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What's In This Guide

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• Days 1-2: Sections 1-6 (core types + pathophysiology)
• Days 3-4: Sections 7-8 (secondary glaucomas + investigations)
• Days 5-6: Sections 9-11 (pharmacology + procedures)
• Day 7: Sections 12-16 (special topics + trials + mnemonics)
• Day 8 (eve of exam): Quick revision of Section 16 (20 high-yield points only)

• It is a standard PDF 1.4 file readable by any PDF viewer (Adobe Reader, Foxit, Preview on Mac, any mobile PDF app)
• The file path in the sandbox is: /home/daytona/workspace/glaucoma-study-guide/glaucoma_study_guide.pdf

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Option 1 — PDF (14 pages, 367 KB)

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Option 2 — Word Document (.docx, 31 KB)

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📝 GLAUCOMA — LONG ANSWER QUESTIONS WITH MARKING SCHEME

20 Marks Each | Ophthalmology PG Year 2 | Exam: 24 June 2026

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Q1. Describe the pathophysiology of Primary Open-Angle Glaucoma (POAG). Discuss its clinical features, investigations, and management. (20 marks)

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MODEL ANSWER

I. DEFINITION (1 mark)

• Retinal nerve fibre layer (RNFL) thinning
• Glaucomatous optic disc changes
• Characteristic visual field loss
• Open anterior chamber angle on gonioscopy
• No identifiable secondary cause

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II. PATHOPHYSIOLOGY (4 marks)

• Aqueous humor outflow is obstructed at the level of the trabecular meshwork (TM)
• Increased resistance to outflow through the TM leads to elevated IOP
• Elevated IOP causes mechanical compression at the lamina cribrosa → axonal damage
• Also causes impaired axoplasmic transport in RGC axons → retrograde degeneration
• Chronic IOP elevation → progressive retinal ganglion cell (RGC) apoptosis → RNFL thinning → optic disc cupping → visual field loss

• Vascular insufficiency — reduced perfusion at the optic nerve head, impaired autoregulation
• Glutamate excitotoxicity — excess glutamate release causes secondary RGC death
• Oxidative stress and mitochondrial dysfunction in TM cells reduce outflow facility
• Neurotrophin deprivation — blockage of BDNF retrograde transport from superior colliculus to RGCs
• These explain why some patients progress despite normal IOP (normal-tension glaucoma spectrum)

• 1.2 million RGC axons pass across retina to optic nerve head
• Arcuate fibres (superotemporal and inferotemporal) are most vulnerable
• Papillomacular bundle fibres are most resistant
• This explains why the first VF defects are arcuate/paracentral, not central

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III. RISK FACTORS (2 marks)

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IV. CLINICAL FEATURES (2 marks)

• Usually asymptomatic until late disease (insidious onset)
• Peripheral field loss noticed late; central vision preserved until very advanced

• Increased C/D ratio — vertical C/D ≥0.7 suspicious; asymmetry >0.2 significant
• Violation of ISNT rule — Inferior > Superior > Nasal > Temporal (any violation = suspect)
• NRR notching — most commonly inferotemporal → corresponds to arcuate scotoma
• RNFL defects — wedge-shaped, best seen on red-free photography
• Disc haemorrhages — flame-shaped at disc margin; inferotemporal; risk factor for progression
• Beta-zone PPA — chorioretinal atrophy adjacent to disc; correlates with RNFL loss
• Nasalisation of vessels, bayoneting sign — baring of circumlinear vessels

1. Isolated paracentral scotoma (within 10°)
2. Nasal step (respects horizontal raphe)
3. Bjerrum/arcuate scotoma (10–20° from fixation)
4. Double arcuate (ring) scotoma
5. Temporal island + central island (advanced)
6. Total blindness

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V. INVESTIGATIONS (4 marks)

• Goldmann Applanation Tonometry (GAT) — gold standard
• Adjusted for CCT: each 10 μm above average (~545 μm) overestimates IOP by ~0.7 mmHg
• Normal range: 10–21 mmHg; diurnal variation 3–5 mmHg

• Essential — confirms open angle, rules out angle-closure or secondary causes
• Shaffer grade 3–4 in POAG; no PAS

• Humphrey Field Analyser (HFA): 24-2 pattern (standard)
• 10-2 pattern for advanced disease (monitoring central island)
• Key indices: Mean Deviation (MD), PSD, VFI, GHT
• MD rate of change (dB/year) used for progression monitoring

• SD-OCT: measures RNFL thickness, GCL (ganglion cell layer), macular volume
• Most sensitive area: inferotemporal RNFL
• Structural changes precede functional (VF) loss by several years
• Probability maps: colour-coded (green/yellow/red)

• Ultrasound pachymetry; average ~545 μm
• Essential for IOP interpretation and OHT risk stratification

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VI. MANAGEMENT (7 marks)

• Target IOP = level below which further damage is unlikely
• Based on: severity of damage, baseline IOP, CCT, rate of progression, age
• Initial reasonable goal: IOP <18 mmHg (AGIS study)
• Each 1 mmHg reduction → ~10% reduction in progression risk (EMGT)

• Wait 5 minutes between two drops to prevent washout
• Fixed combinations (e.g. Cosopt = Timolol + Dorzolamide) improve compliance

• Selective Laser Trabeculoplasty (SLT): Q-switched Nd:YAG 532 nm; selectively targets pigmented TM cells; ~6–8 mmHg IOP reduction; LiGHT trial (2019): SLT as first-line was non-inferior/superior to drops — 74% needed no drops at 3 years
• Can be repeated; effect lasts 2–5 years
• ALT (Argon Laser Trabeculoplasty): Older; not reliably repeatable; largely replaced by SLT

• Indicated when medical/laser therapy fails to achieve target IOP
• Trabeculectomy (gold standard): Creates guarded scleral fistula → subconjunctival bleb
  • Antimetabolites: MMC > 5-FU (potency)
  • Complications: hypotony, bleb failure, blebitis, endophthalmitis (lifelong risk)
• Glaucoma drainage devices: Ahmed valve, Baerveldt — for failed trabeculectomy
• MIGS: iStent, Hydrus — lower risk; combined with phacoemulsification

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MARKING SCHEME SUMMARY

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Q2. Describe the anatomy and physiology of aqueous humor. Discuss the pathophysiology and management of raised intraocular pressure. (20 marks)

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MODEL ANSWER

I. ANATOMY OF AQUEOUS HUMOR (3 marks)

• Produced by the non-pigmented epithelium of the ciliary processes (pars plana + pars plicata)
• Mechanisms:
  1. Active secretion — dominant pathway; Na⁺/K⁺ ATPase and carbonic anhydrase (CA II and CA IV) mediated; accounts for majority of production
  2. Ultrafiltration — driven by hydrostatic pressure gradient
  3. Simple diffusion — minor contribution

• TM structure: Uveal, corneoscleral, and juxtacanalicular (JCT) layers; JCT offers highest resistance
• Schlemm's canal is a modified lymphatic vessel lined by endothelium

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II. PHYSIOLOGY OF IOP (2 marks)

• Normal IOP: 10–21 mmHg (mean ~16 mmHg, SD ~3 mmHg)
• Diurnal variation: 3–5 mmHg (highest in early morning)
• Ocular Perfusion Pressure (OPP) = Mean arterial pressure − IOP; normal >50 mmHg

• Supine position, Valsalva manoeuvre, tight neckwear
• Systemic steroids, topical steroids
• Blinking, tight eyelid closure (artefactual elevation in applanation)

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III. PATHOPHYSIOLOGY OF RAISED IOP IN GLAUCOMA (4 marks)

