Always test each eye separately ^[1]

Why VA is the "vital sign" of the eye: Just as blood pressure quantifies cardiovascular function, VA quantifies the entire visual pathway — from cornea to occipital cortex. An abnormal VA tells you something is wrong; the pattern of abnormality tells you where.

Visual impairment is not defined by acuity alone. The lecture slide identifies five visual functions that can be affected: visual acuity, visual field, contrast sensitivity, colour vision, and stereopsis. ^[1]

Snellen Chart:

6/6 vision is defined as the ability to resolve two points separated by a visual angle of one minute of arc (1/60 of a degree). ^[1]

• The notation "6/X" means: at 6 metres, the patient reads a letter that a normal eye reads at X metres.
• 6/6 = normal; 6/12 = the patient needs to be at 6 m to read what normal sees at 12 m — moderate reduction.

Why the Snellen system works: Letters of different sizes subtend different visual angles at 6 m. The smallest line where each letter subtends exactly 5 arcminutes (with each stroke 1 arcminute) is the 6/6 line.

Visual Acuity Conversion Table (from lecture slide) ^[1]:

The 6/6 (20/20) row corresponds to decimal 1.00 and LogMAR 0.00 — the reference standard.

WHO Criteria for Vision Impairment Severity: ^[1]

These epidemiological categories use presenting visual acuity in the better eye. Severe field constriction is also assessed in the better eye; the better-eye qualifier is essential and was implicit in the slide table. ^[10]

Recording VA worse than 3/60: When a patient cannot read even the largest Snellen letter at 3 m, record descending levels:

1. Counting Fingers (CF) — at specified distance (e.g., CF at 1 m)
2. Hand Movements (HM) — can perceive a moving hand
3. Light Perception (LP) — can detect a light source
4. No Light Perception (NLP) — no detectable vision

Record the eye, testing distance, correction and illumination, for example OD CF at 1 m, unaided. CF/HM/LP/NLP are descriptive bedside levels, not interchangeable Snellen equivalents.

How do you know the refractive error is under-corrected? → Pinhole visual acuity ^[1]

Why it works from first principles: A small aperture blocks many peripheral divergent rays, reduces the retinal blur circle and increases depth of focus. It therefore reduces refractive blur; it does not literally eliminate all refractive error.

Test one eye at a time with the patient's usual distance correction, ask them to move the occluder until they find the aperture, and record the best line. A pinhole is a screen for a refractive contribution, not a diagnostic test for cataract or macular disease.

RAPD — Relative Afferent Pupillary Defect ^[1]

• Ask patient to look to the distance
• Look at the eye you are examining
• Swing from one eye to another
• Looking for reactions — change in size from small to big (dilate) or big to small (constriction)

The Swinging Flashlight Test — Why it works:

The pupillary light reflex is a bilateral, consensual reflex. Light in one eye constricts both pupils equally because the signal crosses at the optic chiasm and pretectal nuclei. When you swing the light from the normal eye to an eye with optic nerve damage:

• The total afferent input drops
• Both pupils therefore dilate (paradoxical dilation of the affected eye when light swings onto it)
• This is the RAPD or "Marcus Gunn pupil"

Technique hidden in the slide demonstration: dim the room, have the patient fixate at distance to avoid the near response, illuminate each eye from the same angle/intensity for about 2–3 seconds, and swing briskly between eyes. Watch both pupils if possible: on moving from the better to the poorer afferent eye, both pupils constrict less or appear to dilate.

Pupillary light reflex pathway (from lecture diagram): ^[1]

1. Light enters the eye → impulses travel along the optic nerve → optic chiasma → optic tract
2. Before reaching the lateral geniculate body, some fibres branch to the midbrain pretectal nucleus
3. Pretectal nucleus projects bilaterally to the Edinger–Westphal nuclei
4. Preganglionic parasympathetic fibres travel in CN III to the ciliary ganglion
5. Postganglionic fibres in the short ciliary nerves innervate the constrictor pupillae → pupillary constriction

Because the pretectal nucleus projects to both Edinger–Westphal nuclei, light in one eye produces both a direct and consensual response — the anatomical basis for the swinging flashlight test.

