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Glaucoma — Complete Exam Answers

Q2 — Short Questions (10 marks total)

Definition of Glaucoma (2 marks)

Glaucoma is a group of ocular disorders characterized by a progressive optic neuropathy, resulting in characteristic optic disc changes and visual field defects, in which raised intraocular pressure (IOP) is the most important risk factor. It is defined by optic nerve damage, not simply by elevated IOP.
More precisely, Primary Open-Angle Glaucoma (POAG) — the commonest type — is defined as a chronic, progressive optic neuropathy of adult onset characterized by:
  • Retinal nerve fibre layer (RNFL) thinning
  • Glaucomatous optic nerve head damage
  • Characteristic visual field loss
  • Open anterior chamber angle
  • Absence of secondary causes
(Kanski's Clinical Ophthalmology)

Classification of Glaucoma (3 marks)

By mechanism of IOP elevation:
TypeMechanism
Open-angleTrabecular meshwork resistance increased; angle remains open
Angle-closureIris blocks trabecular meshwork; angle physically closed
By aetiology:
  1. Primary glaucoma — no identifiable cause
    • Primary Open-Angle Glaucoma (POAG) — most common
    • Primary Angle-Closure Glaucoma (PACG)
  2. Secondary glaucoma — caused by another condition
    • Pseudoexfoliative glaucoma
    • Pigment dispersion glaucoma
    • Lens-induced glaucoma
    • Neovascular glaucoma (rubeotic)
    • Uveitic glaucoma
    • Traumatic glaucoma
  3. Congenital (developmental) glaucoma
    • Primary congenital/infantile glaucoma
    • Glaucoma associated with ocular/systemic anomalies (Sturge-Weber, aniridia, etc.)
By age of onset:
  • Congenital (birth–3 yrs), infantile (3–16 yrs), adult-onset

Management of POAG (5 marks)

Goal: Reduce IOP to a "target IOP" — the level at which progression stops.

1. Medical (First-line)

Drug ClassExampleMechanism
Prostaglandin analoguesLatanoprost, bimatoprost, travoprost↑ uveoscleral outflow
Beta-blockersTimolol 0.5%↓ aqueous production
Carbonic anhydrase inhibitorsDorzolamide (topical), acetazolamide (oral)↓ aqueous production
Alpha-2 agonistsBrimonidine↓ production + ↑ uveoscleral outflow
Miotics (cholinergics)Pilocarpine↑ trabecular outflow
Rho-kinase inhibitorsNetarsudil↑ conventional outflow
Prostaglandin analogues are first-line (most efficacious, once daily, well tolerated).

2. Laser

  • Selective Laser Trabeculoplasty (SLT): First or second-line; stimulates trabecular meshwork; repeatable
  • Argon Laser Trabeculoplasty (ALT): Alternative to SLT

3. Surgical

  • Trabeculectomy (guarded filtration surgery): Creates a drainage bleb; gold standard for surgery; often augmented with Mitomycin C (MMC) or 5-FU
  • Glaucoma Drainage Devices (GDDs): Ahmed, Baerveldt, Molteno tubes — for refractory cases
  • Minimally Invasive Glaucoma Surgery (MIGS): iStent, OMNI, Hydrus — for mild-moderate POAG, combined with cataract surgery
  • Cyclodestructive procedures: Diode laser cycloablation — last resort

Monitoring

Regular visual field testing, OCT of RNFL, IOP measurement, optic disc photography.

Q3 — 4 Marks Each

3a. Anatomy of the Anterior Chamber Angle

The anterior chamber angle (iridocorneal angle) is the drainage angle of the eye, bounded by:
  • Anteriorly: Peripheral cornea (Schwalbe's line = end of Descemet's membrane)
  • Posteriorly: Iris root and ciliary body
  • Structures from anterior to posterior (gonioscopic landmarks):
    1. Schwalbe's line — anterior-most landmark; termination of Descemet's membrane
    2. Trabecular meshwork (TM): Triangular band; pigmented posteriorly; aqueous drains here
    3. Scleral spur — prominent white line; site of ciliary muscle attachment
    4. Ciliary band — grey/brown; variable width
    5. Iris root
Aqueous outflow pathway: Trabecular meshwork → Canal of Schlemm → collector channels → episcleral veins → systemic circulation
This is the conventional (trabecular) outflow pathway (~80%). The uveoscleral pathway (~20%) drains via the ciliary body interstices.

3b. Anti-Glaucoma Drugs

ClassDrugMechanismRoute
Prostaglandin analoguesLatanoprost, bimatoprost, travoprost, tafluprost↑ Uveoscleral outflow via FP receptorTopical
Beta-blockersTimolol, betaxolol, levobunolol↓ Aqueous production (↓ cAMP in ciliary body)Topical
Carbonic anhydrase inhibitorsDorzolamide, brinzolamide (topical); acetazolamide (systemic)↓ Aqueous production (inhibits CA-II in ciliary body)Topical/oral
Alpha-2 adrenergic agonistsBrimonidine, apraclonidine↓ Aqueous production + ↑ uveoscleral outflowTopical
Cholinergic (miotics)PilocarpineCiliary muscle contraction → opens TM → ↑ conventional outflowTopical
Rho-kinase inhibitorsNetarsudil↑ Trabecular + Schlemm's canal outflowTopical
Osmotic agentsMannitol, glycerolAcute IOP reduction (draws water from vitreous)IV/oral

