonstrate optic nerve enhancement, confirm the anatomical site and extent of inflammation, and identify atypical features that may suggest MOG-antibody disease, aquaporin-4-positive neuromyelitis optica spectrum disorder, sarcoidosis, infection, or compressive optic neuropathy, but enhancement of the symptomatic optic nerve does not provide the principal long-term estimate of multiple sclerosis conversion risk. A visual field test in the fellow eye may reveal subclinical dysfunction but does not predict multiple sclerosis as strongly as brain lesion burden, while a family history may modify background susceptibility but cannot replace MRI-based risk stratification. The ONTT also showed that high-dose intravenous corticosteroids accelerate visual recovery without improving the final visual outcome, while standard-dose oral prednisone alone increases the recurrence rate of optic neuritis; importantly, treatment decisions should now incorporate the full neurological assessment, current MRI criteria, and discussion with neurology rather than relying solely on the historical ONTT percentages.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1873,
    "Name": "Macular-sparing homonymous hemianopia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a homonymous hemianopic visual field defect in which central macular vision remains preserved. Which cerebral lobe contains the responsible lesion, and occlusion of which artery is the most likely vascular cause?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eoccipital; posterior cerebral\u003C/strong\u003E, because a highly congruous homonymous hemianopia with macular sparing is a classic localizing sign of a lesion involving the \u003Cstrong\u003Eprimary visual cortex of the occipital lobe\u003C/strong\u003E, most commonly resulting from infarction in the \u003Cstrong\u003Eposterior cerebral artery\u003C/strong\u003E territory. The primary visual cortex is arranged retinotopically along the calcarine fissure: the contralateral visual hemifield is represented throughout the striate cortex, while the central macular field has a disproportionately large cortical representation at the posterior occipital pole. Most of the primary visual cortex is supplied by the calcarine branches of the posterior cerebral artery, so posterior cerebral artery occlusion can destroy the cortical representation of the contralateral hemifield and produce a homonymous hemianopia. Central vision may remain intact when the posterior occipital pole is spared, traditionally explained by collateral or overlapping vascular supply from terminal branches of the middle cerebral artery, although the exact mechanism of macular sparing remains debated and may also reflect incomplete infarction of the macular cortex rather than a universally present dual supply.  The defect is generally highly congruous because corresponding points from the two eyes lie close together in the occipital cortex, and central visual acuity may remain normal despite extensive peripheral hemifield loss. A parietal lesion more typically damages the superior optic radiations and causes a contralateral inferior homonymous quadrantanopia, classically described as \u201Cpie on the floor,\u201D while a temporal lobe lesion involving Meyer\u2019s loop causes a contralateral superior quadrantanopia, or \u201Cpie in the sky.\u201D A middle cerebral artery infarction can damage the optic radiations within the temporal or parietal lobes, but the classic combination of a complete homonymous hemianopia with macular sparing localizes posteriorly to the occipital cortex and most strongly indicates a posterior cerebral artery infarct.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1874,
    "Name": "Apraclonidine",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the primary mechanism of action of apraclonidine?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAlpha adrenergic receptor agonist (alpha 2 \u0026gt; alpha 1)\u003C/strong\u003E, because apraclonidine is predominantly a \u003Cstrong\u003Estrong \u03B12-adrenergic agonist with weaker \u03B11-adrenergic agonist activity\u003C/strong\u003E; ocular \u03B12-receptor stimulation reduces aqueous humor formation through presynaptic inhibition of norepinephrine release and suppression of ciliary body aqueous production, while its limited \u03B11 activity can produce conjunctival blanching and mild mydriasis under appropriate conditions. Its mixed receptor profile explains its important diagnostic role in \u003Cstrong\u003EHorner syndrome\u003C/strong\u003E: in a normal eye, the dominant \u03B12 effect produces little pupillary change or mild miosis, whereas interruption of the oculosympathetic pathway causes denervation supersensitivity and upregulation of postsynaptic \u03B11 receptors in the iris dilator muscle, allowing apraclonidine\u2019s normally weak \u03B11 action to dilate the affected miotic pupil. The normal pupil may remain unchanged or constrict slightly while the Horner pupil dilates, producing the characteristic \u003Cstrong\u003Ereversal of anisocoria\u003C/strong\u003E; \u03B11-mediated contraction of M\u00FCller\u2019s muscle may also improve the mild ptosis.  Denervation supersensitivity may take time to develop, so a very acute Horner syndrome can occasionally give a false-negative result, although positive tests have been documented as early as 48\u201372 hours after onset.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1875,
    "Name": "Sequential NAION in the fellow eye",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient who has developed non-arteritic anterior ischemic optic neuropathy in one eye, which intervention has been definitively shown in large randomized controlled trials to prevent a subsequent episode in the fellow eye?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethere is no well-proven preventative therapy for NAION\u003C/strong\u003E, because no pharmacological or surgical intervention has been demonstrated in adequately powered randomized controlled trials to prevent fellow-eye involvement after unilateral NAION; the estimated risk of sequential involvement is approximately 15\u201320% within five years, but prevention currently depends mainly on identifying and optimizing modifiable systemic risk factors rather than prescribing a specific ocular treatment.  NAION is thought to result from transient hypoperfusion of the short posterior ciliary circulation supplying a structurally crowded optic nerve head, followed by axoplasmic stasis, disc edema, and a compartment-like cycle of further microvascular compression and retinal ganglion-cell axonal loss.  \u003Cstrong\u003Easpirin therapy\u003C/strong\u003E has theoretical antiplatelet and cardiovascular benefits, and retrospective studies have suggested possible short-term reduction in fellow-eye events, but systematic assessment has found the evidence weak, heterogeneous, and insufficient to establish prevention of sequential NAION; aspirin should therefore be used according to the patient\u2019s cardiovascular or cerebrovascular indication and bleeding risk, not solely to prevent fellow-eye NAION.  \u003Cstrong\u003EOral prednisone therapy\u003C/strong\u003E remains controversial for visual recovery in the already affected eye and has not been proven to prevent contralateral disease, while \u003Cstrong\u003EAlphagan (brimonidine) drop therapy\u003C/strong\u003E has no established preventive benefit. Optic nerve sheath decompression is specifically contraindicated as a treatment for acute NAION: the randomized Ischemic Optic Neuropathy Decompression Trial found no visual benefit and a greater risk of visual deterioration compared with observation, establishing that the procedure may be harmful.  Practical risk reduction should include assessment and treatment of diabetes, hypertension, dyslipidemia, smoking, anemia, and obstructive sleep apnea, with avoidance of excessive nocturnal hypotension where clinically appropriate; adherence to CPAP in moderate-to-severe obstructive sleep apnea is particularly important because noncompliance has been associated with increased fellow-eye involvement.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1876,
    "Name": "Postpartum pituitary apoplexy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EOne day after delivery, a 35-year-old develops an abrupt severe headache and binocular diplopia. Visual acuity remains 20/20 in both eyes, but examination demonstrates a pupil-involving right third nerve palsy, a left sixth nerve palsy, and a symmetrical bitemporal hemianopia. Non-contrast head CT reports no acute intracranial abnormality. Which investigation would be most helpful in confirming the underlying diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMRI (magnetic resonance imaging) of the brain\u003C/strong\u003E, because the combination of sudden severe headache, multiple ocular motor cranial neuropathies, and a symmetrical bitemporal hemianopia localizes the lesion to an acutely expanding \u003Cstrong\u003Esellar or parasellar process\u003C/strong\u003E, with the clinical context strongly suggesting \u003Cstrong\u003Epituitary apoplexy\u003C/strong\u003E from hemorrhage or infarction within the pituitary gland, usually in a previously unrecognized adenoma; upward expansion compresses the inferior optic chiasm and produces bitemporal field loss, while lateral extension into the cavernous sinuses can affect cranial nerves III, IV, and VI, explaining the pupil-involving third nerve palsy and contralateral sixth nerve palsy. Pituitary apoplexy is a potentially life-threatening neuroendocrine emergency that may present with severe headache, visual field loss, ophthalmoplegia, altered consciousness, and acute hypopituitarism.  A normal non-contrast CT does not exclude the diagnosis because CT may miss pituitary infarction, a small hemorrhage, or a non-hyperdense sellar lesion; dedicated MRI of the brain and sellar region, ideally with thin-section T1- and T2-weighted sequences and contrast when appropriate, provides superior visualization of the pituitary gland, hemorrhagic or ischemic change, optic chiasm, cavernous sinuses, and associated mass effect.  \u003Cstrong\u003EComputed tomography angiography (CTA) of the brain\u003C/strong\u003E and \u003Cstrong\u003EMRA (magnetic resonance angiography) of the brain\u003C/strong\u003E would be important if an intracranial aneurysm were the leading concern, particularly with a painful pupil-involving third nerve palsy, but an aneurysm would not as readily explain a symmetrical bitemporal hemianopia, which specifically indicates chiasmal compression. \u003Cstrong\u003EElectromyography (EMG)\u003C/strong\u003E may support a diagnosis of neuromuscular junction disease such as myasthenia gravis, but myasthenia does not affect the pupils or visual fields and would not explain the severe acute headache. The postpartum context should not lead to conflation with \u003Cstrong\u003ESheehan syndrome\u003C/strong\u003E, which classically follows severe postpartum hemorrhage and hypotension causing ischemic pituitary necrosis with hypopituitarism, whereas pituitary apoplexy is an acute hemorrhagic or infarctive sellar expansion causing headache, chiasmal dysfunction, and ophthalmoplegia. Because acute ACTH deficiency can cause life-threatening adrenal crisis, urgent endocrine assessment and empirical stress-dose corticosteroids may be required without waiting for imaging when clinical suspicion is high, alongside immediate neurosurgical and endocrine consultation.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1877,
    "Name": "Sixth, seventh, and eighth cranial nerve dysfunction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 50-year-old has experienced four months of progressive horizontal binocular diplopia. Visual acuity, color vision, pupillary responses, intraocular pressure, and confrontation fields are normal. Examination reveals a -2 limitation of left-eye abduction and an incomitant esotropia measuring 15 prism diopters in primary position, increasing to 40 prism diopters in left gaze and decreasing to 5 prism diopters in right gaze. Diminished hearing and weakness of both the upper and lower facial muscles are also present on the left side. Where is the lesion most likely situated?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe cerebellopontine angle\u003C/strong\u003E, because the motility measurements demonstrate a \u003Cstrong\u003Eleft sixth cranial nerve palsy\u003C/strong\u003E: weakness of the left lateral rectus limits abduction and produces an incomitant esotropia that is greatest in left gaze, the field of action of the affected lateral rectus, and smallest in right gaze. The associated ipsilateral hearing impairment localizes additional dysfunction to \u003Cstrong\u003Ecranial nerve VIII\u003C/strong\u003E, while weakness involving both the upper and lower facial muscles indicates an ipsilateral \u003Cstrong\u003Elower motor neuron seventh nerve palsy\u003C/strong\u003E rather than a supranuclear facial lesion, which usually spares the forehead because of bilateral cortical innervation. The anatomical clustering of sixth, seventh, and eighth nerve dysfunction localizes the process to the \u003Cstrong\u003Eleft cerebellopontine angle\u003C/strong\u003E, where cranial nerves VII and VIII traverse the CPA cistern toward the internal auditory canal and the sixth nerve lies nearby as the nerve emerges from the pontomedullary junction; a sufficiently large CPA lesion can therefore produce hearing loss first, followed by facial weakness and abducens palsy through progressive mass effect. The most common CPA mass is a \u003Cstrong\u003Evestibular schwannoma\u003C/strong\u003E, followed by meningioma and epidermoid cyst, although other lesions are possible; vestibular schwannoma classically begins with progressive unilateral sensorineural hearing loss or tinnitus and may involve cranial nerves VII, V, and VI as the lesion enlarges.  Larger lesions may also produce reduced facial or corneal sensation from fifth nerve compression, cerebellar ataxia, long-tract signs, hydrocephalus, or Bruns nystagmus from brainstem and floccular compression.  \u003Cstrong\u003EThe left cerebellar hemisphere\u003C/strong\u003E could cause ipsilateral limb ataxia, dysmetria, intention tremor, or gait disturbance but would not directly explain this combination of sixth, seventh, and eighth cranial neuropathies. \u003Cstrong\u003EThe cerebellar flocculonodular lobe\u003C/strong\u003E is involved in vestibular control and gaze holding, so lesions more typically cause imbalance, gaze-evoked nystagmus, or impaired vestibulo-ocular responses rather than an isolated incomitant sixth nerve palsy with ipsilateral hearing loss and complete facial weakness. \u003Cstrong\u003EThe midbrain\u003C/strong\u003E contains the third and fourth nerve nuclei and fascicles rather than the nuclei or root exit zones of cranial nerves VI, VII, and VIII. Another localization to remember is \u003Cstrong\u003EGradenigo syndrome\u003C/strong\u003E, where petrous apicitis classically causes ipsilateral sixth nerve palsy with severe trigeminal distribution pain and otitis or mastoid disease, but the combination of progressive hearing loss and complete ipsilateral facial weakness in this vignette more strongly indicates \u003Cstrong\u003EThe cerebellopontine angle\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1878,
    "Name": "Prolactinoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich type of secreting pituitary adenoma is most likely to present with optic chiasm compression?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EProlactin secreting adenoma\u003C/strong\u003E, because prolactinomas are the most common functioning pituitary adenomas and, particularly in males, may remain clinically unrecognized until they have enlarged into macroadenomas with suprasellar extension; hyperprolactinemia in males commonly causes relatively nonspecific or underreported symptoms such as reduced libido, erectile dysfunction, infertility, and hypogonadotropic hypogonadism, so diagnosis may be delayed until headache or visual field loss develops. Large prolactinomas may extend upward from the sella and compress the inferior optic chiasm, initially affecting the crossing inferonasal retinal fibers and producing bilateral superotemporal field defects that can progress to complete bitemporal hemianopia; lateral extension into the cavernous sinus may additionally cause ocular motor cranial neuropathies. Clinical reports of giant prolactinomas describe bitemporal field loss from suprasellar extension and optic chiasmal compression, with giant lesions occurring predominantly in males.  By comparison, \u003Cstrong\u003EGrowth hormone (GH) secreting adenoma\u003C/strong\u003E, \u003Cstrong\u003EAdrenocorticotropic hormone (ACTH) secreting adenoma\u003C/strong\u003E, and \u003Cstrong\u003EThyroid stimulating hormone (TSH) secreting adenoma\u003C/strong\u003E usually produce conspicuous endocrine syndromes, namely acromegaly or gigantism, Cushing disease, and central hyperthyroidism, respectively, which often prompt investigation before sufficient enlargement occurs to compress the chiasm; ACTH-secreting adenomas are particularly likely to be microadenomas at diagnosis because even small tumors can produce substantial systemic manifestations. Females with prolactinomas also tend to present earlier with amenorrhea, oligomenorrhea, galactorrhea, or infertility and therefore more commonly have microadenomas at diagnosis, whereas males are more likely to present later with larger invasive tumors and mass-effect symptoms. Prolactinomas are important therapeutically because dopamine agonists, particularly cabergoline, are generally first-line treatment and can rapidly reduce prolactin levels, shrink the tumor, and improve chiasmal visual field defects, although urgent neurosurgical assessment is required when there is pituitary apoplexy, threatened vision without prompt medical response, treatment resistance, or intolerance.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1879,
    "Name": "Apraxia of eyelid opening with preserved vertical saccades",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old with a four-year history of gait difficulty and postural instability reports intermittent inability to reopen the eyelids after voluntary closure. During examination, reopening requires marked frontalis recruitment, although only minimal ptosis remains once the eyelids are elevated. Ocular motility and saccadic velocity are otherwise normal, but fixation is interrupted by more than 20 square-wave jerks per minute. Which diagnosis most appropriately accounts for this clinical pattern?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EParkinson disease\u003C/strong\u003E, because the difficulty initiating eyelid elevation despite preserved levator function once the lids are open represents \u003Cstrong\u003Eapraxia of eyelid opening\u003C/strong\u003E, more accurately described as a supranuclear eyelid-opening disorder involving failure of normal levator palpebrae activation, persistent pretarsal orbicularis oculi activity, or a combination of both; the marked compensatory frontalis contraction and minimal true ptosis help distinguish this from mechanical or neurogenic ptosis. Apraxia of eyelid opening occurs in extrapyramidal disorders, including Parkinson disease, progressive supranuclear palsy, Huntington disease, and Wilson disease, and may coexist with blepharospasm, reduced blink rate, dry eye, and convergence insufficiency. Parkinson disease is also associated with fixation instability and increased square-wave jerks, although very frequent, large-amplitude square-wave jerks are more strongly associated with progressive supranuclear palsy.  The decisive feature against progressive supranuclear palsy in this particular stem is that ocular motility and saccades, especially vertical saccades, are unremarkable after four years of symptoms; progressive supranuclear palsy characteristically produces early slowing of vertical saccades, particularly downward saccades, followed by supranuclear vertical gaze palsy, often with axial rigidity, early backward falls, reduced blink rate, eyelid-opening apraxia, and frequent macro-square-wave jerks.  A functional disorder is less likely because the reproducible frontalis recruitment, parkinsonian gait and postural history, and objective fixation instability provide a coherent organic extrapyramidal pattern, while vascular dementia would require a vascular cognitive or neurological syndrome and does not characteristically produce isolated eyelid-opening apraxia with this ocular motor profile.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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  },
  {
    "Id": 1880,
    "Name": "Microvascular ocular motor cranial neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient thought to have an isolated microvascular palsy of cranial nerve 3, 4, or 6, which clinical feature falls outside the expected temporal course and should prompt reconsideration of the diagnosis, neuroimaging, and a more comprehensive etiologic investigation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EProgression of deficits after 2 weeks\u003C/strong\u003E, because a presumed microvascular ocular motor mononeuropathy results from ischemia of the vasa nervorum supplying cranial nerve 3, 4, or 6 and typically presents acutely in an older patient with vascular risk factors such as diabetes, hypertension, dyslipidemia, smoking, or generalized vascular disease; the paresis may worsen during the first several days, usually reaching maximal severity within approximately one week, but continuing or renewed progression after two weeks is atypical and raises concern for an alternative inflammatory, infiltrative, compressive, neoplastic, infectious, or aneurysmal process requiring thorough evaluation and appropriate neuroimaging. Microvascular palsies generally begin to improve within several weeks and recover substantially or completely within about 6\u201312 weeks, so \u003Cstrong\u003EFailure to recover within 3 weeks\u003C/strong\u003E alone is not necessarily abnormal, although absence of any improvement by approximately 8\u201312 weeks or failure of near-complete recovery by three months should prompt imaging or reassessment.  \u003Cstrong\u003EEye pain\u003C/strong\u003E does not exclude a microvascular mechanism because ipsilateral orbital, brow, or periocular pain is common and may precede or accompany diplopia; however, severe persistent pain, pain accompanied by sensory loss, or pain that continues after the palsy stabilizes should raise concern for conditions such as Tolosa-Hunt syndrome, cavernous sinus disease, aneurysm, or giant cell arteritis.  \u003Cstrong\u003EAge less than 70\u003C/strong\u003E is also not intrinsically inconsistent because the traditional observation threshold is usually older than approximately 50\u201355 years when the palsy is isolated and compatible vascular risk factors are present, although many contemporary specialists favor early MRI in more patients because apparently isolated palsies may occasionally have structural causes. A critical exception is third nerve palsy: a pupil-involving, partial, progressive, painful, or otherwise atypical third nerve palsy requires urgent vascular imaging to exclude a posterior communicating artery aneurysm rather than being presumed microvascular.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1881,
    "Name": "Neurovascular compression syndromes",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed disorder is not classically caused by hyperexcitability of a cranial nerve secondary to compression at or near its root entry or exit zone by an aberrant, ectatic, or dilated intracranial artery?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EBenign essential blepharospasm\u003C/strong\u003E, because benign essential blepharospasm is a bilateral focal dystonia characterized by involuntary synchronous contraction of the orbicularis oculi muscles, sometimes extending to the lower facial and oromandibular muscles as Meige syndrome; its pathophysiology is thought to involve abnormal sensorimotor processing and disinhibition within basal ganglia, brainstem blink-reflex, and cortical networks rather than focal arterial compression of the facial nerve. Ocular surface irritation, dry eye, bright light, fatigue, and stress may exacerbate the spasms, but structural neuroimaging is usually normal, and the principal treatment is periodic botulinum toxin injection into the involved periocular muscles. In contrast, \u003Cstrong\u003ESuperior oblique myokymia\u003C/strong\u003E may result from vascular contact with the cisternal trochlear nerve, causing focal demyelination and ephaptic transmission; this produces brief monocular, high-frequency, low-amplitude torsional or vertical oscillations with episodic oscillopsia or diplopia, and vascular compression has been demonstrated on thin-section MRI in some cases.  \u003Cstrong\u003ETrigeminal neuralgia\u003C/strong\u003E is classically associated with arterial compression of the trigeminal nerve near its root entry zone, most often by the superior cerebellar artery, producing focal demyelination and paroxysmal, electric shock-like facial pain; \u003Cstrong\u003EHemifacial spasm\u003C/strong\u003E commonly results from vascular compression of the facial nerve at its root exit zone, often by the anterior inferior cerebellar, posterior inferior cerebellar, or vertebral artery, producing unilateral involuntary contractions that typically begin around the orbicularis oculi and spread to the lower facial muscles. Symptomatic neurovascular compression is particularly important at the transition between central and peripheral myelin, where chronic pulsatile arterial contact can produce focal demyelination, axonal hyperexcitability, and ephaptic transmission between adjacent nerve fibers.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1882,
    "Name": "Anisocoria",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old noticed unequal pupil sizes one week ago, with the right pupil significantly smaller than the left. There is a one-year history of right upper eyelid drooping, six months of mild left-eye blurring with an outdated spectacle prescription, and a longstanding history of predominantly left-sided migraine without headache during the preceding week. After confirming true anisocoria, which single examination finding is most important for identifying the abnormal pupil and determining the underlying mechanism?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe effect of lighting conditions on her anisocoria\u003C/strong\u003E, because the fundamental first step in evaluating anisocoria is to compare pupil sizes in bright and dim illumination to determine whether the smaller pupil is failing to dilate or the larger pupil is failing to constrict. If anisocoria becomes greater in darkness, the smaller pupil is abnormal because of impaired sympathetic dilation; the differential includes Horner syndrome, pharmacological miosis, posterior synechiae or other mechanical iris restriction, and an old tonic pupil that has become miotic with time. In this patient, a right pupil that remains relatively small in darkness, particularly with dilation lag and mild right ptosis, would strongly support a right Horner syndrome and require assessment for an acquired lesion anywhere along the three-neuron oculosympathetic pathway. If anisocoria becomes greater in bright light, the larger pupil is abnormal because of impaired parasympathetic constriction; important causes include a pupil-involving third nerve palsy, Adie tonic pupil, pharmacological mydriasis, traumatic mydriasis, and structural iris sphincter damage. If the pupil difference remains small and approximately equal in light and darkness, with normal reactions and no associated neurological or ocular abnormality, physiological anisocoria becomes more likely.  \u003Cstrong\u003EThe presence of ptosis\u003C/strong\u003E is clinically important but cannot by itself identify the abnormal pupil, because ptosis may accompany a small pupil in Horner syndrome or a large pupil in a third nerve palsy, and longstanding involutional levator aponeurotic dehiscence may be unrelated to the anisocoria. \u003Cstrong\u003EThe presence of visual blurring\u003C/strong\u003E is also nonspecific and may simply reflect outdated refraction, although impaired accommodation can accompany a tonic pupil or pharmacological mydriasis. \u003Cstrong\u003EThe location of her headache\u003C/strong\u003E may become important after the pupil abnormality has been localized, particularly because a new painful Horner syndrome raises concern for carotid artery dissection and a painful pupil-involving third nerve palsy raises concern for a posterior communicating artery aneurysm, but the historical migraine pattern does not replace examination in light and darkness. The practical FRCS sequence is therefore: confirm anisocoria, measure both pupils in bright and dim illumination while fixation is maintained at distance, identify whether the small or large pupil is abnormal, assess direct and consensual reactions and near responses, look for dilation lag, ptosis, ocular motility abnormalities and iris structural disease, review old photographs, and then select pharmacological testing or urgent imaging according to the localization.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1883,
    "Name": "Spasmus nutans",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is NOT a characteristic of spasmus nutans?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EHigh amplitude horizontal, vertical, or rotary nystagmus\u003C/strong\u003E, because spasmus nutans is classically an acquired nystagmus syndrome of infancy characterized by the triad of \u003Cstrong\u003Enystagmus, head nodding, and torticollis or abnormal head posture\u003C/strong\u003E; the nystagmus is typically \u003Cstrong\u003Ehigh frequency and low amplitude\u003C/strong\u003E, producing a fine \u201Cshimmering\u201D appearance rather than high-amplitude oscillation. The eye movements are usually pendular, may be horizontal, vertical, torsional, or mixed, and are characteristically asymmetric or disconjugate; the amplitude may be so small in one eye that the nystagmus appears monocular, and the waveform or direction may vary with gaze position.  Onset is usually within the first two years of life, most often during the first year, and idiopathic cases are generally benign and self-limiting, with substantial clinical resolution over approximately 1\u20132 years or by 3\u20134 years of age, although subtle eye movement recordings may remain abnormal for longer. The head nodding is typically slower than the ocular oscillation and may occur horizontally, vertically, or obliquely, while torticollis may represent an adaptive attempt to reduce nystagmus asymmetry or improve visual function. A spasmus nutans-like presentation must not automatically be assumed benign because anterior visual pathway tumors, particularly optic pathway or chiasmal glioma, and retinal disorders such as congenital stationary night blindness can occasionally produce a similar asymmetric or monocular, fine nystagmus; atypical features such as persistent strictly monocular nystagmus, optic disc pallor, a relative afferent pupillary defect, poor visual behavior, developmental or neurological abnormalities, onset outside the usual age range, or failure to resolve should prompt MRI of the brain and orbits and, where retinal dysfunction is suspected, electroretinography and genetic assessment.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1884,
    "Name": "Retrochiasmal visual pathway lesions",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAs a general rule of retro-chiasmal optic pathway pathology (lesions located posterior to the optic chiasm), which of the following is true?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMore posteriorly-located lesions result in more congruous visual field deficits.\u003C/strong\u003E, because a unilateral lesion posterior to the optic chiasm ordinarily produces a \u003Cstrong\u003Econtralateral homonymous visual field defect involving both eyes\u003C/strong\u003E, rather than a monocular defect; congruity describes how closely the corresponding field defects in the two eyes match in shape, size, depth, and position. In the anterior retrochiasmal pathway, particularly the optic tract and anterior optic radiations, fibers representing corresponding retinal points in the two eyes remain relatively separated, so a partial lesion is more likely to affect the two eyes unequally and produce an \u003Cstrong\u003Eincongruous\u003C/strong\u003E homonymous defect. As the pathway proceeds posteriorly toward the calcarine cortex, fibers representing corresponding retinal locations become more closely organized, so occipital cortical lesions more often generate highly \u003Cstrong\u003Econgruous\u003C/strong\u003E homonymous hemianopic defects. This is a useful localization rule rather than an absolute law: many optic tract and optic radiation lesions can still produce congruous defects, and a complete homonymous hemianopia has limited anteroposterior localizing value because complete interruption at any point from the optic tract to the visual cortex can produce the same field pattern.  Retrochiasmal pathology is normally binocular because each optic tract and subsequent pathway carries information from the same contralateral visual hemifield of both eyes; the rare exception is \u003Cstrong\u003Emonocular temporal crescent syndrome\u003C/strong\u003E, in which a lesion of the most anterior medial occipital cortex damages the representation of the far peripheral temporal field that has no corresponding nasal-field representation in the fellow eye.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1885,
    "Name": "Resolving presumed microvascular sixth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 65-year-old with a vaguely documented history of hypertension and no primary care provider developed sudden horizontal binocular diplopia and right-eye abduction weakness two months ago. The diplopia improved substantially during the following month and now occurs only occasionally in extreme right gaze. Visual acuity, slit-lamp examination, and fundoscopy are normal; alignment testing demonstrates a 2-prism-diopter esophoria in primary position, orthophoria in left gaze, and an 8-prism-diopter intermittent esotropia in right gaze. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESend the patient to a general internist / primary care physician\u003C/strong\u003E, because the acute onset in an older patient with hypertension, followed by substantial spontaneous improvement over two months, is most consistent with a resolving presumed \u003Cstrong\u003Emicrovascular right sixth nerve palsy\u003C/strong\u003E; the small residual esodeviation that increases in right gaze reflects incomplete recovery of the right lateral rectus, while the 2-prism-diopter esophoria in primary position is small enough to be fused and explains why diplopia is now confined to far right gaze. Microvascular ocular motor palsies are associated with hypertension, diabetes, dyslipidemia, and smoking and usually recover spontaneously within approximately 6\u201312 weeks or, in some cases, 2\u20134 months.  The essential next step is therefore not merely ocular reassurance, but systemic vascular risk assessment through primary care, including accurate blood-pressure measurement, fasting glucose or HbA1c, lipid profile, smoking assessment, cardiovascular evaluation where indicated, and treatment of previously unrecognized or inadequately controlled risk factors; these factors are relevant not only to recurrent cranial mononeuropathy but also to stroke, coronary disease, peripheral vascular disease, and renal disease.  \u003Cstrong\u003EPrescribe Fresnel prisms for his intermittent esotropia\u003C/strong\u003E is not appropriate because the deviation is small in primary gaze, continually improving, and mainly present in extreme right gaze; a fixed prism cannot correct a markedly incomitant deviation in every gaze position and may create diplopia in positions where the patient is currently aligned. \u003Cstrong\u003EReassure the patient and suggest follow-up as needed\u003C/strong\u003E is insufficient because vascular risk factors remain unevaluated and the small residual deficit should be documented until resolution; review in approximately 4\u20138 weeks would be prudent, with neuroimaging reconsidered if improvement stops, the palsy progresses or recurs, additional neurological signs develop, or recovery remains incomplete beyond the expected period. \u003Cstrong\u003EObtain an MRI of the brain\u003C/strong\u003E is not the immediate best step in this improving, isolated, presumed microvascular palsy, although MRI would be indicated for an atypical course, progression, non-isolated findings, papilloedema, younger age, recurrent palsy, or failure to recover as expected.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1886,
    "Name": "Autosomal dominant optic atrophy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed feature is not characteristic of autosomal dominant optic atrophy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Enerve fiber bundle type visual field defects respecting the horizontal meridian\u003C/strong\u003E, because autosomal dominant optic atrophy, also known as \u003Cstrong\u003EKjer optic atrophy\u003C/strong\u003E, is a hereditary mitochondrial optic neuropathy that preferentially damages retinal ganglion cells and the papillomacular bundle, so the characteristic visual field abnormality is a \u003Cstrong\u003Ecentral, centrocecal, or paracentral scotoma\u003C/strong\u003E, rather than an arcuate nerve fiber bundle defect or nasal step respecting the horizontal meridian, which would be more typical of glaucomatous optic neuropathy. ADOA usually begins during the first or second decade, often between 4 and 6 years of age, with slowly progressive, relatively symmetrical bilateral visual loss, dyschromatopsia, and variable intrafamilial severity; many patients retain visual acuity better than 20/200, although severe impairment can occur.  Most cases are caused by heterozygous pathogenic variants in the nuclear \u003Cstrong\u003EOPA1 gene on chromosome 3q28-q29\u003C/strong\u003E, which encodes a dynamin-related mitochondrial GTPase involved in inner mitochondrial membrane fusion, cristae organization, maintenance of mitochondrial DNA, and oxidative phosphorylation; dysfunction leads to mitochondrial fragmentation, oxidative stress, retinal ganglion-cell apoptosis, and preferential papillomacular bundle loss.  The optic discs typically demonstrate temporal pallor or diffuse pallor, often with \u003Cstrong\u003Efocal temporal excavation\u003C/strong\u003E, which may simulate glaucomatous cupping; however, the pallor is disproportionate to the degree of excavation, intraocular pressure is not responsible for the damage, and the field defect is central rather than a classic superior or inferior arcuate defect. Color vision loss is frequently described as blue-yellow or tritan-like, although mixed or generalized dyschromatopsia may occur.  Some patients develop an \u003Cstrong\u003EADOA-plus phenotype\u003C/strong\u003E, with sensorineural hearing loss, peripheral neuropathy, ataxia, myopathy, or chronic progressive external ophthalmoplegia, and the diagnosis should be supported by family history, OCT showing temporal retinal nerve fiber layer and macular ganglion-cell loss, visual fields, electrophysiology when required, exclusion of compressive or nutritional/toxic optic neuropathy, and molecular genetic testing.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1887,