• Increased resistance to outflow at the JCT layer of TM (most common site)
• Structural changes: increased fibrillar material, altered ECM (collagen, fibronectin, laminin), reduced phagocytic activity of TM cells
• Oxidative stress → TM cell dysfunction → reduced outflow facility
• In pseudoexfoliation: fibrillar material clogs TM; in pigmentary glaucoma: melanin granules obstruct TM

• In relative pupillary block: iris-lens apposition → aqueous builds up in posterior chamber → iris bombe → peripheral iris blocks TM
• Appositional closure → if prolonged → PAS (peripheral anterior synechiae) → permanent outflow obstruction
• Mechanisms: Pupillary block (most common), plateau iris, phacomorphic, neovascular

• Steroid-induced: ↑ glycosaminoglycan accumulation in TM → ↓ outflow
• Neovascular: fibrovascular membrane pulls angle closed
• Traumatic: direct TM damage from angle recession

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IV. CLINICAL ASSESSMENT OF RAISED IOP (2 marks)

• GAT (Goldmann Applanation): Gold standard; force needed to applanate 3.06 mm diameter area
• CCT correction: Thin cornea = falsely LOW IOP reading; thick cornea = falsely HIGH reading; each 10 μm above average → ~0.7 mmHg overestimation
• Perkins tonometer: Portable GAT; used for supine/children/OR patients
• iCare rebound: No anaesthetic; excellent for children

• Distinguishes open vs. angle-closure
• Shaffer grading: Grade 4 (wide open) to Grade 0 (closed)
• Dynamic (indentation) gonioscopy: separates appositional from synechial closure

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V. MANAGEMENT OF RAISED IOP (9 marks)

• SLT: First-line option (LiGHT trial); 532 nm Nd:YAG; targets pigmented TM cells; repeatable; ~6–8 mmHg reduction
• ALT: Older; thermal burns in TM; not reliably repeatable
• Laser PI: For angle-closure — creates iris hole to equalise PC/AC pressure
• Laser iridoplasty (ALPI): Plateau iris — shrinks peripheral iris to open angle
• Cyclodiode: Refractory glaucoma — destroys ciliary body to reduce aqueous production

• Gold standard for medically uncontrolled POAG
• Principle: Guarded scleral fistula → subconjunctival filtration bleb
• Steps: Conjunctival flap → lamellar scleral flap (50% depth, 3×3–4 mm) → Kelly punch sclerostomy → peripheral iridectomy → scleral flap sutured (releasable sutures) → bleb formed
• Antimetabolites: MMC (more potent) or 5-FU to reduce fibrosis
• Complications: Early (hypotony, flat AC, choroidal detachment, hyphema); Late (bleb failure, blebitis, endophthalmitis)

• Ahmed valve (with flow restrictor) or Baerveldt (non-valved, larger plate, better long-term IOP)
• Indications: Failed trabeculectomy, NVG, uveitic glaucoma

• iStent, Hydrus: TM bypass; combined with phacoemulsification; mild-moderate glaucoma
• Xen gel stent: Subconjunctival drainage; less invasive than trabeculectomy

• Lens extraction (EAGLE trial: superior to LPI in PAC IOP >29 or PACG)
• Goniotomy/trabeculotomy for congenital glaucoma

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MARKING SCHEME SUMMARY

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Q3. Classify glaucoma. Describe in detail the clinical features, diagnosis, and management of Acute Angle-Closure Glaucoma (AACG). (20 marks)

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MODEL ANSWER

I. CLASSIFICATION OF GLAUCOMA (3 marks)

• Congenital / Developmental
• Acquired

• Open-angle vs. Angle-closure

• Primary (no identifiable cause) vs. Secondary (identifiable ocular/systemic cause)

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II. SPECTRUM OF PRIMARY ANGLE CLOSURE DISEASE (1 mark)

1. PACS: Narrow angle; no PAS; normal IOP; no ONH/VF damage
2. PAC: Narrow angle + IOP >21 or PAS; no ONH/VF damage
3. PACG: Narrow angle + glaucomatous ONH and/or VF damage
4. Acute PACG (AACG): Sudden symptomatic attack

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III. PATHOPHYSIOLOGY OF AACG (2 marks)

• Iris-lens apposition at the pupil blocks aqueous flow from posterior to anterior chamber
• Pressure builds in posterior chamber → iris bombé — forward bowing of peripheral iris
• Peripheral iris occludes the TM → acute IOP rise
• Predisposed anatomy: narrow AC angle, anterior iris root insertion, short axial length, hyperopia

• Plateau iris: Anteriorly rotated ciliary processes push peripheral iris against TM even with pupil fully open
• Phacomorphic: Intumescent lens pushes lens-iris diaphragm anteriorly

• Female sex (3-4× more common in females)
• Lens (hyperopia, thick/intumescent lens)
• Age (average onset ~62 years)
• Shallow anterior chamber, short axial length
• Heredity/family history, East Asian descent

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IV. CLINICAL FEATURES (4 marks)

• Severe, sudden unilateral ocular pain (may be periorbital)
• Frontal headache
• Blurred vision
• Coloured halos around lights (due to corneal epithelial oedema — prismatic effect)
• Nausea and vomiting (vasovagal response to pain; may misdirect to abdominal cause)
• Photophobia

1. Closed angle (gonioscopy or slit-lamp — shallow AC)
2. Acutely raised IOP (often 40–70+ mmHg)
3. Microcystic corneal oedema (epithelial oedema — gives hazy, ground-glass appearance)

• Conjunctival injection — both ciliary (perilimbal) and conjunctival hyperemia
• Fixed, mid-dilated pupil — 4–6 mm, vertically oval, non-reactive to light; iris ischaemia
• Shallow anterior chamber — visible on slit lamp (Van Herick grading)
• Flare and cells in AC (inflammatory response)
• Optic disc — may show hyperaemic oedema acutely
• Fellow eye — narrow, occludable angle (in primary aetiology)
• Sector iris atrophy — after resolved attack (ischaemic)
• Glaukomflecken — anterior subcapsular lens opacities (small grey/white dots) after resolved acute attack; pathognomonic of previous AACG

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V. INVESTIGATIONS (2 marks)

• Tonometry (GAT): IOP markedly elevated, often >40 mmHg
• Gonioscopy: Closed angle (often performed after IOP is lowered or on fellow eye); confirms pupillary block; identifies PAS
• Slit-lamp biomicroscopy: Corneal oedema, AC depth, flare/cells, pupil, lens (glaukomflecken)
• Fundus examination: Optic disc (cupping, hyperaemia, haemorrhages) — often limited by corneal oedema
• Van Herick angle estimation: Peripheral AC depth vs. corneal thickness at slit lamp; grade <1/4 = narrow
• UBM/AS-OCT: If cornea too oedematous; shows iris configuration, angle width, ciliary body position

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VI. MANAGEMENT — EMERGENCY (8 marks)

• Beta-blocker: Timolol 0.5% — ↓ aqueous production
• Alpha-2 agonist: Apraclonidine 1% or Brimonidine 0.2% — ↓ production + ↑ outflow
• Topical CAI: Dorzolamide 2% — ↓ aqueous production
• Pilocarpine 1–2%: Constricts pupil, breaks pupillary block (note: at very high IOP, iris sphincter is ischaemic and pilocarpine may not work; controversial — now omitted by some due to: headache, accommodative spasm, risk of uveitis, potential to worsen angle closure)

• Acetazolamide 500 mg IV or oral — rapidly ↓ aqueous production
• Contraindicated in: sulfonamide allergy, sulfonamide-induced angle closure, severe renal failure

• Mannitol 1–2 g/kg IV over 45 minutes (500 mL of 20% mannitol = 100 g)
• Mechanism: Osmotic dehydration of vitreous → reduces volume → deepens AC
• Contraindicated: Congestive heart failure, renal disease, intracranial bleeding