What does a relative afferent pupillary defect indicate? → Asymmetric optic nerve or retinal disease on the side of the RAPD ^[1]

Key clinical points about RAPD:

• It indicates a unilateral or asymmetric lesion of the optic nerve (or extensive retinal disease)
• It does not usually occur with refractive error or uncomplicated cataract. A very dense asymmetric media opacity can complicate interpretation, so an unexpected RAPD still requires retinal/optic-nerve assessment.
• It DOES occur in: optic neuritis, ischaemic optic neuropathy, glaucoma (advanced unilateral), central retinal artery occlusion (extensive retinal damage), compressive optic neuropathy

Can a patient with bilateral optic neuropathy be associated with an RAPD? ^[1] Answer: YES — if the damage is asymmetric. A patient with bilateral optic neuritis but one side worse than the other will have an RAPD in the worse eye. If damage is perfectly symmetrical, there will be no RAPD (because "relative" means comparing one side to the other).

How to report optic disc examination findings: ^[1]

1. Margin: clear or blurred
2. Neuroretinal rim colour: pink or pale
3. Vertical cup-to-disc ratio

This structured reporting is what examiners expect in OSCE and written answers.

Why each component matters:

The slide's three-item sequence is a minimum. A useful full description is: disc size; margin; rim colour and width; vertical C/D ratio; focal notching; retinal nerve-fibre-layer (RNFL) defects; disc haemorrhage; vessels; and inter-eye asymmetry. A large physiological cup in a large disc may be normal, while a small disc can have glaucoma with a modest C/D ratio. Look for focal superior/inferior rim loss rather than relying on a single numerical cutoff.

Direct vs Indirect Ophthalmoscopy:

Direct ophthalmoscopy / Indirect ophthalmoscopy ^[1]

Confrontation visual field testing is a bedside screening tool. Each eye is tested separately. The examiner compares the patient's visual field to their own (assuming normal fields). This detects:

• Peripheral field loss (glaucoma, retinal detachment)
• Hemianopias (stroke, pituitary tumour)
• Central scotomas (macular disease, optic neuritis)

Tests CN III (SR, IR, MR, IO + LPS), CN IV (SO), CN VI (LR). Diplopia, restriction, or nystagmus may indicate cranial nerve palsy (e.g., diabetic mononeuropathy), thyroid eye disease, or orbital pathology.

Differential Diagnosis of a pale neuroretinal rim (optic neuropathy): ^[1]

Signs of optic disc swelling: ^[1]

• Blurred optic disc margin
• Hyperaemia — dilation of the disc capillaries
• Haemorrhage: nerve fibre layer or retinal haemorrhages
• Dilation and tortuosity of retinal veins
• Soft exudates or cotton wool spots

Why each sign occurs:

• Blurred margin: Axonal swelling from impaired axoplasmic flow (due to raised pressure, inflammation, or ischaemia) causes the nerve fibres at the disc edge to swell and obscure the margin
• Hyperaemia: Vascular engorgement from impaired venous drainage
• Haemorrhages: Rupture of small peripapillary vessels under pressure
• Venous dilation/tortuosity: Back-pressure from impaired venous return
• Cotton wool spots: Ischaemic infarcts of the nerve fibre layer (retinal arteriolar occlusion → ganglion cell ischaemia)

Differential Diagnosis of Optic Disc Swelling: ^[1]

Also consider pseudopapilloedema, especially a crowded hyperopic disc or optic-disc drusen. “Papilloedema” is reserved for disc swelling caused by raised intracranial pressure; it is usually bilateral but may be asymmetric. Disc swelling is a sign, not a diagnosis.