    "Name": "Superior segmental optic nerve hypoplasia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 22-year-old is referred after routine perimetry detects asymptomatic inferior visual field loss in both eyes. Visual acuity, color vision, and pupillary responses are normal. Both optic discs have a similar superior segmental abnormality, and Humphrey 30-2 testing demonstrates nearly identical inferior field defects, while the remainder of the dilated examination is normal. Which listed association is characteristic of this condition?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-08-650c1bb5-ff11-4755-bd97-912d045e08fb.png\u0022\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-08-18546480-8caa-4345-b15b-f2ea5a9816c7.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMaternal diabetes\u003C/strong\u003E, because the bilateral, symmetrical, nonprogressive inferior visual field defects associated with superior segmental optic disc hypoplasia indicate \u003Cstrong\u003Esuperior segmental optic nerve hypoplasia\u003C/strong\u003E, also called \u003Cstrong\u003Etopless disc syndrome\u003C/strong\u003E. This congenital anomaly results from developmental loss or underdevelopment of retinal ganglion cells and axons entering the superior optic nerve head, producing four classically described disc features: superior optic disc pallor, a superior peripapillary scleral halo, superior entrance or displacement of the central retinal artery, and thinning of the superior retinal nerve fiber layer; loss of superior retinal fibers produces the corresponding inferior altitudinal or sectoral visual field defect.  The condition is strongly associated with \u003Cstrong\u003Ematernal diabetes during pregnancy\u003C/strong\u003E, particularly pregestational diabetes, and is thought to reflect a teratogenic effect of intrauterine hyperglycemia on early retinal ganglion-cell and optic nerve development; cases have also been reported following maternal gestational diabetes.  Central visual acuity and color vision remain normal because the temporal papillomacular bundle is relatively preserved, and a relative afferent pupillary defect is usually absent when the anomaly is bilateral and symmetrical. Superior segmental optic nerve hypoplasia can resemble glaucoma because both conditions may show retinal nerve fiber layer thinning with an inferior field defect, but the congenital defect is generally stable, frequently symmetrical, associated with superior disc pallor rather than progressive neuroretinal rim loss, and does not require pressure-lowering treatment; serial OCT and perimetry may be used initially to confirm nonprogression when diagnostic uncertainty remains.  \u003Cstrong\u003EHigh intraocular pressures\u003C/strong\u003E would favor juvenile or secondary glaucoma, where progressive cupping and corresponding nerve fiber bundle loss would be expected. \u003Cstrong\u003ENystagmus\u003C/strong\u003E is more characteristic of severe bilateral generalized optic nerve hypoplasia causing early visual deprivation, not this segmental form with preserved central acuity. \u003Cstrong\u003EAbsence of the septum pellucidum\u003C/strong\u003E is associated with septo-optic dysplasia, which involves generalized optic nerve hypoplasia and may be accompanied by hypothalamic-pituitary dysfunction and neurological abnormalities, rather than isolated superior segmental hypoplasia.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1888,
    "Name": "Pharmacological localization of Horner syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFollowing the observation of anisocoria, the above pharmacological tests are carried out. What is the most likely diagnosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ctable\u003E\u003Cthead\u003E\u003Ctr\u003E\u003Cth\u003ETest condition\u003C/th\u003E\u003Cth align=\u0022right\u0022\u003ERight pupil (mm)\u003C/th\u003E\u003Cth align=\u0022right\u0022\u003ELeft pupil (mm)\u003C/th\u003E\u003C/tr\u003E\u003C/thead\u003E\u003Ctbody\u003E\u003Ctr\u003E\u003Ctd\u003EBaseline\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E4\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E2\u003C/td\u003E\u003C/tr\u003E\u003Ctr\u003E\u003Ctd\u003ECocaine\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E7\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E2\u003C/td\u003E\u003C/tr\u003E\u003Ctr\u003E\u003Ctd\u003EHydroxyamphetamine 1%\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E5\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E1\u003C/td\u003E\u003C/tr\u003E\u003Ctr\u003E\u003Ctd\u003EPhenylephrine 1%\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E3.5\u003C/td\u003E\u003Ctd align=\u0022right\u0022\u003E4\u003C/td\u003E\u003C/tr\u003E\u003C/tbody\u003E\u003C/table\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPost-ganglionic Horner\u2019s\u003C/strong\u003E, because the baseline anisocoria is caused by an abnormally small left pupil, and the pharmacological tests both confirm left oculosympathetic denervation and localize the interruption to the third-order, postganglionic sympathetic neuron. Cocaine blocks norepinephrine reuptake at the iris dilator neuromuscular junction, so the normal right pupil dilates from 4 to 7 mm because endogenous norepinephrine accumulates, whereas the left pupil remains at 2 mm because interruption of the sympathetic pathway leaves insufficient norepinephrine in the synaptic cleft; the resulting increase in anisocoria confirms Horner syndrome but does not localize the lesion.  Hydroxyamphetamine acts indirectly by releasing stored norepinephrine from intact postganglionic sympathetic nerve terminals: a central or preganglionic lesion leaves the third-order neuron intact and therefore permits dilation, but a postganglionic lesion damages the terminal and prevents norepinephrine release, so the left pupil\u2019s failure to dilate localizes the lesion to the third-order neuron.  Dilute phenylephrine 1% has little effect on the normally innervated iris but directly stimulates upregulated \u03B11 receptors in a chronically denervated iris dilator muscle; the left pupil therefore dilates from 2 to 4 mm and reverses the anisocoria, demonstrating denervation supersensitivity and further supporting a postganglionic lesion.  The third-order neuron begins at the superior cervical ganglion, travels along the internal carotid artery through the cavernous sinus, joins the ophthalmic division of the trigeminal nerve and long ciliary nerves, and finally supplies the iris dilator and M\u00FCller muscle; important causes include internal carotid artery dissection, cavernous sinus disease, cluster headache or other trigeminal autonomic cephalalgias, and lesions of the orbital apex.  \u003Cstrong\u003EPreganglionic Horner\u2019s\u003C/strong\u003E would be expected to retain postganglionic norepinephrine stores and therefore dilate with hydroxyamphetamine, while \u003Cstrong\u003EHolme\u2019s Aides pupil\u003C/strong\u003E would produce a relatively large pupil with light-near dissociation and cholinergic supersensitivity rather than a cocaine-confirmed small sympathetic pupil, and \u003Cstrong\u003EPharmacological mydriasis\u003C/strong\u003E would also cause a large poorly constricting pupil rather than the demonstrated left miosis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1889,
    "Name": "Neuroretinitis with a macular star",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA previously healthy 19-year-old develops painless reduction of vision in the left eye over several days, persisting for two weeks. Best-corrected visual acuity is 20/200 in the affected eye, with a mild left relative afferent pupillary defect and impaired color-plate recognition. Fundus examination demonstrates optic disc swelling accompanied by radially arranged macular exudates. Is routine neuroimaging required in this clinical setting, and does this presentation confer an increased risk of subsequently developing multiple sclerosis?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-08-f5f25955-3302-48a9-b8bb-e7e238464b78.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENo neuro-imaging required; No risk of MS over general population\u003C/strong\u003E, because the combination of painless subacute monocular visual loss, dyschromatopsia, a relative afferent pupillary defect, optic disc edema, and hard macular exudates arranged in a stellate pattern is characteristic of \u003Cstrong\u003Eneuroretinitis\u003C/strong\u003E, in which inflammation and vascular leakage at the optic nerve head allow fluid to extend into the peripapillary retina, while lipid-rich material accumulates within the radially arranged outer plexiform or Henle fiber layer to form the macular star; the disc edema usually precedes the star by approximately one to two weeks, so early OCT may demonstrate peripapillary intraretinal or subretinal fluid before the exudates become clinically obvious.  Unlike typical demyelinating optic neuritis, neuroretinitis is usually painless, has conspicuous disc swelling and macular exudation, and is not considered a typical demyelinating event that independently increases the future risk of multiple sclerosis; therefore, routine MRI solely for multiple-sclerosis risk stratification is not required in an otherwise neurologically well patient with a classic neuroretinitis phenotype. Neuroretinitis is a descriptive clinical syndrome rather than a single etiological diagnosis, so the appropriate investigation is directed laboratory testing based on exposure history and systemic features, particularly serology for \u003Cstrong\u003EBartonella henselae\u003C/strong\u003E, a major infectious cause, together with testing for syphilis and consideration of tuberculosis, Lyme disease, toxoplasmosis, toxocariasis, and sarcoidosis where epidemiologically or clinically indicated.  MRI of the brain and orbits should nevertheless be obtained if the presentation is atypical, the diagnosis is uncertain, neurological symptoms are present, visual function continues to deteriorate, the disc swelling is disproportionate or persistent, the macular star is absent despite ongoing disease, or a compressive, infiltrative, demyelinating, or central nervous system inflammatory process is suspected.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1890,
    "Name": "Second-order Horner syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed condition would interrupt the preganglionic sympathetic fibers producing a second-order Horner syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA thoracic aortic aneurysm\u003C/strong\u003E, because the second-order, or preganglionic, sympathetic neuron begins in the intermediolateral cell column at the \u003Cstrong\u003Eciliospinal center of Budge, classically C8\u2013T2\u003C/strong\u003E, exits through the ventral spinal roots, traverses the cervicothoracic sympathetic chain, arches over the pulmonary apex and subclavian artery, and ascends to synapse in the superior cervical ganglion; a thoracic aortic aneurysm can compress or stretch these preganglionic fibers during their intrathoracic course and therefore produce an ipsilateral second-order Horner syndrome. Other important preganglionic causes include an apical lung or Pancoast tumor, mediastinal or thyroid masses, cervical rib, brachial plexus injury, neck or thoracic trauma, and surgery involving the neck, chest, or sympathetic chain.  \u003Cstrong\u003EWallenberg syndrome secondary to ischemic stroke\u003C/strong\u003E interrupts the descending hypothalamospinal sympathetic pathway in the lateral medulla and therefore causes a first-order, central Horner syndrome, usually accompanied by other lateral medullary findings such as vertigo, nystagmus, ipsilateral facial sensory loss, contralateral body pain and temperature loss, dysphagia, hoarseness, and ipsilateral limb ataxia. \u003Cstrong\u003ECluster headache\u003C/strong\u003E produces a third-order Horner syndrome through involvement of the postganglionic sympathetic plexus surrounding the internal carotid artery, often causing transient ipsilateral ptosis and miosis during attacks. \u003Cstrong\u003EA lung cancer metastasis to the cavernous sinus\u003C/strong\u003E also affects the third-order pathway because postganglionic sympathetic fibers travel with the internal carotid artery through the cavernous sinus before joining the ophthalmic division of the trigeminal nerve; cavernous sinus disease may additionally affect cranial nerves III, IV, VI, V1, and V2.  A useful localization mnemonic is\u003Cstrong\u003E\u201CBrain, Breast, Blood vessel\u201D\u003C/strong\u003E: first-order lesions are in the \u003Cstrong\u003Ebrain or cervical cord\u003C/strong\u003E, second-order lesions pass through the \u003Cstrong\u003Ebreast/chest and lung apex\u003C/strong\u003E, and third-order lesions follow the internal carotid \u003Cstrong\u003Eblood vessel\u003C/strong\u003E into the cavernous sinus and orbit.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1891,
    "Name": "Recurrent unilateral headache with delayed visual blurring",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old with moderate hyperopia has experienced recurrent right-sided headaches twice weekly for two months. Each episode begins with right periorbital pain, occurs more frequently at night, lasts 1\u20134 hours, and is followed several minutes later by right-eye visual blurring that persists for approximately one hour after the headache resolves. Visual acuity, pupils, confrontation fields, motility, slit-lamp examination, and undilated fundoscopy are normal between episodes; intraocular pressure is 20 mmHg in each eye, but the cup-to-disc ratios are asymmetrical at 0.45 in the right eye and 0.3 in the left eye. What is the most appropriate next step in the evaluation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EGonioscopy\u003C/strong\u003E, because the combination of moderate hyperopia, recurrent unilateral periorbital headache occurring more commonly at night, and ipsilateral visual blurring that begins \u003Cstrong\u003Eafter\u003C/strong\u003E the pain raises concern for intermittent or subacute angle closure rather than a typical migraine visual aura. Hyperopic eyes frequently have shorter axial lengths, shallower anterior chambers, and more crowded anterior segments; when the pupil becomes physiologically mid-dilated in dim illumination, increased iridolenticular contact can produce relative pupillary block, posterior chamber pressure rises, the peripheral iris bows forward, and the trabecular meshwork becomes transiently occluded. The intraocular pressure may therefore rise during an episode and return to normal once the angle reopens, so an interictal pressure of 20 mmHg and a normal routine slit-lamp examination do not exclude intermittent angle closure. Gonioscopy is essential because it directly assesses angle width, iridotrabecular contact, indentation opening, abnormal angle anatomy, and peripheral anterior synechiae; standard slit-lamp estimation of anterior chamber depth cannot reliably rule out an occludable angle.  The chronology is particularly important: migraine aura usually consists of progressive positive or negative binocular visual phenomena that commonly precede or accompany headache and typically last 5\u201360 minutes, whereas intermittent angle closure may cause unilateral blur or colored halos after ocular or periorbital pain begins and can persist beyond the headache as pressure and corneal function normalize. Intermittent angle closure can closely mimic migraine and may remain undiagnosed until gonioscopy demonstrates narrow or occludable angles.  \u003Cstrong\u003EHumphrey visual fields in both eyes\u003C/strong\u003E and \u003Cstrong\u003ECheck pachymetry\u003C/strong\u003E may subsequently be appropriate because of the asymmetric cup-to-disc ratios and borderline-normal pressure, but neither establishes whether the patient is currently at risk of episodic angle obstruction; the immediate priority is to identify the potentially reversible and sight-threatening angle anatomy. \u003Cstrong\u003EStart a migraine prophylaxis medication\u003C/strong\u003E would be premature before excluding an ocular mechanism, particularly because the visual symptoms follow the headache and the patient has an anatomical risk factor for angle closure. If gonioscopy confirms occludable angles, further assessment should determine the mechanism and presence of synechial or glaucomatous damage, with prophylactic laser peripheral iridotomy considered when pupillary block is responsible.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1892,
    "Name": "Focal occipital lobe seizures",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is true of focal occipital lobe seizures?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThey typically manifest with unformed hallucinations or positive visual phenomena\u003C/strong\u003E, because focal seizures arising from the primary visual cortex commonly produce sudden \u003Cstrong\u003Eelementary visual hallucinations\u003C/strong\u003E, such as multicolored circles, flashing lights, spots, geometric figures, or other unformed shapes. The phenomena usually appear in the visual hemifield contralateral to the epileptic focus and may move horizontally or multiply during the episode. Negative visual symptoms, including focal field loss, transient hemianopia, or complete visual blackout or whiteout, may also occur. By contrast, complex formed hallucinations involving recognizable people, animals, objects, or scenes suggest involvement of the extrastriate visual association cortex or propagation into the temporal or parietal lobes rather than an isolated primary visual cortical seizure.\u003C/p\u003E\n\u003Cp\u003EOccipital visual seizures are usually brief, typically lasting \u003Cstrong\u003Eseconds to less than two minutes\u003C/strong\u003E, rather than only 1\u20132 seconds. This abrupt, short, stereotyped pattern helps distinguish occipital seizures from migraine aura, which usually evolves gradually over several minutes and lasts longer. Associated ocular motor manifestations are common and may include forced eyelid closure, rapid eyelid fluttering, eye deviation, epileptic nystagmus, or head and trunk version, particularly when seizure activity spreads toward the parietal or frontal regions. Therefore, the seizures do not necessarily occur without motor signs.\u003C/p\u003E\n\u003Cp\u003EIn children, occipital seizures may occur as part of \u003Cstrong\u003Echildhood occipital visual epilepsy\u003C/strong\u003E, a self-limited focal epilepsy syndrome in which neurological examination, development, and neuroimaging are usually normal, rather than usually reflecting a tumor or other structural lesion. Structural occipital epilepsy remains an important differential diagnosis, especially with abnormal neurological findings, persistent visual-field defects, an atypical age or seizure pattern, or focal abnormalities on imaging.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1893,
    "Name": "Demyelinating optic neuritis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EApproximately what proportion of eyes with demyelinating optic neuritis exhibit visible optic disc edema during the acute presentation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E35%\u003C/strong\u003E, because typical demyelinating optic neuritis is most commonly \u003Cstrong\u003Eretrobulbar\u003C/strong\u003E, meaning that the inflammatory lesion lies behind the visible optic nerve head; consequently, the optic disc appears normal during the acute presentation in approximately two-thirds of affected eyes, giving rise to the classic description, \u201Cthe patient sees nothing, and the doctor sees nothing.\u201D Visible optic disc edema, also termed anterior optic neuritis or papillitis in this context, occurs in approximately one-third of cases, conventionally quoted as \u003Cstrong\u003E35%.\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EWhen present in typical demyelinating optic neuritis, the disc swelling is generally mild and may be accompanied by hyperemia, but prominent hemorrhages, hard exudates, a macular star, severe swelling, vitreous inflammation, or marked retinal vascular abnormalities should prompt consideration of an alternative or atypical process such as MOG-antibody-associated disease, neuroretinitis, ischemic optic neuropathy, sarcoidosis, infection, or infiltrative optic neuropathy.\u003C/p\u003E\n\u003Cp\u003EThe typical clinical pattern remains acute or subacute monocular visual loss, dyschromatopsia, a relative afferent pupillary defect in unilateral or asymmetric disease, and periocular pain that worsens with eye movement, while the visual field defect may be central, cecocentral, altitudinal, arcuate, or diffuse. MRI of the brain and orbits with gadolinium can demonstrate enhancement of the affected optic nerve and, more importantly for long-term prognosis, identify cerebral white-matter lesions associated with a greater future risk of multiple sclerosis.\u003C/p\u003E\n\u003Cp\u003EA high-yield way to remember the fundus appearance is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EOne-third swollen, two-thirds retrobulbar.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
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  },
  {
    "Id": 1894,
    "Name": "Nuclear innervation of the left superior rectus and left superior oblique muscles",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich oculomotor nuclear complex supplies the left superior rectus muscle, and which trochlear nucleus supplies the left superior oblique muscle, in that order?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe right 3rd nerve nucleus; the right 4th nerve nucleus\u003C/strong\u003E, because both the superior rectus and superior oblique receive \u003Cstrong\u003Econtralateral nuclear innervation\u003C/strong\u003E, although the fibers cross at different anatomical locations.\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Eleft superior rectus\u003C/strong\u003E is supplied by neurons within the \u003Cstrong\u003Eright superior rectus subnucleus of the oculomotor nuclear complex\u003C/strong\u003E. Superior rectus fibers cross within the oculomotor nuclear complex before joining the contralateral oculomotor nerve. By contrast, the medial rectus, inferior rectus, and inferior oblique subnuclei supply the ipsilateral muscles. The levator palpebrae superioris muscles receive bilateral innervation from the single midline central caudal nucleus.\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Eleft superior oblique\u003C/strong\u003E is supplied by the \u003Cstrong\u003Eright trochlear nucleus\u003C/strong\u003E. Trochlear fascicles travel dorsally within the midbrain and decussate in the superior medullary velum before emerging from the dorsal surface of the brainstem. Consequently, a trochlear \u003Cstrong\u003Enuclear or pre-decussation fascicular lesion\u003C/strong\u003E causes contralateral superior oblique weakness, whereas a lesion of the trochlear nerve after emergence from the brainstem causes ipsilateral superior oblique weakness. CN IV is unique because it is the only cranial nerve to exit dorsally and the only ocular motor cranial nerve whose fibers completely decussate before exiting.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1895,
    "Name": "New monocular nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 16-month-old has developed fine, shimmering vertical movement confined to the right eye during the preceding month. Fixation is less reliably maintained with the right eye than with the left, and a trace right relative afferent pupillary defect is present. Ocular alignment and motility are normal, cycloplegic refraction shows \u002B2.00 OD and -1.00 OS, and the anterior segments, optic discs, and retinas appear normal. There is no corresponding movement in the left eye and no associated head nodding or torticollis. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOrder an MRI of the brain and orbits under sedation\u003C/strong\u003E, because newly acquired \u003Cstrong\u003Estrictly monocular nystagmus in an infant\u003C/strong\u003E, particularly when accompanied by asymmetric visual behavior and a relative afferent pupillary defect, is a red flag for organic anterior visual pathway disease and must prompt urgent exclusion of an \u003Cstrong\u003Eoptic nerve, optic chiasmal, or hypothalamic lesion\u003C/strong\u003E, especially an optic pathway glioma. Optic pathway gliomas in young children may initially present with nystagmus and subtle visual dysfunction before optic disc pallor, swelling, proptosis, or obvious funduscopic abnormalities develop; published clinical observations specifically emphasize that monocular acquired nystagmus in a child younger than 2 years should prompt immediate imaging to exclude a chiasmal tumor.\u003C/p\u003E\n\u003Cp\u003EThe fine vertical movement may resemble the \u003Cstrong\u003EHeimann-Bielschowsky phenomenon\u003C/strong\u003E, a monocular vertical pendular oscillation associated with profound or longstanding unilateral visual impairment. However, that description does not establish the cause of the reduced afferent input. In this infant, the nystagmus is recent, fixation is poorer in the right eye, and the trace right afferent pupillary defect provides objective evidence of asymmetric retinal or optic pathway function. These findings cannot safely be attributed to anisometropic amblyopia without first excluding an optic nerve or chiasmal disorder.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe cycloplegic refraction does demonstrate anisometropia and could contribute to amblyopia, but amblyopia alone would not comfortably explain the entire pattern, particularly the afferent pupillary asymmetry and newly developed monocular vertical nystagmus. Once structural disease has been excluded, appropriate optical correction and amblyopia therapy can be instituted according to repeated quantitative or age-appropriate visual assessment. Immediate six-hour patching of the left eye before imaging could delay diagnosis and is an aggressive empiric treatment when the cause of the right afferent dysfunction remains uncertain.\u003C/p\u003E\n\u003Cp\u003EThe absence of head nodding and torticollis also makes classic \u003Cstrong\u003Espasmus nutans\u003C/strong\u003E less convincing. Spasmus nutans usually consists of fine, high-frequency, low-amplitude, often asymmetric or apparently monocular nystagmus accompanied by head nodding and torticollis, but a spasmus nutans-like presentation can itself be produced by optic pathway tumors or retinal dystrophy. Therefore, observation alone is inappropriate when warning signs such as a relative afferent pupillary defect or asymmetric visual function are present.\u003C/p\u003E\n\u003Cp\u003EMRI should include the \u003Cstrong\u003Ebrain and orbits\u003C/strong\u003E, with thin sections through the optic nerves, chiasm, optic tracts, and hypothalamic region, generally with contrast and fat-suppressed orbital sequences according to the pediatric neuroradiology protocol. Because a 16-month-old is unlikely to remain motionless for a diagnostic MRI, sedation or anesthesia is usually necessary under an appropriate pediatric safety pathway.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1896,
    "Name": "Dural venous sinus thrombosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat optic nerve appearance would you expect at the time of diagnosis (2 weeks after symptom onset) in a patient with the imaging study shown above?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-10-ebdb1931-3642-437c-a17d-9448fb101e34.png\u0022\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-10-27b4b419-5574-407a-86c8-260bd37574a1.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPhoto B\u003C/strong\u003E, because the magnetic resonance venography demonstrates a filling defect with absence of the expected high-flow venous signal within the right transverse sinus, consistent with \u003Cstrong\u003Edural venous sinus thrombosis\u003C/strong\u003E. Obstruction of cerebral venous drainage raises venous and intracranial pressure by impairing cerebrospinal fluid absorption at the arachnoid granulations. The increased pressure is transmitted along the optic nerve subarachnoid spaces, producing axoplasmic-flow stasis at the lamina cribrosa and subsequent papilledema. Cerebral venous sinus thrombosis may therefore present with headache, transient visual obscurations, blurred vision, pulsatile tinnitus, diplopia from unilateral or bilateral sixth nerve palsy, seizures, focal neurological deficits, and papilledema.\u003C/p\u003E\n\u003Cp\u003EAt two weeks, the expected appearance is \u003Cstrong\u003Eactive optic disc swelling\u003C/strong\u003E, as shown in Photo B, with marked elevation and hyperemia of the optic nerve head, blurred margins, obscuration of vessels crossing the disc margin, venous congestion, and possible peripapillary hemorrhages or cotton-wool spots. Papilledema is usually bilateral because intracranial pressure is transmitted to both optic nerve sheaths, although the degree may be asymmetric and rare unilateral cases have been reported.\u003C/p\u003E\n\u003Cp\u003EThe other photographs represent different optic nerve states:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto A\u003C/strong\u003E shows a relatively normal optic disc with a small cup-to-disc ratio.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto C\u003C/strong\u003E shows glaucomatous cupping with focal neuroretinal rim loss or notching rather than acute pressure-related swelling.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto D\u003C/strong\u003E shows temporal optic disc pallor, indicating established axonal loss rather than active papilledema.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EOptic pallor would not ordinarily be expected only two weeks after symptom onset. If papilledema is severe or prolonged, secondary optic atrophy may emerge after the swelling subsides, generally over subsequent weeks to months. The disc may transition from hyperemic swelling to pale swelling and eventually to a flat, pale atrophic appearance.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1897,
    "Name": "Cancer-associated retinopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 75-year-old with substantial cigarette and alcohol exposure develops progressive bilateral visual loss over two months, worsening from 20/50 to 20/100, with prominent photopsias in both eyes. Reliable 24-2 perimetry shows generalized depression, and full-field electroretinography demonstrates marked impairment of both rod- and cone-mediated responses. Pupillary responses and fundus examination remain normal. Which investigation is the most appropriate next step in establishing the diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECT of the chest, abdomen, and pelvis\u003C/strong\u003E, because the combination of rapid, painless, bilateral visual deterioration, prominent photopsias, generalized field depression, markedly reduced rod and cone responses on full-field ERG, and an initially normal fundus strongly suggests a \u003Cstrong\u003Eparaneoplastic autoimmune retinopathy\u003C/strong\u003E, particularly cancer-associated retinopathy. In cancer-associated retinopathy, a systemic tumor expresses antigens that resemble retinal proteins, triggering circulating autoantibodies that cross-react with photoreceptors and other retinal cells. Anti-recoverin is the best-known antibody, but antibodies against \u03B1-enolase, transducin, carbonic anhydrase II, arrestin, and several other retinal proteins have also been described. Visual symptoms may precede the recognition of the underlying malignancy, making prompt systemic cancer investigation essential.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe most frequently associated malignancies include \u003Cstrong\u003Esmall-cell lung carcinoma\u003C/strong\u003E, breast carcinoma, and gynecological malignancies, although other lung tumors, lymphoma, prostate, colon, pancreatic, renal, and cutaneous tumors have also been reported. The patient\u2019s age and heavy cigarette exposure make an occult pulmonary malignancy particularly important to exclude. CT imaging of the chest, abdomen, and pelvis therefore provides the most appropriate initial systemic survey, with subsequent oncology-directed PET-CT, biopsy, or other targeted testing if an abnormality is identified. Cancer-associated retinopathy has been reported in association with small-cell lung carcinoma, including cases in which systemic imaging identified the occult tumor after otherwise unexplained rapidly progressive bilateral visual loss.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe normal fundus does not exclude the disorder. Early cancer-associated retinopathy may produce substantial functional retinal impairment before visible structural changes develop. Later findings may include retinal arteriolar attenuation, retinal pigment epithelial disturbance, outer retinal or ellipsoid-zone loss on macular OCT, and optic disc pallor. Full-field ERG is particularly important because it objectively demonstrates widespread retinal dysfunction affecting rods, cones, or both. Cancer-associated retinopathy commonly impairs both systems, often with prominent cone dysfunction, while melanoma-associated retinopathy more characteristically produces an electronegative ERG reflecting ON-bipolar cell dysfunction and frequently causes night blindness, shimmering photopsias, and other positive visual phenomena.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Eoptic nerve optical coherence tomography (OCT)\u003C/strong\u003E would not be the next best test because the clinical and electrophysiological abnormalities localize to the retina rather than the optic nerves; normal pupils despite profound symmetrical bilateral visual loss also favor a relatively symmetric retinal process. Macular OCT may later document outer retinal changes, but optic nerve OCT would not identify the underlying systemic cause. \u003Cstrong\u003Ethyroid function studies\u003C/strong\u003E would not explain marked generalized rod-cone dysfunction on ERG, and thyroid eye disease would usually produce orbital findings such as lid retraction, proptosis, restrictive motility disturbance, or compressive optic neuropathy. \u003Cstrong\u003Efluorescein angiography (FA)\u003C/strong\u003E may remain normal or show nonspecific retinal vascular or pigment epithelial changes and would not establish the paraneoplastic cause or locate the occult malignancy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1898,
    "Name": "Maddox rod findings in right fourth nerve palsy with right hypertropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has right trochlear nerve palsy. During Maddox rod testing, a red Maddox rod is placed over the right eye with its ridges oriented vertically at 90/270 degrees, while the left eye views the white fixation light directly. What position and inclination of the red line should the patient perceive relative to the white light?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA tilted red line below a white light with the right end higher than the left end\u003C/strong\u003E, because the response requires separate interpretation of the \u003Cstrong\u003Evertical deviation\u003C/strong\u003E and the \u003Cstrong\u003Etorsional deviation\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EWith the Maddox rod ridges oriented vertically, the right eye perceives a \u003Cstrong\u003Ehorizontal red line\u003C/strong\u003E, since the streak created by a Maddox rod is perpendicular to the orientation of its cylindrical ridges. The unfiltered left eye perceives the original white point light. Maddox rod testing dissociates the eyes, allowing the position of the two images to reflect the ocular deviation.\u0026nbsp;\u003C/p\u003E\n\u003Ch3\u003E\u003Cspan style=\u0022font-style: italic; font-size: large; text-decoration-line: underline;\u0022\u003EWhy the red line is below the white light:\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EThe right eye is hypertropic, so the fixation target projects onto the \u003Cstrong\u003Esuperior retina\u003C/strong\u003E of the right eye. Because retinal projection is spatially inverted, the right eye perceives the red-line image in the \u003Cstrong\u003Einferior visual field\u003C/strong\u003E. The red line seen by the hypertropic right eye therefore appears \u003Cstrong\u003Ebelow\u003C/strong\u003E the white light seen by the left eye.\u003C/p\u003E\n\u003Cp\u003EA useful rule is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe higher eye sees the lower image.\u003C/strong\u003E\u003C/p\u003E\n\u003Ch3\u003E\u003Cspan style=\u0022font-style: italic; text-decoration-line: underline; font-size: large;\u0022\u003EWhy the right end of the red line is higher:\u003C/span\u003E\u003C/h3\u003E\n\u003Cp\u003EA right fourth nerve palsy weakens the right superior oblique muscle. Because the superior oblique is the principal intorter of the eye in primary position, weakness produces \u003Cstrong\u003Eright ocular excyclotorsion\u003C/strong\u003E in addition to right hypertropia.\u003C/p\u003E\n\u003Cp\u003EThe Maddox rod is physically held at the exact 90/270-degree axis, but the excyclotorted right eye perceives the nominally horizontal red line as tilted in the opposite direction. The perceived line therefore appears relatively incyclotorted, with the \u003Cstrong\u003Eright end higher than the left end\u003C/strong\u003E. Double Maddox rod testing similarly demonstrates excyclotorsion in fourth nerve palsy by requiring rotation of the affected eye\u2019s rod until the perceived line becomes horizontal.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ETherefore:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ERight hypertropia\u003C/strong\u003E \u2192 red line is \u003Cstrong\u003Ebelow\u003C/strong\u003E the white light\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ERight excyclotorsion\u003C/strong\u003E \u2192 red line has its \u003Cstrong\u003Eright end higher\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1899,
    "Name": "See-saw nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich type of nystagmus is not usually associated with pathology of the lower brainstem or cerebellum?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESee-saw nystagmus\u003C/strong\u003E, because this is a rare disconjugate vertical-torsional oscillation in which one eye \u003Cstrong\u003Eelevates and intorts\u003C/strong\u003E while the fellow eye simultaneously \u003Cstrong\u003Edepresses and extorts\u003C/strong\u003E; during the next half-cycle, the vertical and torsional movements reverse.\u003C/p\u003E\n\u003Cp\u003ESee-saw nystagmus is classically associated with \u003Cstrong\u003Eparasellar and diencephalic lesions\u003C/strong\u003E, especially those involving the optic chiasm, and may occur with pituitary or other parasellar masses, chiasmal maldevelopment, mesodiencephalic disease, multiple sclerosis or trauma. Because of the close association with optic chiasmal pathology, see-saw nystagmus may accompany a \u003Cstrong\u003Ebitemporal hemianopia\u003C/strong\u003E, making it one of the forms of nystagmus that can be associated with a visual field defect.\u003C/p\u003E\n\u003Cp\u003EThe remaining patterns are more typically associated with lower brainstem or cerebellar dysfunction:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPeriodic alternating nystagmus\u003C/strong\u003E is a horizontal jerk nystagmus that periodically reverses direction, usually because of instability in the vestibular velocity-storage mechanism involving the cerebellar nodulus and uvula or related brainstem pathways.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EUpbeat nystagmus\u003C/strong\u003E is linked particularly to central vestibular lesions in the medulla and pontomedullary region, although lesions of the midbrain, cerebellar flocculus, or superior cerebellar peduncular pathways may also produce it.\u0026nbsp;\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDownbeat nystagmus\u003C/strong\u003E most strongly suggests dysfunction of the vestibulocerebellum or cervicomedullary junction, with causes including cerebellar degeneration, Chiari malformation, demyelination, nutritional deficiency, and medication toxicity.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EA useful mnemonic is to imagine the eyes physically positioned on a \u003Cstrong\u003Esee-saw\u003C/strong\u003E: the eye moving upward rolls inward, while the eye moving downward rolls outward.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1900,
    "Name": "Old branch retinal artery occlusion involving the macula",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich test is most appropriate for determining whether chronic visual loss is caused by localized macular retinal dysfunction from a branch retinal artery occlusion that occurred five years earlier?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMultifocal electroretinogram (mfERG)\u003C/strong\u003E, because mfERG measures localized retinal electrical function simultaneously across numerous small regions of the posterior pole and produces a topographic map of macular and paramacular function. An old BRAO causes permanent ischemic injury limited to the retinal territory supplied by the affected arterial branch. If the macula was involved, mfERG can demonstrate a corresponding localized reduction in response amplitude and possibly delayed implicit time, even when the acute retinal whitening and other obvious funduscopic findings have disappeared. Studies of BRAO have shown reduced mfERG responses specifically within the affected retinal region, with the location of the electrophysiological abnormality correlating with the corresponding visual field defect.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EFull field electroretinogram (ERG)\u003C/strong\u003E measures the summed electrical response of the entire retina. Because BRAO affects only a limited retinal territory, the normal function of the remaining retina can dominate the response, and the full-field ERG may remain normal despite clinically important localized macular dysfunction. This distinction is specifically reported in BRAO, where full-field ERG may be normal while mfERG responses are reduced in the arterial distribution.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EVisual evoked potential (VEP)\u003C/strong\u003E records the occipital cortical response to visual stimulation and assesses the integrity of the visual pathway as a whole. An abnormal result would not reliably distinguish localized macular retinal damage from optic nerve or post-retinal visual pathway dysfunction. \u003Cstrong\u003EPotential acuity meter (PAM)\u003C/strong\u003E estimates potential macular acuity by projecting a visual target through relatively clear areas of the ocular media, mainly helping predict visual potential when cataract or another media opacity is present; the patient\u2019s question instead requires objective localization of chronic retinal dysfunction.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1901,