• Supine position (gravity helps lens-iris fall back)
• Analgesics + antiemetics (treat pain and vomiting)
• Dark room (allows some pupillary constriction)

• Performed once cornea clears and IOP is controlled (usually 1–5 days after attack)
• Nd:YAG laser (or combined with argon) creates full-thickness hole in peripheral iris
• Equalises pressure between posterior and anterior chambers → iris flattens → angle opens
• Fellow eye: Prophylactic PI — 40–80% risk of AACG in 5–10 years if untreated
• If PI not possible due to persistent oedema/inflammation: surgical iridectomy

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MARKING SCHEME SUMMARY

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Q4. Describe trabeculectomy — its indications, surgical technique, use of antimetabolites, and complications. (20 marks)

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MODEL ANSWER

I. DEFINITION AND PRINCIPLE (1 mark)

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II. INDICATIONS (2 marks)

• Failure of conservative therapy — IOP not at target despite maximum tolerated medical therapy + laser
• Progressive deterioration despite seemingly adequate IOP control (including poor adherence)
• Primary therapy — advanced disease requiring very low target IOP (especially younger patients)
• Patient preference — desire to be free of chronic medication
• Specific conditions: Neovascular glaucoma, inflammatory glaucoma, pseudoexfoliation glaucoma with uncontrolled IOP

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III. PREOPERATIVE PREPARATION (1 mark)

• IOP lowering: Maximum medical therapy preoperatively; pilocarpine 2% to constrict pupil
• Anticoagulants: Stop aspirin/warfarin where safe (reduces intraoperative haemorrhage)
• Conjunctival assessment: Site of surgery (superior, away from previous surgery/scarring)
• Informed consent: Specifically include risk of late endophthalmitis (lifelong); cataract acceleration; visual loss from hypotony

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IV. SURGICAL TECHNIQUE — STEP-BY-STEP (6 marks)

1. Bridle suture — superior cornea or superior rectus muscle for globe fixation
2. Conjunctival flap — either:
   • Fornix-based (incision at limbus, flap opened superiorly) — better bleb diffusion
   • Limbus-based (incision posterior to limbus, flap hinged forward) — more watertight closure
3. Haemostasis — episcleral tissue cleared; major vessels cauterised with bipolar cautery
4. Antimetabolite application (MMC/5-FU) if planned — at this stage
5. Lamellar scleral flap — incisions through ~50% of scleral thickness; shape: rectangular (3×3–4 mm), trapezoidal, or triangular; dissected anteriorly into clear cornea
6. Paracentesis — made in temporal peripheral clear cornea (AC access, IOP control, BSS injection)
7. Sclerostomy — AC entered along trapdoor base; deep scleral block excised using Kelly punch (or Vannas scissors); creates internal fistula
8. Peripheral iridectomy — prevents iris prolapse into sclerostomy (blockage of internal opening); usually created; may be omitted in pseudophakic (small residual risk of iris prolapse)
9. Flap suturing — superficial scleral flap sutured at posterior corners ± radial edges with releasable or lysable sutures (argon/Nd:YAG laser suture lysis postoperatively to titrate flow)
10. Patency testing — BSS injected through paracentesis; confirms fistula patent; IOP checked
11. Conjunctival closure — conjunctiva/Tenon capsule sutured water-tightly; irrigation to form bleb; check for leakage (Seidel test)
12. End-of-procedure: Atropine 1% drop instilled; subconjunctival steroid + antibiotic injection
13. Postoperative regime: Topical antibiotic + steroid QID × 2 weeks → steroid alone × 8–12 weeks

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V. ANTIMETABOLITES (4 marks)

• Alkylating agent — cross-links DNA → inhibits fibroblast proliferation; irreversible cell cycle arrest
• More potent than 5-FU
• Application: Cellulose sponges soaked in MMC (concentration 0.1–0.4 mg/mL) applied under conjunctival flap and/or over scleral flap for 1–5 minutes, then thoroughly washed
• Indications (high-risk cases): Young patients, Afro-Caribbean descent, aphakia, prior conjunctival surgery/inflammation, uveitic glaucoma, neovascular glaucoma, failed trabeculectomy
• Complications: Avascular, thin-walled bleb (poorly vascularised → infection risk); hypotony maculopathy; bleb leak; blebitis (incidence up to 5%/year); late endophthalmitis

• Antimetabolite — inhibits thymidylate synthetase → blocks DNA synthesis; S-phase specific
• Less potent than MMC; more manageable
• Application: Intraoperative sponge OR postoperative subconjunctival injections (5 mg in 0.1 mL) given on alternate days × 5 doses
• Indications: Moderate-risk cases; also used for rescuing failing blebs postoperatively
• Complications: Persistent corneal epithelial defect (most characteristic); bleb leakage; punctate keratopathy

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VI. COMPLICATIONS (6 marks)

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MARKING SCHEME SUMMARY

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Q5. Classify and describe secondary glaucomas. Give the pathophysiology, clinical features, and management of Neovascular Glaucoma and Pseudoexfoliation Glaucoma. (20 marks)

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MODEL ANSWER

I. CLASSIFICATION OF SECONDARY GLAUCOMA (3 marks)

• Neovascular glaucoma (fibrovascular membrane)
• ICE syndrome (endothelial membrane)
• Epithelial ingrowth

• Pseudoexfoliation glaucoma
• Pigmentary glaucoma
• Steroid-induced glaucoma
• Inflammatory/uveitic glaucoma (trabecular oedema, debris)
• Angle recession glaucoma

• Sturge-Weber syndrome
• Carotid-cavernous fistula
• Superior vena cava obstruction

• Neovascular glaucoma (PAS formation)
• Phacomorphic glaucoma
• Phacolytic glaucoma
• Malignant glaucoma (ciliolenticular block)
• Topiramate-induced

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II. NEOVASCULAR GLAUCOMA (NVG) — DETAILED (8 marks)

• Proliferative diabetic retinopathy (most common; 1/3 of NVG cases)
• Central retinal vein occlusion (CRVO) (especially ischaemic type; 1/3 of NVG)
• Ocular ischaemic syndrome (carotid artery disease; 1/3 of NVG)
• Less common: CRAO, sickle cell retinopathy, radiation retinopathy, CRVO in young

• Retinal ischaemia → upregulation of VEGF (Vascular Endothelial Growth Factor), PDGF
• VEGF diffuses to anterior segment → neovascularization of iris (rubeosis iridis) and angle
• Stage 1 (Pre-glaucoma): Fine tufts of new vessels at pupil margin; angle open on gonioscopy
• Stage 2 (Open-angle NVG): Vessels in angle — open angle but high IOP from fibrovascular membrane obstructing TM
• Stage 3 (Angle-closure NVG): Fibrovascular membrane contracts → PAS → synechial angle closure → very high IOP

• Painful red eye with very high IOP
• Rubeosis iridis — dilated, irregular vessels on iris surface, beginning at pupil margin
• Corneal oedema (from acutely elevated IOP)
• AC flare/cells
• Gonioscopy: Vessels on angle walls → later PAS → closed angle
• Signs of underlying retinal disease (diabetic changes, CRVO signs on fundus)

• Gonioscopy — essential for staging
• Fundus examination / FFA — identify underlying retinal ischaemia
• Carotid Doppler — if ocular ischaemic syndrome suspected
• Blood glucose, HbA1c — diabetic workup