Glaucoma, a neurodegenerative disease of the optic nerve, is the leading cause of irreversible blindness worldwide. ^[1] With 76 million glaucoma patients in 2020 worldwide, the need for early detection is pressing. ^[1]

Why glaucoma is a "silent" disease:

Glaucoma patients are not aware of visual impairment/blindness even at the advanced stages! ^[1]

This is because:

1. Glaucoma preferentially damages peripheral visual field first (mid-peripheral arcuate scotomas)
2. The fellow eye and perceptual “filling in” can conceal missing information
3. Central VA is preserved until very late stages
4. Chronic open-angle glaucoma is usually painless

What the lecture's paired street/football images mean: a glaucoma scotoma is not necessarily perceived as a black patch. Objects may simply disappear into apparently continuous background, which is why patients can miss hazards without noticing a hole in vision. The staged “tunnel vision” pictures are an intuition aid, not a literal or diagnostic simulation of an individual patient's field.

Diagnosis:

1. Glaucoma is a chronic progressive optic neuropathy. ^[1] 2. Clinical diagnosis of glaucoma is predicated on the detection of a thinned retinal nerve fibre layer (RNFL) and narrowed neuroretinal rim. (World Glaucoma Association Consensus Statement) ^[1]

This means glaucoma is diagnosed by characteristic optic-nerve/RNFL damage, with corresponding functional assessment, not by intraocular pressure (IOP) alone. IOP is the major modifiable risk factor, but:

• Some patients have glaucoma with normal IOP ("normal tension glaucoma")
• Some patients have high IOP without glaucoma ("ocular hypertension")

Current standard for detection and monitoring:

Structure: Optical coherence tomography (OCT) is the prevailing technology to detect retinal nerve fibre layer (RNFL) thinning. ^[1] Function: Visual field testing determines the extent of functional loss. ^[1]

How to read the OCT figure on the slide:

• The peripapillary RNFL thickness trace normally has two superior/inferior peaks (the “double hump”).
• Colour coding compares the patient with the machine's normative database; green does not guarantee health and red does not guarantee disease.
• The en-face reflectance image highlights a wedge-shaped RNFL defect that should anatomically correspond to rim loss and a visual-field defect.
• Check signal strength, segmentation, centration, refractive error and scan artefact before interpreting. Apparent structure–function discordance is common in early disease and must be followed longitudinally.

Cataract ^[1] — Examined by slit lamp examination

What is a cataract? Opacification of the crystalline lens. It is the most common cause of reversible blindness worldwide and the most common cause of visual impairment overall.

Why cataracts form:

• Age-related (most common): Cumulative oxidative damage → protein denaturation and aggregation in lens fibres → loss of transparency
• Diabetic: Hyperglycaemia activates the polyol (sorbitol) pathway via aldose reductase → sorbitol accumulates in lens → osmotic swelling → lens fibre disruption ^[3]
• Steroid-induced: Posterior subcapsular cataract — glucocorticoids alter lens epithelial cell metabolism
• Traumatic, congenital, radiation-induced

Types:

Reading the lecture images: a mature cataract can make the pupil look white and abolish the red reflex, but earlier cataracts require a slit lamp. Direct illumination shows the opacity; an optical section localises it within the lens, while retroillumination outlines cortical or posterior subcapsular opacities against the red reflex.

Diagnosis: Slit lamp examination — look for lens opacity and assess the red reflex (diminished or absent in dense cataract). A white pupil has an important differential, particularly in a child, and should not be assumed to be cataract without examination.

Management: Surgical removal (phacoemulsification) with intraocular lens (IOL) implant when VA impairs function. There is no effective medical treatment.