    "Name": "Optic disc drusen",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed condition or demographic factor is not associated with small optic disc drusen?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Etuberous sclerosis (TS)\u003C/strong\u003E, because tuberous sclerosis is associated with \u003Cstrong\u003Eretinal astrocytic hamartomas\u003C/strong\u003E, not true optic disc drusen. When an astrocytic hamartoma develops on or adjacent to the optic nerve head, the elevated, calcified, nodular lesion may resemble optic disc drusen clinically, particularly when the hamartoma has the classic opaque, multinodular\u003Cstrong\u003E\u201Cmulberry-like\u201D\u003C/strong\u003E appearance. However, the hamartoma is a glial tumor composed of astrocytes, whereas optic disc drusen are acellular, calcified deposits situated within the prelaminar optic nerve head. Therefore, tuberous sclerosis may produce an important \u003Cstrong\u003Edrusen mimic\u003C/strong\u003E, but is not itself a recognized association of small optic disc drusen.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Eretinitis pigmentosa (RP)\u003C/strong\u003E is associated with an increased prevalence of optic disc drusen. In some affected eyes, retinal and retinal pigment epithelial atrophy surrounding the disc may make buried or marginal drusen more clinically apparent. Recent EDI-OCT-based studies have found optic disc drusen substantially more frequently in patients with retinitis pigmentosa than in the general population, although reported prevalence varies according to the RP subtype and imaging method used.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Epseudoxanthoma elasticum (PXE)\u003C/strong\u003E is a well-established association. PXE produces abnormal mineralization of elastic tissue and calcification of Bruch membrane, causing peau d\u2019orange and angioid streaks. Optic disc drusen are markedly more prevalent in PXE, with one recent cohort identifying drusen in approximately 30.7% of patients; their presence also correlated with greater angioid-streak length and therefore with the extent of Bruch membrane calcification.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ECaucasian race\u003C/strong\u003E is also associated with a higher recognized prevalence of optic disc drusen, whereas optic disc drusen are diagnosed less commonly in non-Caucasian populations. This may reflect anatomical, genetic, and ascertainment factors, but it remains a classical epidemiological association.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1902,
    "Name": "Isolated unilateral mydriasis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old notices sudden right pupillary dilation without headache, ptosis, diplopia, trauma, or known medication exposure. Examination confirms that the right pupil constricts poorly in bright light, but visual function, ocular alignment, motility, and the remainder of the ocular examination are normal. What is the most appropriate next diagnostic step?\u0026nbsp;\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPilocarpine testing\u003C/strong\u003E, because the anisocoria becomes substantially greater in bright light, indicating that the larger right pupil is abnormal and is failing to constrict appropriately. The absence of ptosis, diplopia, ocular misalignment, or limitation of extraocular movements makes an oculomotor nerve palsy unlikely, while the slightly irregular oval pupil and trace light response suggest either a \u003Cstrong\u003Etonic pupil with segmental iris sphincter paralysis\u003C/strong\u003E or pharmacological blockade of the sphincter pupillae. An isolated dilated pupil is rarely the sole manifestation of a compressive third nerve palsy, which generally produces at least subtle ptosis or ocular motor dysfunction; uncal herniation is also incompatible with the patient\u2019s alert mental state and otherwise normal neurological examination.\u003C/p\u003E\n\u003Cp\u003ETesting should begin with dilute pilocarpine, usually \u003Cstrong\u003E0.1% or 0.125%\u003C/strong\u003E, instilled into both eyes as an internal control. Parasympathetic denervation of the ciliary ganglion or short ciliary nerves produces postsynaptic cholinergic supersensitivity, so an Adie tonic pupil typically constricts significantly to dilute pilocarpine, whereas the normal pupil generally changes little. The characteristic clinical findings of a tonic pupil include poor constriction to light, better tonic constriction during near effort, slow redilation after near fixation, and sectoral palsy or vermiform movements of the iris sphincter visible at the slit lamp.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIf the dilated right pupil does not constrict to dilute pilocarpine, full-strength pilocarpine, usually \u003Cstrong\u003E1%\u003C/strong\u003E, should then be used. An intact but non-supersensitive iris sphincter should constrict to full-strength pilocarpine. Failure of the dilated pupil to constrict despite full-strength pilocarpine strongly supports \u003Cstrong\u003Eanticholinergic pharmacological mydriasis\u003C/strong\u003E, where muscarinic receptors have been blocked by agents such as atropine, scopolamine, tropicamide, ipratropium, or inadvertent contact with anticholinergic plants or cosmetics.\u003C/p\u003E\n\u003Cp\u003EA useful sequence is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EConstricts to dilute pilocarpine:\u003C/strong\u003E supports a tonic pupil due to denervation supersensitivity\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENo response to dilute, but constricts to 1% pilocarpine:\u003C/strong\u003E parasympathetic dysfunction remains possible, including an incompletely denervated pupil\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENo response to 1% pilocarpine:\u003C/strong\u003E supports pharmacological anticholinergic blockade\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EMRA or CTA would be urgently indicated if examination demonstrated a painful, partial, pupil-involving third nerve palsy or other neurological abnormalities suggesting a posterior communicating artery aneurysm. Immediate ICU admission would be reserved for evidence of altered consciousness, herniation, or another unstable neurological emergency. In this alert patient with truly isolated mydriasis and normal ocular motility, the most appropriate next step is \u003Cstrong\u003EPilocarpine testing\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1903,
    "Name": "Sella turcica",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich structure lies within the sella turcica, and which skull bone forms the sella turcica?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethe pituitary gland; the sphenoid bone\u003C/strong\u003E, because the sella turcica is a saddle-shaped depression on the superior surface of the \u003Cstrong\u003Ebody of the sphenoid bone\u003C/strong\u003E, within the middle cranial fossa. Its deepest central portion is the \u003Cstrong\u003Ehypophyseal or pituitary fossa\u003C/strong\u003E, which contains the pituitary gland. The sella is bounded anteriorly by the tuberculum sellae and posteriorly by the dorsum sellae, with the anterior and posterior clinoid processes situated around it.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe optic chiasm does not sit within the sella turcica. It lies \u003Cstrong\u003Esuperior and slightly anterior to the pituitary gland\u003C/strong\u003E, above the diaphragma sellae and near the chiasmatic groove. This anatomical relationship explains why a pituitary macroadenoma extending superiorly into the suprasellar region can compress the optic chiasm, initially producing bilateral superotemporal visual field loss that may progress to a complete bitemporal hemianopia.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1904,
    "Name": "Riddoch phenomenon",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with profound cortical visual loss following bilateral occipital strokes can detect large moving targets despite being unable to see stationary targets. What is this finding called?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERiddoch phenomenon\u003C/strong\u003E, because this describes preservation of the ability to detect, and sometimes determine the direction of, \u003Cstrong\u003Emoving visual stimuli within an otherwise blind visual field\u003C/strong\u003E, despite an inability to perceive stationary targets. It occurs after damage to the primary visual cortex and represents a dissociation between motion perception and other components of conscious vision. Moving objects may be perceived only as vague, shadow-like outlines without clear color, form, or detail.\u003C/p\u003E\n\u003Cp\u003EThe proposed mechanism is preservation of alternative visual pathways that bypass the damaged primary visual cortex and transmit motion-related information through subcortical structures to the extrastriate motion-processing cortex.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EPulfrich phenomenon\u003C/strong\u003E is an illusion in which a target moving from side to side appears to follow an elliptical path in depth because visual conduction is delayed in one eye relative to the other, classically following asymmetric optic neuritis. \u003Cstrong\u003ECharles Bonnet syndrome\u003C/strong\u003E consists of formed or unformed visual hallucinations in a person with significant visual impairment but without the perceptual preservation of real moving targets. \u003Cstrong\u003EAnton syndrome\u003C/strong\u003E is cortical blindness accompanied by denial or lack of awareness of the visual loss, often with confabulation about what is being seen.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1905,
    "Name": "Bilateral superior arcuate visual field defects",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old with vague, slowly progressive visual symptoms has visual acuity of 20/25 in both eyes. Humphrey perimetry\u0027s pictures are below. Which listed condition most likely produces the demonstrated pattern?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-10-ff2334bd-d3b2-490e-8ae1-e64b7987163a.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EGlaucoma\u003C/strong\u003E, because the fields are displayed separately for each eye rather than from the patient\u2019s binocular perspective. When interpreted correctly, the dark defects involve the \u003Cstrong\u003Esuperior nasal field of each eye\u003C/strong\u003E, producing bilateral superior arcuate or nasal-step-type loss rather than a true bitemporal superior quadrantanopia. Glaucoma damages retinal ganglion-cell axons according to the anatomical course of retinal nerve fiber bundles, so early defects include paracentral scotomas, nasal steps, temporal wedges, and arcuate defects that arch from the blind spot toward the nasal field and characteristically respect the \u003Cstrong\u003Ehorizontal meridian\u003C/strong\u003E. With progression, superior and inferior arcuate defects may enlarge and join to form double arcuate loss.\u003C/p\u003E\n\u003Cp\u003EThe apparent resemblance to a chiasmal field defect is a presentation trap. The defect in the left-eye plot does not remain strictly confined by the vertical meridian, and the overall configuration follows nerve fiber bundle anatomy more closely than a neurological hemifield boundary. Genuine chiasmal compression produces bitemporal defects that respect the \u003Cstrong\u003Evertical meridian\u003C/strong\u003E, whereas glaucomatous defects primarily obey the horizontal retinal raphe. A useful rule is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHorizontal meridian:\u003C/strong\u003E consider retinal nerve fiber layer or optic nerve head disease, especially glaucoma\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EVertical meridian:\u003C/strong\u003E consider chiasmal or retrochiasmal neurological disease\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EHowever, visual fields should always be correlated with optic disc examination, retinal nerve fiber layer and ganglion-cell OCT, intraocular pressure, gonioscopy, and repeat perimetry because an isolated field can occasionally be misleading.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EPituitary adenoma\u003C/strong\u003E usually enlarges superiorly from below the optic chiasm and preferentially affects the crossing inferior nasal retinal fibers, causing bilateral superotemporal visual field loss that may progress to complete bitemporal hemianopia. \u003Cstrong\u003ECraniopharyngioma\u003C/strong\u003E usually compresses the chiasm from above and may preferentially produce bilateral inferotemporal field loss, although the precise pattern varies with tumor position. Both conditions should produce defects that more convincingly respect the vertical meridian. \u003Cstrong\u003EOccipital lobe stroke\u003C/strong\u003E produces a contralateral homonymous hemianopia or quadrantanopia, meaning loss on the same side of visual space in both eyes, often with a highly congruous pattern and possible macular sparing, rather than mirrored superior nasal arcuate defects. Bitemporal defects are associated with chiasmal lesions, while homonymous defects indicate retrochiasmal disease.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1906,
    "Name": "Light-induced central scotoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old with hypertension, hypercholesterolemia, and diabetes develops a large right central scotoma whenever exposed to bright light. The scotoma persists for several minutes after leaving the bright environment. Intermittent periocular and ocular pain improves when lying down. Visual acuity and pupillary function are normal, but several mid-peripheral dot-blot retinal hemorrhages are present in each quadrant of the right eye. Which diagnostic test is most appropriate?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFluorescein angiography (FA)\u003C/strong\u003E, because the combination of \u003Cstrong\u003Elight-induced monocular visual loss, dull ocular or periocular pain, vascular risk factors, and scattered mid-peripheral dot-blot hemorrhages\u003C/strong\u003E strongly suggests chronic ocular hypoperfusion from \u003Cstrong\u003Eocular ischemic syndrome\u003C/strong\u003E, usually secondary to severe ipsilateral common or internal carotid artery stenosis or occlusion. Light exposure sharply increases photoreceptor metabolic activity and retinal oxygen demand. When ocular perfusion is critically reduced, the retinal circulation cannot meet this increased demand, producing a central scotoma or visual dimming that persists until the photoreceptors recover after the patient leaves the bright environment. This is termed light-induced amaurosis and is a hemodynamic manifestation of severe carotid disease rather than the usual embolic mechanism of amaurosis fugax.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EFluorescein angiography is the most appropriate listed test because it can directly demonstrate the characteristic retinal and choroidal perfusion abnormalities of ocular ischemic syndrome. The most specific finding is \u003Cstrong\u003Edelayed or patchy choroidal filling\u003C/strong\u003E, while other findings include prolonged retinal arteriovenous transit time, delayed retinal arterial filling, vascular staining, and late optic disc or retinal vascular leakage. Mid-peripheral intraretinal hemorrhages are a typical clue and result from chronic venous stasis and retinal hypoperfusion.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe ocular pain results from ischemia of the globe and extraocular tissues and may occur despite normal visual acuity, intraocular pressure, and pupillary function between attacks. Improvement on lying down further supports a perfusion-dependent process because the supine position can temporarily improve ocular blood flow. Normal acuity does not exclude early ocular ischemic syndrome, particularly when the visual disturbance is episodic and provoked by increased metabolic demand.\u003C/p\u003E\n\u003Cp\u003EOnce ocular hypoperfusion is demonstrated or strongly suspected, the evaluation must proceed urgently to the carotid circulation with \u003Cstrong\u003Ecarotid duplex ultrasonography\u003C/strong\u003E, followed when necessary by CTA or MRA of the head and neck. Ocular ischemic syndrome may be the presenting manifestation of advanced carotid atherosclerosis and indicates increased risks of cerebral infarction and cardiovascular disease, requiring coordinated ophthalmic, neurological, vascular, and primary-care assessment.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMRI of the brain\u003C/strong\u003E would not directly assess retinal or choroidal circulation and would be more appropriate if a central neurological lesion were suspected. \u003Cstrong\u003ECT of the orbits\u003C/strong\u003E evaluates orbital structural disease but would not explain light-triggered retinal dysfunction with mid-peripheral hemorrhages. \u003Cstrong\u003ETraditional electroretinogram (ERG)\u003C/strong\u003E assesses generalized retinal function and may be abnormal in advanced ocular ischemia, but it neither demonstrates the vascular filling delay nor provides the most direct confirmation of the suspected mechanism.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1907,
    "Name": "Goldmann perimetry",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the surface area of the Goldmann V4e stimulus used to confirm this absolute visual field defect?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E64 mm2\u003C/strong\u003E, because the Roman numeral in Goldmann perimetry identifies the \u003Cstrong\u003Estimulus size\u003C/strong\u003E. Each successive Roman-numeral size has twice the diameter and therefore four times the area of the preceding stimulus:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003E0:\u003C/strong\u003E 1/16 mm\u00B2\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EI:\u003C/strong\u003E 1/4 mm\u00B2\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EII:\u003C/strong\u003E 1 mm\u00B2\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIII:\u003C/strong\u003E 4 mm\u00B2\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIV:\u003C/strong\u003E 16 mm\u00B2\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EV:\u003C/strong\u003E 64 mm\u00B2\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EGoldmann size V has a diameter of approximately 1.72\u00B0 and an area of \u003Cstrong\u003E64 mm\u00B2\u003C/strong\u003E, whereas the commonly used Goldmann size III stimulus has a diameter of approximately 0.43\u00B0 and an area of 4 mm\u00B2.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIn the designation \u003Cstrong\u003EV4e\u003C/strong\u003E:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EV\u003C/strong\u003E indicates the largest standard target size, with an area of \u003Cstrong\u003E64 mm\u00B2\u003C/strong\u003E.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003E4\u003C/strong\u003E indicates the highest standard luminance step.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003Ee\u003C/strong\u003E indicates the least dense filter within that luminance step, making V4e the largest and brightest standard Goldmann stimulus. Goldmann kinetic perimetry standardizes stimulus sizes from I to V and intensities from 1a to 4e.\u0026nbsp;\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EAn absolute scotoma is an area with no detectable visual sensitivity. Failure to perceive even the large, bright V4e stimulus supports an absolute rather than relative defect.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMnemonic: \u201CQuarter, one, four, sixteen, sixty-four\u201D\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EI \u2192 \u00BC, II \u2192 1, III \u2192 4, IV \u2192 16, V \u2192 64\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1908,
    "Name": "Anton syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with bilateral occipital strokes has profound cortical visual loss but denies being blind and behaves as though vision is normal. What is this condition called?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAnton syndrome\u003C/strong\u003E, because Anton syndrome, also called \u003Cstrong\u003EAnton-Babinski syndrome\u003C/strong\u003E or \u003Cstrong\u003Evisual anosognosia\u003C/strong\u003E, is characterized by cortical blindness accompanied by a lack of awareness or denial of the visual deficit. Patients may behave as though sighted and often confabulate visual information, such as claiming to read letters or describe objects despite producing consistently incorrect responses.\u003C/p\u003E\n\u003Cp\u003EThe bilateral occipital infarctions explain the cortical blindness. Severe hypotension and blood loss during coronary artery bypass surgery may produce posterior cerebral artery or watershed ischemia affecting both occipital visual cortices. Because the lesion lies posterior to the pathways mediating the pupillary light reflex, the pupils remain normally reactive despite profound visual loss. The optic discs, retinas, and other ocular structures may also appear normal because the primary pathology is cortical rather than ocular.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe defining feature is not merely cortical blindness, but the patient\u2019s \u003Cstrong\u003Edenial of blindness despite objective evidence\u003C/strong\u003E, often accompanied by confabulation. The mechanism is incompletely understood, but may involve disruption of connections between visual association areas and networks responsible for awareness, memory, language, and metacognitive monitoring.\u003C/p\u003E\n\u003Cp\u003EThe alternatives describe different phenomena:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPulfrich phenomenon\u003C/strong\u003E is an illusion in which a horizontally moving object appears to travel along an elliptical path in depth because visual signal transmission is delayed asymmetrically between the two eyes.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ERiddoch phenomenon\u003C/strong\u003E is preserved perception of moving targets within an otherwise blind visual field.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ECharles Bonnet syndrome\u003C/strong\u003E consists of visual hallucinations in a patient with substantial visual loss who retains insight that the hallucinations are not real. This preservation of insight distinguishes Charles Bonnet syndrome from Anton syndrome.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1909,
    "Name": "Ocular tilt reaction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a right hypertropia that increases on right head tilt and left gaze, but the right hypertropic eye is incyclotorted\u0026nbsp;and the left eye is excyclotorted. What is the most likely diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOcular tilt reaction\u003C/strong\u003E, because the right hypertropia initially resembles a right fourth nerve palsy on the Parks-Bielschowsky three-step test, but the torsional finding points away from fourth nerve palsy. A right trochlear nerve palsy weakens the right superior oblique, producing right hypertropia together with \u003Cstrong\u003Eright excyclotorsion\u003C/strong\u003E. In this case, the right hypertropic eye is \u003Cstrong\u003Eincyclotorted\u003C/strong\u003E, while the left hypotropic eye is more markedly excyclotorted. This pattern is characteristic of a \u003Cstrong\u003Eskew deviation within an ocular tilt reaction\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe ocular tilt reaction is a triad of:\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003E\u003Cstrong\u003ESkew deviation\u003C/strong\u003E, producing vertical ocular misalignment\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EConjugate ocular torsion\u003C/strong\u003E, with both eyes rotating toward the side of the hypotropic eye\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHead tilt toward the hypotropic eye\u003C/strong\u003E\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cp\u003ETherefore, when the right eye is hypertropic and incyclotorted while the left eye is hypotropic and excyclotorted, both eyes have rotated toward the left, predicting an associated leftward head tilt.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003ESkew deviation is a \u003Cstrong\u003Esupranuclear disorder\u003C/strong\u003E caused by asymmetric disruption of the otolith-ocular pathways carrying graviceptive vestibular information from the utricle through the vestibular nuclei, brainstem, medial longitudinal fasciculus, cerebellum, and interstitial nucleus of Cajal. The vertical deviation may be comitant or incomitant and can reproduce all three steps of the Parks-Bielschowsky test, making torsional assessment essential. Common causes include brainstem or cerebellar ischemia, demyelination, tumor, inflammation, trauma, and peripheral vestibular disease. In an older patient with poorly controlled diabetes and hypertension and an acute two-week history, a posterior fossa ischemic lesion must be excluded urgently.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe \u003Cstrong\u003Eupright-supine test\u003C/strong\u003E can provide additional evidence. A reduction in the vertical deviation of at least 50% on moving from the upright to the supine position supports skew deviation because the otolith-mediated gravitational drive is reduced when supine. Trochlear nerve palsy generally shows little change. This test has high specificity, although a negative result does not exclude skew deviation.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA useful distinguishing rule is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EHypertropic eye excyclotorted:\u003C/strong\u003E consider ipsilateral fourth nerve palsy\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EHypertropic eye incyclotorted:\u003C/strong\u003E consider skew deviation or ocular tilt reaction\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1910,
    "Name": "Total volume of the adult orbit",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the approximate total volume of the adult bony orbit?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E30 cc\u003C/strong\u003E, because the adult bony orbit has an approximate volume of \u003Cstrong\u003E30 cubic centimetres\u003C/strong\u003E, equivalent to \u003Cstrong\u003E30 mL\u003C/strong\u003E. The orbit is shaped like a four-sided pyramid, with its broad base at the orbital rim and its apex directed posteriorly toward the optic canal. Its average dimensions are approximately \u003Cstrong\u003E40 mm in width, 35 mm in height, and 40\u201345 mm in depth\u003C/strong\u003E.\u003C/p\u003E\n\u003Cp\u003EThe globe occupies only about \u003Cstrong\u003E6.5\u20137 mL\u003C/strong\u003E of the orbital volume. The remaining space contains orbital fat, the extraocular muscles, optic nerve, lacrimal gland, blood vessels, cranial nerves, fascia, and connective tissues. Thus, the volume ratio of the orbit to the globe is approximately \u003Cstrong\u003E4.5:1\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThis measurement has clinical importance because small changes in orbital contents can produce visible globe displacement. An orbital mass, hemorrhage, inflammation, or extraocular muscle enlargement increases the volume of orbital contents and may cause proptosis. Conversely, orbital wall fractures or surgical orbital decompression increase the effective bony orbital volume and may produce or treat globe displacement.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1911,
    "Name": "Right abducens nucleus lesion",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich additional neurological deficit commonly accompanies a lesion involving the right abducens nucleus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA right facial palsy\u003C/strong\u003E, because the abducens nucleus lies in the dorsal caudal pons, immediately beneath the facial colliculus. The fascicles of the facial nerve travel dorsally and loop around the ipsilateral abducens nucleus, forming the internal genu of the facial nerve and creating the surface elevation known as the facial colliculus. A lesion involving the right abducens nucleus therefore commonly damages the adjacent right facial nerve fascicles, producing a \u003Cstrong\u003Eright lower motor neuron facial palsy\u003C/strong\u003E affecting both the upper and lower face.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EImportantly, an abducens \u003Cstrong\u003Enuclear\u003C/strong\u003E lesion does not cause merely an isolated abduction deficit. The abducens nucleus contains:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EMotor neurons supplying the ipsilateral lateral rectus\u003C/li\u003E\n\u003Cli\u003EInternuclear neurons that cross the midline and ascend through the contralateral medial longitudinal fasciculus to the medial rectus subnucleus of the oculomotor complex\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EConsequently, a right abducens nuclear lesion prevents both \u003Cstrong\u003Eabduction of the right eye\u003C/strong\u003E and \u003Cstrong\u003Eadduction of the left eye during right gaze\u003C/strong\u003E, producing a \u003Cstrong\u003Eright horizontal conjugate gaze palsy\u003C/strong\u003E. The vestibulo-ocular reflex is also unable to overcome a complete nuclear gaze palsy.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EBy contrast, an isolated abduction deficit in the right eye localizes to the \u003Cstrong\u003Eright sixth nerve fascicle or peripheral abducens nerve\u003C/strong\u003E, after the internuclear neurons responsible for conjugate gaze have separated. A left gaze paralysis would result from a lesion involving the left abducens nucleus or left paramedian pontine reticular formation. A right gaze preference is not the expected finding because destructive involvement of the right abducens nucleus causes inability to look right, so the eyes may rest deviated toward the left.\u003C/p\u003E\n\u003Cp\u003EA useful mnemonic is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003E\u201CSix sits inside Seven.\u201D\u003C/strong\u003E\u003C/p\u003E\n\u003Cp\u003EThe facial nerve fascicle loops around the abducens nucleus, so a nuclear sixth nerve lesion frequently causes:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Eipsilateral gaze palsy \u002B ipsilateral lower motor neuron facial palsy\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1912,
    "Name": "Early toxic or nutritional optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich visual field defect typically develops early in slowly progressive toxic or nutritional optic neuropathy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECecocentral and/or central defects\u003C/strong\u003E, because slowly progressive toxic and nutritional optic neuropathies preferentially damage the small-calibre retinal ganglion-cell axons of the \u003Cstrong\u003Epapillomacular bundle\u003C/strong\u003E, which carries visual information from the macula to the temporal optic disc. This selective injury initially produces a \u003Cstrong\u003Ecentral scotoma\u003C/strong\u003E, affecting fixation, or a \u003Cstrong\u003Ececocentral scotoma\u003C/strong\u003E, extending from fixation to the physiological blind spot. The defects are usually bilateral, relatively symmetrical, and accompanied by central visual blurring and dyschromatopsia that may be disproportionate to the reduction in visual acuity.\u003C/p\u003E\n\u003Cp\u003EThe optic discs may initially appear normal or mildly hyperemic. With continued toxic exposure or nutritional deficiency, temporal pallor develops because of papillomacular bundle loss, eventually progressing to more diffuse optic atrophy. A relative afferent pupillary defect is generally absent because both optic nerves are affected symmetrically. When routine 30-2 perimetry is normal or equivocal despite suggestive symptoms, a central 10-2 field can better demonstrate the early central or cecocentral defects.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EGlobal depression\u003C/strong\u003E may occur in severe or advanced toxic optic neuropathy and can accompany acute profound toxic injury, particularly methanol poisoning, but it is not the characteristic early field pattern of a slowly progressive process. \u003Cstrong\u003EArcuate defect\u003C/strong\u003E follows retinal nerve fiber bundle anatomy and is classically associated with glaucoma, although it can occur in other optic nerve disorders. \u003Cstrong\u003ERing scotoma\u003C/strong\u003E is more typical of retinal disease, particularly retinitis pigmentosa and other rod-predominant retinal degenerations.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1913,
    "Name": "Adie tonic pupil",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA dilated, slightly irregular pupil reacts poorly to light but constricts better during near fixation and then slowly redilates. Which pharmacological response would confirm her diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EDramatic pupillary constriction to pilocarpine 0.125% in the left eye\u003C/strong\u003E, because the clinical findings are characteristic of a \u003Cstrong\u003Eleft Adie tonic pupil\u003C/strong\u003E: unilateral mydriasis, a slightly irregular pupil from segmental sphincter paralysis, poor light response, better constriction during near fixation, and slow tonic redilation after shifting fixation back to a distant target. This combination represents \u003Cstrong\u003Elight-near dissociation\u003C/strong\u003E with tonicity. Blurred near vision results from accompanying parasympathetic denervation of the ciliary muscle and impaired accommodation.\u003C/p\u003E\n\u003Cp\u003EAdie tonic pupil results from postganglionic parasympathetic injury involving the \u003Cstrong\u003Eciliary ganglion or short ciliary nerves\u003C/strong\u003E. Denervation causes upregulation of muscarinic receptors in the iris sphincter, producing \u003Cstrong\u003Echolinergic denervation supersensitivity\u003C/strong\u003E. Consequently, dilute pilocarpine at 0.125%, which ordinarily has little effect on a normally innervated pupil, produces marked constriction of the affected tonic pupil.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe differential diagnosis can be distinguished pharmacologically:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EAn \u003Cstrong\u003EAdie tonic pupil\u003C/strong\u003E constricts excessively to dilute pilocarpine because of denervation supersensitivity.\u003C/li\u003E\n\u003Cli\u003EA pupil affected by a \u003Cstrong\u003Ethird nerve palsy\u003C/strong\u003E generally requires full-strength pilocarpine to constrict and should be accompanied by ptosis or ocular motor dysfunction, which are absent here.\u003C/li\u003E\n\u003Cli\u003EA pupil with \u003Cstrong\u003Eanticholinergic pharmacological mydriasis\u003C/strong\u003E fails to constrict even with 1% pilocarpine because its muscarinic receptors are blocked.\u003C/li\u003E\n\u003Cli\u003EA structurally damaged iris may show an irregular pupil and incomplete constriction, but the characteristic light-near dissociation and slow redilation favor a tonic pupil.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1914,
    "Name": "NAION",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003EA 75-year-old with several vascular risk factors develops sudden, painless inferior visual field loss in the right eye, with right optic disc swelling and evidence of right optic nerve dysfunction. Which pictured optic disc would most likely be found in the unaffected left eye?\u003C/div\u003E\u003Cdiv style=\u0022line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-12-ab578aba-98bd-4d61-acdb-b4b031bc29ce.png\u0022\u003E\u003C/div\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPhoto A\u003C/strong\u003E, because the presentation is characteristic of \u003Cstrong\u003Enon-arteritic anterior ischemic optic neuropathy\u003C/strong\u003E: sudden painless monocular visual loss noticed on awakening, an inferior altitudinal field defect, impaired color vision, a relative afferent pupillary defect, and acute optic disc edema in an older patient with diabetes, hypertension, smoking, hypercholesterolemia, and peripheral vascular disease. NAION results from transient hypoperfusion of the short posterior ciliary circulation, producing ischemic axonal swelling within a structurally crowded optic nerve head. The swelling further compresses the surrounding microcirculation, creating a compartment-like cycle of ischemia and axoplasmic-flow stasis.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe unaffected fellow eye usually demonstrates the underlying anatomical predisposition known as a\u003Cstrong\u003E\u201Cdisc at risk\u201D\u003C/strong\u003E, consisting of a small or absent physiological cup, a low cup-to-disc ratio, and tightly crowded neuroretinal tissue. Photo A shows this crowded optic disc with a very small cup and no active swelling. Because optic disc anatomy is commonly similar between the two eyes, examining the fellow disc is especially helpful when acute edema obscures the cup in the affected eye.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe inferior field defect indicates superior optic nerve head involvement because visual field and retinal anatomy are inverted. NAION commonly produces altitudinal, arcuate, nasal-step, or central defects, with altitudinal loss being the classic pattern.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe remaining photographs are less consistent:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto B\u003C/strong\u003E shows severe sectoral or diffuse optic disc edema rather than an unaffected fellow disc.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto C\u003C/strong\u003E shows glaucomatous excavation with focal inferior neuroretinal rim notching.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPhoto D\u003C/strong\u003E shows temporal optic disc pallor, indicating established papillomacular bundle or optic nerve axonal loss.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1915,
    "Name": "Voluntary nystagmoid movements",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich finding does \u003Cstrong\u003Enot reliably help\u003C/strong\u003E distinguish voluntary eye oscillations from pathological involuntary eye movements?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ELack of oscillopsia\u003C/strong\u003E, because oscillopsia is inconsistent in voluntary nystagmoid movements and may be either present or absent. Some patients report that the surroundings remain stable, whereas others experience transient blurring or apparent movement of the visual environment during the oscillations. Therefore, the absence of oscillopsia does not reliably establish that the movements are voluntary, and its presence does not exclude voluntary oscillations.\u003C/p\u003E\n\u003Cp\u003EVoluntary \u201Cnystagmus\u201D is more accurately classified as a \u003Cstrong\u003Evoluntary saccadic oscillation resembling ocular flutter\u003C/strong\u003E, because it consists of rapid, back-to-back horizontal saccades without the slow phase required for true nystagmus. The movements are typically conjugate, high-frequency, low-amplitude, and sustainable for only several seconds because generating them requires considerable effort.\u003C/p\u003E\n\u003Cp\u003EThe other findings are useful diagnostic clues:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EAssociated facial grimacing and eyelid flutter\u003C/strong\u003E support voluntary effort and recruitment of neighbouring facial muscles.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EDisappearance of oscillations with distraction\u003C/strong\u003E is helpful because performing a competing cognitive or motor task may interrupt the voluntary oscillations.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EAssociated convergence movements\u003C/strong\u003E are helpful because voluntary oscillations are frequently initiated by convergence effort or activation of the near triad, sometimes accompanied by pupillary constriction.\u0026nbsp;\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EAdditional clues include abrupt onset and termination, the ability to reproduce the movement on request, inability to sustain it for long, absence of other neurological or ocular motor abnormalities, and a longstanding benign history. In contrast, pathological ocular flutter or opsoclonus is involuntary, may persist without effort or convergence, and requires assessment for inflammatory, infectious, toxic, metabolic, or paraneoplastic disease.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1916,