• Anti-VEGF injection (intravitreal bevacizumab/ranibizumab) — rapidly causes regression of new vessels; given before PRP or surgery; "buying time"
• Panretinal photocoagulation (PRP) — treats underlying retinal ischaemia; reduces VEGF load; first-line for preventing and treating NVG
• Medical IOP lowering — topical agents; avoid miotics (worsen inflammation)
• Cyclodiode laser — if no visual potential; destroys ciliary body → ↓ aqueous production
• Surgery:
  • Trabeculectomy: Poor success rate due to progressive scarring
  • GDD (Glaucoma drainage device): Ahmed valve or Baerveldt — best surgical option
  • Pre-treatment with anti-VEGF before surgery improves success
• End-stage (no visual potential): Cyclodiode laser; retrobulbar alcohol/chlorpromazine for pain; enucleation if absolutely necessary

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III. PSEUDOEXFOLIATION GLAUCOMA (PXG) — DETAILED (7 marks)

• PXM is produced by abnormal basement membrane metabolism (from epithelial cells of lens, ciliary body, iris, TM, conjunctiva, and systemically)
• LOXL1 gene mutations are the strongest genetic risk factor
• PXM deposits in TM → obstruction of outflow → raised IOP
• IOP fluctuations are characteristically marked (one of the highest IOP variabilities)

• Anterior lens capsule: Classic pattern — central disc of PXM + peripheral ring with a clear zone between (ring-and-disc pattern, best seen on retroillumination)
• Pupil margin: Loss of pigment, poor dilation (sphincter involvement)
• Corneal endothelium: Pigment dusting (not Krukenberg spindle — that's pigmentary glaucoma)
• Iris: PXM on iris surface; transillumination defects (less prominent than pigmentary)
• Zonules: Fragile, degenerated — risk of lens subluxation and phacodonesis
• TM: Marked TM pigmentation, especially on Sampaolesi's line (anterior to Schwalbe's line)

• Asymmetric IOP elevation (often unilateral onset)
• IOP fluctuations are particularly marked
• Poor pupil dilation (requires iris hooks at surgery)

• Worst natural history of common glaucoma types: −3.13 dB/year without treatment
• Responds well to IOP lowering (laser or medical)

• GAT + diurnal IOP curve (captures fluctuation)
• Gonioscopy: TM pigmentation, Sampaolesi line (pigment anterior to Schwalbe's)
• Slit lamp: Lens capsule pattern (dilation needed — may require phenylephrine 10%)
• OCT-RNFL: Rapid RNFL thinning expected

• Medical: Prostaglandin analogues (good response); combination therapy often needed
• Laser: SLT — excellent response in PXG (pigmented TM responds well)
• Surgery: Trabeculectomy with MMC (if medical/laser fails)
  • Special precautions: iris hooks for poor pupil; extra care with capsulorrhexis (fragile zonules); capsular tension rings if zonular weakness; risk of vitreous loss is higher
• Monitoring: More frequent (every 3 months) due to rapid progression

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IV. OTHER SECONDARY GLAUCOMAS — BRIEF (2 marks)

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MARKING SCHEME SUMMARY

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Q6. Describe Normal Tension Glaucoma — its definition, pathogenesis, clinical features, investigations, and management. How does it differ from POAG? (20 marks)

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MODEL ANSWER

I. DEFINITION (1 mark)

• IOP is consistently ≤21 mmHg (within the statistically normal range)
• Typical glaucomatous changes of the optic nerve head and visual fields are present
• Open anterior chamber angle on gonioscopy
• All secondary causes of optic neuropathy are excluded

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II. EPIDEMIOLOGY AND DEMOGRAPHICS (1 mark)

• Accounts for ~30–40% of open-angle glaucoma in Western populations
• More common in Japanese populations (up to 90% of OAG)
• More common in females than males
• Average age of presentation: 60–70 years

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III. PATHOGENESIS (4 marks)

• Impaired optic nerve head blood flow — reduced perfusion due to local vascular dysregulation
• Nocturnal systemic hypotension — most strongly implicated; marked BP dip during sleep → reduced OPP → ischaemia of optic nerve; 24-hour ABP monitoring reveals nocturnal dip
• Vasospasm: Migraine, Raynaud's phenomenon — episodic reduction in ONH perfusion
• Obstructive sleep apnea — intermittent hypoxia and hypercapnia
• Low mean arterial pressure — reduced ocular perfusion pressure (OPP = MAP − IOP)
• Carotid artery disease — reduced ipsilateral perfusion

• Lamina cribrosa abnormalities — altered connective tissue structure; increased mechanical stress on axons even at normal IOP
• Thin lamina cribrosa (LC) with increased compliance may be more susceptible to pressure-related damage
• Parapapillary atrophy is more extensive in NTG (reflects choroidal ischaemia)

• Autoantibodies against optic nerve antigens found in NTG patients
• OPA1 gene mutations — associated with dominant optic atrophy; some NTG patients may have overlap
• Tau protein and neurodegeneration — NTG may share pathways with neurodegenerative diseases

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IV. CLINICAL FEATURES — HOW NTG DIFFERS FROM POAG (4 marks)

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V. INVESTIGATIONS (4 marks)

• GAT (IOP confirmed ≤21 mmHg on multiple occasions at different times of day)
• Gonioscopy — confirms open angle, no PAS
• Disc photography + OCT-RNFL (often shows inferotemporal damage preferentially)
• Humphrey VF (24-2 and 10-2 — defects often deep, close to fixation)

• 24-hour ambulatory blood pressure (ABP) monitoring — identify nocturnal dip; BP dip >10% systolic = significant; major modifiable vascular risk factor
• Carotid duplex imaging — identify stenosis reducing perfusion
• Blood pressure and systemic vascular assessment — orthostatic hypotension, cardiac disease
• Blood tests to exclude non-glaucomatous optic neuropathy:
  • Vitamin B12 and red cell folate
  • Full blood count (anaemia)
  • ESR/CRP (inflammatory)
  • Treponemal serology (syphilis) including VDRL
  • Lyme disease serology
  • Serum ACE level (sarcoidosis)
  • Plasma protein electrophoresis (paraproteinaemia)
  • Autoantibody screen (ANA, ANCA, etc.)

1. VA loss out of proportion to optic disc cupping
2. Loss of colour vision on Ishihara testing
3. VF loss NOT consistent with RNFL dropout pattern
4. Pallor of neuroretinal rim (pallor > cupping)
5. Rapid progression despite confirmed normal pressure

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VI. MANAGEMENT (6 marks)

• Documented VF/disc progression
• Advanced damage (split fixation, threat to central vision)
• Long life expectancy
• Patient preference after counselling

• Prostaglandin analogues — usual first choice; potent; once daily; uveoscleral outflow
• SLT — reasonable first-line (LiGHT trial); no drops, no compliance issues; IOP reduction adequate in many
• Add second agent if needed (brimonidine, CAI, beta-blocker with care)

• Brimonidine (alpha-2 agonist): Preferred in NTG; may have neuroprotective effect (activates alpha-2 receptors → upregulates survival pathways: BDNF release, reduced glutamate excitotoxicity); CNTGS sub-study showed less VF progression with brimonidine vs timolol
• Betaxolol (selective β1 blocker): Preferred over timolol if beta-blocker chosen; timolol at bedtime can cause nocturnal systemic BP dip → worsens ONH ischaemia; betaxolol has less nocturnal BP effect; also has calcium channel blocking properties → vasodilatory
• Calcium channel blockers (systemic): May improve ONH blood flow (nifedipine); used in selected patients with vasospasm/migraine (adjunct — not proven in large RCTs)
• Avoid pilocarpine (miosis, RD risk, compliance issues)

• Refer if nocturnal hypotension found on ABP monitoring (reduce antihypertensive dose at night; avoid evening diuretics)
• Treat OSA (CPAP)
• Migraine management
• Carotid endarterectomy if significant stenosis
• Encourage regular aerobic exercise (improves vascular autoregulation)
• Avoid yoga head-stands (elevate IOP)