Undercorrected refractive error ^[1] — the most common cause of visual impairment globally (the answer to the opening poll question)

Types of refractive error:

Reading the ray diagrams:

• In myopia, parallel distance rays focus in front of the retina; a minus/concave lens diverges them before they enter the eye.
• In hyperopia, the relaxed eye would focus rays behind the retina; a plus/convex lens converges them. A young patient may mask hyperopia by accommodation, so the slide's “near blur only” image is deliberately simplified.
• Axial length is a common explanation (long eye in myopia, short eye in hyperopia), but corneal/lenticular power also matters.

Why astigmatism causes blur: The simplified “rugby-ball cornea” shows two principal meridians with different optical powers, producing two focal lines rather than one point focus. Astigmatism may be corneal or lenticular. Regular astigmatism is corrected with a cylindrical/toric lens; the streaked lights and doubled bridge on the slides demonstrate direction-dependent blur rather than a unique diagnostic appearance. ^[1]

Complications related to myopia: ^[1]

• Glaucoma
• Retinal detachment
• Myopic choroidal neovascularization
• Myopic macular atrophy

Why myopia predisposes to these complications: In myopic eyes, the axial length is increased → the retina is stretched thinner → peripheral retinal degeneration → tears/holes → retinal detachment. The vitreous is also more liquefied → posterior vitreous detachment occurs earlier. The optic nerve head is larger and more susceptible to glaucomatous damage. Scleral stretching at the macula causes macular atrophy.

Complications related to hyperopia: ^[1]

• Primary angle-closure glaucoma

Why hyperopia predisposes to angle-closure: Hyperopic eyes are shorter → the anterior chamber is shallower → the peripheral iris is closer to the trabecular meshwork → the angle is narrower → risk of pupillary block (when the mid-dilated pupil apposes the lens, aqueous cannot flow from posterior to anterior chamber → iris bows forward → angle closes → IOP spikes).

Distinguishing refractive error from other causes of poor VA:

Pinhole visual acuity — improvement indicates that refractive blur contributes to the reduced VA. ^[1]

The lecture shows sequential images of a scene through varying refractive errors vs through a cataract vs corrected. The key teaching point is that both cataract and refractive error blur vision, but:

• Refractive error: usually improves with pinhole and can be quantified by refraction
• Cataract: response is variable; diagnose by red reflex/slit-lamp examination, not by a pinhole rule

Age-related macular degeneration ^[1]

Two types:

Dry AMD — geographic atrophy and drusen ^[1] Wet AMD — treated with anti-VEGF intravitreal injection ^[1]

Clinical presentation:

• Gradual painless central visual loss
• Metamorphopsia — distortion of straight lines (detected with Amsler grid)

Amsler Grid — metamorphopsia ^[1]

Why metamorphopsia occurs: Macular structural distortion changes photoreceptor alignment → straight lines appear wavy. Test the Amsler grid one eye at a time with near correction. New distortion or a central missing patch needs prompt macular assessment; the grid supports symptom monitoring but does not replace examination/OCT.

Pathology — cross-sectional view (from lecture diagrams): ^[1]

• Non-neovascular (“dry”) AMD: Conventional drusen lie between the RPE basal lamina and Bruch's membrane. Progressive loss of outer retina, RPE and choriocapillaris produces geographic atrophy — sharply demarcated pallor with visible underlying choroidal vessels.
• Neovascular (“wet”) AMD: Macular neovascularisation can produce sub-RPE, subretinal or intraretinal fluid, haemorrhage, pigment-epithelial detachment and later fibrosis; “wet” is a useful label but does not specify the vessel compartment.

Reading the fundus–OCT pair on the slide: the colour photograph localises the macular haemorrhagic/exudative lesion; the cross-sectional OCT demonstrates distortion/elevation of the RPE–retina complex with retinal fluid. OCT therefore reveals anatomy that a two-dimensional photograph cannot and is central to monitoring treatment response.