    "Name": "Left lateral medullary infarction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 75-year-old with significant vascular risk factors, including smoking, hypertension, diabetes, and hyperlipidaemia, develops acute oscillopsia, disequilibrium, facial and bodily sensory disturbance, and gait difficulty. T2-weighted and diffusion-weighted MRI sequences are below . Which listed ophthalmic abnormality would be expected on the basis of the anatomical structures affected?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-14-65a24931-7c16-426b-b56b-08afc52097c3.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ELeft Horner syndrome\u003C/strong\u003E, because the MRI shows an acute infarction of the left dorsolateral medulla, producing \u003Cstrong\u003Elateral medullary syndrome, also called Wallenberg syndrome\u003C/strong\u003E. The associated oscillopsia, disequilibrium, crossed face and body sensory disturbance, and difficulty walking support this localization. Wallenberg syndrome most commonly results from occlusion of the vertebral artery or posterior inferior cerebellar artery.\u003C/p\u003E\n\u003Cp\u003EThe descending first-order sympathetic fibers travel from the hypothalamus through the ipsilateral brainstem before reaching the ciliospinal center of Budge at C8\u2013T2. A left lateral medullary infarction interrupts these fibers before they cross, producing a \u003Cstrong\u003Eleft central Horner syndrome\u003C/strong\u003E. The expected findings are:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ELeft miosis\u003C/li\u003E\n\u003Cli\u003EMild left upper eyelid ptosis\u003C/li\u003E\n\u003Cli\u003EPossible left lower-eyelid reverse ptosis\u003C/li\u003E\n\u003Cli\u003ELeft facial anhidrosis\u003C/li\u003E\n\u003Cli\u003EAnisocoria that is greater in darkness\u003C/li\u003E\n\u003Cli\u003EDilation lag of the left pupil\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThe pupillary light reaction remains intact because the parasympathetic pathway is unaffected.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EOther findings of lateral medullary syndrome result from involvement of neighboring structures:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EVestibular nuclei:\u003C/strong\u003E vertigo, nausea, nystagmus, and oscillopsia\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EInferior cerebellar peduncle:\u003C/strong\u003E ipsilateral limb and gait ataxia, with falling toward the lesion\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESpinal trigeminal nucleus and tract:\u003C/strong\u003E ipsilateral facial loss of pain and temperature\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ESpinothalamic tract:\u003C/strong\u003E contralateral body loss of pain and temperature\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003ENucleus ambiguus:\u003C/strong\u003E dysphagia, hoarseness, palatal weakness, and reduced gag reflex\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EOtolith-ocular pathways:\u003C/strong\u003E skew deviation or ocular tilt reaction with vertical diplopia\u0026nbsp;\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003E\u003Cstrong\u003ELeft oculomotor palsy\u003C/strong\u003E is incorrect because the oculomotor nucleus and fascicles are located in the midbrain, not the medulla. \u003Cstrong\u003ELeft trochlear nerve palsy\u003C/strong\u003E also localizes to the midbrain or the peripheral fourth nerve. \u003Cstrong\u003ERight gaze palsy\u003C/strong\u003E generally requires damage to the right paramedian pontine reticular formation or right abducens nucleus in the pons, neither of which is involved by an isolated left lateral medullary infarction.\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-08-14-514a40a1-977c-4825-b964-5e1057bfc402.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1917,
    "Name": "Superior limbic keratoconjunctivitis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 65-year-old with cardiovascular comorbidity reports two months of ocular irritation and binocular visual blurring despite best-corrected acuity of 20/25 in each eye. The slit-lamp examination reveals superior bulbar conjunctival injection with a papillary reaction adjacent to the superior limbus. Which investigation would be the most appropriate next step?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-14-89b1892b-cd60-4142-91de-9c9cc559d8c7.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThyroid-stimulating immunoglobulin testing.\u0026nbsp;\u003C/strong\u003E\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EThe photograph shows the right eye positioned higher than the left, indicating a vertical deviation, together with greater left upper-eyelid retraction. Although the patient describes \u201Cblurred vision,\u201D the preservation of monocular acuity at 20/25 in each eye and worsening under binocular conditions suggest that the symptom may represent poorly described binocular diplopia from restrictive vertical strabismus. Thyroid eye disease commonly produces restrictive motility disturbance because of extraocular muscle enlargement and fibrosis, with the inferior and medial rectus muscles frequently involved.\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003EThe slit-lamp findings support \u003Cstrong\u003Esuperior limbic keratoconjunctivitis\u003C/strong\u003E, a chronic inflammatory disorder involving the superior bulbar conjunctiva, superior limbus, and adjacent upper cornea. Typical findings include superior bulbar conjunctival injection, upper tarsal papillary reaction, redundant superior conjunctiva, superior corneal or limbal staining, and sometimes filamentary keratitis. SLK has a well-established association with thyroid dysfunction and Graves ophthalmopathy.\u003C/p\u003E\n\u003Cp\u003EThyroid-stimulating immunoglobulin testing is therefore appropriate, ideally as part of a broader thyroid assessment including:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ETSH\u003C/li\u003E\n\u003Cli\u003EFree T4 and, where indicated, free T3\u003C/li\u003E\n\u003Cli\u003ETSH-receptor antibodies or thyroid-stimulating immunoglobulins\u003C/li\u003E\n\u003Cli\u003EOrbital imaging if restrictive myopathy, proptosis, apical crowding, or compressive optic neuropathy is suspected\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThyroid eye disease can occur in euthyroid patients, so normal routine thyroid hormone levels would not completely exclude the diagnosis. Thyroid-stimulating immunoglobulin or TSH-receptor antibody testing may provide evidence of the underlying autoimmune process.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EReassurance\u003C/strong\u003E or \u003Cstrong\u003Ereassurance with artificial tears\u003C/strong\u003E alone would be inadequate because lubrication may improve surface irritation but would not investigate the combination of eyelid retraction, vertical misalignment, and SLK. \u003Cstrong\u003EEdrophonium testing\u003C/strong\u003E is inappropriate because myasthenia gravis can produce variable vertical strabismus and ptosis, but true eyelid retraction and SLK are not characteristic. In addition, edrophonium can cause clinically significant bradycardia and arrhythmia, making the test particularly unsuitable in a patient with previous myocardial infarction. If myasthenia remained a concern, safer initial evaluation would include fatigability testing, the ice-pack test when ptosis is present, acetylcholine-receptor antibodies, and possibly single-fiber electromyography.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 9,
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  },
  {
    "Id": 1918,
    "Name": "Large right middle cerebral artery infarction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old with diabetes and hypertension sustains an extensive right middle cerebral artery infarction involving the right frontal, parietal, and temporal lobes. The stroke produces several possible ocular motor and visual consequences. Which listed deficit is most likely to show marked spontaneous improvement during the first week after the infarction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERight gaze deviation\u003C/strong\u003E, because involvement of the right frontal eye field temporarily disrupts the cortical drive responsible for generating conjugate saccades toward the left. Each frontal eye field normally directs both eyes toward the contralateral side through projections to the contralateral paramedian pontine reticular formation. Destruction of the right frontal eye field therefore removes the drive for leftward gaze, while activity from the intact left frontal eye field remains relatively unopposed, causing both eyes to deviate toward the right cerebral lesion. This is conventionally described as the patient\u003Cstrong\u003E\u201Clooking toward the hemispheric lesion and away from the hemiparesis.\u201D\u003C/strong\u003E Ipsilesional eye and head deviation is well recognized in acute right hemispheric stroke.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe important feature is that gaze deviation from an acute destructive frontal eye field lesion is usually \u003Cstrong\u003Etransient\u003C/strong\u003E. Other cortical and subcortical ocular motor networks rapidly compensate for the unilateral loss of supranuclear drive, so the resting gaze deviation may improve markedly over several days and often resolves within the first week. This rapid recovery contrasts with the more persistent structural visual and pursuit deficits caused by damage elsewhere in the same large infarct.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ELeft homonymous hemianopia\u003C/strong\u003E would result from damage to the right optic radiations passing through the temporal and parietal lobes. This produces loss of the left visual hemifield in both eyes. Although patients may develop compensatory scanning strategies and some spontaneous field improvement may occur over time, a dense homonymous defect from extensive destruction of the optic radiations would not ordinarily be expected to resolve dramatically within one week.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ESmooth pursuit to the right\u003C/strong\u003E would be impaired, rather than preserved, by right parietal cortical damage. Each parietal-occipital pursuit network predominantly supports smooth tracking toward the ipsilateral side. Thus, a right parietal lesion impairs rightward smooth pursuit, often causing the eyes to lag behind a target moving toward the right and requiring corrective saccades. Pursuit depends on a distributed network involving visual motion areas, parietal and frontal cortex, pontine nuclei, cerebellum, and brainstem ocular motor pathways, and a structural deficit from extensive parietal infarction is not expected to recover as dramatically as the acute frontal gaze deviation.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA useful localization contrast is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EDestructive frontal eye field lesion:\u003C/strong\u003E eyes deviate \u003Cstrong\u003Etoward\u003C/strong\u003E the cerebral lesion\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EIrritative frontal eye field seizure:\u003C/strong\u003E eyes deviate \u003Cstrong\u003Eaway from\u003C/strong\u003E the epileptic focus\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPontine horizontal gaze-centre lesion:\u003C/strong\u003E eyes deviate \u003Cstrong\u003Eaway from\u003C/strong\u003E the pontine lesion\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1919,
    "Name": "ocular myasthenia gravis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old presents with a three-month history of intermittent binocular diplopia. After maintaining upgaze for approximately 45 seconds, the patient developed the findings in the image below. Which diagnosis most appropriately explains this fatigable ocular finding and the fluctuating binocular symptoms?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-14-6c45f45e-2270-43a5-a686-1eb43f475b52.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMyasthenia gravis\u003C/strong\u003E, because the image following approximately 45 seconds of sustained upgaze shows marked left upper-eyelid ptosis, demonstrating \u003Cstrong\u003Efatigability of the levator palpebrae superioris\u003C/strong\u003E. Fluctuating binocular diplopia over several months, together with ptosis that appears or worsens during sustained activity, is characteristic of ocular myasthenia gravis. Myasthenic weakness commonly varies during the examination, worsens with repetitive use or later in the day, and improves following rest.\u003C/p\u003E\n\u003Cp\u003EMyasthenia gravis is an autoimmune disorder of neuromuscular transmission, most often caused by antibodies against the postsynaptic acetylcholine receptor and less commonly by antibodies against muscle-specific kinase or LRP4. The reduction in functional postsynaptic receptors lowers the neuromuscular junction\u2019s safety factor. Repeated stimulation progressively exhausts effective transmission, explaining why maintained upgaze causes increasing ptosis. The extraocular muscles and levator palpebrae are particularly vulnerable because of their high firing rates and specialized neuromuscular physiology.\u003C/p\u003E\n\u003Cp\u003EThe ocular motor pattern may imitate virtually any pupil-sparing ocular motor nerve palsy or supranuclear disorder. The deviation can be horizontal, vertical, or torsional and may change between examinations. Pupillary responses remain normal because the iris sphincter and dilator muscles are autonomically innervated smooth muscles rather than skeletal muscles supplied through the somatic neuromuscular junction.\u003C/p\u003E\n\u003Cp\u003EAdditional supportive examination findings include:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EImprovement of ptosis after rest or sleep\u003C/li\u003E\n\u003Cli\u003EImprovement following an ice-pack test\u003C/li\u003E\n\u003Cli\u003ECogan lid twitch after returning rapidly from downgaze to primary position\u003C/li\u003E\n\u003Cli\u003EOrbicularis oculi weakness\u003C/li\u003E\n\u003Cli\u003EVariable or alternating ptosis\u003C/li\u003E\n\u003Cli\u003EChanging patterns of incomitant strabismus\u003C/li\u003E\n\u003Cli\u003EEnhanced ptosis in the opposite eyelid when the more ptotic eyelid is manually elevated\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EA positive ice-pack test is generally defined as improvement in eyelid elevation by more than approximately 2 mm after applying ice to the closed eyelid for about two minutes. Subsequent investigation may include serum acetylcholine-receptor antibodies, MuSK and LRP4 antibodies where appropriate, repetitive nerve stimulation, and particularly single-fiber electromyography when clinical suspicion remains high despite negative serology.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EGiant cell arteritis\u003C/strong\u003E may cause ischemic visual loss and diplopia in an older patient, but it does not characteristically produce isolated, activity-dependent ptosis during sustained upgaze. \u003Cstrong\u003EDecompensated congenital exophoria\u003C/strong\u003E may produce intermittent binocular diplopia but would not cause progressive unilateral eyelid drooping. \u003Cstrong\u003ELeft microvascular cranial nerve 3 palsy\u003C/strong\u003E would produce a relatively fixed pattern of ptosis and impaired adduction, elevation, and depression, rather than markedly fluctuating weakness brought out by sustained gaze.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1920,
    "Name": "optic perineuritis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 22-year-old develops acute left visual loss over two days with severe pain exacerbated by eye movement. Visual acuity is 20/25 in the affected eye, with preserved color vision, a left relative afferent pupillary defect, diffuse constriction of the left visual field, anterior chamber inflammation, and moderate left optic disc swelling. Contrast-enhanced orbital MRI is below.\u0026nbsp; Which form of optic neuropathy best accounts for the clinical and radiological findings?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-14-ecda55e8-f32a-4568-956a-114a5a1b69c9.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EOptic perineuritis\u003C/strong\u003E, because the contrast-enhanced, fat-suppressed coronal orbital MRI demonstrates prominent circumferential enhancement and slight thickening of the \u003Cstrong\u003Eleft optic nerve sheath\u003C/strong\u003E, with relative sparing of the optic nerve substance. This indicates inflammation centred on the meningeal sheath surrounding the optic nerve rather than primary inflammation of the axons and myelin within the nerve. Optic perineuritis is an orbital inflammatory disorder that commonly presents with unilateral visual disturbance, severe periocular pain or pain on eye movement, a relative afferent pupillary defect, visual field loss, and optic disc oedema. Orbital inflammatory findings such as anterior uveitis, scleritis, extraocular muscle inflammation, proptosis, or motility disturbance may coexist.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe characteristic MRI pattern is \u003Cstrong\u003Eperineural enhancement\u003C/strong\u003E surrounding a relatively spared optic nerve. On axial post-contrast fat-suppressed images, enhancement along both sides of the optic nerve may produce the \u003Cstrong\u003Etram-track sign\u003C/strong\u003E; on coronal images, circumferential sheath enhancement produces the \u003Cstrong\u003Edoughnut sign\u003C/strong\u003E. These appearances are highly suggestive of optic perineuritis, although similar sheath enhancement may occur with optic nerve sheath meningioma, sarcoidosis, lymphoma, leukaemic infiltration, IgG4-related disease, granulomatosis with polyangiitis, tuberculosis, and syphilis. Imaging must therefore be interpreted alongside the tempo, inflammatory findings, and systemic investigation.\u003C/p\u003E\n\u003Cp\u003EDemyelinating optic neuritis remains an important clinical mimic because both disorders may present with acute visual loss, pain on eye movement, and a relative afferent pupillary defect. However, demyelinating optic neuritis usually shows enhancement \u003Cstrong\u003Ewithin the optic nerve substance\u003C/strong\u003E, commonly affects central vision and color vision, and frequently produces a central or cecocentral scotoma. In this patient, preserved color vision, diffuse rather than central field loss, visible disc swelling, anterior chamber inflammation, and sheath-dominant enhancement favour optic perineuritis. Unlike typical demyelinating optic neuritis, isolated optic perineuritis does not carry the same conventional association with future multiple sclerosis.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EOptic perineuritis may be idiopathic or secondary to systemic inflammatory, infectious, infiltrative, or neoplastic disease. The investigation should therefore be guided by the clinical context and may include tests for syphilis, tuberculosis, sarcoidosis, IgG4-related disease, ANCA-associated vasculitis, systemic lupus erythematosus, lymphoma, and other orbital inflammatory disorders.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe disorder generally responds rapidly to systemic corticosteroids, but treatment usually requires a sufficiently high dose followed by a \u003Cstrong\u003Eslow, prolonged taper\u003C/strong\u003E because rapid reduction or premature discontinuation is associated with relapse. This differs from typical demyelinating optic neuritis, which is often self-limiting and in which corticosteroids primarily accelerate recovery without substantially altering the final visual outcome.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIschemic optic neuropathy\u003C/strong\u003E is unlikely in a 22-year-old with severe pain on eye movement, anterior chamber inflammation, and sheath enhancement. \u003Cstrong\u003ENutritional optic neuropathy\u003C/strong\u003E usually causes slowly progressive, painless, symmetrical bilateral visual loss with dyschromatopsia and central or cecocentral scotomas, rather than acute unilateral painful disc swelling.\u003C/p\u003E\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-08-14-988c9b09-9c63-48c6-82d8-eb7baf879f01.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1921,
    "Name": "Marcus Gunn jaw-winking syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn Marcus Gunn jaw-winking syndrome, which muscle of mastication is synkinetically linked to the levator palpebrae superioris when the ptotic eyelid elevates during forced mouth closure, and which muscle is implicated when eyelid elevation occurs during mouth opening?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EInternal pterygoid; external pterygoid\u003C/strong\u003E, because Marcus Gunn jaw-winking syndrome is a congenital \u003Cstrong\u003Etrigemino-oculomotor synkinesis\u003C/strong\u003E in which motor activity intended for a muscle supplied by the mandibular division of the trigeminal nerve is aberrantly linked to the oculomotor innervation of the levator palpebrae superioris. Consequently, contraction of the relevant muscle of mastication causes simultaneous elevation or retraction of the congenitally ptotic upper eyelid.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EWhen the upper eyelid elevates during \u003Cstrong\u003Eforced closure of the mouth\u003C/strong\u003E, the synkinetic connection involves the \u003Cstrong\u003Einternal pterygoid\u003C/strong\u003E, also called the medial pterygoid. This muscle contributes to elevation and closure of the mandible, so forced mouth closure activates both the internal pterygoid and the aberrantly linked levator palpebrae superioris.\u003C/p\u003E\n\u003Cp\u003EWhen the upper eyelid elevates during \u003Cstrong\u003Eopening of the mouth\u003C/strong\u003E, the connection involves the \u003Cstrong\u003Eexternal pterygoid\u003C/strong\u003E, also called the lateral pterygoid. The external pterygoid assists in depressing and protruding the mandible and is the muscle most commonly implicated in the classic jaw-winking response.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe phenomenon may be elicited by:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EOpening the mouth\u003C/li\u003E\n\u003Cli\u003EMoving the jaw to the contralateral side\u003C/li\u003E\n\u003Cli\u003EProtruding the mandible\u003C/li\u003E\n\u003Cli\u003EChewing\u003C/li\u003E\n\u003Cli\u003ESucking\u003C/li\u003E\n\u003Cli\u003ETeeth clenching\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThe external pterygoid-levator connection is the more common pattern, while internal pterygoid-levator synkinesis is less frequent. The underlying abnormality is congenital misdirection or anomalous central connection between motor fibers associated with \u003Cstrong\u003ECN V3\u003C/strong\u003E and the superior division of \u003Cstrong\u003ECN III\u003C/strong\u003E, rather than a primary myopathy of the levator muscle. \u003Ca href=\u0022https://eyewiki.org/Marcus-Gunn_jaw_winking_ptosis\u0022\u003E[\u003C/a\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1922,
    "Name": "dural venous sinus thrombosis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat diagnosis is apparent in the imaging study shown above?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-15-bc62c31a-6414-4f0b-b4f5-216952502bc3.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EDural venous sinus thrombosis\u003C/strong\u003E, because the images are from a magnetic resonance venography study and demonstrate absence of the expected flow-related signal within the \u003Cstrong\u003Eright transverse sinus\u003C/strong\u003E, producing a venous filling defect. The contralateral transverse sinus remains well opacified, making the asymmetry conspicuous. Loss of normal venous flow signal on MRV is a characteristic finding of thrombotic occlusion, although source images must always be reviewed to distinguish true thrombosis from congenital transverse sinus hypoplasia or flow-related artefact.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA thrombus obstructs cerebral venous drainage, raising venous pressure and impairing cerebrospinal-fluid absorption at the arachnoid granulations. Clinical manifestations may therefore include headache, papilloedema, transient visual obscurations, sixth nerve palsy, pulsatile tinnitus, seizures, focal neurological deficits, altered consciousness, or venous infarction. Unlike arterial infarction, a venous infarct may cross conventional arterial boundaries and is more likely to become haemorrhagic.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EArterial venous malformation\u003C/strong\u003E would demonstrate a vascular nidus with abnormal feeding arteries and early-draining veins rather than an isolated absence of flow in a dural sinus. \u003Cstrong\u003EStroke\u003C/strong\u003E is a clinical and radiological consequence rather than the specific vascular diagnosis shown here, and arterial stroke is primarily identified by parenchymal diffusion restriction or arterial occlusion. \u003Cstrong\u003EAneurysm\u003C/strong\u003E is a focal arterial dilatation and is generally evaluated with arterial imaging such as CTA, MRA, or catheter angiography rather than appearing as a dural venous filling defect on MRV.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1923,
    "Name": "Low-flow dural sinus fistula versus high-flow carotid-cavernous fistula",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen comparing an indirect, low-flow dural arteriovenous fistula involving the cavernous sinus with a direct, high-flow carotid-cavernous fistula, which feature is more characteristic of the low-flow lesion?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESpontaneous idiopathic onset\u003C/strong\u003E, because low-flow cavernous sinus dural arteriovenous fistulas are \u003Cstrong\u003Eindirect fistulas\u003C/strong\u003E formed by abnormal communications between small meningeal branches of the internal carotid artery, external carotid artery, or both and the cavernous sinus. These lesions often develop spontaneously without a preceding traumatic event, particularly in older adults, and usually produce a gradual, relatively mild clinical presentation. Direct high-flow carotid-cavernous fistulas instead represent a direct communication between the intracavernous internal carotid artery and cavernous sinus and are most commonly associated with craniofacial trauma or skull-base fracture, although spontaneous rupture of a cavernous internal carotid aneurysm is another recognized cause.\u003C/p\u003E\n\u003Cp\u003EThe other listed findings can occur in \u003Cstrong\u003Eboth\u003C/strong\u003E low-flow and high-flow fistulas because both elevate pressure within the cavernous sinus and may impair normal orbital venous drainage:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003EElevated intraocular pressure\u003C/strong\u003E may result from raised episcleral venous pressure and, less commonly, secondary angle closure or neovascular mechanisms. It is therefore not specific to a low-flow fistula.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EArterialization of the conjunctiva\u003C/strong\u003E produces dilated, tortuous corkscrew episcleral vessels and may occur with either fistula type, although it is often more pronounced and rapidly apparent in a direct high-flow fistula.\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EPresence of a cranial bruit\u003C/strong\u003E is more characteristic of a direct high-flow carotid-cavernous fistula because the large-volume shunt produces turbulent flow. A low-flow indirect fistula may have no audible bruit. Direct fistulas classically produce the triad of pulsatile proptosis, conjunctival chemosis, and an orbital or cranial bruit.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003ELow-flow indirect fistulas may present insidiously with chronic red eye, corkscrew episcleral vessels, mild proptosis, diplopia from ocular motor nerve dysfunction, raised intraocular pressure, or orbital discomfort and can consequently be mistaken for conjunctivitis, thyroid eye disease, or orbital inflammation. Some indirect fistulas undergo spontaneous thrombosis and closure, permitting observation in selected low-risk cases. However, progressive visual loss, uncontrolled intraocular pressure, severe proptosis, cranial neuropathy, retinal or choroidal ischemia, or cortical venous reflux requires urgent neurovascular assessment. Digital subtraction angiography remains the definitive investigation for characterizing the arterial supply, venous drainage, and associated risk before endovascular treatment.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1924,
    "Name": "Distinguishing cavernous sinus pathology from orbital apex pathology",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the primary clinical feature that aides in distinguishing a lesion of the cavernous sinus from a lesion of the orbital apex?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe presence or absence of optic nerve involvement\u003C/strong\u003E, because the orbital apex contains both the \u003Cstrong\u003Eoptic canal\u003C/strong\u003E and the \u003Cstrong\u003Esuperior orbital fissure\u003C/strong\u003E. A lesion at the orbital apex can therefore affect the optic nerve together with cranial nerves III, IV, and VI and the ophthalmic division of cranial nerve V, producing ophthalmoplegia accompanied by an optic neuropathy. By contrast, the optic nerve does not pass through the cavernous sinus, so a lesion confined to the cavernous sinus usually spares optic nerve function.\u003C/p\u003E\n\u003Cp\u003EOptic nerve involvement should be assessed by looking for:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EReduced visual acuity\u003C/li\u003E\n\u003Cli\u003EDyschromatopsia\u003C/li\u003E\n\u003Cli\u003EA relative afferent pupillary defect in unilateral or asymmetric disease\u003C/li\u003E\n\u003Cli\u003EReduced contrast sensitivity\u003C/li\u003E\n\u003Cli\u003EA central, cecocentral, or other optic neuropathic visual field defect\u003C/li\u003E\n\u003Cli\u003EOptic disc swelling or subsequent optic atrophy, although the disc may initially appear normal\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThe combination of optic neuropathy and multiple ocular motor cranial neuropathies is therefore the defining clinical pattern of \u003Cstrong\u003Eorbital apex syndrome\u003C/strong\u003E, also called Jacod syndrome.\u003C/p\u003E\n\u003Cp\u003ECranial nerves III, IV, VI, and V1 are present in or adjacent to both anatomical regions. Consequently, \u003Cstrong\u003EV1 involvement\u003C/strong\u003E does not reliably separate the two sites. Similarly, the oculomotor nerve divides into superior and inferior divisions before entering the orbit, so a divisional third nerve pattern does not reliably distinguish an anterior cavernous sinus lesion from orbital apex pathology.\u003C/p\u003E\n\u003Cp\u003ESympathetic fibers accompany the intracavernous internal carotid artery and may be affected by cavernous sinus disease, producing a partial Horner syndrome. However, sympathetic involvement is not the most dependable discriminator because clinical expression may be subtle, and a lesion can extend across adjacent anatomical compartments.\u003C/p\u003E\n\u003Cp\u003EThe distinction is useful but not absolute. A disease process centred in the cavernous sinus may extend anteriorly into the orbital apex and involve the optic nerve, while an orbital process may extend posteriorly into the cavernous sinus. When the clinical findings overlap or localization remains uncertain, contrast-enhanced MRI of the brain and orbits with thin sections through the cavernous sinus and orbital apex is required.\u003C/p\u003E\n\u003Cp\u003E\u003Cbr\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1925,
    "Name": "Upgaze-induced intraocular pressure",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen evaluating suspected inferior rectus restriction, such as in thyroid-associated orbitopathy, intraocular pressure is measured in primary position and then repeated during attempted upgaze. What minimum rise in intraocular pressure during upgaze is considered clinically significant evidence of mechanical restriction?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eupgaze IOP 5 points higher than primary gaze\u003C/strong\u003E, because an increase of approximately \u003Cstrong\u003E5 mmHg or more\u003C/strong\u003E on attempted elevation is considered significant and supports mechanical restriction of the inferior rectus muscle. A markedly enlarged or fibrotic inferior rectus resists elevation of the globe. During attempted upgaze, contraction of the superior rectus against the nonrelaxing inferior rectus mechanically compresses the globe and produces a transient rise in measured intraocular pressure. Thyroid eye disease is a classic cause because inflammatory enlargement followed by fibrosis commonly affects the inferior rectus and produces restricted elevation, hypotropia, and elevated pressure in upgaze.\u003C/p\u003E\n\u003Cp\u003EThe measurement should be performed using the same tonometer and technique in primary gaze and upgaze, avoiding excessive eyelid manipulation or pressure on the globe. A smaller rise can occur physiologically or from measurement variability, whereas a difference of at least 5 mmHg is more supportive of restriction. This finding is supportive rather than independently diagnostic and should be interpreted alongside reduced elevation, incomitant vertical deviation, forced-duction testing, saccadic velocity assessment, and orbital imaging.\u003C/p\u003E\n\u003Cp\u003EThis test helps distinguish \u003Cstrong\u003Erestrictive\u003C/strong\u003E from \u003Cstrong\u003Eparetic\u003C/strong\u003E strabismus:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EIn inferior rectus restriction, attempted upgaze produces mechanical resistance, a positive forced-duction test, and a significant rise in intraocular pressure.\u003C/li\u003E\n\u003Cli\u003EIn superior rectus weakness, elevation is reduced because of inadequate muscle force, but there is no opposing mechanical tether, so the gaze-related pressure rise is usually absent.\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 9,
    "Category": null,
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  },
  {
    "Id": 1926,
    "Name": "Orbital trauma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn which clinical scenario is CT imaging preferable to MRI imaging?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E23-year-old involved in a motor vehicle accident with double vision and periocular swelling in the right eye\u003C/strong\u003E, because acute orbital trauma requires rapid assessment of the bony orbital walls and associated soft-tissue complications. A thin-section non-contrast CT of the orbits provides excellent visualization of orbital fractures, displaced bone fragments, herniation of orbital contents, extraocular muscle or soft-tissue entrapment, retrobulbar haemorrhage, orbital emphysema, globe injury, and most radiopaque foreign bodies. CT is also fast, widely available, and less affected by patient movement, making CT particularly suitable for emergency trauma assessment.\u003C/p\u003E\n\u003Cp\u003EThe combination of diplopia and periocular swelling raises particular concern for an orbital wall fracture with extraocular muscle or adjacent soft-tissue entrapment. An orbital floor fracture may entrap the inferior rectus or perimuscular connective tissue and cause restricted elevation, vertical diplopia, nausea, vomiting, or an oculocardiac reflex. A medial wall fracture may involve the medial rectus and cause horizontal diplopia. CT can demonstrate the fracture and the relationship between the extraocular muscles, orbital fat, and fracture defect, although clinical motility examination and forced-duction testing remain important because radiological tissue herniation does not necessarily prove functional entrapment.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003E40-year-old female with acute monocular vision loss and eye pain worse with eye movement\u003C/strong\u003E has a clinical pattern suggestive of optic neuritis. MRI of the brain and orbits with gadolinium, fat suppression, and dedicated optic nerve sequences is preferable because MRI can demonstrate optic nerve enhancement and identify cerebral demyelinating lesions relevant to diagnosis and future multiple sclerosis risk. CT has poor sensitivity for inflammation within the optic nerve.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003E60-year-old with an acute onset internuclear ophthalmoplegia (INO) on clinical exam\u003C/strong\u003E requires MRI because an INO localizes to the medial longitudinal fasciculus within the pons or midbrain. Diffusion-weighted MRI is more sensitive than CT for a small acute brainstem infarct, while T2-weighted and FLAIR imaging can detect demyelination or another intrinsic brainstem lesion.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003E4-year-old with a 2 month history of ataxia and running into objects\u003C/strong\u003E also requires MRI of the brain because the progressive course raises concern for posterior fossa, brainstem, cerebellar, or visual pathway pathology. MRI provides better soft-tissue contrast and posterior fossa resolution and avoids ionizing radiation, which is particularly important in children. Sedation may be required if the child cannot remain still, but this does not make CT diagnostically preferable for a progressive neurological presentation.\u003C/p\u003E\n\u003Cp\u003EA useful imaging rule is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\u003Cstrong\u003ECT:\u003C/strong\u003E trauma, fractures, acute haemorrhage, calcification, orbital foreign body, and rapid emergency assessment\u003C/li\u003E\n\u003Cli\u003E\u003Cstrong\u003EMRI:\u003C/strong\u003E optic nerve, chiasm, brainstem, posterior fossa, demyelination, inflammation, and most non-traumatic neurological disorders\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EMRI must not be performed until a metallic intraorbital foreign body has been excluded when penetrating orbital trauma is possible, because movement of a ferromagnetic object within the magnetic field could cause further ocular injury.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1927,
    "Name": "Pupil-involving third nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient develops an acute third cranial nerve palsy with pupillary involvement, raising concern for external compression by an intracranial aneurysm. At which arterial junction is the causative aneurysm most commonly located?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EAt the junction of the posterior communicating artery and the internal carotid artery\u003C/strong\u003E, because an aneurysm arising at the internal carotid artery-posterior communicating artery junction lies immediately adjacent to the oculomotor nerve during the nerve\u2019s subarachnoid course. Enlargement or directional projection of the aneurysm can compress the nerve and produce an acute, often painful third nerve palsy. This is the most common and clinically important aneurysmal site associated with isolated oculomotor palsy.\u003C/p\u003E\n\u003Cp\u003EAfter emerging from the ventral midbrain, the third nerve travels through the interpeduncular and ambient cisterns between the posterior cerebral and superior cerebellar arteries. The nerve then passes close to the posterior communicating artery and enters the roof of the cavernous sinus. This anatomical relationship explains why an aneurysm arising near the origin of the posterior communicating artery from the internal carotid artery can readily compress the nerve.\u003C/p\u003E\n\u003Cp\u003EThe parasympathetic pupillomotor fibers lie superficially in the dorsomedial peripheral portion of the oculomotor nerve during its subarachnoid course. External compression therefore tends to affect these fibers early, producing ipsilateral mydriasis with impaired or absent light reaction. Compression of the remaining somatic motor fibers may cause:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EPtosis from levator palpebrae superioris weakness\u003C/li\u003E\n\u003Cli\u003EImpaired adduction from medial rectus weakness\u003C/li\u003E\n\u003Cli\u003EImpaired elevation from superior rectus and inferior oblique weakness\u003C/li\u003E\n\u003Cli\u003EImpaired depression from inferior rectus weakness\u003C/li\u003E\n\u003Cli\u003EA \u201Cdown and out\u201D resting ocular position caused by unopposed lateral rectus and superior oblique activity\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EBy contrast, microvascular ischemia classically affects the central somatic fibers while relatively sparing the superficial parasympathetic fibers. However, this distinction is not absolute. Pupil sparing does not reliably exclude an aneurysm, particularly in a partial or evolving third nerve palsy, and microvascular palsies can occasionally show minor pupillary involvement. Modern management therefore favours urgent vascular imaging for any acute acquired third nerve palsy when aneurysm is clinically possible.\u003C/p\u003E\n\u003Cp\u003ECTA or MRA can identify most clinically significant aneurysms, but catheter digital subtraction angiography remains appropriate when non-invasive imaging is negative or equivocal despite strong clinical suspicion. Prompt investigation is essential because an enlarging posterior communicating artery aneurysm may rupture and produce life-threatening subarachnoid haemorrhage.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EAneurysms at the basilar tip, posterior cerebral artery, superior cerebellar artery, or cavernous internal carotid artery can also affect the third nerve, but these locations are less common causes of an isolated pupil-involving third nerve palsy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1928,