• If IOP remains above target despite maximum medical + laser therapy
• Trabeculectomy (± MMC) — same as POAG but target IOP much lower (often <12–14 mmHg)
• GDD for refractory cases

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MARKING SCHEME SUMMARY

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Q7. Describe the clinical features, investigations, and medical management of glaucoma. Discuss the mechanism of action, uses, and side effects of anti-glaucoma drugs. (20 marks)

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MODEL ANSWER

I. CLINICAL FEATURES OF GLAUCOMA (4 marks)

• POAG: Usually asymptomatic until late; peripheral VF loss (not noticed early due to binocular overlap and neural compensation); late: central vision threat, "tunnel vision"
• NTG: Similar to POAG; visual symptoms at similar stage
• AACG: Acute pain, red eye, coloured halos, nausea/vomiting
• PACG (chronic): Intermittent blurring, halos, mild eye ache

• Increased C/D ratio — vertical C/D ≥0.7; asymmetry >0.2 significant
• ISNT rule violation — normal NRR: Inferior > Superior > Nasal > Temporal
• Notching of NRR — most commonly inferotemporal
• RNFL defects — wedge-shaped (red-free photography)
• Disc haemorrhages — risk factor; more common in NTG
• Beta-zone PPA — adjacent chorioretinal atrophy

1. Paracentral scotoma (within 10°)
2. Nasal step (horizontal raphe)
3. Arcuate (Bjerrum) scotoma (10–20°)
4. Ring scotoma
5. Temporal island / central island

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II. INVESTIGATIONS (3 marks)

• GAT (gold standard): Force to applanate 3.06 mm corneal area
• CCT pachymetry: Corrects for corneal effect on IOP readings; thin CCT = falsely low IOP
• Diurnal IOP phasing (multiple readings throughout day) — captures fluctuation

• Differentiates open vs. angle-closure
• Identifies secondary causes (NVG vessels, PXM, pigment, PAS)
• Shaffer grading 0–4

• HFA 24-2 (standard), 10-2 (advanced), 30-2
• MD, PSD, VFI, GHT — global indices
• Reliability indices: FP <15%, FN <33%, FL <20%

• RNFL thickness (inferotemporal most sensitive)
• Precedes VF change by years — "structure before function"

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III. MEDICAL MANAGEMENT AND PHARMACOLOGY (13 marks)

• Drugs: Latanoprost (0.005%), Bimatoprost (0.01/0.03%), Travoprost (0.004%), Tafluprost (0.0015% — preservative-free)
• Mechanism: Agonists at FP (prostaglandin F2α) receptors on ciliary muscle → remodelling of extracellular matrix (MMP induction) → increased permeability of uveoscleral pathway → ↑ uveoscleral outflow; some also ↑ trabecular outflow
• IOP reduction: 25–35% (most potent class); once daily — given at night (circadian rhythm)
• Side effects:
  • Iris colour change — increased iris pigmentation (FP receptor stimulation of melanocytes); irreversible; monocular use → heterochromia
  • Eyelash hypertrichosis — longer, thicker, more lashes (same pathway — serendipitously discovered → bimatoprost approved for eyelash growth/Latisse)
  • Periorbital fat atrophy — sunken appearance
  • Eyelid pigmentation (skin darkening)
  • Conjunctival hyperemia (most common)
  • Anterior uveitis (rare; use cautiously in uveitic glaucoma)
  • CME in aphakic/pseudophakic eyes (use with caution)
  • Mnemonic: PALE FISH (Periorbital fat atrophy, Arterial BP, Lash hypertrichosis, Eyelid darkening, Fore/uveitis, Iris pigmentation, Superficial keratitis, Hyperemia)

• Drugs: Timolol 0.25%/0.5% (non-selective), Betaxolol 0.25%/0.5% (β1-selective), Carteolol (with ISA)
• Mechanism: Block β2 receptors on ciliary body non-pigmented epithelium → ↓ cAMP → ↓ active secretion of aqueous humor
• IOP reduction: 20–30%; applied BD (OD for gel-forming formulation)
• Side effects:
  • Ocular: Dry eye, superficial punctate keratitis, reduced tear production
  • Systemic (most important): Bradycardia, heart block, bronchospasm (β2 blockade in lungs), hypotension, reduced exercise tolerance, sexual dysfunction, CNS depression
  • Betaxolol: β1-selective — relative safety in asthma/COPD; also has calcium channel blocking effect → vasodilatory; preferred in NTG (less nocturnal BP dip)
• Contraindications: Asthma (absolute), COPD (relative), 2nd/3rd degree heart block, sinus bradycardia, uncontrolled heart failure, beta-blocker-treated diabetics
• Special note: Timolol gel-forming solution (Timoptol-XE) — once daily; ↓ systemic absorption

• Drugs: Brimonidine 0.1%/0.15%/0.2%, Apraclonidine 0.5%/1%
• Mechanism: Stimulate pre- and post-synaptic α2 receptors in ciliary body → ↓ cAMP → ↓ aqueous production; also ↑ uveoscleral outflow; additionally ↓ episcleral venous pressure
• IOP reduction: 20–25%; applied BD-TID
• Additional effects: Brimonidine may have neuroprotective effect — activates RGC survival pathways (upregulates BDNF, reduces glutamate excitotoxicity)
• Side effects:
  • Allergic follicular conjunctivitis (up to 30% with brimonidine — major limitation; class effect)
  • Dry mouth, dry nose
  • Sedation, fatigue (CNS penetration)
  • Lid retraction (alpha-1 activity of apraclonidine)
  • Tachyphylaxis (apraclonidine especially)
• Contraindications:
  • Infants and neonates (absolute): Brimonidine crosses BBB → CNS depression, bradycardia, hypotension, apnea (potentially fatal)
  • MAO inhibitors (dangerous interaction — hypertensive crisis)
  • Concomitant systemic alpha-2 agonists

• Topical: Dorzolamide 2% (BD-TID), Brinzolamide 1% (BD-TID)
• Oral: Acetazolamide 125–250 mg QID (up to 500 mg BD), Methazolamide 25–50 mg BD-TID
• Mechanism: Inhibit carbonic anhydrase II and IV in ciliary body non-pigmented epithelium → ↓ bicarbonate ion production → ↓ Na+ and water transport → ↓ active aqueous secretion
• IOP reduction: 15–20%
• Topical side effects: Stinging/burning (especially dorzolamide), metallic taste, transient blurring, corneal decompensation with corneal endothelial disease
• Oral side effects: Paresthesias (fingers/toes — most common; potassium wasting), GI upset (nausea, diarrhoea), malaise, renal stones (hypocitraturia — use with caution in stone formers), hypokalemia, urinary frequency, aplastic anaemia (rare but potentially fatal — idiosyncratic), depression
• Contraindications: Sulfonamide allergy (all CAIs are sulfonamide derivatives — risk of Stevens-Johnson syndrome, aplastic anaemia); severe renal/hepatic failure; first trimester of pregnancy
• Acetazolamide used acutely (IV 500 mg) for AACG; chronic use limited by side effects

• Drug: Pilocarpine 0.5–4% (QID), Carbachol (less common)
• Mechanism: Directly stimulate M3 muscarinic receptors → ciliary muscle contraction → tightens trabecular meshwork → opens Schlemm's canal → ↑ conventional outflow; also constricts pupil (may help in pupillary block)
• IOP reduction: 20–25%
• Side effects:
  • Brow ache (ciliary muscle spasm — especially initially)
  • Accommodative spasm (myopisation — worse in young patients)
  • Miosis (poor vision in dim light; difficult night driving)
  • Retinal detachment (traction on vitreous base → peripheral tears — especially in high myopes)
  • Increased salivation/sweating (systemic cholinergic effects)
  • Potential to worsen uveitic glaucoma
• Contraindications: Aphakic/pseudophakic pupillary block; high myopia with risk of RD