Why anti-VEGF works: VEGF signalling promotes vascular permeability and neovascular growth. Intravitreal anti-VEGF suppresses leakage/activity and can stabilise or improve vision, but treatment commonly requires a loading and repeated monitoring/injection strategy rather than a single injection. [4,12]

Diabetic retinopathy ^[1]

DR is covered in detail in the GC 042 lecture. Key points from this lecture and supporting sources:

Pathophysiology (from first principles): ^{[3] [5]}

1. Chronic hyperglycaemia → metabolic damage to retinal capillary pericytes and endothelial cells
2. Microangiopathy: Loss of pericytes → microaneurysm formation → dot-and-blot haemorrhages
3. Capillary leakage: Breakdown of blood-retinal barrier → hard exudates (lipoprotein deposits) → retinal oedema
4. Ischaemia: Capillary occlusion → cotton wool spots (nerve fibre layer infarcts) → venous beading → IRMA (intraretinal microvascular abnormalities)
5. Neovascularization: Ischaemia → VEGF upregulation → new fragile vessels grow (proliferative DR) → vitreous haemorrhage → tractional retinal detachment

Classification:

Lecture-slide screening grid (scheme-specific): ^[1]

NVD = neovascularisation at disc; NVE = neovascularisation elsewhere.

Do not merge this grid with the international clinical disease-severity scale above. The slide uses an R0–R4/M0–M2 screening/referral scheme and even labels a lesion “flame exudate”; the correct morphologic term is flame-shaped haemorrhage (hard exudates are yellow lipid deposits). Grade definitions and recall intervals vary across screening programmes and editions, and macular referral now also depends on OCT, VA and local pathways. Current ADA guidance recommends prompt ophthalmology referral for any DME, moderate-or-worse NPDR, or any PDR. ^[13]

Reading the DR photographs:

• NPDR: microaneurysms are tiny red dots; dot/blot haemorrhages lie deeper in the retina; hard exudates are sharply defined yellow lipid; cotton-wool spots are fluffy white nerve-fibre-layer infarcts.
• PDR: the defining change is fragile new vessels on or near the disc (NVD) or elsewhere (NVE), not simply “more haemorrhages.” These can bleed into the vitreous or form fibrovascular tissue that pulls the retina off.
• DME: can coexist with any retinopathy grade, so a peripheral DR grade alone does not state whether the macula is safe.

Important ocular complications of DM (beyond retinopathy): ^[3]

• Diabetic macular oedema (commonest cause of vision loss in DM)
• Neovascular glaucoma — rubeosis iridis (new vessels on iris → angle closure)
• Vitreous haemorrhage — blood in the vitreous, commonly from fragile preretinal new vessels in PDR or from a retinal tear/PVD; causes sudden floaters, haze or marked visual loss and may obscure the red reflex/fundus view. Media opacity alone does not create an RAPD, but an RAPD may be present if the underlying eye also has severe asymmetric retinal ischaemia, retinal detachment or optic-nerve disease. If the retina cannot be seen, urgent assessment may require B-scan ultrasonography. [1,14]
• CN III, IV, VI palsies (diabetic mononeuropathy)
• Cataract (sorbitol accumulation)
• ↑ eye infections

Subconjunctival haemorrhage ^[1]

• Bleeding from small conjunctival/episcleral vessels → bright red, flat discolouration of the sclera
• Painless, no visual disturbance, no photophobia
• Usually self-limiting (resolves in 7–14 days) ^[4]
• Causes: idiopathic (most common), minor trauma (rubbing), hypertension, coagulopathy/anticoagulants, Valsalva (coughing, straining), conjunctivitis
• No treatment needed — reassurance
• Check BP and bleeding history if recurrent ^[4]

The slide image shows a sharply demarcated sheet of blood under the conjunctiva, with a clear cornea and normal-looking pupil. Pain, photophobia, reduced VA, trauma/foreign body or an irregular pupil should prompt a search for a more serious diagnosis rather than reassurance alone.