    "Name": "Number of retinal ganglion cell axons",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EApproximately how many retinal ganglion cell axons converge at the optic disc to form each human optic nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E1.2 million\u003C/strong\u003E, because each optic nerve is formed by approximately \u003Cstrong\u003E1.0 to 1.2 million unmyelinated retinal ganglion cell axons\u003C/strong\u003E converging at the optic disc and passing through the lamina cribrosa. The axons become myelinated by oligodendrocytes only after leaving the globe, beginning in the retrolaminar optic nerve.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe retina contains roughly 100 million photoreceptors, so substantial convergence occurs as signals pass from rods and cones through bipolar and amacrine cells to retinal ganglion cells. Convergence is minimal near the fovea, supporting high spatial resolution, but becomes much greater in the peripheral retina, where one ganglion cell may receive information derived from many photoreceptors.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1929,
    "Name": "Crossing Goldmann isopters",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient reports reduced peripheral vision in both eyes. Goldmann kinetic perimetry demonstrates severe bilateral field constriction. Which diagnosis best explains this visual field pattern?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cbr\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-15-f598e068-d62c-4fac-b4ff-509bad28f1f9.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFunctional vision loss\u003C/strong\u003E, because the Goldmann field demonstrates \u003Cstrong\u003Ecrossing and overlapping isopters\u003C/strong\u003E, an internally inconsistent response pattern that cannot be explained by normal visual physiology or a stable organic visual pathway lesion.\u003C/p\u003E\n\u003Cp\u003EAn isopter represents the boundary within which a stimulus of a specified size and luminance is perceived. In the displayed field:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EThe \u003Cstrong\u003Epurple line\u003C/strong\u003E represents the \u003Cstrong\u003EV4e\u003C/strong\u003E stimulus.\u003C/li\u003E\n\u003Cli\u003EThe \u003Cstrong\u003Ebrown line\u003C/strong\u003E represents the \u003Cstrong\u003EIII4e\u003C/strong\u003E stimulus.\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThe V4e stimulus is substantially larger than the III4e stimulus and should therefore be visible farther into the peripheral field. Under genuine physiological conditions, the V4e isopter must consistently remain outside the III4e isopter.\u0026nbsp;\u003Cspan style=\u0022letter-spacing: 0.14994px;\u0022\u003EIn this field, the purple V4e isopter passes inside the brown III4e isopter at several locations. This would imply that the patient detected the smaller III4e target at a location where the larger V4e target of the same luminance was not detected. That reversal is physiologically incompatible with a reproducible organic field defect and indicates variable responses during testing.\u003C/span\u003E\u003C/p\u003E\n\u003Cp\u003EOther Goldmann patterns supporting functional visual loss include:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ESpiralling isopters during repeated testing\u003C/li\u003E\n\u003Cli\u003EStar-shaped fields\u003C/li\u003E\n\u003Cli\u003ETubular or \u201Cgun-barrel\u201D constriction that remains unchanged when testing distance increases\u003C/li\u003E\n\u003Cli\u003ETarget fields produced when the same isopter is plotted repeatedly\u003C/li\u003E\n\u003Cli\u003EMarked inconsistency between confrontation fields, behaviour, and formal perimetry\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EThese patterns provide \u003Cstrong\u003Epositive evidence of functional inconsistency\u003C/strong\u003E, rather than making the diagnosis solely because all investigations are normal. Repeated kinetic testing can document nonorganic constriction because patients with functional loss may perceive the same stimulus considerably farther inward on a second presentation, whereas patients with organic disease generally reproduce the original boundary.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EEnd-stage glaucoma\u003C/strong\u003E, \u003Cstrong\u003Eretinitis pigmentosa\u003C/strong\u003E, and \u003Cstrong\u003Eend-stage pseudotumor cerebri\u003C/strong\u003E can all produce severe bilateral peripheral constriction with a residual central island. However, an organic field should retain orderly stimulus hierarchy, with the larger, brighter stimulus producing the outermost isopter and no repeated crossing of isopters. Organic examples of advanced retinal or glaucomatous disease may show small central islands, peripheral islands, arcuate loss, or ring scotomas, but the responses remain anatomically and psychophysically coherent.\u003C/p\u003E\n\u003Cp\u003EFunctional visual loss can coexist with genuine ocular or neurological pathology. The diagnosis should therefore be supported by a complete examination, including visual acuity consistency tests, pupils, color vision, optic disc and retinal assessment, OCT, and targeted electrophysiology or neuroimaging when clinically indicated.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1930,
    "Name": "Palinopsia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is NOT associated with palinopsia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Epapilledema\u003C/strong\u003E, because palinopsia is a pathological visual perseveration in which an image persists or recurs after the causative visual stimulus has been removed. Unlike a normal physiological afterimage, the recurrent image may be prolonged, unusually vivid, delayed, or reproduced repeatedly. Palinopsia is broadly divided into \u003Cstrong\u003Ehallucinatory\u003C/strong\u003E and \u003Cstrong\u003Eillusory\u003C/strong\u003E forms, which have different clinical characteristics and anatomical implications.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EHallucinatory palinopsia\u003C/strong\u003E usually produces formed, high-resolution, long-lasting images that may appear after a delay or in a different location from the original stimulus. It is associated with focal posterior cortical dysfunction, particularly lesions of the parietal-occipital region, and with epileptic activity involving the visual association cortex. Structural causes include infarction, haemorrhage, tumour, arteriovenous malformation, cortical dysplasia, and abscess.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EIllusory palinopsia\u003C/strong\u003E generally causes brief, indistinct, low-resolution afterimages or visual trailing that remain influenced by light intensity, contrast, fixation, and movement. Recognized associations include migraine, visual snow syndrome, head trauma, hallucinogen persisting perception disorder, and several prescription medications. \u003Cstrong\u003EMedications including topiramate, clomiphene, and trazodone\u003C/strong\u003E have all been reported to cause palinopsia, particularly visual trailing.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMigraine associated visual phenomena\u003C/strong\u003E may include illusory palinopsia, particularly in migraine with aura.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Epapilledema\u003C/strong\u003E is optic disc swelling caused by raised intracranial pressure and typically produces transient visual obscurations, enlargement of the blind spot, peripheral field loss, and, in advanced disease, progressive visual impairment. It is not itself a recognized cause of palinopsia. If palinopsia occurs in a patient who also has papilledema, an associated intracranial lesion, seizure disorder, medication effect, or migraine phenomenon should be considered rather than attributing the visual perseveration directly to the papilledema.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1931,
    "Name": "CSCR",
    "Body": "\u003Cspan style=\u0022font-weight: bold;\u0022\u003EWhich medication has shown potential benefit in the treatment of chronic central serous chorioretinopathy (CSCR) through antagonism of mineralocorticoid receptors in the choroid?\u003C/span\u003E",
    "Explanation": "\u003Cul\u003E\u003Cli\u003E\u003Cp\u003E\u003Cstrong\u003EEplerenone\u003C/strong\u003E is a \u003Cstrong\u003Eselective mineralocorticoid receptor (MR) antagonist\u003C/strong\u003E that was investigated as a treatment for \u003Cstrong\u003Echronic CSCR\u003C/strong\u003E (\u0026gt;4 months duration).\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003EEarly evidence came from a \u003Cstrong\u003Enon-randomized pilot study\u003C/strong\u003E involving \u003Cstrong\u003E13 patients\u003C/strong\u003E with chronic, non-fluctuating CSCR.\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003EAfter \u003Cstrong\u003E3 months of treatment\u003C/strong\u003E, mean central macular thickness decreased significantly from \u003Cstrong\u003E352 \u00B1 139 \u00B5m\u003C/strong\u003E to \u003Cstrong\u003E189 \u00B1 99 \u00B5m\u003C/strong\u003E.\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003EThese encouraging results required confirmation in larger randomized controlled trials before eplerenone could be recommended as standard therapy.\u003C/p\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003EProposed mechanism of action:\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cstrong\u003EMineralocorticoid receptor antagonism\u003C/strong\u003E reverses the upregulation of the \u003Cstrong\u003Eendothelial vasodilatory potassium channel (KCa2.3)\u003C/strong\u003E within the choroid.\u003C/li\u003E\u003Cli\u003EThis reduces \u003Cstrong\u003Echoroidal vasodilatation\u003C/strong\u003E, which is believed to play a key role in the pathogenesis of CSCR.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003EWhy the other options are incorrect:\u003C/p\u003E\u003Cul\u003E\u003Cli\u003E\u003Cstrong\u003EBevacizumab\u003C/strong\u003E may occasionally be used in chronic CSCR (particularly if secondary CNV develops), but \u003Cstrong\u003Eits mechanism is anti-VEGF\u003C/strong\u003E, not mineralocorticoid receptor antagonism.\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003EHydrochlorothiazide\u003C/strong\u003E has \u003Cstrong\u003Enot been specifically studied\u003C/strong\u003E as a treatment for chronic CSCR.\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003EAldosterone\u003C/strong\u003E is itself a \u003Cstrong\u003Emineralocorticoid agonist\u003C/strong\u003E and would activate mineralocorticoid receptors, increasing KCa2.3 activity rather than inhibiting it.\u003C/li\u003E\u003C/ul\u003E\u003C/li\u003E\u003Cli\u003E\u003Cp\u003E\u003Cstrong\u003ESpironolactone\u003C/strong\u003E, another mineralocorticoid receptor antagonist, has also been investigated as a potential treatment for chronic CSCR.\u003C/p\u003E\u003C/li\u003E\u003C/ul\u003E\u003Ch3\u003EHigh-Yield FRCOphth Pearls\u003C/h3\u003E\u003Cul\u003E\u003Cli\u003E\u003Cstrong\u003EEplerenone = Mineralocorticoid receptor antagonist.\u003C/strong\u003E\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003EMechanism:\u003C/strong\u003E Reduces choroidal vascular hyperpermeability by antagonising mineralocorticoid receptors.\u003C/li\u003E\u003Cli\u003E\u003Cstrong\u003EModern update:\u003C/strong\u003E Although early studies were promising, subsequent higher-quality evidence (e.g. the \u003Cstrong\u003EVICI trial\u003C/strong\u003E) did \u003Cstrong\u003Enot\u003C/strong\u003E demonstrate superiority of eplerenone over placebo for chronic CSCR. Consequently, \u003Cstrong\u003Eeplerenone is no longer routinely recommended\u003C/strong\u003E, and \u003Cstrong\u003Ehalf-dose or half-fluence photodynamic therapy (PDT)\u003C/strong\u003E is now considered the preferred evidence-based treatment for chronic CSCR.\u003C/li\u003E\u003C/ul\u003E",
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    "Category": null,
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  },
  {
    "Id": 1932,
    "Name": "Persistent vertical diplopia after cataract surgery",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old with diabetes and hypertension develops binocular diplopia immediately after uncomplicated left cataract surgery, despite having no preoperative strabismus. Two months later, visual acuity is 20/20 in both eyes, but the left eye has a -2 elevation deficit. There is a moderate right hypertropia in primary position that increases in upgaze and resolves in downgaze. Which perioperative factor most likely caused this persistent\u0026nbsp; strabismus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERetrobulbar injection\u003C/strong\u003E, because the immediate onset of diplopia after cataract surgery, followed by persistent limitation of left-eye elevation and an incomitant vertical deviation that is greatest in upgaze, is characteristic of \u003Cstrong\u003Eanaesthetic-related injury to the left inferior rectus muscle\u003C/strong\u003E. The right hypertropia is equivalent to a left hypotropia. Restriction of the left eye by a shortened or fibrotic inferior rectus becomes most evident when the patient attempts elevation, causing the right eye to appear increasingly hypertropic in upgaze. The deviation resolves in downgaze because downgaze does not require lengthening of the restricted left inferior rectus.\u003C/p\u003E\n\u003Cp\u003ERetrobulbar or peribulbar anaesthesia can damage an extraocular muscle through direct needle trauma, intramuscular haemorrhage, local anaesthetic myotoxicity, or high local drug concentration within or around the muscle. Inferotemporal needle placement makes the inferior rectus particularly vulnerable. The initial injury may produce muscle paresis and transient hypertropia of the injected eye, but subsequent healing with contracture and fibrosis can reverse the deviation, producing hypotropia with restricted elevation.\u003C/p\u003E\u003Col\u003E\n\u003C/ol\u003E\n\u003Cp\u003EThe diagnosis is supported by a positive forced-duction test when the left globe is passively elevated. Orbital imaging may reveal inferior rectus enlargement acutely or focal atrophy and fibrosis later. Saccadic velocity testing may also help distinguish restriction from paresis: restrictive disease typically preserves the initial velocity of the attempted upward saccade before the eye is mechanically arrested, whereas superior rectus or third nerve paresis reduces saccadic force and velocity.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThyroid associated ophthalmopathy\u003C/strong\u003E can produce an almost identical pattern through enlargement and fibrosis of the inferior rectus, causing hypotropia and restricted elevation. However, thyroid-related restriction would not typically begin immediately after cataract surgery and would usually be accompanied by other supportive features, such as lid retraction, proptosis, conjunctival injection, raised intraocular pressure in upgaze, or characteristic extraocular muscle enlargement on imaging.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMicrovascular partial CN III palsy\u003C/strong\u003E is less likely because weakness of the superior rectus and inferior oblique would produce impaired elevation through a paretic mechanism rather than restrictive inferior rectus tethering. A partial third nerve palsy may also affect adduction, depression, or eyelid elevation, and would not be specifically linked to the immediate postoperative onset.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EBrainstem stroke\u003C/strong\u003E could cause skew deviation or an ocular motor palsy, but the absence of additional neurological signs, the immediate temporal relationship to retrobulbar anaesthesia, and the isolated restrictive elevation deficit argue strongly against this diagnosis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1933,
    "Name": "Post-radiation ocular neuromyotonia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old underwent pituitary adenoma resection followed by cranial radiotherapy two years ago. The patient now experiences recurrent episodes of binocular vertical and horizontal diplopia lasting 15 seconds to two minutes. Examination during an attack demonstrates involuntary contraction of the right medial and inferior rectus muscles, while follow-up MRI shows only chronic postoperative and post-radiation changes. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea trial of carbamazepine therapy\u003C/strong\u003E, because the recurrent, brief episodes of tonic contraction affecting the right medial and inferior rectus muscles after previous sellar surgery and cranial radiotherapy are characteristic of \u003Cstrong\u003Eocular neuromyotonia involving the right oculomotor nerve\u003C/strong\u003E. Ocular neuromyotonia causes intermittent sustained contraction of one or more extraocular muscles, producing paroxysmal strabismus and binocular diplopia lasting seconds to minutes. Prior cranial irradiation, particularly for sellar or parasellar disease, is the most frequent association, and onset may occur months to many years after treatment.\u003C/p\u003E\n\u003Cp\u003EBoth the medial rectus and inferior rectus are innervated by the inferior division of cranial nerve III. Their simultaneous spasm during an attack therefore strongly localizes the hyperexcitability to the right oculomotor nerve rather than representing independent muscle disease. Episodes may arise spontaneously or be provoked by maintaining eccentric gaze in the field of action of the involved muscles, with the eye remaining tonically deviated when attempting to return to primary position. The normal or near-normal examination between attacks and the absence of a new structural lesion on MRI are typical.\u003C/p\u003E\n\u003Cp\u003ETreatment should begin under appropriate medical supervision because carbamazepine can cause dizziness, somnolence, diplopia, hyponatraemia, blood dyscrasias, hepatic dysfunction, and serious cutaneous reactions. Baseline and follow-up full blood count, liver function, sodium, medication-interaction review, and relevant pharmacogenetic risk assessment should be considered according to local prescribing guidance.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003ETensilon (edrophonium) test\u003C/strong\u003E is not the best next step because myasthenia gravis produces fluctuating weakness rather than visible tonic spasm of muscles supplied by a single ocular motor nerve. \u003Cstrong\u003EStrabismus surgery\u003C/strong\u003E is unsuitable as initial treatment because the deviation is episodic rather than stable, although surgery may occasionally be considered for persistent interictal misalignment or medically refractory disease. \u003Cstrong\u003EPsychiatry consultation for a functional disorder\u003C/strong\u003E is inappropriate because the recurrent, anatomically coherent contraction of right oculomotor-innervated muscles following cranial irradiation provides a well-recognized organic diagnosis.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1934,
    "Name": "Ethambutol-associated toxic optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 70-year-old with controlled hypertension and longstanding treated hypothyroidism has been receiving multiple antimicrobial agents for pulmonary \u003Cem\u003EMycobacterium avium\u003C/em\u003E complex infection for approximately one year. Over the previous two months, the patient has developed progressive, painless, symmetrical visual deterioration to 20/100 in each eye, with acquired bilateral color-vision impairment despite normal anterior segment, retinal, and optic disc examinations. Automated perimetry and Contrast-enhanced MRI of the brain and orbits are below. Which listed mechanism most likely accounts for the visual dysfunction?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-16-9c1eca2a-dd2c-44af-81cd-4f91df910697.png\u0022\u003E\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-16-d54e2866-3997-4a35-84b7-db79fdaab995.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMedication-related toxicity of retinal ganglion cell mitochondria\u003C/strong\u003E, because the temporal relationship to prolonged multidrug treatment for \u003Cem\u003EMycobacterium avium\u003C/em\u003E complex infection, together with painless symmetrical loss of central acuity, acquired dyschromatopsia, bitemporal and central field loss, initially normal optic discs, and unrevealing MRI, strongly supports \u003Cstrong\u003Eethambutol-induced toxic optic neuropathy\u003C/strong\u003E. Ethambutol is commonly included in therapy for nontuberculous mycobacterial infections and can produce bilateral optic neuropathy through disruption of retinal ganglion-cell and optic nerve mitochondrial function ; the papillomacular bundle is particularly susceptible, accounting for reduced central acuity, dyschromatopsia, and central or cecocentral scotomata. Ethambutol optic neuropathy is usually retrobulbar at presentation, so substantial visual dysfunction may precede temporal pallor or OCT retinal nerve fibre layer thinning, while macular ganglion-cell\u2013inner plexiform layer loss can emerge earlier and may provide a more sensitive structural marker.  Although central and cecocentral defects are most typical, ethambutol can also produce a bitemporal pattern that respects the vertical meridian, possibly because decussating nasal retinal ganglion-cell axons within the chiasm share particular metabolic vulnerability; reported cases confirm that ethambutol toxicity can cause bitemporal hemianopia and, rarely, visible chiasmal signal abnormality, although MRI is usually normal.  The normal coronal post-contrast image argues against \u003Cstrong\u003EPituitary macroadenoma-related compression of the optic chiasm\u003C/strong\u003E and \u003Cstrong\u003ETuberculum sellae meningioma-related compression of the optic chiasm\u003C/strong\u003E, both of which should generally produce a demonstrable sellar, suprasellar, or anterior skull-base mass with chiasmal displacement or compression; \u003Cstrong\u003EDemyelinating lesion of the optic chiasm\u003C/strong\u003E would be unusual in a 70-year-old without a personal demyelinating history and would usually produce an intrinsic chiasmal T2 signal abnormality or enhancement during the acute inflammatory phase, while a first cousin with multiple sclerosis does not establish a demyelinating cause.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1935,
    "Name": "NAION",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn patients presenting with acute non-arteritic anterior ischemic optic neuropathy confined to one eye, what approximate risk of developing NAION in the fellow eye over the subsequent five years was reported by the Ischemic Optic Neuropathy Decompression Trial follow-up study?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E12-19%\u003C/strong\u003E, because the Ischemic Optic Neuropathy Decompression Trial follow-up study documented new NAION in the fellow eye in \u003Cstrong\u003E14.7% of patients at risk\u003C/strong\u003E during a median follow-up of 5.1 years, conventionally rounded to an approximately \u003Cstrong\u003E15% five-year risk\u003C/strong\u003E and therefore falling within the stated range. The study followed 326 patients whose fellow eyes were initially free from NAION; fellow-eye involvement occurred in 48 patients, with diabetes and presenting visual acuity of 20/200 or worse in the first affected eye associated with increased risk, whereas age, sex, smoking history, and aspirin use were not significantly associated with fellow-eye involvement in that cohort.  NAION is believed to arise from transient hypoperfusion of the short posterior ciliary circulation supplying a structurally crowded optic nerve head, followed by ischaemic axonal swelling, axoplasmic-flow stasis, and secondary compression of the microcirculation within a small or absent physiological cup, the classic\u003Cstrong\u003E\u201Cdisc at risk.\u201D\u003C/strong\u003E Systemic associations include diabetes, hypertension, dyslipidaemia, smoking, obstructive sleep apnoea, anaemia, and possibly excessive nocturnal hypotension, so management should include investigation and optimisation of modifiable vascular and sleep-related risk factors.  No treatment has been proven to prevent fellow-eye NAION: aspirin should be prescribed according to the patient\u2019s cardiovascular or cerebrovascular indication rather than solely for NAION prevention, and optic nerve sheath decompression is not beneficial and may be harmful. The approximately 15% five-year risk in NAION contrasts with untreated arteritic anterior ischaemic optic neuropathy from giant cell arteritis, in which the fellow eye may become involved rapidly, often within days, making immediate high-dose corticosteroid therapy essential when arteritic disease is suspected.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1936,
    "Name": "Diabetic papillopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 25-year-old with poorly controlled type I diabetes is referred after bilateral optic disc swelling is detected incidentally. Visual acuity remains 20/25 in both eyes, with moderate non-proliferative diabetic retinopathy, bilateral hyperaemic disc edema, and fine telangiectatic vessels over the disc surfaces. Which additional historical or examination finding would be inconsistent with diabetic papillopathy and should prompt consideration of an alternative diagnosis?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Esuperior arcuate visual field defects on Humphrey visual field (HVF) testing OU\u003C/strong\u003E, because diabetic papillopathy is generally a mild, self-limiting optic nerve head disorder characterized by hyperaemic disc swelling with little or no optic nerve dysfunction; patients may be asymptomatic or report mild visual blurring, central acuity is usually preserved, and visual fields are often normal apart from enlargement of the physiological blind spot caused by the swollen optic nerve head, whereas reproducible superior arcuate defects represent anatomically organized retinal nerve fiber bundle loss and imply significant axonal dysfunction that is not characteristic of uncomplicated diabetic papillopathy. Diabetic papillopathy is a diagnosis of exclusion and may represent the mild end of an ischemic optic nerve head spectrum, with NAION at the more destructive end; the distinction rests mainly on functional impairment, because NAION produces a relative afferent pupillary defect in unilateral or asymmetric disease, dyschromatopsia, and altitudinal or arcuate field defects, followed by optic atrophy, while diabetic papillopathy typically resolves over several months with minimal permanent optic nerve damage.  \u003Cstrong\u003Ethe absence of an afferent pupillary defect (APD)\u003C/strong\u003E supports rather than opposes the diagnosis, especially when the involvement is bilateral and symmetrical, because an RAPD measures interocular asymmetry and may be absent even when both optic nerves are affected; \u003Cstrong\u003Eleakage from the optic disc telangiectasias on fluorescein angiography (FA)\u003C/strong\u003E is also compatible with diabetic papillopathy, as the dilated surface capillaries and swollen disc characteristically show fluorescein leakage, although these telangiectasias should be distinguished from neovascularization of the disc, which extends above the disc surface and may leak into the vitreous; and \u003Cstrong\u003Eno subjective visual complaints\u003C/strong\u003E is common because diabetic papillopathy is frequently identified incidentally and usually causes minimal functional disturbance. Diabetic papillopathy can occur in either type I or type II diabetes and is not strictly determined by glycaemic control or the severity of diabetic retinopathy; macular edema may coexist and, when present, may account for reduced acuity more than the optic nerve swelling itself.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1937,
    "Name": "Presumed amblyopia in an adult",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 25-year-old attending for a routine examination has best-corrected visual acuity of 20/20 in the right eye and 20/40 in the left eye, with no current visual symptoms, normal fundus appearances, and a longstanding history that the left eye has always seen less well. Which additional finding would be disproportionate to a diagnosis of uncomplicated amblyopia and therefore warrant further investigation for organic visual pathway disease?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea 3\u002B afferent pupillary defect (APD) in the left eye\u003C/strong\u003E, because the history of lifelong unilateral reduction in vision with a normal ocular examination is compatible with amblyopia, particularly if supported by childhood strabismus or significant anisometropia; however, a dense 3\u002B relative afferent pupillary defect would be markedly disproportionate to the relatively mild acuity difference of 20/20 versus 20/40 and should raise concern for an additional asymmetric organic lesion affecting the left retina, optic nerve, chiasm, or optic tract. Amblyopia is a developmental disorder of visual processing caused by abnormal visual experience during the sensitive period, and the diagnosis requires both an amblyogenic factor and exclusion of structural pathology; although small measurable RAPDs have been reported in some patients with unilateral amblyopia, their occurrence is variable and the relationship between RAPD magnitude and amblyopic acuity is inconsistent, so a pronounced RAPD must not simply be attributed to amblyopia without investigating for an organic afferent defect.  The accompanying mild reduction to 20/40 does not explain a 3\u002B RAPD, because RAPD magnitude generally reflects interocular asymmetry in afferent retinal or optic nerve function rather than Snellen acuity alone; severe optic neuropathy may occasionally preserve central acuity if peripheral or sectoral fibers are predominantly affected, making formal color testing, contrast sensitivity, automated perimetry, macular and retinal nerve fiber layer OCT, and careful optic nerve examination necessary even when the fundus initially appears normal. RAPD is classically associated with asymmetric optic neuropathies such as demyelinating, ischemic, compressive, infiltrative, hereditary, or glaucomatous disease and with extensive asymmetric retinal pathology.  \u003Cstrong\u003Ea 5 prism diopter microesotropia with a history of strabismus surgery as a child\u003C/strong\u003E provides a plausible childhood amblyogenic mechanism through longstanding foveal suppression and abnormal binocular development, while \u003Cstrong\u003Ea refraction of -2.00 diopters OD and -6.00 diopters OS\u003C/strong\u003E demonstrates substantial anisometropic myopia that could similarly produce left anisometropic amblyopia if uncorrected during childhood; neither finding automatically requires neuroimaging when the history, examination, and functional tests are otherwise coherent.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1938,
    "Name": "One-and-a-half syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old develops acute horizontal diplopia following a recent stroke. Visual acuity and pupillary responses are normal. Ocular motility testing shows that the left eye cannot move horizontally in either direction, while the right eye retains only abduction; vertical eye movements remain intact. In which listed anatomical region is the causative lesion most likely located?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Epons\u003C/strong\u003E, because this ocular motor pattern defines a \u003Cstrong\u003Eleft one-and-a-half syndrome\u003C/strong\u003E, produced by a unilateral lesion of the left dorsal pontine tegmentum involving both the left horizontal gaze centre, either the paramedian pontine reticular formation or abducens nucleus, and the adjacent left medial longitudinal fasciculus. Damage to the left horizontal gaze centre causes the \u201Cone,\u201D which is a complete conjugate gaze palsy toward the left: the left eye cannot abduct and the right eye cannot adduct during attempted left gaze. Damage to the left medial longitudinal fasciculus causes the additional \u201Chalf,\u201D an internuclear ophthalmoplegia during attempted right gaze: the left eye cannot adduct because the signal from the right abducens nucleus cannot reach the left medial rectus subnucleus, while the right eye can still abduct and may demonstrate abducting nystagmus. The left eye is therefore unable to move horizontally in either direction, while the only preserved horizontal movement is abduction of the right eye. Vertical gaze remains normal because the rostral midbrain vertical gaze centres, including the rostral interstitial nucleus of the medial longitudinal fasciculus and posterior commissure pathways, are not involved. One-and-a-half syndrome is classically caused by a unilateral pontine lesion, most commonly ischemic stroke in an older patient, although demyelination, hemorrhage, tumor, trauma, vascular malformation, and infection are recognized causes.  \u003Cstrong\u003Ecerebellum\u003C/strong\u003E lesions may cause gaze-evoked nystagmus, dysmetria, impaired smooth pursuit, or skew deviation but do not usually produce this precise horizontal conjugate gaze palsy plus ipsilateral internuclear ophthalmoplegia; \u003Cstrong\u003Emidbrain\u003C/strong\u003E lesions more typically affect vertical gaze, the third or fourth cranial nerve fascicles, or the rostral medial longitudinal fasciculus without simultaneously damaging the pontine horizontal gaze centre; and \u003Cstrong\u003Ethalamus\u003C/strong\u003E lesions may cause vertical gaze abnormalities, skew deviation, or higher-order visual deficits but do not contain the abducens nucleus or paramedian pontine reticular formation. A useful mnemonic is\u003Cstrong\u003E\u201COne plus half equals pons\u201D\u003C/strong\u003E: the \u201Cone\u201D is the ipsilateral horizontal gaze palsy, and the \u201Chalf\u201D is the ipsilateral internuclear ophthalmoplegia. If the lesion also involves the fascicles of the ipsilateral facial nerve as they loop around the abducens nucleus, the patient develops an ipsilateral lower motor neuron facial palsy, producing \u003Cstrong\u003Eeight-and-a-half syndrome: one-and-a-half plus cranial nerve VII\u003C/strong\u003E.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1939,
    "Name": "Acute myeloid leukemia with infiltrative optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 23-year-old with recently diagnosed acute myelogenous leukemia develops profound visual loss in the right eye over one day. Visual acuity is reduced to hand movements, a right relative afferent pupillary defect is present, and the right optic disc is pale, swollen, and irregularly nodular, while the left-eye examination is normal. What is the most appropriate immediate investigation and specialist referral?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECall a radiation oncology consult and order an MRI orbits STAT\u003C/strong\u003E, because acute profound monocular visual loss with a relative afferent pupillary defect and a pale, swollen, nodular optic nerve in a patient with acute myelogenous leukemia should be presumed to represent \u003Cstrong\u003Eleukemic infiltration of the optic nerve\u003C/strong\u003E until proved otherwise. Direct infiltration by malignant leukocytes can involve the optic nerve substance, nerve sheath, optic disc, or perineural tissues and may occur despite apparent hematological remission or negative bone marrow findings because the optic nerve can function as a pharmacological sanctuary with limited penetration of systemic chemotherapy. Optic nerve involvement constitutes central nervous system leukemia and is a neuro-oncological emergency, as treatment delay can lead to rapid, irreversible axonal loss and profound permanent visual impairment.  Urgent contrast-enhanced MRI of the brain and orbits with fat-suppressed, thin-section sequences is required to assess optic nerve enlargement, intrinsic or sheath enhancement, perineural infiltration, orbital extension, chiasmal involvement, and other central nervous system disease; however, normal imaging would not completely exclude leukemic infiltration if the clinical suspicion remained high. Further assessment commonly includes lumbar puncture for cerebrospinal fluid cytology and flow cytometry when safe, repeat bone marrow evaluation, complete blood count and peripheral smear, and systemic restaging, but negative CSF or marrow studies do not exclude isolated optic nerve infiltration. \u003Cstrong\u003EStart IV acyclovir immediately\u003C/strong\u003E would be appropriate for suspected severe herpetic infection in an immunocompromised patient, but the nodular infiltrative optic disc appearance and leukemia history provide no specific evidence for herpetic optic neuropathy or retinitis. \u003Cstrong\u003EOrder a chest / abdomen / pelvis CT\u003C/strong\u003E may form part of systemic restaging, but it does not take priority over urgent evaluation and treatment of the sight-threatening optic nerve lesion. \u003Cstrong\u003EOrder a STAT OCT of the optic nerve\u003C/strong\u003E would document disc swelling, peripapillary fluid, and structural involvement but would neither establish the full extent of infiltration nor alter the immediate need for MRI and oncological management.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1940,
    "Name": "Optic Neuritis Treatment Trial",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAccording to the Optic Neuritis Treatment Trial, which therapeutic benefit was demonstrated when acute optic neuritis was treated with high-dose intravenous methylprednisolone followed by oral prednisone, compared with placebo or standard-dose oral prednisone alone?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFaster visual recovery in the affected eye\u003C/strong\u003E, because the ONTT demonstrated that high-dose intravenous methylprednisolone followed by oral prednisone accelerated the early recovery of visual function after typical acute demyelinating optic neuritis, particularly during the first two weeks, but did not improve the eventual visual acuity, visual field, color vision, or contrast-sensitivity outcome compared with placebo. The original regimen was intravenous methylprednisolone 250 mg every six hours for three days, equivalent to 1 g daily, followed by oral prednisone 1 mg/kg/day for 11 days and then a short taper. By six months, the treatment groups had similarly favorable visual outcomes, and the early advantage of intravenous treatment had largely disappeared by approximately one month.  The intravenous regimen also produced a temporary reduction in the rate of conversion to clinically definite multiple sclerosis, particularly in patients whose baseline brain MRI showed two or more demyelinating white-matter lesions, but this protective effect diminished by approximately three years and did not translate into a sustained reduction in multiple sclerosis risk at ten years.  Standard-dose oral prednisone alone, at 1 mg/kg/day, neither accelerated recovery nor improved the final visual outcome and was associated with approximately twice the rate of recurrent optic neuritis compared with placebo or intravenous methylprednisolone followed by oral prednisone. Therefore, this standard-dose oral regimen should not be used alone for a first episode of typical demyelinating optic neuritis, although this historical finding should not be confused with contemporary bioequivalent high-dose oral corticosteroid regimens.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1941,
    "Name": "Physiologic anisocoria ",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EApproximately what proportion of otherwise healthy individuals demonstrate a physiologic anisocoria during routine penlight examination?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E20%\u003C/strong\u003E, because physiologic anisocoria, also termed simple or essential anisocoria, is a common benign normal variant affecting approximately one in five individuals. The interocular difference is generally small, usually no greater than 1 mm, with normal direct and consensual light responses, preserved near responses, and no associated ptosis, ocular motility deficit, visual dysfunction, or neurological abnormality. A difference of approximately 0.2\u20130.4 mm may be clinically detectable under suitable examination conditions, although the measured asymmetry can fluctuate between visits and the identity of the larger pupil may occasionally alternate.  Physiologic anisocoria classically remains approximately equal in bright and dim illumination because neither the parasympathetic constrictor pathway nor the sympathetic dilator pathway is pathologically impaired, but mild variation with illumination can occur and does not alone establish Horner syndrome. The is therefore to measure both pupils while the patient fixates at distance, compare the anisocoria in light and darkness, assess direct, consensual, and near responses, look for dilation lag, ptosis, ocular motor abnormalities, and structural iris disease, and review old photographs whenever available. Anisocoria that increases in darkness indicates relative failure of the smaller pupil to dilate and raises concern for sympathetic dysfunction such as Horner syndrome, whereas anisocoria that increases in bright light indicates relative failure of the larger pupil to constrict and suggests parasympathetic dysfunction, pharmacological mydriasis, or iris sphincter damage. Physiologic anisocoria is diagnosed when the asymmetry is small and stable, pupillary reactions are normal, and no pathological ocular or neurological features are present.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1942,