• Drug: Netarsudil 0.02% (Rhopressa) — once daily
• Mechanism: Inhibits Rho-kinase (ROCK) → reduces actomyosin contractility in TM cells → ↑ conventional outflow (most novel mechanism); also ↓ episcleral venous pressure and ↓ aqueous production
• IOP reduction: 15–20%
• Side effects: Conjunctival hyperemia (most common), corneal verticillata (whorl-like corneal pigment deposits, reversible), subconjunctival haemorrhage
• Available as fixed combination with latanoprost (Rocklatan/Vyzulta)

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MARKING SCHEME SUMMARY

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Q8. Describe Primary Congenital Glaucoma — its aetiology, clinical features, investigations, and management. Add a note on developmental glaucomas associated with systemic syndromes. (20 marks)

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MODEL ANSWER

I. DEFINITION (1 mark)

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II. AETIOLOGY AND GENETICS (2 marks)

• Mechanism: Trabeculodysgenesis — the mesodermal/neural crest cells that form the TM fail to differentiate fully; persistent anterior insertion of the iris into the TM; impaired aqueous outflow from birth
• Genetics:
  • Most cases sporadic
  • ~10–40% have genetic basis
  • CYP1B1 gene (chromosome 2p21): Codes for cytochrome P450 enzyme; AR inheritance; accounts for >50% of familial PCG; higher frequency in Middle East and Roma populations
  • LTBP2 gene mutations also described
• Increased frequency in: Consanguineous marriages; Middle Eastern/Roma populations; male sex (65% cases)

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III. CLASSIC CLINICAL TRIAD (3 marks)

1. Buphthalmos ("ox eye") — Enlarged eye due to elevated IOP distending the pliable infant sclera and cornea (child's eye is more elastic than adult's); normal neonatal corneal diameter is 9.5–10.5 mm; >12 mm at birth = diagnostic; >13 mm at 1 year = abnormal
2. Epiphora (watering eyes) — Corneal oedema and epithelial irritation from elevated IOP → reflex tearing; must be distinguished from nasolacrimal duct obstruction (NLD obstruction has no corneal changes)
3. Photophobia and Blepharospasm — Due to corneal oedema causing painful light sensitivity; infant buries face in pillow/mother's shoulder; characteristic finding

• Haab's striae — Horizontal or oblique breaks in Descemet's membrane caused by corneal stretching from acute IOP rise; appear as parallel, whitish-grey lines on the cornea; pathognomonic of PCG (parallel vs. cornea forceps trauma which are vertical/oblique; Haab's are horizontal)
• Corneal oedema — cloudy/hazy cornea; initially reversible, later permanent scarring
• Increased axial length — eye elongates (myopisation); unlike adults where ONH damage occurs first
• Elevated IOP — variable; may not be consistently elevated (episodic)
• Optic disc cupping — increased C/D ratio; importantly in children reversible with IOP normalisation (unlike adults)
• Myopia — from axial elongation

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IV. INVESTIGATIONS (2 marks)

• IOP measurement — Perkins applanation or Tonopen (infant probes); iCare (no anaesthesia)
  • Normal infant IOP under GA: ~8–10 mmHg (GA lowers IOP); readings >15 mmHg under GA are significant
• Corneal diameter — horizontal WTW diameter; calipers; >12 mm suspicious
• Corneal clarity — document degree of oedema
• Gonioscopy — high insertion of iris root; abnormal angle configuration; Barkan membrane (abnormal tissue across angle)
• Refraction — axial myopia (retinoscopy)
• Optic disc assessment — C/D ratio; cupping
• B-scan ultrasound — axial length measurement (monitor buphthalmos)
• Pachymetry — CCT (thin in PCG; affects IOP interpretation)

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V. MANAGEMENT (6 marks)

• Indication: PCG with clear cornea (allows visualisation of angle)
• Technique: Knife introduced through corneal stab incision; under direct gonioscopic view; incision made through abnormal trabecular tissue into Schlemm's canal; performed over 90–120° of angle
• Success rate: 70–90% in primary PCG with clear cornea
• Advantage: Preserves conjunctiva (important for later surgery)
• Can be repeated (another 90°) if IOP not controlled

• Indication: PCG with cloudy cornea (cannot perform goniotomy)
• Technique: External surgical access to Schlemm's canal through limbal incision; trabeculotome passed into Schlemm's canal and rotated into AC — tears open TM from outside
• Success rate similar to goniotomy
• Advantage: No need to see angle; can be done with any corneal clarity
• Gonioscopy-assisted transluminal trabeculotomy (GATT): Modern technique; suture passed 360° around Schlemm's canal via single goniotomy incision; then pulled through TM; less invasive

• For more severe/refractory cases
• Provides both angle opening and filtration
• Higher risk of complications including choroidal detachment

• If above procedures fail
• Ahmed valve (most commonly used in paediatric refractory glaucoma)

• Last resort for refractory/end-stage
• Reduces aqueous production

• Used to temporarily lower IOP before surgery or if surgery is delayed
• Topical beta-blockers (Timolol) — used with caution (systemic absorption → bradycardia, bronchospasm in infants; use lowest concentration)
• Topical CAIs (Dorzolamide) — safe in infants
• Prostaglandins — less effective in paediatric glaucoma; may affect ocular growth
• Brimonidine — ABSOLUTELY CONTRAINDICATED in infants/neonates and children under 2 years (crosses BBB → CNS depression, apnea, bradycardia, hypotension — potentially fatal)
• Oral acetazolamide (2–5 mg/kg TID) — for short-term use

• Regular EUA every 3–6 months (under GA if needed)
• Amblyopia management (patching, spectacles — very important; axial myopia + corneal scarring cause deprivation amblyopia)
• Strabismus treatment if present
• Genetic counselling for family

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VI. DEVELOPMENTAL GLAUCOMAS WITH SYSTEMIC SYNDROMES (6 marks)

• Sporadic (no hereditary pattern)
• Features: Port-wine stain (facial haemangioma — trigeminal distribution), ipsilateral leptomeningeal angioma (intracranial calcification — "tram-track"), seizures, mental retardation, contralateral hemiplegia
• Glaucoma: ~30% develop glaucoma; 60% before age 2 (buphthalmos); remainder at any age
• Mechanisms:
  • Infants: Trabeculodysgenesis (same as PCG)
  • Older children/adults: Raised episcleral venous pressure from arteriovenous communications in episcleral haemangioma
• Management: Medical; goniotomy; combined trabeculotomy-trabeculectomy
• Surgical risk: High risk of choroidal effusion and suprachoroidal haemorrhage — sudden IOP reduction causes uveal expansion into decompressed suprachoroidal space; must reform AC slowly; consider drainage of choroidal effusion if needed

• Absence of iris (incomplete — iris remnant usually present on gonioscopy)
• Genetics: PAX6 gene mutation (AD, chromosome 11p13)
• Sporadic form: Associated with Wilms tumour (nephroblastoma) — WAGR syndrome (Wilms tumour, Aniridia, GU anomalies, mental Retardation)
• Glaucoma: ~50% develop glaucoma; mechanism — progressive encroachment of iris stump onto TM (late-onset open angle)
• Management: GDD offers best chance; trabeculectomy with MMC often fails; medical adjunct

• AD; NF1 gene (chromosome 17q)
• Glaucoma: Rare; usually unilateral; congenital; ~50% of NF1 glaucoma have ipsilateral plexiform neurofibroma of upper lid
• Mechanisms: Congenital angle anomaly; ectropion uveae