Pterygium ^[1]

• Triangular fibrovascular growth of conjunctiva that extends onto the cornea (from nasal side, toward centre)
• UV exposure is the major risk factor (hence more common in tropical/equatorial regions)
• Can cause astigmatism, visual obstruction if it encroaches on the visual axis
• Management: observation for mild cases; surgical excision with conjunctival autograft if threatening visual axis or causing significant astigmatism (recurrence rate is high without graft)

On the slide, the triangular fibrovascular tissue crosses the limbus onto the cornea, usually from the nasal side. Distinguish it from a pinguecula, which remains on the conjunctiva and does not invade the cornea.

Dry eye disease — punctate epithelial erosion ^[1]

The traditional teaching model divides the tear film into three layers:

1. Lipid layer (outermost) — produced by Meibomian glands (tarsal glands) → prevents evaporation
2. Aqueous layer (middle) — produced by lacrimal gland → provides lubrication, nutrients, antimicrobial factors
3. Mucin layer (innermost) — produced by conjunctival goblet cells → allows aqueous layer to adhere to corneal epithelium

This remains useful for exams, although modern physiology treats the aqueous and mucin components as an interacting mucoaqueous phase beneath a superficial lipid layer rather than three perfectly discrete strata.

Dry eye disease occurs when:

• Aqueous deficiency: Reduced lacrimal gland secretion (e.g., Sjögren's syndrome, ageing, post-radiation)
• Evaporative: Meibomian gland dysfunction (most common cause), blepharitis, reduced blink rate (screen use)
• Mucin deficiency: Damage to goblet cells (e.g., chemical burns, cicatricial pemphigoid, Stevens-Johnson syndrome)

Symptoms: Gritty/sandy sensation, burning, foreign body sensation, paradoxical tearing (reflex watering), worse in dry/windy environments

Reading the fluorescein image: the numerous tiny green points are areas where fluorescein pools in superficial epithelial disruption—superficial punctate keratopathy. The staining pattern (inferior, interpalpebral or diffuse) helps suggest exposure/toxic/dry-eye mechanisms but is not specific by itself.

Signs: punctate epithelial staining (fluorescein under cobalt-blue illumination), reduced tear break-up time and, in selected cases, reduced tear production on Schirmer testing. Cutoffs and interpretation depend on technique and clinical context.

Management: Artificial tears, warm compresses for MGD, punctal plugs in severe cases, cyclosporine A drops for inflammatory dry eye

Meibomian gland dysfunction ^[1]

• The most common cause of evaporative dry eye
• Meibomian glands (sebaceous glands in the tarsal plate) produce the lipid layer of the tear film
• Obstruction → lipid deficiency → rapid tear film evaporation → dry eye
• Associated with blepharitis, rosacea
• The slide close-up shows capped/plugged meibomian orifices and altered secretions at the lid margin. Management starts with warm compresses, lid hygiene and lubricants; anti-inflammatory or antimicrobial treatment is selected for the individual phenotype rather than used routinely for every patient.

Floaters ^[1]

What floaters are: Shadows cast on the retina by opacities in the vitreous humour. They move with eye movement and are most noticeable against bright backgrounds.

Common causes:

• Posterior vitreous detachment (PVD): Most common cause in adults > 50. The vitreous shrinks and separates from the retina → collagen fibres clump → cast shadows. Usually benign.
• Vitreous haemorrhage: Sudden shower of floaters → think DR, retinal tear
• Inflammatory cells (vitritis): In posterior uveitis
• Retinal tear or detachment: Floaters + flashes of light (photopsia) = RED FLAG

A Weiss ring—the ring-like posterior hyaloid remnant from separation around the optic disc—supports a PVD but its absence does not exclude one. The slide's eye diagram makes the key mechanism visible: an opacity in the vitreous is perceived because it casts a moving shadow on the retina. ^[1]

Risk quantification (JAMA systematic review presented in lecture): ^[1]