    "Name": "Idiopathic intracranial hypertension",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 30-year-old obese patient with a two-year history of headaches and bilateral optic disc edema has previously been diagnosed with idiopathic intracranial hypertension, although the earlier medical records are limited. Which additional symptom or examination finding would be atypical for uncomplicated idiopathic intracranial hypertension and should prompt reassessment for an alternative intracranial or neurological disorder?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Evertical binocular diplopia\u003C/strong\u003E, because the characteristic ocular motor disturbance in idiopathic intracranial hypertension is \u003Cstrong\u003Ehorizontal binocular diplopia\u003C/strong\u003E caused by unilateral or bilateral sixth nerve dysfunction; raised intracranial pressure can stretch the abducens nerve along its long intracranial course, particularly where the nerve passes over the petrous apex and through Dorello\u2019s canal, producing an esotropia that is greater at distance and on gaze toward the affected lateral rectus. Vertical binocular diplopia instead suggests dysfunction involving a cyclovertical muscle, the third or fourth cranial nerve, the otolith-ocular pathways causing skew deviation, the neuromuscular junction, or a restrictive orbital process, and therefore constitutes an atypical localizing neurological feature that should prompt reconsideration of an uncomplicated IIH diagnosis and renewed evaluation for cerebral venous sinus thrombosis, brainstem or posterior fossa disease, meningeal inflammation or infiltration, demyelination, and other secondary causes of raised intracranial pressure. Classic IIH manifestations include headache, pulsatile tinnitus, transient visual obscurations, papilledema, visual field loss, and horizontal diplopia from sixth nerve palsy or divergence insufficiency.  \u003Cstrong\u003Ebilateral superior arcuate scotomas\u003C/strong\u003E do not exclude IIH because papilledema can produce nerve fiber bundle defects, including arcuate loss, particularly as axonal injury progresses; early abnormalities more commonly include enlargement of the blind spot and inferonasal loss, but arcuate defects may occur in established disease.  \u003Cstrong\u003Ean afferent pupillary defect\u003C/strong\u003E may occur when papilledema and optic nerve damage are markedly asymmetric, despite the usual bilateral involvement, because an RAPD reflects unequal afferent function rather than the presence or absence of raised intracranial pressure. \u003Cstrong\u003Efrequent nausea and vomiting\u003C/strong\u003E are compatible with raised intracranial pressure and may accompany severe headache, so these symptoms do not dissuade from the diagnosis. Although rare reports describe third nerve palsy, fourth nerve palsy, skew deviation, and other atypical ocular motor manifestations in patients labelled as having IIH, such findings are not considered routine and should be treated as red flags until an alternative cause has been excluded.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1943,
    "Name": "Congenital nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich statement is inconsistent with the typical characteristics of congenital nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPredominantly a conjugate, vertical nystagmus\u003C/strong\u003E, because congenital nystagmus, now usually termed \u003Cstrong\u003Einfantile nystagmus syndrome\u003C/strong\u003E, is predominantly a bilateral, conjugate, horizontal ocular oscillation that develops at birth or within the first six months of life and typically remains horizontal in upgaze and downgaze; a predominantly vertical nystagmus is therefore atypical and should prompt investigation for an acquired central ocular motor disorder, retinal or optic nerve disease, medication toxicity, or another neurological cause rather than being attributed automatically to infantile nystagmus syndrome.  A \u003Cstrong\u003Enull point\u003C/strong\u003E or broader null zone is characteristic and represents the gaze position at which nystagmus intensity is lowest and foveation, and therefore visual acuity, is usually best; if this position lies away from primary gaze, the patient may adopt a compensatory face turn, chin elevation or depression, or occasionally head tilt to maintain the eyes within the null zone. Infantile nystagmus may demonstrate \u003Cstrong\u003Ependular, jerk, or more complex waveforms\u003C/strong\u003E, and the waveform may evolve during infancy from predominantly pendular oscillation to a jerk pattern with increasing-velocity slow phases and foveation periods.  Nystagmus intensity commonly increases with fixation effort, attention, fatigue, anxiety, and viewing distant targets; near fixation may dampen the oscillation through convergence, which explains why distance acuity may be more impaired than near acuity and why convergence prisms or base-out prism testing can be useful in selected patients. Oscillopsia is usually absent despite continuous eye movement because infantile onset permits sensory adaptation and periods of relatively stable foveation.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1944,
    "Name": "Relative afferent pupillary defect",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAssuming that all examination findings not specified are normal, which patient is least likely to show an RAPD when the afferent pupillary responses of the two eyes are compared using the swinging-flashlight test?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea 50-year old who awoke from a complicated 12-hour spine surgery with light perception vision in both eyes. Both optic nerves and the MRI of the brain/orbits are normal one day after surgery. A spinning OKN drum fails to elicit any nystagmus from either eye.\u003C/strong\u003E, because an RAPD is a \u003Cstrong\u003Erelative measure of interocular asymmetry\u003C/strong\u003E in afferent pupillomotor input rather than a direct measure of the absolute severity of bilateral visual loss; the postoperative patient has equally profound visual impairment in both eyes, absent optokinetic responses bilaterally, and normal-appearing optic discs immediately after prolonged spinal surgery, a pattern consistent with \u003Cstrong\u003Ebilateral posterior ischemic optic neuropathy\u003C/strong\u003E, in which ischemic injury occurs behind the optic nerve head and the discs may initially appear normal, with optic pallor developing only after several weeks. If both optic nerves are affected to a similar degree, illumination of either eye generates equally reduced afferent input, so the swinging-flashlight test detects no interocular difference and therefore no RAPD, although both eyes have severe absolute afferent dysfunction; this is why a normal swinging-flashlight test does not exclude severe bilateral symmetrical optic neuropathy.  The patient with traumatic near-total right optic nerve cupping has severe unilateral right optic neuropathy and would be expected to show a marked right RAPD; the patient with headache, jaw claudication, light-perception vision, and a pale swollen right disc has a presentation highly suspicious for arteritic anterior ischemic optic neuropathy from giant cell arteritis and would also have a dense right RAPD; and the child with a right optic nerve glioma, reduced right acuity, and right optic atrophy has asymmetric compressive optic neuropathy and should demonstrate a right RAPD. The key FRCS principle is that the RAPD reflects the \u003Cstrong\u003Edifference between the two afferent pathways\u003C/strong\u003E: unilateral or asymmetrical retinal or optic nerve dysfunction produces an RAPD, whereas severe but symmetrical bilateral disease may produce sluggish or reduced pupillary responses in both eyes without a relative defect.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1945,
    "Name": "Relative afferent pupillary defect",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the most accurate means to quantify the severity of an afferent pupillary defect (APD) in the clinic?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENeutral density filters\u003C/strong\u003E, because these filters permit the magnitude of an RAPD to be quantified objectively in \u003Cstrong\u003Elogarithmic units\u003C/strong\u003E by progressively reducing the intensity of light entering the eye with the stronger afferent response until the pupillary reactions elicited by stimulating either eye become equal. For example, in a patient with a right RAPD, the neutral density filter is placed over the normal left eye, beginning with the lowest density, commonly 0.3 log units, while the swinging-flashlight test is repeated; increasingly dense filters are then placed over the left eye until transfer of the light between the eyes no longer produces relative pupillary dilation, and the filter density required to neutralize the asymmetry represents the severity of the right RAPD.\u0026nbsp;\u003Cstrong\u003EThe time required for release of the pupil upon swinging a light to the abnormal eye\u003C/strong\u003E and \u003Cstrong\u003EThe speed and extent of reactivity of the pupil to light in the abnormal eye\u003C/strong\u003E contribute to descriptive clinical grading but are observer-dependent and do not produce a calibrated measurement of afferent asymmetry. \u003Cstrong\u003EThe visual acuity in the abnormal eye\u003C/strong\u003E cannot quantify an RAPD because central acuity assesses foveal resolution, whereas the pupillary light reflex integrates afferent input from a much wider area of the retina and optic nerve; therefore, profound peripheral or optic nerve dysfunction may produce a dense RAPD despite relatively preserved acuity, while severe but symmetrical bilateral visual loss may produce no RAPD. Quantification with neutral density filters is clinically valuable because serial changes can document progression or recovery of an asymmetric optic neuropathy or extensive retinal disorder alongside visual fields, color vision, contrast sensitivity, and OCT.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1946,
    "Name": "Rebound nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EPathology of what structure results in rebound nystagmus?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe cerebellum\u003C/strong\u003E, because rebound nystagmus is a characteristic cerebellar ocular motor sign that appears transiently when the eyes return toward primary position after sustained eccentric gaze, usually following gaze-evoked nystagmus. Stable eccentric gaze requires the pulse generated by the\u0026nbsp; saccadic system to be converted into a sustained step of tonic ocular motor innervation by the neural velocity-to-position integrator, which must counteract the elastic restoring forces of the orbital tissues that pull the eyes back toward primary position; the horizontal neural integrator includes the nucleus prepositus hypoglossi and medial vestibular nucleus, while the vertical and torsional integrator is centred around the interstitial nucleus of Cajal, but both systems are calibrated and stabilized by the vestibulocerebellum, particularly the flocculus and paraflocculus. Cerebellar dysfunction makes the integrator \u201Cleaky,\u201D so during eccentric gaze the eyes drift slowly back toward primary position and corrective fast phases return the eyes toward the eccentric target, producing gaze-evoked nystagmus; during sustained eccentric fixation, the cerebellum attempts to adapt to this persistent drift by shifting the gaze-holding set point, but when the eyes return to primary position, the adaptive signal briefly persists and becomes inappropriate, causing a transient slow drift toward the previously held eccentric position with corrective fast phases in the opposite direction. Rebound nystagmus therefore beats opposite to the preceding gaze-evoked nystagmus and usually decays within seconds. Rebound nystagmus is strongly associated with cerebellar loss of function, although physiological gaze-evoked and rebound nystagmus can occur in healthy individuals when testing is performed at excessive gaze eccentricities, particularly beyond approximately 30 degrees, so bedside assessment should avoid extreme end gaze.  \u003Cstrong\u003EThe midbrain\u003C/strong\u003E contains important vertical gaze and pupillary pathways but is not the characteristic localization for rebound nystagmus; \u003Cstrong\u003EThe paramedian pontine reticular formation\u003C/strong\u003E generates ipsilateral horizontal saccades, and a destructive lesion causes an ipsilateral horizontal conjugate gaze palsy rather than this adaptive gaze-holding abnormality; and \u003Cstrong\u003EThe frontal eye field\u003C/strong\u003E provides supranuclear drive for contralateral saccades, with a destructive lesion causing transient gaze deviation toward the cerebral lesion rather than rebound nystagmus. A useful sequence is: \u003Cstrong\u003Eeccentric gaze produces gaze-evoked nystagmus, return to primary position produces transient nystagmus in the opposite direction, and the combination points to cerebellar gaze-holding dysfunction.\u003C/strong\u003E \u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1947,
    "Name": "Cavernous sinus fistulas",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn both indirect low-flow dural fistulas and direct high-flow carotid-cavernous fistulas, retrograde transmission of cavernous sinus pressure through which orbital venous structure produces dilated, arterialized conjunctival and episcleral vessels?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe superior ophthalmic vein\u003C/strong\u003E, because both carotid-cavernous fistulas and cavernous sinus dural arteriovenous fistulas introduce arterial blood into the low-pressure cavernous sinus venous system, raising cavernous sinus pressure and reversing or obstructing normal orbital venous drainage. The superior ophthalmic vein is the principal venous channel draining the superior orbit into the cavernous sinus; reflux of arterialized blood from the cavernous sinus into this vein transmits elevated pressure anteriorly to the episcleral and conjunctival venous plexuses, producing the characteristic dilated, tortuous \u003Cstrong\u003Ecorkscrew vessels\u003C/strong\u003E, conjunctival chemosis, orbital congestion, proptosis, and sometimes pulsatile exophthalmos. Raised episcleral venous pressure also reduces aqueous outflow through Schlemm canal and may cause secondary ocular hypertension or glaucoma. Imaging commonly demonstrates enlargement and early enhancement of the superior ophthalmic vein, and reversal of flow can be detected with Doppler imaging, although superior ophthalmic vein enlargement is supportive rather than specific because cavernous sinus thrombosis and other causes of impaired orbital venous drainage can produce a similar appearance.  The \u003Cstrong\u003Einferior ophthalmic vein\u003C/strong\u003E also communicates with the cavernous sinus and pterygoid plexus and may contribute to orbital drainage, but superior ophthalmic venous reflux is the classic mechanism and radiological marker associated with anterior orbital and conjunctival arterialization. The \u003Cstrong\u003Epterygoid venous plexus\u003C/strong\u003E provides an alternative posterior-inferior drainage route from the cavernous sinus and does not directly account for the characteristic anterior conjunctival corkscrew vessels. The \u003Cstrong\u003Esphenoparietal venous plexus\u003C/strong\u003E drains superficial cerebral and dural venous territories toward the cavernous sinus rather than serving as the principal orbital venous conduit responsible for conjunctival congestion.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1948,
    "Name": "Junctional scotoma",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 45-year-old notices that vision in the left eye is dimmer and more blurred than in the right eye. There is no ocular pain, headache, or associated neurological symptom. Best-corrected visual acuity is 20/20 in the right eye and 20/100 with eccentric fixation in the left eye; the pupils are equal and reactive, but a dense left relative afferent pupillary defect is present. Both optic discs have sharp margins, small physiological cups, and temporal pallor. Perimetry is shown below. Which listed disorder most likely accounts for this pattern of visual dysfunction?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-18-8d23ed48-6ec5-4893-8de8-a12aae8848cb.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPituitary adenoma\u003C/strong\u003E, because the combination of severe central and temporal field loss in the left eye with a superior temporal defect in the right eye constitutes a \u003Cstrong\u003Ejunctional scotoma\u003C/strong\u003E, localizing the lesion to the junction of the left optic nerve and the anterior optic chiasm. Compression of the left optic nerve accounts for the reduced left visual acuity, eccentric fixation, temporal pallor, dense left RAPD, and extensive left field loss, while involvement of crossing inferonasal retinal fibers from the right eye produces the right superotemporal defect; this pattern has traditionally been explained by compression of \u003Cstrong\u003EWilbrand\u2019s knee\u003C/strong\u003E, although modern anatomical work suggests that the clinically observed junctional field pattern may result from combined compression of the ipsilateral optic nerve and adjacent anterior chiasmal crossing fibers rather than a consistent physiological loop of contralateral fibers into the optic nerve. Sellar and parasellar masses are the principal causes of junctional scotoma, and \u003Cstrong\u003Epituitary adenoma is the most common\u003C/strong\u003E, typically enlarging superiorly from the sella to compress the optic nerve-chiasm junction or the inferior surface of the chiasm; functioning tumors may present earlier with endocrine symptoms, whereas nonfunctioning macroadenomas may remain clinically silent until visual loss, field defects, or headache develops.  \u003Cstrong\u003EArteritic anterior ischemic optic neuropathy\u003C/strong\u003E would usually occur in an older patient with sudden profound visual loss, a pale swollen optic disc during the acute phase, and often systemic features of giant cell arteritis; the sharply marginated discs and contralateral superotemporal field defect do not fit that diagnosis. \u003Cstrong\u003ETemporal lobe tumor\u003C/strong\u003E classically affects Meyer\u2019s loop and produces a contralateral superior homonymous quadrantanopia, with corresponding defects on the same side of visual space in both eyes, rather than asymmetric monocular optic nerve dysfunction with a junctional pattern. \u003Cstrong\u003EGlaucomatous optic neuropathy\u003C/strong\u003E produces progressive neuroretinal rim thinning and cupping with arcuate or nasal-step defects respecting the horizontal meridian; the cup-to-disc ratio of 0.3, temporal pallor, marked acuity and color-related afferent dysfunction, and field loss respecting the vertical meridian argue strongly against glaucoma.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1949,
    "Name": "Heerfordt syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 30-year-old presents with a one-week history of malaise, fever, photophobia, and bilateral lower motor neuron facial weakness. Ocular examination demonstrates bilateral nongranulomatous uveitis, while the external photograph is below. Which named syndrome is defined by this combination of manifestations?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-18-d02d43db-f05b-42d7-a3c6-631db272c6d6.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EHeerfordt syndrome\u003C/strong\u003E, because the combination of \u003Cstrong\u003Euveitis, parotid-gland enlargement, facial nerve palsy, and fever\u003C/strong\u003E constitutes Heerfordt-Waldenstr\u00F6m syndrome, also called \u003Cstrong\u003Euveoparotid fever\u003C/strong\u003E, a distinctive but uncommon manifestation of sarcoidosis. The complete syndrome contains all four components, whereas an incomplete form may be diagnosed when only some of the principal features are present. Facial weakness results from granulomatous involvement of the facial nerve and may be unilateral, sequential, or bilateral; parotid involvement is frequently bilateral and may be painless, while ocular inflammation most commonly takes the form of anterior uveitis, although intermediate, posterior, or panuveitic involvement can occur.  Although sarcoid uveitis is classically granulomatous with mutton-fat keratic precipitates and iris nodules, a nongranulomatous anterior uveitis does not exclude ocular sarcoidosis, so the absence of granulomatous slit-lamp features should not outweigh the highly characteristic systemic constellation. Heerfordt syndrome strongly suggests sarcoidosis but is not, by itself, definitive histopathological proof; evaluation should exclude infectious and inflammatory mimics and assess systemic involvement with chest imaging, serum calcium and organ-function testing, while tissue biopsy from an accessible involved site should demonstrate \u003Cstrong\u003Enoncaseating granulomas\u003C/strong\u003E after exclusion of tuberculosis, fungal infection, lymphoma, and other granulomatous disorders.  \u003Cstrong\u003ELofgren syndrome\u003C/strong\u003E is a different acute sarcoid phenotype characterized by erythema nodosum, bilateral hilar lymphadenopathy, and ankle-predominant periarthritis or arthritis, rather than the uveoparotid-facial palsy pattern. \u003Cstrong\u003ERaymond syndrome\u003C/strong\u003E is a ventral pontine syndrome producing an ipsilateral sixth nerve palsy with contralateral hemiparesis, while \u003Cstrong\u003EClaude syndrome\u003C/strong\u003E results from a dorsal midbrain lesion involving the third nerve fascicle and superior cerebellar peduncular pathways, producing an ipsilateral third nerve palsy with contralateral cerebellar ataxia. A useful mnemonic is\u003Cstrong\u003E\u201CPUFF\u201D\u003C/strong\u003E, representing \u003Cstrong\u003EParotid enlargement, Uveitis, Facial palsy, and Fever\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1950,
    "Name": "Cranial dysinnervation disorders",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed ocular motor disorder, unlike the other conditions is not associated with congenital absence or developmental malformation of a cranial nerve nucleus or its peripheral nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESuperior oblique myokymia\u003C/strong\u003E, because superior oblique myokymia is an acquired ocular motor hyperexcitability disorder characterized by brief, recurrent, unilateral, high-frequency, low-amplitude contractions of the superior oblique muscle, producing monocular torsional or vertical oscillopsia and sometimes diplopia; the underlying mechanism is thought to involve focal hyperexcitability of the trochlear nerve, possibly from segmental demyelination and ephaptic transmission near its root-exit zone, with vascular compression by the superior cerebellar artery or, much less commonly, a cyst, tumor, or previous trauma implicated in selected cases, but there is no congenital agenesis of the trochlear nucleus.  In contrast, \u003Cstrong\u003ECongenital fibrosis of the extraocular muscles\u003C/strong\u003E belongs to the congenital cranial dysinnervation disorders and reflects abnormal development of the ocular motor nuclei, cranial nerves, or their axonal guidance pathways, particularly involving the oculomotor nerve and its innervated muscles; although the older description emphasized oculomotor nuclear agenesis, modern genetic understanding includes developmental abnormalities caused by pathogenic variants.  \u003Cstrong\u003EDuane syndrome\u003C/strong\u003E is also a congenital cranial dysinnervation disorder, most commonly associated with hypoplasia or absence of the abducens nucleus or nerve and aberrant innervation of the lateral rectus by branches of the oculomotor nerve; this produces limited abduction and/or adduction, with medial and lateral rectus co-contraction causing globe retraction and palpebral fissure narrowing during attempted adduction. \u003Cstrong\u003EMobius syndrome\u003C/strong\u003E is characterized principally by congenital dysfunction or developmental absence of the abducens and facial nuclei or nerves, producing bilateral abduction limitation with esotropia and congenital bilateral lower motor neuron facial weakness.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1951,
    "Name": "Idiopathic intracranial hypertension",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the listed visual field abnormalities, which pattern occurs most frequently in patients with idiopathic intracranial hypertension, particularly in association with papilloedema?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Epartial arcuate defects\u003C/strong\u003E, because visual field loss in idiopathic intracranial hypertension primarily reflects pressure-related dysfunction of retinal ganglion-cell axons at the swollen optic nerve head, producing defects that follow retinal nerve fibre bundle anatomy; analysis of 660 baseline visual fields from 165 participants in the Idiopathic Intracranial Hypertension Treatment Trial showed that localized nerve fibre bundle-type loss predominated, and a \u003Cstrong\u003Epartial arcuate defect combined with enlargement of the blind spot\u003C/strong\u003E was the single most frequent classification, accounting for approximately 31.5% of hemifield classifications, with localized inferior hemifield loss more common than superior loss.  Enlargement of the physiological blind spot is a classic early finding because elevation of the peripapillary retina displaces the functional disc margin outward, but enlarged blind spot alone was less frequent than partial arcuate nerve fibre bundle loss in the IIHTT cohort. With increasing severity or chronicity, papilloedema can produce nasal steps, arcuate defects, paracentral loss, generalized constriction, and eventually severe diffuse field depression or a residual central island from secondary optic atrophy; central visual acuity is often preserved until late because papillomacular bundle function is relatively resistant during the earlier stages. The IIHTT clinical baseline report similarly identified an enlarged blind spot with a partial inferior arcuate defect as the typical common field pattern.  \u003Cstrong\u003Eparacentral scotomas\u003C/strong\u003E occur but were considerably less common, \u003Cstrong\u003Enasal steps\u003C/strong\u003E may develop as part of nerve fibre bundle damage but were not the predominant isolated pattern, and \u003Cstrong\u003Ealtitudinal\u003C/strong\u003E loss should raise stronger consideration of anterior ischaemic optic neuropathy or another sectoral optic neuropathy when the clinical context is not otherwise typical of IIH.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1952,
    "Name": "Infiltrative optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich listed disorder is not classically associated with infiltration of the optic nerve or its sheath?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Evaricella zoster virus (VZV)\u003C/strong\u003E, because infiltrative optic neuropathy results from direct invasion or accumulation of neoplastic cells, inflammatory granulomas, or infectious granulomatous tissue within the optic nerve, optic nerve sheath, or adjacent meninges, often causing rapidly progressive visual loss, dyschromatopsia, a relative afferent pupillary defect, visual field loss, optic disc swelling or nodular infiltration, and optic nerve or sheath enlargement and enhancement on contrast-enhanced MRI. \u003Cstrong\u003Elymphoma\u003C/strong\u003E is a recognized neoplastic cause and may infiltrate the optic nerve, sheath, chiasm, or leptomeninges, sometimes producing severe visual loss despite an initially normal fundus; cerebrospinal fluid cytology may be negative, so repeated CSF analysis, flow cytometry, systemic imaging, and occasionally biopsy may be required when suspicion remains high.  \u003Cstrong\u003Esarcoidosis\u003C/strong\u003E is also a well-established infiltrative cause because noncaseating granulomatous inflammation may involve the optic nerve, optic chiasm, nerve sheath, orbital apex, or meninges, producing optic disc swelling, optic perineuritis, compressive-appearing optic neuropathy, or optic atrophy.  \u003Cstrong\u003Etuberculosis (TB)\u003C/strong\u003E can produce granulomatous infiltration of the optic nerve or sheath, including an optic nerve tuberculoma with nerve thickening, enhancement, and occasionally ring enhancement with central necrosis.  In contrast, \u003Cstrong\u003Evaricella zoster virus (VZV)\u003C/strong\u003E can certainly cause optic neuropathy, but the principal mechanisms are inflammatory optic neuritis, perineuritis, or VZV vasculopathy producing ischemic injury to the optic nerve rather than direct infiltrative replacement of the nerve by cellular or granulomatous tissue; VZV may also cause retinal necrosis, orbital inflammation, cranial neuropathies, and ocular motor disturbances, but it is not classified as a typical cause of infiltrative optic neuropathy.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1953,
    "Name": "Leber hereditary optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the listed mitochondrial DNA point mutations associated with Leber hereditary optic neuropathy, which is the most prevalent primary pathogenic mutation worldwide?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E11778\u003C/strong\u003E, because the mitochondrial DNA point mutation \u003Cstrong\u003Em.11778\u003C/strong\u003E\u0026nbsp;\u0026nbsp;is the most common primary pathogenic mutation causing Leber hereditary optic neuropathy, accounting for approximately 70% of cases worldwide.  The three principal LHON mutations are \u003Cstrong\u003Em.11778\u003C/strong\u003E, \u003Cstrong\u003Em.3460\u003C/strong\u003E, and \u003Cstrong\u003Em.14484\u003C/strong\u003E, which together account for approximately 90% of molecularly confirmed cases and are therefore routinely included in initial genetic testing panels; \u003Cstrong\u003E5780\u003C/strong\u003E is not one of the three major primary LHON mutations.  LHON is transmitted through mitochondrial DNA and therefore follows \u003Cstrong\u003Ematernal inheritance\u003C/strong\u003E: a carrier mother may transmit the mutation to all children, whereas an affected father does not transmit the mutation to offspring; penetrance is incomplete and sex-dependent, so only a proportion of carriers become visually affected, with environmental mitochondrial stressors such as smoking and heavy alcohol exposure increasing the likelihood of conversion. Clinically, LHON usually causes painless, subacute central visual loss in one eye followed by the fellow eye within weeks or months, with dyschromatopsia and central or cecocentral scotomata; the acute fundus may show peripapillary telangiectatic microangiopathy, vascular tortuosity, and retinal nerve fibre layer pseudoedema without fluorescein leakage, followed later by temporal and then diffuse optic atrophy. The \u003Cstrong\u003Em.14484\u003C/strong\u003E\u0026nbsp;mutation generally carries the most favourable probability of spontaneous visual recovery, whereas \u003Cstrong\u003Em.11778\u003C/strong\u003E\u0026nbsp;is both the most common mutation and traditionally associated with a less favourable natural visual prognosis.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1954,
    "Name": "Traumatic optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn otherwise healthy 25-year-old sustains blunt trauma to the left side of the face and immediately reports monocular visual loss. Best-corrected visual acuity is 20/20 in the right eye and 20/150 in the left eye. Pupillary light reactions are brisk and symmetrical without a relative afferent pupillary defect; ocular motility and confrontation fields are normal, and slit-lamp and fundus examinations show no ocular abnormality. Which finding is incompatible with unilateral traumatic optic neuropathy ?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EHe did not demonstrate an APD\u003C/strong\u003E, because unilateral traumatic optic neuropathy causing genuine reduction of left-eye vision to 20/150 should produce a left relative afferent pupillary defect when the fellow retina and optic nerve are normal; traumatic injury reduces afferent pupillomotor input from the affected eye, so during the swinging-flashlight test both pupils constrict normally when the right eye is illuminated but constrict less, or appear to redilate, when the light is transferred to the left eye. The RAPD is therefore the most important objective bedside sign supporting unilateral indirect traumatic optic neuropathy and may remain detectable even when the fundus appears normal.  Visual acuity in traumatic optic neuropathy is highly variable, ranging from mild reduction to no light perception, so \u003Cstrong\u003EHis vision should be worse than 20/150 with TON\u003C/strong\u003E is incorrect. Absence of optic disc edema does not exclude the diagnosis because the common indirect form usually injures the intracanalicular or posterior orbital optic nerve through forces transmitted from frontal or facial trauma; the optic disc is therefore often normal acutely, with pallor developing after several weeks, whereas visible disc swelling is more likely with anterior direct injury.  A grossly full confrontation field also does not exclude traumatic optic neuropathy because confrontation testing is insensitive to central, cecocentral, paracentral, or subtle nerve-fibre-bundle defects, and formal automated or kinetic perimetry may detect abnormalities that finger-counting confrontation misses. The lack of an RAPD in this case is particularly important because the reported visual loss is unilateral and substantial, the right afferent pathway is normal, and no retinal or media abnormality explains the interocular acuity difference; this internal inconsistency should prompt careful reassessment of refraction, macular function, testing reliability, and possible functional visual loss rather than acceptance of traumatic optic neuropathy.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
    "ExamAnswers": null
  },
  {
    "Id": 1955,
    "Name": "Cocaine testing for unilateral Horner syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient with a right upper-lobe lung malignancy has mild right upper-lid ptosis and a smaller right pupil, with the anisocoria becoming more pronounced in darkness. When cocaine 10% is used to confirm suspected unilateral Horner syndrome, which listed post-instillation finding most accurately defines a positive test?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E\u0026gt; 1 mm anisocoria 30 minutes after instillation of two drops of cocaine 10% OU\u003C/strong\u003E, because cocaine confirms Horner syndrome by blocking reuptake of norepinephrine from the synaptic cleft at the junction between the postganglionic sympathetic nerve terminal and the iris dilator muscle; in the normal left eye, continuously released norepinephrine therefore accumulates and produces substantial pupillary dilation, whereas interruption of the right oculosympathetic pathway means that little norepinephrine reaches the right iris dilator, so cocaine has little substrate on which to act and the affected pupil dilates poorly. The diagnostically meaningful endpoint is therefore the \u003Cstrong\u003Eabsolute anisocoria after cocaine has been instilled into both eyes\u003C/strong\u003E, rather than the amount of dilation of the suspected eye in isolation; post-cocaine anisocoria of approximately 1 mm or greater strongly supports Horner syndrome, although published thresholds vary between more than 0.5 mm and approximately 0.8\u20131.0 mm depending on the protocol and population studied.  Cocaine must be placed in \u003Cstrong\u003Eboth eyes\u003C/strong\u003E because the normal fellow pupil acts as the internal control, allowing direct comparison under identical conditions; testing only the right eye cannot reliably distinguish sympathetic denervation from poor drug penetration, dark iris pigmentation, mechanical iris restriction, inadequate dosage, or individual variability in pharmacological response. \u003Cstrong\u003EReversal of anisocoria\u003C/strong\u003E is not the expected cocaine response: this is characteristic of \u003Cstrong\u003Eapraclonidine\u003C/strong\u003E, whose weak \u03B11-agonist effect becomes pronounced in the denervated Horner pupil because of postsynaptic adrenergic supersensitivity, allowing the affected pupil to dilate more than the normal pupil and potentially improving the ptosis through stimulation of M\u00FCller muscle. Cocaine confirms the presence of oculosympathetic dysfunction but does not localize it to the central, preganglionic, or postganglionic neuron; in this clinical setting, an apical lung lesion may interrupt the second-order sympathetic fibers ascending over the lung apex before the superior cervical ganglion, producing a preganglionic Horner syndrome and possibly associated lower brachial plexus symptoms in Pancoast syndrome. A high-yield distinction is: \u003Cstrong\u003Ecocaine enlarges the anisocoria, while apraclonidine reverses the anisocoria\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1956,
    "Name": "Ductions and versions",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 20-year-old has intermittent binocular diplopia during prolonged near work when fatigued. Old photographs demonstrate a longstanding right head tilt from early childhood. Examination shows a left hypertropia that increases in downgaze and right gaze. Monocular assessment of each eye reveals an apparently full range of movement, whereas binocular gaze testing demonstrates a prominent elevation of the left eye in far right gaze. How should the duction and version findings be classified?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENormal ductions with abnormal versions\u003C/strong\u003E, because \u003Cstrong\u003Eductions\u003C/strong\u003E assess the movement of each eye separately with the fellow eye occluded, whereas \u003Cstrong\u003Eversions\u003C/strong\u003E assess conjugate binocular movements with both eyes viewing; the stem explicitly states that ocular rotations appear full during monocular testing, so the ductions are normal, but binocular testing demonstrates an abnormal upshoot of the left eye in right gaze, so the versions are abnormal. The overall pattern suggests a decompensated congenital left fourth nerve palsy: the left hypertropia is greater in right gaze, where the left eye is adducted and the weak left superior oblique should depress it, and is greater in downgaze, where failure of superior oblique depression becomes more evident; the longstanding right head tilt is a compensatory posture that places the head away from the affected left side, reducing the vertical and torsional misalignment, while intermittent symptoms during late-night reading reflect eventual failure of the unusually large vertical fusional amplitudes commonly acquired in congenital fourth nerve palsy.  The prominent left-eye upshoot in far right gaze represents apparent \u003Cstrong\u003Eleft inferior oblique overaction\u003C/strong\u003E, which frequently develops secondary to longstanding left superior oblique weakness and is most evident in adduction because the inferior oblique has its greatest elevating effect when the eye is adducted; this abnormality may be subtle or missed when each eye is examined separately but becomes conspicuous during versions because binocular fixation invokes \u003Cstrong\u003EHering\u2019s law of equal innervation\u003C/strong\u003E to the left inferior oblique and its yoke muscle, the right superior rectus, accentuating the asymmetric elevation. Secondary inferior oblique overaction in congenital fourth nerve palsy is well recognized and should be distinguished from primary inferior oblique overaction by the accompanying positive head-tilt pattern, hypertropia maximal in contralateral gaze, and other evidence of superior oblique dysfunction.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1957,