• Spectrum: Axenfeld anomaly (posterior embryotoxon + iris strands) → Rieger anomaly (+ iris atrophy/corectopia) → Rieger syndrome (+ systemic: dental hypoplasia, facial boning abnormalities, periumbilical skin)
• Genetics: PITX2, FOXC1 gene mutations; AD
• Glaucoma: 50% develop glaucoma (typically juvenile onset)

• Central corneal opacity (leucoma) with defects in Descemet's and corneal endothelium
• Often associated with corneolenticular adhesions
• Glaucoma in ~50%; complex management

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MARKING SCHEME SUMMARY

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Q9. Describe the visual field changes in glaucoma. Discuss gonioscopy and tonometry in detail. (20 marks)

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MODEL ANSWER

I. ANATOMICAL BASIS OF VISUAL FIELD DEFECTS IN GLAUCOMA (2 marks)

• 1.2 million RGC axons travel across the retina to the optic nerve head
• Fibres from the temporal retina follow an arcuate path around the papillomacular bundle — they do not cross the horizontal raphe
• The arcuate fibres (superotemporal and inferotemporal) are most vulnerable to glaucomatous damage
• The papillomacular bundle is most resistant (central vision preserved until very late)
• The horizontal raphe separates superior and inferior arcuate fibres → explains nasal step
• Nasal retinal fibres follow a straight course to the disc

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II. VISUAL FIELD DEFECTS IN GLAUCOMA (5 marks)

• Humphrey Field Analyser (HFA): Standard automated static threshold perimetry
  • 24-2 pattern: 54 test points; central 24° temporal, 30° nasal; standard for glaucoma
  • 10-2 pattern: 68 points in central 10°; for advanced disease (central island, split fixation monitoring)
  • 30-2 pattern: More peripheral; alternative to 24-2
• Global indices:
  • MD (Mean Deviation): Average deviation across all tested points from age-matched normal; expressed in dB; negative = worse; -6 dB = moderate loss; >-12 dB = severe
  • PSD (Pattern Standard Deviation): Irregularity of the field; elevated in focal glaucomatous loss (e.g. arcuate scotoma); low in diffuse loss (e.g. cataracts)
  • VFI (Visual Field Index): 0–100%; 100% = normal; used for trend analysis; weighted for central points
  • GHT (Glaucoma Hemifield Test): Compares five matched zones in superior and inferior hemifields; "Outside normal limits" = statistically significant asymmetry
• Reliability criteria: FP <15%, FN <33%, FL <20% — test unreliable if exceeded
• Progression analysis:
  • Pointwise linear regression — change in dB/year at each point
  • Trend analysis — VFI over time; MD rate of change >1 dB/year = rapid progressor
  • Event analysis (GCP, Guided Progression Analysis — GPA)
• Alternative perimetric tests:
  • SITA (Swedish Interactive Threshold Algorithm) — faster, less fatiguing
  • Frequency Doubling Technology (FDT) — tests magnocellular pathway; detects early damage
  • Short-Wavelength Automated Perimetry (SWAP) — tests blue-yellow pathway

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III. GONIOSCOPY (7 marks)

• Koeppe lens — provides erect, direct view of angle; used with patient supine; allows bimanual indentation
• Barkan lens — similar; used for surgical goniotomy

• Goldmann 3-mirror lens (3 mirrors at different angles — for peripheral retina + angle + equatorial retina); single mirror for angle view; requires gonioscopic solution (methylcellulose); magnification × 1.27 correction for disc measurement
• Zeiss 4-mirror lens — 4 mirrors; no gonioscopic solution; used for indentation gonioscopy; each mirror shows opposite angle; smaller contact area
• Sussman 4-mirror — handheld; similar to Zeiss but non-cornea contact

1. Schwalbe's line — anterior termination of Descemet's membrane; marks anterior border of TM; may be prominent in posterior embryotoxon (Axenfeld-Rieger syndrome)
2. Trabecular meshwork (TM) — anterior TM (non-pigmented/uveal TM) and posterior TM (pigmented corneoscleral + juxtacanalicular); most important structure; posterior TM is most pigmented and most functionally significant; contains Schlemm's canal behind it
3. Schwalbe's line to scleral spur = TM zone (~0.5–0.6 mm)
4. Scleral spur — whitish line; most posterior TM landmark; attachment of longitudinal ciliary muscle; important reference point in grading
5. Ciliary band — dark brown/grey band; represents anterior ciliary body; most posterior visible structure; width related to iris insertion
6. Iris root — most posterior; configuration (flat, steep, bombe) important

• Iris insertion level (A–E: anterior to posterior)
• Angular width (degrees)
• Iris configuration (flat, steep/convex, plateau, concave/bowed back)

• Zeiss/Sussman lens gently pressed on cornea → increases AC pressure → pushes peripheral iris back → opens appositional closure
• Appositional closure: Opens with indentation (iris not stuck)
• Synechial closure (PAS): Cannot be opened with indentation (iris permanently adhered)
• Essential to differentiate these — critical for management decisions

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IV. TONOMETRY (6 marks)

• Principle (Imbert-Fick principle): For a perfectly rigid sphere: Force (P) = IOP × Area of contact
  • Actual equation modified for corneal rigidity and tear film: Goldmann used 3.06 mm diameter area where surface tension and corneal rigidity forces cancel each other out
• Technique: Fluorescein + local anaesthetic; cobalt blue slit lamp light → two semicircles in the eyepiece; adjust dial until inner edges of semicircles just touch → reading in mmHg
• Sources of error:
  • CCT: Thin cornea = falsely low; thick cornea = falsely high (each 10 μm from ~545 μm average → ~0.7 mmHg error)
  • Corneal rigidity (keratoconus — low; post-LASIK — low; post-RK — unpredictable)
  • Excessive fluorescein/tear lake → thick prism rings → overestimate
  • Very low tear film → underestimate
  • Corneal oedema → underestimate
  • Calibration error
  • Breath-holding, Valsalva, tight neckwear → artificially elevated
• Calibration check: GAT should be checked with calibration bar weekly (0, 2, 6 positions)

• Central Corneal Thickness (CCT) is the most important variable affecting GAT accuracy
• Average CCT: ~545 μm
• Measured by: Ultrasound pachymetry (contact; most accurate); Orbscan (non-contact); Pentacam; Scheimpflug; optical coherence
• Correction tables or formulae available (Ehlers, Shah, etc.) — approximately 0.7 mmHg per 10 μm deviation from average
• Clinical importance:
  • Thin CCT: Patient with IOP "21 mmHg" may actually have IOP >24 mmHg — undertreated
  • Thick CCT: Patient with IOP "26 mmHg" may actually have IOP <22 mmHg — over-treated
  • OHTS: Thin CCT was the strongest single predictor of conversion from OHT to POAG

• Diurnal IOP phasing — multiple readings throughout the day (8am, 12pm, 4pm, 8pm); identifies peak IOP and fluctuation; IOP variability >6 mmHg is significant
• Seasonal variation (higher in winter)
• Ocular Pulse Amplitude (OPA) — difference between peak and trough IOP during cardiac cycle; measured by Pascal DCT; elevated OPA may indicate increased ocular blood flow

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MARKING SCHEME SUMMARY

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Q10. Write about the laser procedures in glaucoma. Discuss in detail Selective Laser Trabeculoplasty (SLT) and Laser Peripheral Iridotomy (LPI). (20 marks)

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MODEL ANSWER

I. OVERVIEW OF LASER PROCEDURES IN GLAUCOMA (3 marks)

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II. SELECTIVE LASER TRABECULOPLASTY (SLT) — IN DETAIL (10 marks)

• Developed by Latina and Park in 1995 as an evolution of ALT
• ALT caused thermal coagulation burns → scarring of TM → not reliably repeatable; SLT overcomes this by selective targeting

