Macula and retina flashcards
24 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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What is the first-line treatment for wet (neovascular) age-related macular degeneration?
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Intravitreal anti-VEGF injections (e.g. ranibizumab, aflibercept, faricimab).
Why? VEGF drives choroidal neovascularisation and increases vessel permeability; blocking it reduces leakage and bleeding. NICE: refer to a macula service within 1 working day and start treatment within 14 days; the agents are judged equivalent, so the cheapest suitable one is used.
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Which component of high-dose antioxidant supplements for dry AMD should smokers avoid, and why?
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Beta-carotene (vitamin A precursor) — it increases lung cancer risk in smokers.
Why? Later formulations (AREDS2) replaced beta-carotene with lutein and zeaxanthin; zinc and vitamins C and E remain.
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What does the "4-2-1 rule" define in diabetic retinopathy, and what does each number refer to?
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Severe non-proliferative (pre-proliferative) DR: haemorrhages in all 4 quadrants, venous beading in ≥2 quadrants, or IRMA in ≥1 quadrant (any one).
Why? These are signs of significant capillary closure and ischaemia, the step before VEGF-driven new vessels.
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What is the first-line treatment for proliferative diabetic retinopathy?
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Panretinal laser photocoagulation (PRP).
Why? PRP destroys ischaemic peripheral retina, reducing VEGF drive for new vessels. Anti-VEGF is added if PDR stays active after complete PRP.
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What is the first-line treatment for centre-involving diabetic macular oedema with reduced vision and a central retinal thickness of 400 micrometres or more?
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Intravitreal anti-VEGF injections (e.g. aflibercept, ranibizumab, faricimab).
Why? NICE: below 400 micrometres, consider anti-VEGF or macular laser; centre-involving oedema with good vision, laser or observation; non-centre-involving oedema, macular laser. A steroid implant is considered if response at 12 months is poor.
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Which fundal finding defines grade IV hypertensive retinopathy (Keith–Wagener–Barker)?
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Papilloedema (optic disc swelling).
Why? Grade I: arteriolar narrowing/silver wiring; II: AV nicking; III: flame haemorrhages, cotton-wool spots, hard exudates; IV: grade III plus papilloedema (malignant hypertension).
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What is the earliest symptom of retinitis pigmentosa?
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Night blindness (nyctalopia).
Why? Rods degenerate first, then cones; peripheral (tunnel) vision is lost next and central vision late. Fundus: bone-spicule pigmentation, thin vessels, waxy pale disc.
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Name the mitochondrial disorder with retinitis pigmentosa, external ophthalmoplegia, ptosis and heart block, starting before age 20.
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Kearns–Sayre syndrome.
Why? Mitochondrial disease affects high-energy tissues: retina, extraocular muscles, conducting system and inner ear (SNHL).
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What is the most common systemic association of angioid retinal streaks?
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Pseudoxanthoma elasticum.
Why? Angioid streaks are cracks in a brittle Bruch's membrane radiating from the disc; they can lead to choroidal neovascularisation and visual loss.
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Which gene and chromosome locus are linked with retinoblastoma?
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RB1 on chromosome 13q14.
Why? RB1 is a tumour suppressor; retinoblastoma is the commonest primary eye cancer in children under 5 and presents with leukocoria.
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What is the most important modifiable risk factor for age-related macular degeneration?
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Smoking.
Why? Age is the biggest risk factor overall. Smoking raises the risk of AMD and of blindness from it, so stopping smoking is part of managing both dry and wet AMD.
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What is the hallmark fundoscopic finding of dry AMD?
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Drusen — yellow deposits between the retinal pigment epithelium and Bruch's membrane.
Why? Dry AMD (about 90%) progresses slowly to geographic atrophy. Wet AMD (about 10%) is choroidal neovascularisation with leakage and bleeding, and progresses fast.
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Which simple chart detects the distortion of straight lines (metamorphopsia) caused by macular disease?
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The Amsler grid.
Why? Wavy or missing lines on the grid suggest macular fluid, as in wet AMD, and need urgent referral.
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According to NICE, what is the first-line imaging test for suspected wet (neovascular) AMD?
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Optical coherence tomography (OCT); fluorescein angiography is added if OCT does not exclude neovascularisation.
Why? OCT shows fluid within and under the retina quickly and without injection; it is also used to monitor anti-VEGF response.
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Faricimab, used for wet AMD and diabetic macular oedema, blocks which two targets?
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VEGF-A and angiopoietin-2 (Ang-2).
Why? It is a bispecific antibody; blocking both pathways stabilises vessels and can allow longer gaps between injections than older anti-VEGF drugs such as ranibizumab and aflibercept.
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What is the most serious sight-threatening complication of an intravitreal anti-VEGF injection?
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Endophthalmitis.
Why? Other risks include a rise in IOP, retinal tear/detachment and lens injury. Patients are told to report a painful red eye or falling vision urgently.
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An 82-year-old man with advanced macular degeneration in both eyes sees vivid images of people and patterns. He knows they are not real and has no other psychiatric or cognitive symptoms. What is the diagnosis?
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Charles Bonnet syndrome.
Why? Complex visual hallucinations with preserved insight in people with significant visual loss. Reassurance is the main treatment.
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What is the earliest clinical sign of diabetic retinopathy?
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Microaneurysms.
Why? They are outpouchings of weakened capillary walls. Mild NPDR = microaneurysms only; dot-blot haemorrhages and hard exudates appear as it progresses.
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From what age does the NHS diabetic eye screening programme invite people with diabetes?
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From age 12.
Why? Screening uses digital retinal photographs after dilating drops. It is yearly, or every 2 years for people with no retinopathy on their last two consecutive screens (phased in across England from October 2023; already in place in Scotland, Wales and Northern Ireland).
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When should a pregnant woman with pre-existing diabetes have retinal assessment?
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After her first antenatal appointment and again at 28 weeks — plus at 16–20 weeks if any retinopathy is found at booking.
Why? Retinopathy can progress rapidly in pregnancy, especially with quick tightening of glucose control.
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Flame haemorrhages, cotton-wool spots and hard exudates, without disc swelling, indicate which Keith–Wagener–Barker grade?
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Grade III.
Why? Grade III plus papilloedema is grade IV (malignant hypertension). Cotton-wool spots are nerve-fibre-layer infarcts.
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Which substance accumulates in Refsum disease, causing retinitis pigmentosa, peripheral neuropathy and ataxia?
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Phytanic acid.
Why? It is an autosomal recessive defect of phytanic acid breakdown; other features include sensorineural deafness, ichthyosis, anosmia and arrhythmias.
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What is the most common presenting sign of retinoblastoma?
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Leukocoria (a white pupillary reflex).
Why? Strabismus is the next most common. Any child with an absent or white red reflex needs urgent ophthalmology referral.
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Which lipid-lowering drug does NICE (2024) suggest ophthalmologists consider to slow non-proliferative diabetic retinopathy in type 2 diabetes?
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Fenofibrate (an off-label use).
Why? It reduced retinopathy progression in trials. NICE does not recommend blood pressure drugs in people without hypertension just to protect the retina, and makes no statin recommendation for this.