Sudden painless visual loss flashcards
16 high-yield MRCP Part 1 cards from the Intellect Medicos Ophthalmology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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A 74-year-old woman has new temporal headache and jaw claudication, and woke with painless loss of vision in her right eye. The right disc is pale, chalky-white and swollen. What is the first-line management?
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Start high-dose glucocorticoid immediately, before biopsy/ultrasound — with visual loss, IV methylprednisolone (0.5–1 g daily for up to 3 days) then oral prednisolone.
Why? This is arteritic AION from giant cell arteritis occluding the short posterior ciliary arteries. Steroids aim to protect the other eye; lost vision rarely recovers.
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Besides ESR/CRP, what is the first-line confirmatory test for suspected giant cell arteritis in the UK?
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Urgent temporal (± axillary) artery ultrasound looking for a "halo" sign, or temporal artery biopsy (at least 1 cm long).
Why? Fast-track GCA pathways often use ultrasound first; biopsy can miss skip lesions. Do them promptly (ideally within a week of starting steroids), because steroids gradually reduce their sensitivity.
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Which biologic is NICE-approved for relapsing or refractory giant cell arteritis, and what is its target?
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Tocilizumab — an IL-6 receptor monoclonal antibody.
Why? It is steroid-sparing and allows faster steroid tapering. NICE funds it only for relapsing or refractory GCA, given with a steroid taper, and stopped after at most 1 year of continuous treatment.
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What is the classic fundal appearance of central retinal artery occlusion?
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A cherry-red spot at the macula on a pale, swollen retina.
Why? The ischaemic inner retina turns pale, but the thin fovea still shows the intact choroidal circulation underneath. There is also an RAPD.
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What is the first-line management of acute central retinal artery occlusion?
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Treat as a stroke equivalent: emergency same-day referral (eye / stroke service), urgent ESR/CRP to exclude GCA, and vascular work-up (ECG for AF, carotid imaging).
Why? Most CRAO is embolic from carotid atheroma or AF, so these patients are at high risk of stroke. No reperfusion therapy has proven benefit outside trials.
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Which haematological condition should be looked for in central retinal vein occlusion?
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Polycythaemia (hyperviscosity) — check a full blood count.
Why? Other risk factors are age over 50, hypertension, diabetes and glaucoma. Fundus: widespread flame and dot-blot haemorrhages, swollen disc, cotton-wool spots.
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What is the first-line treatment for macular oedema caused by retinal vein occlusion?
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Intravitreal anti-VEGF injections (e.g. ranibizumab, aflibercept, faricimab); a dexamethasone implant is an alternative.
Why? Vein blockage causes ischaemia and VEGF release, which makes the macula leak. Ischaemic CRVO with new vessels needs panretinal laser.
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A short-sighted 55-year-old man has new flashes and floaters, followed by a dark curtain spreading across his vision from one side. What is the most likely diagnosis and the first-line management?
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Rhegmatogenous retinal detachment — emergency same-day ophthalmology referral for surgical repair.
Why? A retinal tear lets fluid lift the retina; it is most urgent while the macula is still attached. The fundus shows an elevated grey retina.
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Which optic disc anatomy predisposes to non-arteritic anterior ischaemic optic neuropathy?
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A small, crowded disc with little or no cup (a "disc at risk").
Why? Other risk factors are vascular: hypertension, diabetes and older age. Vision loss is typically noticed on waking.
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In arteritic anterior ischaemic optic neuropathy the swollen disc is ______; in non-arteritic AION it is hyperaemic (pink).
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pale, chalky white
Why? Arteritic AION is due to GCA occluding the short posterior ciliary arteries; non-arteritic AION is atherosclerotic small-vessel disease.
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In arteritic anterior ischaemic optic neuropathy the swollen disc is pale, chalky white; in non-arteritic AION it is ______.
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hyperaemic (pink)
Why? Arteritic AION is due to GCA occluding the short posterior ciliary arteries; non-arteritic AION is atherosclerotic small-vessel disease.
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What is the most common cause of central retinal artery occlusion?
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Embolism from carotid artery atherosclerosis.
Why? AF is the other main embolic source. GCA and antiphospholipid syndrome are less common causes, but GCA must always be excluded in older patients.
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Which serious complication can follow ischaemic central retinal vein occlusion, typically about 3 months later?
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Neovascular glaucoma (new vessels on the iris and angle — rubeosis iridis).
Why? Retinal ischaemia drives VEGF release; new vessels block the drainage angle. It is treated with panretinal laser (± anti-VEGF) and IOP-lowering drugs.
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What is the commonest cause of vitreous haemorrhage in adults?
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Proliferative diabetic retinopathy.
Why? Fragile new vessels bleed into the vitreous, causing sudden floaters or "smoke", a reduced red reflex and no view of the fundus. Other causes: retinal tear/PVD, trauma, vein occlusion.
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What is the usual starting dose of oral prednisolone for giant cell arteritis without visual symptoms (BSR)?
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40–60 mg daily.
Why? Start immediately on clinical suspicion, then taper slowly once symptoms and inflammatory markers settle. With acute or intermittent visual loss, IV methylprednisolone 0.5–1 g daily for up to 3 days may be given first.
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A 70-year-old man had 5 minutes of painless loss of vision in his left eye, "like a curtain coming down", which fully recovered. He has no headache or jaw claudication and takes no antiplatelets. What is the first-line management?
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Treat as a TIA: aspirin 300 mg immediately and specialist TIA assessment within 24 hours.
Why? Amaurosis fugax is transient retinal ischaemia, usually embolic from carotid atheroma, so carotid imaging is key. Check ESR/CRP to exclude GCA in anyone over 50.