• Laser: Q-switched Nd:YAG, 532 nm (frequency-doubled/KTP) — green wavelength; nanosecond pulse duration (~3 ns)
• Spot size: 400 μm
• Energy: Typically 0.4–1.4 mJ (titrated to produce fine champagne bubbles without overt coagulation — "threshold bubbling")
• Mechanism:
  • 532 nm wavelength is specifically absorbed by melanin granules in pigmented TM cells (selectively photothermal)
  • Nanosecond pulses: energy deposited faster than thermal relaxation time of melanin granules → thermal damage confined to pigmented cells; adjacent non-pigmented cells, collagen, Schlemm's canal — not damaged
  • This is in contrast to ALT which uses longer pulses → coagulative damage to all TM cells
  • Biological effect: Selective damage triggers macrophage recruitment, cytokine release (IL-1, TNF-α), matrix metalloproteinase activation → remodelling of TM extracellular matrix → increased permeability and outflow facility
  • Repopulation of TM cells from stem cells in angle — explains repeatability

• First-line therapy for POAG/OHT — supported by LiGHT trial
• Adjunct when medications insufficient
• Patient non-compliant or intolerant to medications
• Before escalating to surgery
• NTG (IOP lowering)
• Secondary OAG with pigmented TM (PXG, pigmentary glaucoma — often excellent response)
• Post-trabeculectomy with elevated IOP

• Angle-closure glaucoma (not open angle)
• Heavily scarred/pale TM (will not respond — no melanin to target)
• Uveitic glaucoma (relative — may worsen inflammation)
• Corneal oedema (poor view)

• Topical pre-treatment: Apraclonidine 0.5% or 1% (30 minutes before) → prevents post-laser IOP spike
• Anaesthesia: Topical LA (proxymetacaine/lidocaine 4%)
• Lens: Goldmann single-mirror gonioscopy lens with coupling solution
• Patient position: Slit lamp, sitting
• Treatment area: 180° or 360° of TM (360° slightly more effective; similar safety)
• Spots: 50 spots per 180° (100 spots for 360°); non-overlapping
• Endpoint: Fine champagne bubbles ("popcorn" appearance) = adequate energy; avoid coagulation blanching
• Energy titration: Start low (0.4–0.6 mJ); increase until micro-bubble formation; if overt coagulation/intense bubbling → reduce energy
• Post-laser: Apraclonidine 1% immediately after; check IOP after 1 hour; NSAIDs/prednisolone for inflammation if needed

• IOP reduction: ~20–30% (6–8 mmHg absolute reduction) — equivalent to one topical agent
• LiGHT Trial (2019): Randomised 718 patients with newly diagnosed POAG/OHT; SLT vs. topical medication
  • SLT was non-inferior to drops as first-line therapy
  • At 3 years: 74% in SLT group required no drops; 58% in drops group required no additional medications
  • More disease progression events in drops group vs. SLT group
  • Conclusion: SLT should be offered as first-line treatment for newly diagnosed POAG/OHT
• Duration: Effect typically lasts 2–5 years; can be retreated (unlike ALT)
• Retreatment success rate similar to initial treatment

• Transient IOP spike (prevented by pre-treatment with apraclonidine) — occurs 1–3 hours post-laser
• Transient anterior uveitis (mild; resolves in 1–2 days; NSAIDs/topical steroids)
• Transient discomfort during procedure
• Peripheral anterior synechiae (rare; if excessive energy)
• Persistent IOP elevation (rare)
• No permanent structural changes to TM — distinguishes from ALT

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III. LASER PERIPHERAL IRIDOTOMY (LPI) — IN DETAIL (7 marks)

• Equalises pressure between posterior and anterior chambers
• Iris flattens (iris bombé relieved)
• Peripheral iris falls away from TM → opens narrow/closed angle

• Acute angle closure (AACG) — definitive treatment after IOP control; performed 1–5 days after attack when cornea clears
• Primary angle closure (PAC) — prevents progression to PACG
• PACS (Primary Angle Closure Suspect) — prophylactic in high-risk cases (narrow angle on gonioscopy; occludable angle in fellow eye)
• Fellow eye after unilateral AACG — 40–80% risk of attack in 5–10 years if not treated
• Chronic angle-closure glaucoma (PAC/PACG) — stops further PAS formation
• Before pupil dilation in narrow-angle eyes (prophylactic)

• Laser: Nd:YAG (1064 nm or frequency-doubled) — photodisruption (plasma-mediated)
• Pre-procedure:
  • Pilocarpine 1–2% → constricts pupil → thins peripheral iris → easier penetration; stretches crypt areas (facilitates PI)
  • Wait 30 min → topical anaesthetic
  • Apraclonidine 1% (30 min before) → prevents post-laser IOP spike
• Lens: Abraham (fundus contact lens with +66D button) or Wise (annular) — provides magnification and focal spot
• Position: Superior iris, under upper lid (bleb hides behind lid; reduces visual symptoms from PI); alternatively temporal
• Targeting: Iris crypt (thin area; less pigment); 11 o'clock or 1 o'clock position
• Parameters: 1–15 mJ energy; 1–3 shots per spot; usually 1–3 bursts total; aim for through-and-through penetration
• Endpoint: Pigment plume (brown "mushroom cloud") through the hole; retroillumination confirms full-thickness penetration (dark hole with transillumination from behind); flow of aqueous pigment into AC
• Post-procedure:
  • Apraclonidine 1% immediately after
  • Check IOP at 1 hour
  • Topical prednisolone/dexamethasone QID × 1 week
  • Follow-up gonioscopy after 4–6 weeks (confirm angle opening)

• For darkly pigmented or thick irides (e.g. Asian patients)
• Argon pre-treatment: Burns on iris to thin it and create a crater (absorbs pigment); reduces energy needed for YAG penetration; reduces bleeding risk
• Then YAG to complete full-thickness perforation

• Clinically: Transillumination through the hole (retroillumination with slit lamp)
• Gonioscopy: Opening/widening of the angle after PI (confirms functional PI)
• UBM/AS-OCT: Can confirm patent PI and assess angle opening; EAGLE trial used OCT to confirm

• IOP spike (transient — prevented by apraclonidine)
• Hyphema/bleeding — more common with YAG alone; reduced by pre-argon or direct pressure with lens
• Uveitis (mild; resolves in days)
• Dysphotopsia — linear shadow/glare if PI not fully covered by upper lid (avoid at 3 or 9 o'clock); affects 2–4% of patients
• Cataract — direct laser hit on anterior lens capsule (usually insignificant)
• Corneal burn — if PI placed too anteriorly (close to cornea); rare
• Plateau iris — angle may still be occludable after PI if ciliary processes are anteriorly rotated; requires ALPI

• Plateau iris syndrome: Angle remains narrow/closes despite patent PI; ALPI needed
• PAS already formed: Cannot reverse PAS (synechial closure) — only prevents further PAS formation
• Mixed mechanism (lens-induced): Phacomorphic component needs lens extraction
• EAGLE trial conclusion: Clear lens extraction > LPI in PAC (IOP >29 mmHg) or PACG — superior efficacy, cost-effectiveness, and quality of life; LPI still appropriate for PACS and lower-risk PAC
• Failed/occluded PI: May need repeat PI or surgical iridectomy

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MARKING SCHEME SUMMARY

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QUICK REFERENCE — ALL 10 QUESTIONS AT A GLANCE

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1. Convert all 10 answers into a downloadable Word document (.docx)?
2. Add 5 more questions on specific topics (e.g., pseudoexfoliation, pigmentary glaucoma, malignant glaucoma)?
3. Generate short-note questions (5 marks each) for the same topics?