    "Name": "Bilateral optic disc swelling",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 18-year-old taking isotretinoin develops a new headache over three weeks and is found to have bilateral optic disc swelling. Central visual acuity, pupillary responses, ocular motility, and static visual fields remain normal. Fundus examination is shown below. What is the most appropriate next step in the investigation and management of this presentation?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-19-1031b495-37e7-4aaf-9b08-6bf8a6f6a3cb.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMRI / MRV\u003C/strong\u003E, because the fundus photographs show bilateral optic disc edema with venous congestion and obscuration of vessels as the vessels cross the elevated disc margins, with a possible inferior peripapillary hemorrhage in the right eye. In the setting of a new headache, this appearance should be managed as \u003Cstrong\u003Epapilledema from raised intracranial pressure until proved otherwise\u003C/strong\u003E. Preserved acuity, normal pupils, full ocular movements, and normal static perimetry do not exclude early papilledema because central visual function may remain normal initially. Papilledema refers specifically to optic disc swelling caused by increased intracranial pressure and requires urgent investigation for potentially serious intracranial disease.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EMRI of the brain with contrast should be performed urgently to exclude:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EAn intracranial mass or infiltrative lesion\u003C/li\u003E\n\u003Cli\u003EHydrocephalus\u003C/li\u003E\n\u003Cli\u003EIntracranial hemorrhage\u003C/li\u003E\n\u003Cli\u003EMeningeal inflammation or infiltration\u003C/li\u003E\n\u003Cli\u003EStructural abnormalities causing raised intracranial pressure\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EMR venography should be obtained concurrently to exclude \u003Cstrong\u003Ecerebral venous sinus thrombosis\u003C/strong\u003E, which can closely mimic idiopathic or medication-induced intracranial hypertension. MRI and MRV should precede lumbar puncture because the presence of a mass lesion, obstructive hydrocephalus, or another cause of dangerous intracranial pressure gradients must first be excluded.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIf MRI and MRV reveal no causative structural or venous abnormality, the next investigation is a \u003Cstrong\u003Elumbar puncture\u003C/strong\u003E, performed in the lateral decubitus position, to measure the opening pressure and analyze the cerebrospinal fluid. A diagnosis of idiopathic or medication-associated intracranial hypertension requires elevated opening pressure with normal cerebrospinal fluid composition and no alternative cause identified by neuroimaging.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIsotretinoin is a vitamin A derivative and is a recognized precipitant of secondary intracranial hypertension. The medication should therefore be discontinued in liaison with the prescribing clinician while the urgent investigation proceeds. This presentation should not immediately be labelled idiopathic intracranial hypertension because a plausible medication-related secondary cause is present, and structural and venous causes have not yet been excluded.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Eacetaminophen or a NSAID for her mild headaches\u003C/strong\u003E would treat only the symptom and could delay investigation of potentially sight-threatening or life-threatening raised intracranial pressure. \u003Cstrong\u003Eoral acetazolamide for her mild headaches\u003C/strong\u003E is premature because acetazolamide is used to lower intracranial pressure and protect visual function, not simply as headache analgesia, and the cause of the disc edema must first be assessed. \u003Cstrong\u003Elumbar puncture\u003C/strong\u003E is required after reassuring neuroimaging, but it is not the first step when intracranial mass, hydrocephalus, or venous sinus thrombosis has not yet been excluded.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1958,
    "Name": "Autosomal dominant optic atrophy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong the listed inherited disorders that may cause optic nerve dysfunction and progressive visual loss, which is recognized as the most prevalent hereditary optic neuropathy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eautosomal dominant optic atrophy (ADOA)\u003C/strong\u003E, because ADOA, also known as \u003Cstrong\u003EKjer optic atrophy\u003C/strong\u003E, is regarded as the most common inherited optic neuropathy encountered in clinical practice, with reported prevalence estimates ranging from approximately 1 in 10,000 to 1 in 50,000 depending on the population studied.  Most molecularly confirmed cases are caused by heterozygous pathogenic variants in \u003Cstrong\u003EOPA1 on chromosome 3q28\u2013q29\u003C/strong\u003E, although OPA1 variants account for only approximately 50\u201360% of clinically diagnosed dominant optic atrophy and rarer genetic causes include OPA3-associated disease. The typical phenotype is insidious, bilateral, relatively symmetrical visual loss beginning in the first or second decade, often with reduced central acuity, dyschromatopsia, central or cecocentral scotomata, and temporal optic disc pallor or focal temporal excavation; severity is highly variable within and between families because penetrance and expressivity are incomplete, and some patients remain mildly affected while others develop substantial visual disability. Approximately one-fifth of affected OPA1 carriers may develop an \u003Cstrong\u003EADOA-plus phenotype\u003C/strong\u003E, including sensorineural hearing loss, peripheral neuropathy, ataxia, myopathy, or chronic progressive external ophthalmoplegia.  \u003Cstrong\u003ELeber\u0027s hereditary optic neuropathy (LHON)\u003C/strong\u003E is another major hereditary mitochondrial optic neuropathy, but it typically causes painless, subacute, sequential central visual loss, predominantly in young adults, and follows maternal mitochondrial inheritance rather than autosomal dominant transmission. \u003Cstrong\u003EWolfram syndrome (DIDMOAD)\u003C/strong\u003E is usually an autosomal recessive \u003Cstrong\u003EWFS1-related\u003C/strong\u003E neurodegenerative disorder characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, while \u003Cstrong\u003EBehr syndrome\u003C/strong\u003E describes a syndromic optic atrophy phenotype associated with neurological abnormalities such as ataxia, pyramidal signs, peripheral neuropathy, spasticity, and developmental impairment rather than the most prevalent isolated hereditary optic neuropathy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1959,
    "Name": "Postoperative bilateral visual loss",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 60-year-old with no previous ocular disease develops profound bilateral visual loss immediately after a prolonged coronary artery bypass procedure. Visual acuity is reduced to hand movements in both eyes, the pupillary responses are sluggish with light-near dissociation, and the remainder of the neuro-ophthalmic examination, including the acute dilated fundus appearance, is normal. Which diagnosis best explains this postoperative visual loss?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPosterior ischemic optic neuropathy\u003C/strong\u003E, because the immediate, profound, bilateral visual loss following prolonged cardiac surgery, together with severely impaired pupillary responses and an initially normal optic disc appearance, localizes the ischemic injury to the \u003Cstrong\u003Eretrobulbar portion of both optic nerves\u003C/strong\u003E rather than the visible optic nerve heads. Perioperative posterior ischemic optic neuropathy results from inadequate oxygen delivery to the posterior optic nerves during a prolonged operation, usually through a multifactorial interaction between systemic hypotension, anemia or haemodilution, hypovolemia, reduced cardiac output, prolonged surgical duration, vascular disease, and impaired autoregulation; cardiac and lengthy prone spinal operations are the principal surgical settings in which perioperative ischemic optic neuropathy is recognized.  The acute fundus remains normal because the ischemic segment lies behind the lamina cribrosa, but optic disc pallor typically develops after several weeks as retrograde axonal degeneration reaches the optic nerve head. This distinguishes posterior ischemic optic neuropathy from \u003Cstrong\u003EArteritic anterior ischemic optic neuropathy\u003C/strong\u003E and \u003Cstrong\u003ENon-arteritic anterior ischemic optic neuropathy\u003C/strong\u003E, both of which involve the anterior optic nerve and should produce visible acute disc edema, with arteritic disease typically causing chalky pallid swelling and non-arteritic disease usually producing hyperemic or segmental swelling, often with peripapillary hemorrhages. The bilateral light-near dissociation is compatible with severe symmetrical optic neuropathy because the diminished afferent input produces a weak light response while the near response may remain relatively preserved through a different supranuclear pathway; a relative afferent pupillary defect may be absent when both optic nerves are affected equally, despite devastating bilateral disease. \u003Cstrong\u003EDorsal midbrain syndrome\u003C/strong\u003E can cause light-near dissociation, but it would usually be accompanied by supranuclear upgaze limitation, convergence-retraction movements, eyelid retraction, or skew deviation and would not adequately explain sudden bilateral hand-movements vision after cardiac bypass with a normal fundus.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1960,
    "Name": "Alternating abducting hypertropia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a gaze-dependent vertical deviation that reverses between the two eyes: the right eye becomes hypertropic in right gaze, while the left eye becomes hypertropic in left gaze. Which listed diagnosis most accurately accounts for this pattern of alternating abducting hypertropia?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESkew deviation\u003C/strong\u003E, because the hypertropic eye in each lateral gaze is the \u003Cstrong\u003Eabducting eye\u003C/strong\u003E, producing a right hypertropia in right gaze and a left hypertropia in left gaze, a pattern termed \u003Cstrong\u003Ealternating skew deviation\u003C/strong\u003E or \u003Cstrong\u003Ealternating abducting hypertropia\u003C/strong\u003E. Skew deviation is a supranuclear vertical misalignment caused by disruption of prenuclear graviceptive vestibulo-ocular pathways linking the otolith organs, vestibular nuclei, cerebellum, medial longitudinal fasciculus, and rostral midbrain structures responsible for vertical alignment and ocular torsion; unlike a single cyclovertical muscle palsy, the deviation may be comitant, incomitant, alternating, or gaze dependent. Alternating abducting hypertropia is particularly associated with lesions affecting the cerebellar flocculus or paraflocculus, cerebellar pathways, cervicomedullary junction, or pretectal region, and may accompany downbeat nystagmus, gaze-evoked nystagmus, or ataxia.\u0026nbsp;\u003Cstrong\u003EBilateral CN IV palsy\u003C/strong\u003E produces the opposite alternating pattern, an \u003Cstrong\u003Eadducting hypertropia\u003C/strong\u003E: the right eye becomes hypertropic in left gaze and the left eye becomes hypertropic in right gaze because superior oblique weakness is maximal when the affected eye is adducted; bilateral fourth nerve palsy is also commonly associated with excyclotorsion, a V-pattern, and hypertropia alternating with ipsilateral head tilt. \u003Cstrong\u003Eunilateral complete CN III palsy\u003C/strong\u003E produces ptosis, ophthalmoplegia, and a fixed \u201Cdown and out\u201D eye, rather than symmetric alternating hypertropia in horizontal gaze, although a partial third nerve palsy affecting vertical recti may create gaze-dependent vertical deviations. \u003Cstrong\u003EBilateral inferior rectus restriction\u003C/strong\u003E would also produce the reverse pattern because restriction is most evident when the inferior rectus must lengthen during elevation of the abducted eye, resulting in relative hypotropia of the abducting eye and therefore apparent hypertropia of the fellow adducting eye. A useful distinction is: \u003Cstrong\u003Eabducting eye hypertropic indicates alternating skew; adducting eye hypertropic suggests bilateral fourth nerve palsy\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1961,
    "Name": "Visual extinction",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFollowing a recent right parietal lobe stroke, a patient correctly detects finger-counting targets presented individually in every visual-field quadrant of either eye. When targets are presented simultaneously in the right and left visual hemifields, however, the patient consistently fails to perceive the target on the left side in both eyes. Which term describes this stimulus-dependent visual deficit?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Eextinction\u003C/strong\u003E, because visual extinction is an attentional disorder in which a patient can identify a contralesional stimulus when it is presented alone but fails to report that same stimulus when an ipsilesional stimulus is presented simultaneously; in this case, the patient detects isolated targets throughout both visual fields, demonstrating that the primary retinogeniculocalcarine pathways are functionally intact, but during double simultaneous stimulation the right-sided target competes successfully for attentional resources and the left-sided target is \u201Cextinguished,\u201D creating the appearance of a left homonymous field defect. Visual extinction is most commonly associated with damage to the nondominant right parietal attention network and affects the visual hemispace contralateral to the lesion, although analogous extinction may occur in tactile or auditory modalities; the finding is related to, but milder and more stimulus-dependent than, hemispatial neglect, because the patient may attend to the left side adequately when no competing right-sided stimulus is present. Research in patients with unilateral parietal lesions confirms that extinction is maximal when contralesional and ipsilesional targets are presented simultaneously and reflects impaired allocation of limited attentional resources rather than a primary sensory field defect.  \u003Cstrong\u003Egaze preference\u003C/strong\u003E describes a spontaneous tendency to direct the eyes toward one side while voluntary gaze in other directions remains possible and does not depend on simultaneous target presentation. \u003Cstrong\u003Evisual allesthesia\u003C/strong\u003E refers to displacement or transposition of a visual stimulus from its true location, often into the opposite hemifield, rather than failure to perceive a competing stimulus. \u003Cstrong\u003Ethe Pulfrich phenomenon\u003C/strong\u003E is a binocular motion illusion caused by unequal visual processing latency between the eyes, classically after unilateral or asymmetric optic neuropathy, in which a target moving laterally appears to follow an elliptical path in depth.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1962,
    "Name": "Bilateral optic nerve hypoplasia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 14-month-old has displayed pendular ocular oscillations since approximately 3 months of age and is small for age, with substantial delay across developmental milestones. Visual assessment demonstrates fixation with intermittent following in both eyes, reactive pupils without an afferent pupillary defect, full ocular motility, and no strabismus. The maculae, retinal vessels, and peripheral retinas appear normal, but both optic nerve heads are shown below with his coronal MRI scans. What is the most appropriate next step in management?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-19-e8d14405-3f36-47dd-a3a9-3cdf153a5b44.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EEndocrine consultation\u003C/strong\u003E, because the fundus photographs demonstrate bilateral optic nerve hypoplasia, with small optic discs surrounded by a relative peripapillary halo or \u003Cstrong\u003Edouble-ring sign\u003C/strong\u003E, while the coronal MRI demonstrates absence of the septum pellucidum; together with poor visual behaviour, infantile pendular nystagmus, poor growth, and global developmental delay, these findings indicate septo-optic dysplasia, also called de Morsier syndrome, a developmental spectrum defined by the presence of at least two components of the classical triad of optic nerve hypoplasia, midline cerebral abnormalities, and hypothalamic-pituitary dysfunction. Optic nerve hypoplasia reflects a congenital reduction in retinal ganglion-cell axons, and the apparent outer disc boundary represents the expected scleral canal while the smaller inner ring delineates the true hypoplastic nerve; visual function can range from near normal to profound impairment and does not correlate reliably with apparent optic disc size, while bilateral symmetrical disease explains why no RAPD is present despite significant visual dysfunction.  The immediate management priority is comprehensive pediatric endocrine assessment because hypothalamic-pituitary abnormalities may cause growth hormone deficiency, central hypothyroidism, ACTH deficiency with potentially life-threatening adrenal insufficiency, hypogonadotropic hypogonadism, and arginine vasopressin deficiency; growth hormone deficiency is particularly common, but deficiencies may evolve over time, so normal initial testing does not eliminate the need for longitudinal endocrine surveillance.  \u003Cstrong\u003EElectroretinogram (ERG)\u003C/strong\u003E would be appropriate if an occult retinal dystrophy were suspected in an infant with nystagmus and poor vision, but the visible bilateral optic nerve hypoplasia and midline MRI abnormality already provide an afferent explanation and make endocrine evaluation more urgent; \u003Cstrong\u003EFluorescein angiography (FA)\u003C/strong\u003E would not clarify a developmental optic nerve anomaly or pituitary risk when the retinal vasculature and peripheral retina are normal; and \u003Cstrong\u003EGenetic counseling\u003C/strong\u003E may be considered later, particularly if other congenital abnormalities or a suggestive family history are present, but most cases are sporadic and currently identifiable genetic variants explain only a minority, so genetic evaluation must not delay assessment for treatable and potentially dangerous hormone deficiencies.\u0026nbsp;\u003C/p\u003E\u003Cp\u003E\u003Cimg src=\u0022/upload-2026-08-19-6c670394-fb54-446c-9bfc-c7b65933a27d.png\u0022\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1963,
    "Name": "Migraine visual aura",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhat is the usual duration of a fully reversible visual disturbance occurring as part of a migrainous aura?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E10-60 minutes\u003C/strong\u003E, because a typical visual migraine aura develops gradually over several minutes and usually resolves completely within one hour; the visual phenomenon often begins near fixation as a small positive disturbance, such as scintillation, flashing lights, a zigzag or fortification pattern, and then expands or migrates across the visual field, frequently leaving a negative scotoma behind it as cortical spreading depression propagates through the occipital visual cortex. The formal diagnostic framework defines an individual aura symptom as lasting \u003Cstrong\u003E5\u201360 minutes\u003C/strong\u003E, so \u003Cstrong\u003E10-60 minutes\u003C/strong\u003E is the closest available answer.  A cortical visual aura is usually \u003Cstrong\u003Ebinocular and homonymous\u003C/strong\u003E, although patients may mistakenly describe the disturbance as monocular because the phenomenon affects one side of visual space; genuinely monocular visual loss requires consideration of retinal ischemia, carotid disease, retinal vasospasm, or the rare diagnosis of retinal migraine, which should only be made after other causes of amaurosis fugax have been excluded.  Duration is an important diagnostic discriminator: visual obscurations lasting only seconds are more typical of papilledema or optic disc drusen and may be precipitated by postural change, while abrupt negative monocular loss lasting seconds to several minutes raises concern for amaurosis fugax; occipital seizures generally produce abrupt, brief, stereotyped positive visual phenomena lasting seconds to a few minutes, whereas visual symptoms persisting for one or two days are atypical for ordinary aura and require evaluation for persistent aura, migrainous infarction, stroke, or another neurological disorder.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1964,
    "Name": "Thyroid-associated orbitopathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich mechanism most commonly causes optic nerve dysfunction in patients who develop sight-threatening thyroid-associated orbitopathy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ECompression of the optic nerve at the orbital apex from enlarged extraocular muscles\u003C/strong\u003E, because dysthyroid optic neuropathy most commonly occurs when autoimmune orbital inflammation causes marked enlargement of the extraocular muscles, particularly their posterior bellies, producing crowding at the confined bony orbital apex and mechanical compression of the optic nerve together with compromise of its microvascular perfusion. Orbital fibrocytes expressing TSH and IGF-1 receptors are activated by the autoimmune process, leading to cytokine-mediated inflammation, hydrophilic glycosaminoglycan accumulation, interstitial edema, and eventual fibrosis within the extraocular muscles; because the orbital apex provides little capacity for outward tissue expansion, relatively modest posterior muscle enlargement may compress the optic nerve even when anterior proptosis is mild.  The inferior and medial recti are commonly enlarged, but the risk of optic neuropathy depends particularly on the degree of \u003Cstrong\u003Eapical crowding\u003C/strong\u003E rather than the absolute amount of proptosis. Stretch optic neuropathy from extreme proptosis is a recognized but uncommon mechanism, while ischemic compromise may contribute secondarily to the predominant compressive process.  Direct mononuclear inflammatory infiltration of the optic nerve is not the usual mechanism: inflammatory cells infiltrate orbital connective tissue and extraocular muscles, but the optic neuropathy results mainly from external compression and associated vascular compromise rather than cellular invasion of the nerve. Thyroid hormone dysregulation does not directly produce mitochondrial optic nerve dysfunction, and dysthyroid optic neuropathy may occur in patients who are biochemically euthyroid because orbital disease activity does not necessarily parallel circulating thyroid hormone levels. Clinically, early warning signs include impaired color vision, reduced contrast sensitivity, central or paracentral field defects, a relative afferent pupillary defect in asymmetric disease, and reduced visual acuity, although central acuity may initially remain relatively preserved; CT or MRI typically demonstrates muscle-belly enlargement with tendon sparing and apical crowding, and established dysthyroid optic neuropathy requires urgent treatment with high-dose intravenous corticosteroids and orbital decompression when response is inadequate or vision is immediately threatened.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1965,
    "Name": "Anterior optic chiasmal compression",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich combination of visual field abnormalities may result from a lesion compressing the anterior optic chiasm at its junction with one optic nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EFull field visual loss in one eye with a superotemporal deficit in the contralateral eye\u003C/strong\u003E, because this pattern represents a \u003Cstrong\u003Ejunctional scotoma\u003C/strong\u003E, which localizes to the junction of the ipsilateral optic nerve and anterior optic chiasm. Compression of the optic nerve produces severe ipsilateral visual dysfunction, which may range from a central or cecocentral scotoma to extensive or complete monocular field loss, together with reduced visual acuity, dyschromatopsia, and an ipsilateral relative afferent pupillary defect. Simultaneous involvement of adjacent crossing inferonasal retinal fibres from the contralateral eye produces a contralateral \u003Cstrong\u003Esuperotemporal field defect\u003C/strong\u003E, because inferonasal retinal fibres represent the superotemporal visual field. Sellar and parasellar masses, particularly pituitary adenomas, are the most common causes, although meningioma, craniopharyngioma, aneurysm, inflammatory disease, and infiltrative lesions may produce the same localization pattern.  The classical anatomical explanation invokes \u003Cstrong\u003EWilbrand\u2019s knee\u003C/strong\u003E, in which crossing inferonasal fibres were believed to loop anteriorly for a short distance into the contralateral optic nerve before turning posteriorly through the chiasm.  \u003Cstrong\u003ESymmetric bitemporal hemianopia of both entire temporal fields\u003C/strong\u003E is more typical of central chiasmal compression after more extensive involvement of crossing nasal retinal fibres; \u003Cstrong\u003EA bitemporal hemianopic type defect of the central 5-10 degrees only\u003C/strong\u003E is not the characteristic junctional pattern; and \u003Cstrong\u003EBilateral mostly inferotemporal deficits respecting the vertical midline\u003C/strong\u003E would imply preferential damage to superior nasal retinal fibres, as may occur with compression of the chiasm from above rather than the usual anterior junctional lesion.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1966,
    "Name": "Aberrant regeneration of the third nerve",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich of the following is NOT a manifestation of aberrant regeneration seen following damage to the 3rd nerve?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EEyelid retraction upon abduction\u003C/strong\u003E, because acquired aberrant regeneration of the third cranial nerve, also termed \u003Cstrong\u003Eoculomotor synkinesis or misdirection\u003C/strong\u003E, occurs when damaged oculomotor axons regenerate into inappropriate fascicles, causing simultaneous activation of structures that share third-nerve innervation; levator palpebrae fibers may become linked to fibers intended for the medial rectus or inferior rectus, producing elevation or retraction of a previously ptotic upper eyelid during \u003Cstrong\u003Eadduction\u003C/strong\u003E or \u003Cstrong\u003Edepression\u003C/strong\u003E, the latter classically producing the pseudo-von Graefe sign, while parasympathetic fibers intended for the sphincter pupillae may become linked to somatic motor fibers supplying the medial or inferior rectus, causing \u003Cstrong\u003Emiosis upon adduction\u003C/strong\u003E or \u003Cstrong\u003Emiosis upon depression\u003C/strong\u003E, termed pupil-gaze dyskinesia.  Abduction, however, is generated by the lateral rectus, which is supplied by the sixth cranial nerve rather than the third cranial nerve; aberrant regeneration confined to the damaged oculomotor nerve therefore cannot link lateral rectus activation to the levator palpebrae superioris, making eyelid retraction during abduction an implausible manifestation. Aberrant third-nerve regeneration most commonly follows traumatic, surgical, aneurysmal, or compressive injury that disrupts axonal architecture, while primary oculomotor synkinesis without a recognized preceding palsy should raise concern for a slowly progressive compressive lesion such as an intracavernous aneurysm, meningioma, or schwannoma; it is not expected after an uncomplicated microvascular third-nerve palsy because the endoneurial architecture generally remains sufficiently preserved to permit orderly recovery, so its later appearance should prompt neuroimaging and reconsideration of the original diagnosis.  This acquired misdirection must be distinguished from congenital synkinesis, such as Duane retraction syndrome or Marcus Gunn jaw-winking, in which anomalous developmental innervation may involve different cranial nerves.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1967,
    "Name": "Toxic-nutritional optic neuropathy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAn 80-year-old with longstanding tobacco and alcohol exposure and a poor diet has developed slowly progressive, symmetrical visual loss in both eyes over one year, with serial deterioration in visual acuity and color discrimination. Both eyes show similar field abnormalities, while the macular examination is normal. The displayed visual field demonstrates a central defect extending toward the physiological blind spot. Which optic nerve appearance would be expected?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-19-87559d04-c269-4eaa-8244-64396ed7e23f.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EImage D\u003C/strong\u003E, because the slowly progressive, painless, symmetrical reduction in visual acuity and color vision, combined with a normal macular examination and a bilateral \u003Cstrong\u003Ececocentral scotoma\u003C/strong\u003E, localizes dysfunction to the papillomacular bundles and is characteristic of a toxic-nutritional optic neuropathy; the small-calibre retinal ganglion-cell axons carrying central macular information have high metabolic requirements and are particularly vulnerable to impaired mitochondrial oxidative phosphorylation caused by nutritional deficiency and toxic exposure, so chronic alcohol use, poor dietary intake, and smoking may act synergistically through deficiencies of vitamin B12, folate, thiamine, copper, and other nutrients, together with direct or indirect mitochondrial toxicity. The field defect is cecocentral because papillomacular axons extend between fixation and the optic disc, linking the central scotoma to the physiological blind spot; peripheral fields are relatively preserved until advanced disease. Toxic-nutritional optic neuropathy is initially retrobulbar, so the discs may appear normal or mildly hyperaemic, but continued axonal loss produces \u003Cstrong\u003Etemporal optic disc pallor\u003C/strong\u003E, followed in advanced cases by diffuse optic atrophy, making Image D the appearance that best matches the demonstrated field. The absence of an RAPD would not exclude severe disease because the involvement is bilateral and symmetrical.  Image A represents a relatively normal crowded optic disc or \u201Cdisc at risk,\u201D which may predispose to NAION but does not explain symmetrical progressive cecocentral loss; Image B shows marked hyperaemic disc edema with surrounding exudative change, more compatible with active papilloedema or another acute swollen-disc process, where early fields more commonly show blind-spot enlargement and peripheral nerve-fibre-bundle loss; and Image C shows glaucomatous excavation with focal neuroretinal rim notching, which would be expected to produce arcuate defects, nasal steps, or paracentral loss respecting the horizontal meridian rather than an isolated symmetrical cecocentral scotoma. The appropriate work-up should include a detailed dietary, medication, alcohol, tobacco, gastrointestinal, and occupational history, together with full blood count, vitamin B12 and metabolites, folate, thiamine, copper, and other investigations guided by the clinical context; management requires removal of relevant toxic exposure and prompt replacement of confirmed deficiencies, because early treatment may allow slow visual recovery, whereas established optic atrophy may be irreversible.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1968,
    "Name": "Cocaine testing in Horner syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EHow does cocaine usage aid in diagnosis of Horner syndrome?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EIt blocks re-uptake of norepinephrine at the pre-synaptic terminal\u003C/strong\u003E, because cocaine inhibits the norepinephrine transporter on postganglionic sympathetic nerve terminals, preventing reuptake of norepinephrine from the neuroeffector junction between the long ciliary sympathetic fibers and the iris dilator muscle; in a normally innervated eye, norepinephrine continues to be released, accumulates within the junction, and stimulates postsynaptic \u03B11-adrenergic receptors, producing contraction of the iris dilator and pupillary dilation. In Horner syndrome, interruption anywhere along the oculosympathetic pathway reduces norepinephrine delivery from the postganglionic terminal, so little transmitter is present for cocaine to retain and the affected miotic pupil dilates poorly, whereas the normally innervated fellow pupil dilates substantially; cocaine is therefore instilled bilaterally, and development or enlargement of post-cocaine anisocoria confirms sympathetic denervation but does not localize the lesion to the first-, second-, or third-order neuron.  Cocaine does not release stored norepinephrine, which is the mechanism of \u003Cstrong\u003Ehydroxyamphetamine\u003C/strong\u003E and historically permits differentiation of postganglionic from central or preganglionic Horner syndrome; cocaine also has no diagnostic action through acetylcholine, which is the parasympathetic neurotransmitter acting on the iris sphincter to produce miosis. A useful pharmacological distinction is: \u003Cstrong\u003Ecocaine blocks norepinephrine reuptake and enlarges anisocoria, hydroxyamphetamine releases stored norepinephrine, and apraclonidine exploits \u03B11-receptor denervation supersensitivity to reverse anisocoria\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1969,
    "Name": "Acute divergence insufficiency",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA previously healthy 40-year-old develops a two-week history of almost continuous horizontal binocular diplopia accompanied by headache. The diplopia is present in all directions of distance gaze but disappears during reading. Visual acuity and ocular motility are normal, and alternate-cover testing demonstrates a comitant 6-prism-diopter esotropia at distance in primary position and lateral gazes, with orthophoria at near. What is the most appropriate next management step?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMRI of the brain\u003C/strong\u003E, because the distance esotropia with orthophoria at near, full abduction, and an equal deviation in primary and lateral gazes is a \u003Cstrong\u003Edivergence insufficiency-type pattern\u003C/strong\u003E, but the acute onset over two weeks in a 40-year-old with a new headache makes it unsafe to assume that the deviation is benign or age-related. The field of single binocular vision at near is preserved because convergence remains intact, whereas inadequate divergence produces horizontal diplopia at distance; however, similar findings may arise from subtle bilateral sixth nerve dysfunction, raised intracranial pressure, posterior fossa or brainstem disease, meningeal pathology, cerebellar disease, demyelination, myasthenia gravis, or another neurological process. Secondary divergence insufficiency requires more urgent investigation than the benign, slowly progressive form usually encountered in older adults.  MRI of the brain should therefore be obtained to evaluate the brainstem, posterior fossa, meninges, and intracranial structures, with contrast and additional orbital or venographic sequences guided by subsequent findings; the examination should also include careful assessment for papilloedema, abduction saccadic velocity, incomitance on repeat measurements, fatigability, neurological signs, and symptoms of raised intracranial pressure, with acetylcholine-receptor antibody testing considered if ocular myasthenia remains clinically plausible. \u003Cstrong\u003EReassurance and ground-in prisms\u003C/strong\u003E may eventually be appropriate if imaging and neurological assessment are reassuring and the deviation persists, but permanent prisms should not precede investigation because the alignment may evolve or resolve and the current acute headache is a red flag. \u003Cstrong\u003EStrabismus surgery\u003C/strong\u003E is premature after only two weeks and is generally reserved for a persistent, stable deviation after an adequate observation period, while \u003Cstrong\u003EContact lenses\u003C/strong\u003E do not address the underlying divergence deficit or correct the distance esotropia.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1970,
    "Name": "Benign episodic pupillary mydriasis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhich neurological disorder is most commonly associated with recurrent, fully reversible episodes of isolated pupillary dilation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMigraine headaches\u003C/strong\u003E, because benign episodic pupillary mydriasis is a transient autonomic pupillary disturbance characterized by recurrent, usually unilateral but occasionally bilateral, pupil dilation that resolves spontaneously; episodes may last from minutes to hours and may cause blurred vision, photophobia, difficulty with near accommodation, or periocular discomfort, but the neurological and ocular examinations are normal between attacks. The condition has a well-described association with a personal or family history of migraine, although pupillary dilation does not have to occur simultaneously with the headache and may precede, accompany, follow, or occur independently of a migraine episode.  The precise mechanism remains uncertain but probably reflects transient imbalance between sympathetic and parasympathetic pupillary control.  \u003Cstrong\u003EAdie\u0027s tonic pupil\u003C/strong\u003E produces a persistently enlarged pupil with segmental sphincter palsy, light-near dissociation, tonic near constriction, slow redilation, and cholinergic denervation supersensitivity to dilute pilocarpine rather than brief, fully reversible episodes. \u003Cstrong\u003EMyasthenia gravis\u003C/strong\u003E causes fatigable ptosis and variable diplopia but does not affect the pupils because the iris muscles are autonomically innervated smooth muscles. \u003Cstrong\u003ETrigeminal neuralgia\u003C/strong\u003E causes brief attacks of severe electric shock-like facial pain without a characteristic association with isolated episodic mydriasis. Before diagnosing a benign migraine-associated phenomenon, clinicians must exclude a pupil-involving third nerve palsy, pharmacological mydriasis, Adie tonic pupil, intermittent angle closure, iris sphincter injury, and other neurological causes, particularly when episodes are associated with ptosis, diplopia, ophthalmoplegia, severe headache, neck pain, or other neurological deficits.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1971,
    "Name": "Apraclonidine testing",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 75-year-old Caucasian female presents to your clinic because she recently noticed that her pupils were different sized. You examine the patient and note anisocoria that is greater in the dark compared to the light. The top photo shows the patient\u2019s exam before you apply drops in both eyes to confirm your suspected diagnosis. The bottom photo shows the patient\u2019s exam 30 minutes after drop application. Which pupil is abnormal and what drops were applied?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-19-d2aceb19-399f-4b4d-90f5-b63489357412.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ERight pupil; apraclonidine 1% drops\u003C/strong\u003E, because anisocoria that increases in darkness indicates impaired dilation of the smaller pupil, localizing the abnormality to the sympathetic pathway; the smaller right pupil and subtle ipsilateral upper-eyelid ptosis therefore indicate a right Horner syndrome. Apraclonidine is predominantly an \u03B12-adrenergic agonist with weak \u03B11-adrenergic activity: in the normally innervated left eye, presynaptic \u03B12 stimulation reduces norepinephrine release and may cause slight miosis or little pupillary change, whereas sympathetic denervation in the right eye produces postsynaptic \u03B11-receptor supersensitivity in the iris dilator muscle, allowing apraclonidine\u2019s normally weak \u03B11 effect to cause marked dilation of the right Horner pupil. The right pupil consequently becomes larger than the left, producing the characteristic \u003Cstrong\u003Ereversal of anisocoria\u003C/strong\u003E shown in the lower photograph; \u03B11-mediated contraction of the denervated M\u00FCller muscle also elevates the right upper eyelid and improves the mild ptosis.  \u003Cstrong\u003ELeft pupil; apraclonidine 1% drops\u003C/strong\u003E is incorrect because the left pupil is initially larger and dilates normally in darkness, while the right pupil is miotic and fails sympathetic dilation; \u003Cstrong\u003ELeft pupil; pilocarpine 1% drops\u003C/strong\u003E is incompatible with the image because pilocarpine stimulates muscarinic receptors and causes miosis rather than reversal of anisocoria through dilation of the Horner pupil; and \u003Cstrong\u003ERight pupil; cocaine 10% drops\u003C/strong\u003E is incorrect because cocaine blocks norepinephrine reuptake, causing the normal pupil to dilate while the Horner pupil dilates poorly, thereby increasing rather than reversing the baseline anisocoria. Apraclonidine confirms oculosympathetic paresis but does not localize the lesion to the central, preganglionic, or postganglionic neuron, and a negative test in a very acute Horner syndrome does not reliably exclude the diagnosis because denervation supersensitivity may not yet be sufficiently established, although positive responses have been documented within several days of onset.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1972,