• Among patients with acute-onset floaters/flashes referred to ophthalmology, the prevalence of retinal tear is 14 % (95 % CI 12–16 %)
• Subjective visual reduction is the most important symptom predicting retinal tear (LR 5.0)
• Vitreous haemorrhage on slit-lamp examination has the highest positive LR for retinal tear (LR 10)
• Absence of vitreous pigment on examination is the best negative predictor (LR 0.23)
• Patients initially diagnosed with uncomplicated PVD still carried a 3.4 % risk of a later retinal tear within 6 weeks; ≥10 new floaters or subjective visual reduction at re-presentation increased concern

These figures come from the 2009 JAMA evidence review reproduced in the lecture and describe referred patients, not a population-screening probability. They support—not replace—the clinical action: acute monocular flashes/floaters need a prompt dilated peripheral retinal examination, preferably indirect ophthalmoscopy with scleral depression. Vitreous pigment (“tobacco dust”) or haemorrhage strongly raises suspicion; a curtain/field defect or reduced central vision is a same-day emergency. Follow-up and explicit return precautions remain important even when the initial examination shows uncomplicated PVD. ^[15]

Retinal tear with detachment ^[1]

Why this is an emergency: Once the retina detaches from the underlying RPE, photoreceptors lose their blood supply and undergo irreversible degeneration. If the macula is involved ("macula-off"), prognosis for visual recovery is significantly worse.

Pathophysiology:

1. PVD → vitreous traction on retina → retinal tear
2. Liquefied vitreous flows through the tear → separates sensory retina from RPE → rhegmatogenous retinal detachment

Symptoms:

• New floaters (sudden onset, shower of spots)
• Flashes of light (photopsia) — caused by vitreous traction stimulating the retina mechanically
• "Curtain" or shadow descending across visual field — as detachment progresses

Risk factors: High myopia, prior eye surgery, trauma, lattice degeneration, family history, PVD

Reading the final fundus photograph: the horseshoe/flap tear is the entry point; the adjacent grey, elevated, corrugated retina represents neurosensory retina separated by subretinal fluid. Finding one tear does not end the examination—the peripheral retina must be searched for additional breaks.

Management: urgent/same-day ophthalmological assessment when detachment or an acute symptomatic tear is suspected. Surgical repair options include:

• Laser photocoagulation / cryotherapy (for tears without detachment)
• Pneumatic retinopexy, scleral buckle, or pars plana vitrectomy (for detachment)

The Red Eye lecture classifies red eye by location and urgency. Key discriminators for the exam:

The five major conditions used to structure this lecture are:

1. Uncorrected refractive error
2. Cataract
3. Glaucoma
4. AMD
5. Diabetic retinopathy

These overlap with the dominant global causes, but their rank depends on whether the outcome is blindness or MSVI, the age group, year and region.

GBD 2020 data (presented in lecture): Leading global causes of blindness in people aged ≥ 50 years (2020) ^[1]:

Leading causes of moderate and severe vision impairment (MSVI): uncorrected refractive error (86.1 million) and cataract (78.8 million). Note that the ranking differs between blindness (cataract #1) and MSVI (refractive error #1). ^[1]

2021 Fourth Summative MCQ Q13: A 54-year-old lady on hydroxychloroquine for 8 years complains of bilateral progressive blurring of vision. Most likely cause = C. Bull's eye maculopathy ^[7]

Hydroxychloroquine accumulates in the RPE → damage to photoreceptors → characteristic ring of RPE depigmentation around the fovea ("bull's eye"). Risk increases with cumulative dose (> 5 years or > 5 mg/kg/day). Annual screening with OCT and visual field testing is recommended after 5 years of use.

2017 Fourth Summative SAQ Q3: A 30-year-old woman with "sand in eye" sensation and xerostomia, anti-Ro/anti-La positive → Sjögren's syndrome ^[8]

Sjögren's causes keratoconjunctivitis sicca (dry eye from lacrimal gland lymphocytic infiltration) and xerostomia (dry mouth from salivary gland infiltration). ^[9]