    "Name": "Periodic alternating nystagmus",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn periodic alternating nystagmus, what is the usual duration of a complete cycle comprising a nystagmus-free interval, a jerk nystagmus phase in one direction, another neutral interval, a jerk nystagmus phase in the opposite direction, and return to the initial neutral phase?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E2-4 minutes\u003C/strong\u003E, because periodic alternating nystagmus is a conjugate horizontal jerk nystagmus in which the direction of the fast phase reverses at regular intervals; during one complete cycle, nystagmus develops in one direction with a crescendo-decrescendo pattern over approximately 60\u201390 seconds, passes through a brief neutral or nystagmus-free interval, then develops in the opposite direction for a similar duration before returning to another neutral phase, giving a total cycle time of approximately \u003Cstrong\u003E2\u20134 minutes\u003C/strong\u003E.  This must be distinguished from the shorter interval required merely for the nystagmus to reverse from one direction to the other, which is approximately 1\u20132 minutes and represents only half of the complete cycle. The oscillation reflects instability of the vestibular velocity-storage mechanism combined with maladaptation of the neural network responsible for cancelling sustained vestibular nystagmus, usually following dysfunction of the vestibulocerebellum, particularly the nodulus and uvula; acquired causes include cerebellar degeneration, multiple sclerosis, posterior-fossa tumors or infarction, Chiari malformation, encephalitis, Wernicke encephalopathy, and medication toxicity, while congenital periodic alternating nystagmus may occur with infantile nystagmus syndrome, albinism, or other sensory visual disorders.  Detection requires prolonged observation in primary gaze because a brief examination may sample only one directional phase and lead to misclassification as ordinary horizontal jerk nystagmus; observing for at least two minutes, and preferably documenting a complete cycle with eye-movement recordings, increases diagnostic sensitivity. The shifting null zone may produce periodic alternating face turns, which is surgically important because a conventional Kestenbaum procedure directed toward a presumed fixed null point may fail or worsen the abnormal head posture unless the null point remains consistently asymmetric throughout the cycle. Baclofen is the classic pharmacological treatment for symptomatic acquired periodic alternating nystagmus because it can stabilize the velocity-storage mechanism and reduce or abolish the periodic reversals.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1973,
    "Name": "Congenital right fourth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EIn a patient with a longstanding congenital right trochlear nerve palsy, which finding would be inconsistent?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EExotropia on down gaze\u003C/strong\u003E, because a right fourth nerve palsy weakens the right superior oblique muscle, whose actions are intorsion, depression in adduction, and abduction. The right eye consequently becomes hypertropic and excyclotorted, with the hypertropia increasing in \u003Cstrong\u003Eleft gaze\u003C/strong\u003E, where the right eye is adducted, and on \u003Cstrong\u003Eright head tilt\u003C/strong\u003E, when the weakened intorting effect of the right superior oblique cannot balance the right superior rectus. Diplopia is also typically greater in downgaze, particularly during reading or descending stairs.\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003ELeft head tilt\u003C/strong\u003E is expected because tilting the head away from the affected right side reduces the right hypertropia and excyclotorsion. A longstanding contralateral head tilt may be visible in childhood photographs and can produce facial asymmetry over time.\u003C/p\u003E\n\u003Cp\u003EA \u003Cstrong\u003ERight gaze preference\u003C/strong\u003E may also be expected. In right gaze, the affected right eye is abducted, so vertical movement depends mainly on the right superior and inferior recti rather than the weak right superior oblique. This gaze position therefore reduces the vertical misalignment compared with left gaze, where the affected right eye is adducted and superior oblique weakness is maximally demonstrated.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EVertical fusional amplitudes of 8 diopters\u003C/strong\u003E support a congenital rather than an acute acquired fourth nerve palsy. Normal vertical fusional amplitudes are small, usually approximately 2\u20133 prism diopters, but patients with congenital fourth nerve palsy may develop unusually large vertical fusional reserves that compensate for the longstanding hypertropia. The deviation may remain asymptomatic until these reserves decompensate because of fatigue, illness, ageing, or prolonged near work.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EExotropia on down gaze\u003C/strong\u003E is not expected because superior oblique weakness removes an abducting force that is particularly relevant in downgaze. This allows relatively unopposed adducting action of the inferior recti, producing \u003Cstrong\u003Eesotropia in downgaze\u003C/strong\u003E, not exotropia. The esodeviation is therefore greater in downgaze and less in upgaze, creating a \u003Cstrong\u003EV-pattern\u003C/strong\u003E horizontal deviation. This V pattern is especially prominent in bilateral fourth nerve palsy but may also occur in unilateral disease.\u003C/p\u003E\n\u003Cp\u003EA useful summary is:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003ERight fourth nerve palsy \u2192 \u003Cstrong\u003Eright hypertropia\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003EWorse in \u003Cstrong\u003Eleft gaze\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003EWorse on \u003Cstrong\u003Eright head tilt\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003ECompensatory \u003Cstrong\u003Eleft head tilt\u003C/strong\u003E\u003C/li\u003E\n\u003Cli\u003ELarge vertical fusion suggests \u003Cstrong\u003Econgenital\u003C/strong\u003E disease\u003C/li\u003E\n\u003Cli\u003ELoss of superior oblique abduction \u2192 \u003Cstrong\u003Eesotropia in downgaze\u003C/strong\u003E\u003C/li\u003E\u003C/ul\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1974,
    "Name": "Carotid endarterectomy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAmong patients with asymptomatic carotid narrowing, complete carotid occlusion, or recurrent right-eye amaurosis fugax associated with varying degrees of ipsilateral carotid stenosis, which patient is expected to obtain the greatest reduction in future ipsilateral ischemic events from carotid endarterectomy?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EA 70-year-old male with a history of recurrent amaurosis fugax OD and 80% right carotid stenosis\u003C/strong\u003E, because recurrent right monocular transient visual loss constitutes \u003Cstrong\u003Esymptomatic right carotid-territory ischemia\u003C/strong\u003E, and severe ipsilateral carotid stenosis provides the strongest evidence-based indication for carotid endarterectomy. Amaurosis fugax commonly results from embolic material arising from an atherosclerotic ipsilateral internal carotid plaque and entering the ophthalmic and retinal circulation. Carotid endarterectomy removes the causative plaque and reduces the risk of subsequent retinal or cerebral ischemic events. Contemporary vascular guidelines continue to recommend carotid endarterectomy for suitable symptomatic patients with substantial ipsilateral stenosis, provided the expected perioperative stroke and mortality risk is acceptably low.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EThe greatest benefit demonstrated by the NASCET evidence occurs in patients with recent retinal or hemispheric ischemic symptoms and \u003Cstrong\u003Esevere 70\u201399% ipsilateral carotid stenosis\u003C/strong\u003E. This patient\u2019s recurrent right-eye amaurosis fugax and 80% right carotid stenosis therefore represent the highest-risk, most clearly beneficial combination among the choices. The patient requires urgent stroke and vascular assessment, confirmation of stenosis severity and anatomy with appropriate vascular imaging, optimal medical therapy, and consideration of early carotid endarterectomy if medically and surgically suitable.\u003C/p\u003E\n\u003Cp\u003EThe other choices are less suitable:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EA 70-year-old male with asymptomatic 60% carotid stenosis bilaterally\u003C/strong\u003E may be considered for intervention only in carefully selected circumstances. The absolute benefit is substantially smaller than in symptomatic severe stenosis and must be balanced against perioperative risk, life expectancy, plaque characteristics, and the effectiveness of contemporary medical therapy.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EA 70-year-old male with a history of recurrent amaurosis fugax OD and a complete right carotid occlusion\u003C/strong\u003E would not usually benefit from conventional carotid endarterectomy. Once the artery is completely occluded, there is no patent residual lumen for routine plaque removal and flow restoration, and attempted revascularization has a low success rate with substantial procedural risk.\u003C/p\u003E\n\u003C/li\u003E\n\u003Cli\u003E\n\u003Cp\u003E\u003Cstrong\u003EA 70-year-old male with a history of recurrent amaurosis fugax OD and 50% right carotid stenosis\u003C/strong\u003E has symptomatic moderate stenosis. Carotid endarterectomy may provide some benefit in selected patients with 50\u201369% stenosis, particularly when performed promptly and with low perioperative risk, but the benefit is less substantial than that associated with symptomatic 70\u201399% stenosis. Current guidelines specifically address symptomatic patients with 50\u201399% carotid stenosis, but the magnitude of benefit increases with stenosis severity until near-occlusion or complete occlusion changes the risk-benefit balance.\u0026nbsp;\u003C/p\u003E\n\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EA useful examination principle is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003ESymptomatic severe stenosis benefits most; complete occlusion is too late for routine CEA.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1975,
    "Name": "Right RAPD following NAION",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EFollowing a recent right non-arteritic anterior ischemic optic neuropathy, examination demonstrates a right relative afferent pupillary defect. Assuming that both efferent parasympathetic pathways and iris sphincters are intact, which pupillary response would be expected when each eye is illuminated separately?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea relatively diminished consensual pupillary constriction in the left eye when shining a light in the right eye\u003C/strong\u003E, because right NAION reduces the afferent pupillomotor signal carried from the right retina through the damaged right optic nerve to the pretectal nuclei. Since each pretectal nucleus projects bilaterally to both Edinger-Westphal nuclei, the reduced right afferent input results in diminished parasympathetic output to \u003Cstrong\u003Eboth\u003C/strong\u003E pupils when the right eye is illuminated. Consequently, the right pupil shows a diminished direct response and the left pupil shows a correspondingly diminished consensual response.\u003C/p\u003E\n\u003Cp\u003EWhen light is directed into the normal left eye, the intact left afferent pathway activates both Edinger-Westphal nuclei normally. Both pupils therefore constrict briskly, including a normal consensual constriction of the right pupil. This confirms that the right oculomotor parasympathetic efferent pathway, ciliary ganglion, short ciliary nerves, and iris sphincter remain functional. The abnormality lies in the right \u003Cstrong\u003Eafferent\u003C/strong\u003E pathway, not the right efferent pathway.\u003C/p\u003E\n\u003Cp\u003EDuring the swinging-flashlight test:\u003C/p\u003E\n\u003Col\u003E\n\u003Cli\u003EIllumination of the left eye produces brisk bilateral constriction.\u003C/li\u003E\n\u003Cli\u003EMoving the light from the left eye to the right eye reduces bilateral afferent drive.\u003C/li\u003E\n\u003Cli\u003EBoth pupils constrict less or appear to redilate despite continued illumination.\u003C/li\u003E\n\u003Cli\u003EThis bilateral redilation when the light reaches the right eye identifies a right RAPD.\u0026nbsp;\u003C/li\u003E\n\u003C/ol\u003E\n\u003Cp\u003EA relative afferent pupillary defect does \u003Cstrong\u003Enot\u003C/strong\u003E cause anisocoria. Pupil size is determined principally by the balance between sympathetic dilator and parasympathetic sphincter activity, whereas an RAPD reflects asymmetry of retinal or optic nerve input to the light reflex. The pupils should therefore remain approximately equal in size in light and darkness unless a separate efferent, pharmacological, or structural iris abnormality is present.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003Ea relatively diminished consensual pupillary constriction in the right eye when shining a light in the left eye\u003C/strong\u003E would imply impaired right parasympathetic efferent function. In an isolated right NAION, illumination of the normal left eye supplies normal bilateral afferent input, so the right pupil should constrict normally through its intact consensual pathway.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1976,
    "Name": "Giant cell arteritis with sectoral choroidal ischemia",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EThe fundus photo and two fluorescein angiography (FA) images shown above were taken from a patient with giant cell arteritis (GCA) and vision loss in the left eye. In this patient, occlusion of which specific vessel is responsible for her vision loss?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-21-e0e782cf-c023-498a-bce6-8334b28a6e71.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EPosterior ciliary artery\u003C/strong\u003E, because the early fluorescein angiographic image demonstrates a large, sharply demarcated temporal region of absent choroidal fluorescence despite filling of the retinal circulation, followed by delayed filling of the same choroidal territory in the later image; this sectoral choroidal hypoperfusion localizes the vascular obstruction to a \u003Cstrong\u003Eposterior ciliary artery\u003C/strong\u003E, which supplies both the choroid and, through its short posterior ciliary branches, the prelaminar and laminar optic nerve head. Giant cell arteritis is a granulomatous vasculitis affecting medium- and large-calibre arteries with elastic tissue, and the posterior ciliary arteries are particularly susceptible; occlusion of branches supplying the optic nerve head produces arteritic anterior ischemic optic neuropathy, whereas occlusion of a branch predominantly supplying the temporal choroid can produce sectoral choroidal ischemia or infarction with profound angiographic filling delay even when the initial fundus appearance is relatively subtle. Markedly delayed or patchy choroidal filling on fluorescein angiography in an older patient with acute visual loss is therefore a major warning sign for GCA.  \u003Cstrong\u003ECentral retinal artery\u003C/strong\u003E occlusion would primarily cause diffuse inner retinal ischemia, retinal whitening, a cherry-red spot, marked attenuation of the retinal arteries, and delayed retinal arterial filling rather than an isolated sectoral choroidal filling defect. \u003Cstrong\u003EOphthalmic artery\u003C/strong\u003E occlusion would compromise both retinal and choroidal circulations, producing much more extensive nonperfusion with severe combined retinal and choroidal ischemia. \u003Cstrong\u003ECentral retinal vein\u003C/strong\u003E occlusion would produce venous dilation and tortuosity, widespread retinal hemorrhages, cotton-wool spots, and delayed venous transit rather than sharply demarcated choroidal hypoperfusion. GCA can cause several ocular ischemic syndromes, including arteritic anterior ischemic optic neuropathy, posterior ischemic optic neuropathy, central or branch retinal artery occlusion, cilioretinal artery occlusion, ocular ischemic syndrome, choroidal infarction, and ocular motor ischemia, but the vascular territory displayed here specifically identifies the \u003Cstrong\u003EPosterior ciliary artery\u003C/strong\u003E.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
    "ExamQuestions": null,
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  },
  {
    "Id": 1977,
    "Name": "Normal levator function",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EWhen levator palpebrae superioris function is assessed clinically by measuring upper-eyelid excursion from maximal downgaze to maximal upgaze, what range is considered normal?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003E\u0026gt;12-16 mm\u003C/strong\u003E, because levator function is measured as the total vertical excursion of the upper-eyelid margin from maximal downgaze to maximal upgaze while the examiner firmly immobilizes the eyebrow to eliminate compensatory frontalis activity; normal levator excursion is generally approximately \u003Cstrong\u003E12\u201316 mm\u003C/strong\u003E, with many references describing around 15 mm as normal, although grading thresholds vary slightly between texts.  Levator function must be distinguished from \u003Cstrong\u003EMRD1\u003C/strong\u003E, which measures upper-eyelid position in primary gaze rather than muscle excursion, and from palpebral fissure height, which can be influenced by lower-eyelid position. This measurement is central to determining the mechanism of ptosis and selecting surgery: preserved levator function with a high or absent lid crease and lid lag on downgaze is characteristic of aponeurotic dehiscence, whereas reduced excursion suggests a myogenic, congenital, or neurogenic process. Levator function below approximately 12 mm is therefore atypical, although the clinical significance depends on the degree of reduction and associated findings; severe congenital or myogenic ptosis may show poor excursion of 4 mm or less, often requiring frontalis suspension rather than levator advancement or resection. The levator palpebrae superioris is the principal voluntary upper-eyelid elevator and is supplied by the superior division of cranial nerve III, while M\u00FCller muscle contributes only approximately 1\u20132 mm of sympathetically mediated elevation, so pharmacological stimulation of M\u00FCller muscle does not substitute for assessing true levator excursion.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1978,
    "Name": "Chronic congenital fourth nerve palsy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 40-year-old has experienced intermittent binocular diplopia for one year, initially occurring only with fatigue late in the day but now requiring considerable effort to fuse two diagonally separated images. There is no ptosis or anisocoria. Measurements demonstrate a comitant right hypertropia of 10 prism diopters. Childhood photographs consistently show a previously unrecognized left head tilt, although this posture is absent from photographs taken during the past 20 years. Brain MRI is normal, and the clinical diagnosis is a congenital fourth nerve palsy that has recently decompensated. Which physiological adaptation explains why the current deviation is comitant despite originating from a longstanding unilateral superior oblique weakness?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ESpread of comitance\u003C/strong\u003E, because an untreated congenital fourth nerve palsy is initially incomitant, with the hypertropia greatest in the field of action of the weak superior oblique, but prolonged adaptation over many years can redistribute the vertical deviation across different gaze positions until the measurements become relatively similar, a process termed spread of comitance; in a right superior oblique palsy, the primary weakness initially produces right hypertropia that is greatest in left gaze, downgaze, and right head tilt, but chronic secondary changes develop within the extraocular motor system, including contracture of the ipsilateral superior oblique antagonist, the right inferior oblique, followed by altered innervational demands and secondary changes in the contralateral yoke and antagonist muscles, so the original gaze-dependent difference becomes progressively less conspicuous and the deviation may eventually appear comitant. This does not mean that the congenital palsy has resolved; rather, the ocular motor system has recalibrated around the longstanding paresis, and the patient may remain asymptomatic for decades because congenital fourth nerve palsy is commonly accompanied by unusually large vertical fusional amplitudes, often far exceeding the normal 2\u20133 prism diopters. With ageing, fatigue, illness, or reduced fusional reserve, compensation may fail and diplopia emerges despite the deviation having become more comitant. The historical left head tilt is an important clue because a patient with a right fourth nerve palsy typically tilts the head toward the contralateral shoulder to reduce the right hypertropia and excyclotorsion, while longstanding torticollis may diminish as facial asymmetry, sensory adaptation, and spread of comitance develop. \u003Cstrong\u003EHering\u0027s Law\u003C/strong\u003E describes equal innervation to yoke muscles in the two eyes and contributes to secondary deviation patterns but does not itself name the chronic conversion of an incomitant deviation into a comitant one. \u003Cstrong\u003ESherington\u0027s law\u003C/strong\u003E describes reciprocal innervation within the same eye, whereby contraction of an agonist is accompanied by relaxation of its antagonist. \u003Cstrong\u003EInhibitional paresis of the contralateral antagonist\u003C/strong\u003E is a specific consequence of Hering\u2019s and Sherrington\u2019s laws: if the paretic eye is used for fixation, altered innervation to its overacting antagonist changes the drive to the contralateral yoke muscle, and reciprocal inhibition may make the contralateral antagonist appear weak; this may complicate the motility pattern but does not best explain the generalized comitance in this longstanding congenital palsy.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": true,
    "CategoryId": 10,
    "Category": null,
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  },
  {
    "Id": 1979,
    "Name": "Pharmacological mydriasis",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA 30-year-old presents with a two-day history of isolated left mydriasis without headache, ptosis, diplopia, trauma, or reported medication exposure. The left pupil is round, measures 8 mm in darkness, and shows no constriction to either light or near stimulation; visual acuity, pupils apart from the anisocoria, ocular alignment, and motility are otherwise normal. If topical anticholinergic exposure is suspected, which response to pilocarpine would definitively support pharmacological pupillary dilation?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003ENo pupillary response to pilocarpine 1% in the left eye\u003C/strong\u003E, because topical antimuscarinic agents such as atropine, tropicamide, cyclopentolate, or scopolamine produce mydriasis and cycloplegia by competitively blocking muscarinic receptors on the iris sphincter and ciliary muscle; when those receptors remain pharmacologically occupied, even full-strength pilocarpine cannot stimulate meaningful sphincter contraction, so the affected pupil remains dilated despite pilocarpine 1%, while the normal fellow pupil constricts and acts as an internal control.  The differential diagnosis of an isolated, poorly reactive large pupil includes a tonic pupil, parasympathetic dysfunction from a third nerve lesion, traumatic or surgical sphincter damage, and pharmacological mydriasis. A tonic pupil results from postganglionic parasympathetic denervation at the ciliary ganglion or short ciliary nerves and, after denervation supersensitivity develops, typically shows marked constriction to dilute pilocarpine 0.125%; however, lack of response to dilute pilocarpine is not definitive for pharmacological blockade because supersensitivity may be absent in an acute tonic pupil, the dilution may be inaccurate, or the response may be subtle. In a pupil affected by a third nerve palsy, the iris sphincter remains pharmacologically accessible and should constrict to pilocarpine 1%, while examination would usually reveal at least partial ptosis, impaired adduction, elevation or depression, or ocular misalignment; the completely normal motility and eyelid examination therefore make compressive third nerve palsy less likely, although urgent vascular imaging remains necessary if painful mydriasis, ophthalmoplegia, ptosis, or other neurological signs develop. A structurally damaged iris may also respond incompletely to full-strength pilocarpine, but slit-lamp examination would generally reveal sphincter tears, an irregular pupil, transillumination defects, inflammation, or evidence of previous trauma or surgery, whereas the perfectly round pupil and normal anterior segment in this case favour receptor blockade. Inadvertent exposure may arise from scopolamine patches, aerosolized ipratropium, mydriatic drops, anticholinergic plant material such as \u003Cem\u003EDatura\u003C/em\u003E, or hand-to-eye transfer of another person\u2019s medication, and healthcare workers may be particularly vulnerable to accidental exposure during medication handling.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1980,
    "Name": "Neurological causes of an irregularly shaped pupil",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EAfter excluding structural iris abnormalities such as surgical damage, synechiae, coloboma, sphincter tears, iridodialysis, and iris neovascularization, which pair of neurological conditions may produce episodic distortion or displacement of the pupil?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EMidbrain pathology and migraine\u003C/strong\u003E, because two neurological causes of an irregular pupil are \u003Cstrong\u003Emidbrain corectopia\u003C/strong\u003E and the migraine-associated \u003Cstrong\u003Etadpole pupil\u003C/strong\u003E. Midbrain corectopia is a rare pupil-position abnormality associated with diffuse or focal midbrain dysfunction and may be unilateral or bilateral, fixed or episodic; the proposed mechanism is unequal supranuclear inhibition of pupillomotor output from the Edinger-Westphal nuclear complex, producing asymmetric segmental contraction of the iris sphincter and displacement of the pupil away from its normal central position, with reported episodic cycles of distortion followed by spontaneous recovery. The tadpole pupil is a different paroxysmal phenomenon in which one segment of the iris dilator muscle contracts excessively, creating a transient peaked, elongated, or tadpole-shaped pupil; episodes are usually unilateral, last seconds to minutes, may occur in clusters, and have a recognized association with migraine, although the pupillary episode may occur before, during, after, or independently of headache.  Tadpole pupil has also been reported with ipsilateral Horner syndrome, suggesting that sympathetic denervation hypersensitivity may contribute in some patients, but the mechanism remains incompletely established.  \u003Cstrong\u003EMyasthenia gravis\u003C/strong\u003E does not affect pupil size, shape, or reactivity because the iris sphincter and dilator are autonomically innervated smooth muscles rather than skeletal muscles supplied through the nicotinic neuromuscular junction; \u003Cstrong\u003Eoptic nerve meningioma\u003C/strong\u003E may cause progressive optic neuropathy, optociliary shunt vessels, visual field loss, and optic atrophy but does not characteristically distort the pupil; and \u003Cstrong\u003Einternuclear ophthalmoplegia\u003C/strong\u003E results from a medial longitudinal fasciculus lesion and affects horizontal conjugate gaze rather than iris anatomy or autonomic pupillary control.\u0026nbsp;\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "HighYield": false,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1981,
    "Name": "Acute papilloedema versus other causes of optic disc oedema",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient presents with acute optic disc swelling whose ophthalmoscopic appearance could represent papilloedema from raised intracranial pressure or oedema caused by an ischemic, inflammatory, infiltrative, or hypertensive optic nerve process. Which clinical assessment provides the most useful initial distinction between these diagnostic categories?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe visual function of the optic nerve in question (acuity, fields, color vision)\u003C/strong\u003E, because acute papilloedema and other causes of true optic disc oedema can have substantially overlapping funduscopic appearances, including disc elevation, hyperaemia, obscuration of the disc margins and surface vessels, venous congestion, loss of the physiological cup, and peripapillary flame-shaped haemorrhages. The appearance of the disc alone therefore may not reliably identify the underlying mechanism.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003EIn early papilloedema, optic nerve function is generally preserved despite striking disc swelling. Central visual acuity, colour vision, and pupillary responses are usually normal, while the earliest visual field abnormality is commonly enlargement of the physiological blind spot from elevation of the peripapillary retina. Transient visual obscurations may occur, but persistent reduction in central acuity and dyschromatopsia usually indicate advanced or fulminant papilloedema with secondary axonal injury rather than uncomplicated early disease.\u003C/p\u003E\n\u003Cp\u003EBy contrast, optic disc oedema caused by an intrinsic optic neuropathy usually produces early and measurable optic nerve dysfunction. Depending on the cause, examination may reveal:\u003C/p\u003E\n\u003Cul\u003E\n\u003Cli\u003EReduced visual acuity\u003C/li\u003E\n\u003Cli\u003EDyschromatopsia or red desaturation\u003C/li\u003E\n\u003Cli\u003EReduced contrast sensitivity\u003C/li\u003E\n\u003Cli\u003EA central, cecocentral, arcuate, or altitudinal visual field defect\u003C/li\u003E\n\u003Cli\u003EA relative afferent pupillary defect in unilateral or asymmetric disease\u003C/li\u003E\n\u003C/ul\u003E\n\u003Cp\u003EFor example, optic neuritis commonly produces central dysfunction and colour desaturation, while anterior ischemic optic neuropathy often produces an altitudinal or arcuate field defect. Thus, the relationship between the degree of swelling and the severity of visual dysfunction is more diagnostically valuable than hyperaemia or haemorrhage alone.\u0026nbsp;\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe presence or absence of optic nerve hyperemia\u003C/strong\u003E is not sufficiently discriminatory because both acute papilloedema and several inflammatory, ischemic, vascular, and infiltrative causes of disc oedema can appear hyperaemic.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe presence or absence of optic nerve gliosis\u003C/strong\u003E is not the key distinction in an acute presentation. Gliosis develops with longstanding or recurrent optic nerve injury and may give a chronically elevated disc a pale, grey, or glistening appearance.\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe presence or absence of peripapillary hemorrhages\u003C/strong\u003E is also unreliable because haemorrhages may occur in papilloedema, anterior ischemic optic neuropathy, central retinal vein occlusion, malignant hypertension, and other causes of disc swelling.\u003C/p\u003E\n\u003Cp\u003EA useful principle is:\u003C/p\u003E\n\u003Cp\u003E\u003Cstrong\u003EMarked swelling with relatively preserved visual function suggests early papilloedema, whereas swelling accompanied by substantial early acuity, colour, pupillary, or field dysfunction suggests an intrinsic optic neuropathy.\u003C/strong\u003E\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
    "Choices": [],
    "HighYield": true,
    "CategoryId": 8,
    "Category": null,
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  },
  {
    "Id": 1982,
    "Name": "Millard-Gubler syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EMillard-Gubler syndrome is NOT associated with which of the following findings?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EIpsilateral ataxia\u003C/strong\u003E, because Millard-Gubler syndrome is a crossed ventral pontine syndrome caused by a unilateral lesion involving the fascicles of cranial nerves VI and VII together with the descending corticospinal tract before its decussation in the caudal medulla; involvement of the ipsilateral abducens fascicle produces weakness of the lateral rectus with an ipsilateral abduction deficit and horizontal diplopia, involvement of the ipsilateral facial fascicle produces a lower motor neuron facial palsy affecting both the upper and lower facial muscles, and interruption of the corticospinal tract produces contralateral spastic hemiparesis or hemiplegia. Some modern descriptions regard ipsilateral facial paralysis with contralateral hemiparesis as the core syndrome and describe sixth nerve involvement as variable when the lesion extends medially, but the classic examination triad includes ipsilateral sixth and seventh nerve palsies with contralateral hemiplegia.  \u003Cstrong\u003EIpsilateral ataxia\u003C/strong\u003E is not a defining feature because the lesion is primarily ventral and does not characteristically involve the cerebellar peduncles or cerebellar connections; prominent ataxia instead suggests extension into adjacent pontocerebellar pathways or a different crossed brainstem syndrome. \u003Cstrong\u003EClaude syndrome\u003C/strong\u003E, for example, results from a dorsal midbrain lesion involving the oculomotor fascicles and superior cerebellar peduncular pathways, producing an ipsilateral third nerve palsy with contralateral cerebellar ataxia. A useful mnemonic for Millard-Gubler syndrome is\u003Cstrong\u003E\u201CFace and eye on the lesion side, limbs weak on the opposite side\u201D\u003C/strong\u003E: ipsilateral facial palsy and abduction deficit occur with contralateral hemiplegia.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  },
  {
    "Id": 1983,
    "Name": "Axial orbital MRI anatomy",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EOn the displayed axial FLAIR MRI at the level of the posterior orbits and midbrain, arrow \u201CA\u201D points to a tubular structure within the superior orbit. Which listed anatomical structure is indicated?\u003C/div\u003E\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Cimg src=\u0022/upload-2026-08-21-9544b3d5-e038-44d6-b213-f3c7b8f81dca.png\u0022\u003E\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003EThe superior ophthalmic vein (SOV)\u003C/strong\u003E, because arrow \u201CA\u201D points to the normal tubular vascular structure coursing posteriorly through the superior intraconal orbit, anatomically positioned above the optic nerve and below the superior rectus muscle. The SOV originates superomedially near the anterior orbit from venous tributaries that include the supraorbital, supratrochlear, and angular veins, then passes posterolaterally through the superior orbit, exits via the superior orbital fissure, and drains into the cavernous sinus; it is the largest and most consistently identifiable orbital vein and is usually visible on both axial and coronal CT or MRI.  The SOV should not be mistaken for \u003Cstrong\u003EThe optic nerve (ON)\u003C/strong\u003E, which is the more substantial structure extending from the posterior globe toward the optic canal and is indicated by arrow \u201CB\u201D; arrow \u201CC\u201D points to the left optic tract posterior to the chiasmal region, while arrow \u201CD\u201D points to the midbrain, whose paired cerebral peduncles create the characteristic axial \u201CMickey Mouse\u201D configuration. \u003Cstrong\u003EThe oculomotor nerve (CN3)\u003C/strong\u003E emerges from the ventral midbrain into the interpeduncular cistern and courses between the posterior cerebral and superior cerebellar arteries before entering the cavernous sinus, so it is neither situated within the superior orbital compartment at arrow \u201CA\u201D nor as conspicuous on routine FLAIR imaging as the orbital vein. \u003Cstrong\u003EThe trochlear nerve (CN4)\u003C/strong\u003E is substantially smaller, emerges dorsally from the midbrain, winds around the brainstem, and travels within the lateral wall of the cavernous sinus before entering the orbit through the superior orbital fissure, making it unlikely to correspond to the relatively prominent tubular structure shown. The SOV is clinically important because enlargement or abnormal enhancement can indicate disturbed cavernous sinus or orbital venous drainage, particularly in carotid-cavernous fistula, cavernous sinus thrombosis, SOV thrombosis, orbital inflammation, thyroid eye disease, or an orbital vascular malformation; however, the vein shown here is not pathologically enlarged.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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    "Category": null,
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  },
  {
    "Id": 1984,
    "Name": "Right one-and-a-half syndrome",
    "Body": "\u003Cdiv style=\u0022color: rgb(0, 0, 0); letter-spacing: normal; font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003EA patient has a right-sided one-and-a-half syndrome. Which statement correctly describes the resulting pattern of horizontal ocular motility?\u003C/div\u003E",
    "Explanation": "\u003C!--StartFragment--\u003E\u003Cdiv style=\u0022font-family: \u0026quot;Segoe UI\u0026quot;; line-height: 20px;\u0022\u003E\u003Ch2\u003EAnswer\u003C/h2\u003E\n\u003Cp\u003E\u003Cstrong\u003Ethere will be an abducting nystagmus of the left eye\u003C/strong\u003E, because a right one-and-a-half syndrome combines a \u003Cstrong\u003Eright horizontal conjugate gaze palsy\u003C/strong\u003E, the \u201Cone,\u201D with a \u003Cstrong\u003Eright internuclear ophthalmoplegia\u003C/strong\u003E, the \u201Chalf.\u201D A lesion involving the right paramedian pontine reticular formation or right abducens nucleus prevents rightward conjugate gaze: the right eye cannot abduct because the right lateral rectus receives no effective drive, and the left eye cannot adduct because the right abducens internuclear neurons cannot transmit the conjugate gaze command through the left medial longitudinal fasciculus to the left medial rectus subnucleus. Simultaneous involvement of the adjacent right medial longitudinal fasciculus prevents the right eye from adducting during attempted left gaze because the horizontal signal arising from the left abducens nucleus cannot ascend to the right medial rectus subnucleus. The right eye therefore has no effective horizontal movement, while the only preserved horizontal movement is \u003Cstrong\u003Eabduction of the left eye during attempted left gaze\u003C/strong\u003E; this abducting left eye characteristically develops dissociated abducting nystagmus, reflecting the internuclear ophthalmoplegia component and increased conjugate innervational drive under Hering\u2019s law. Vertical eye movements are generally preserved because the rostral midbrain vertical gaze centres are unaffected, so the statement that all gaze positions of the right eye are impaired would be incorrect if it includes vertical gaze. The only horizontal movement is neither right-eye abduction nor left-eye adduction. A useful localization rule is: \u003Cstrong\u003Ethe side of the syndrome is the immobile eye, while the fellow eye retains abduction with nystagmus\u003C/strong\u003E. One-and-a-half syndrome localizes to the ipsilateral dorsal pontine tegmentum and is most commonly caused by ischemic or hemorrhagic stroke in older patients and demyelination in younger patients, with tumors, infection, trauma, and vascular malformations as additional causes.\u003C/p\u003E\u003C/div\u003E\u003C!--EndFragment--\u003E",
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  }
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