3c. Management of Angle Closure Attack (Acute Angle Closure Crisis)

Acute angle closure is an ophthalmological emergency. IOP can reach 50–80 mmHg.
Immediate medical management:
  1. Systemic IOP reduction (to break the attack):
    • IV acetazolamide 500 mg stat (inhibits aqueous production)
    • IV mannitol 1–2 g/kg over 45 min (hyperosmotic agent)
  2. Topical agents:
    • Timolol 0.5% (β-blocker)
    • Brimonidine 0.1–0.2%
    • Pilocarpine 2–4% — given after IOP begins to fall (not when IOP very high, as iris ischaemia prevents miosis)
  3. Analgesia + antiemetics (nausea/vomiting common)
  4. Supine positioning — may help deepen the angle
Definitive treatment (after IOP controlled):
  • Nd:YAG laser peripheral iridotomy (PI) — creates a hole in peripheral iris to bypass pupillary block; prevents further attacks; also performed prophylactically in the fellow eye
  • If cornea hazy: medical treatment first; topical glycerol to clear cornea before laser
  • Surgical peripheral iridectomy if laser fails

3d. Lens-Induced Glaucoma

These are forms of secondary glaucoma caused by pathological changes in the lens:
TypeMechanismIOP Mechanism
Phacomorphic glaucomaIntumescent (swollen) mature cataract → lens enlarges → pushes iris forward → pupillary block → angle closureAngle-closure mechanism
Phacolytic glaucomaHypermature cataract → lens proteins leak through intact capsule → macrophages engorge on lens proteins → block TMOpen-angle mechanism
Phacoantigenic (phacoanaphylactic) uveitisLens proteins incite autoimmune reaction (secondary uveitis) → secondary glaucomaInflammatory
Lens particle glaucomaAfter trauma or surgery → lens fragments block TMOpen-angle mechanism
Treatment: Definitive treatment is removal of the offending lens (cataract extraction) + IOP-lowering agents in the interim.

3e. Optic Disc Changes in Glaucoma

The glaucomatous optic disc shows characteristic changes due to loss of retinal ganglion cell axons:
  1. Increased cup-to-disc (C:D) ratio — normal C:D < 0.5; suspicious if > 0.6; abnormal C:D asymmetry (>0.2 between eyes) is significant
  2. Neuroretinal rim (NRR) thinning — follows the ISNT rule (Inferior > Superior > Nasal > Temporal thickness normally); glaucoma violates this rule
  3. Focal NRR notching — especially inferotemporal and superotemporal
  4. Disc haemorrhages (Drance/splinter haemorrhages) — at disc margin, particularly inferotemporal; strongly predictive of progression
  5. Retinal nerve fibre layer (RNFL) defects — wedge-shaped arcuate defects visible with red-free light
  6. Laminar dot sign — pores of the lamina cribrosa become visible in deep cupping
  7. Baring of circumlinear vessels — vessels course over the rim without NRR support
  8. Parapapillary atrophy (PPA) — beta zone (chorioretinal atrophy) is associated with glaucoma progression
  9. Bayoneting of vessels — vessels disappear at the disc margin and reappear on the floor of the cup

Q4 — 2 Marks Each

4A. Congenital Triad of Glaucoma

Primary congenital glaucoma (buphthalmos) presents with the classic triad:
  1. Epiphora (excessive tearing / lacrimation)
  2. Photophobia (light sensitivity — due to corneal oedema)
  3. Blepharospasm (involuntary eyelid closure)
Additional features: Large eye (buphthalmos/"ox eye"), corneal oedema/haziness, Haab's striae (horizontal breaks in Descemet's membrane), raised IOP.

4B. 3 Side Effects of Prostaglandin Analogues

  1. Conjunctival hyperaemia (red eye) — most common
  2. Iris darkening (increased iris pigmentation) — due to ↑ melanin in stromal melanocytes (irreversible)
  3. Periorbital fat atrophy (Prostaglandin-associated periorbitopathy, PAP) — deepening of upper lid sulcus, ptosis, enophthalmos; may be asymmetric if used in one eye only
  4. Hypertrichosis (eyelash growth — longer, thicker, darker eyelashes) — basis for bimatoprost cosmetic use
  5. Anterior uveitis — in susceptible patients
  6. Cystoid macular oedema (CME) — rare; especially in aphakic eyes
(3 required: most testable = conjunctival hyperaemia, iris pigmentation, periorbital fat atrophy/eyelash growth)

4C. Surgical Procedures of Glaucoma

  1. Trabeculectomy (guarded filtering surgery) — gold standard; creates scleral flap and sclerostomy to allow sub-conjunctival filtration bleb; ± MMC/5-FU
  2. Glaucoma Drainage Devices (GDDs/tube surgery) — Ahmed, Baerveldt, Molteno; diverts aqueous to equatorial bleb via silicone tube
  3. Goniotomy / Trabeculotomy — for congenital glaucoma; opens trabecular meshwork directly
  4. Cyclodestructive procedures — Diode laser cycloablation/cyclocryotherapy; destroys ciliary body to reduce aqueous production; last resort
  5. MIGS (Minimally Invasive Glaucoma Surgery): iStent (trabecular micro-bypass), OMNI (canaloplasty + trabeculotomy), XEN gel stent, Hydrus microstent
  6. Peripheral iridectomy / laser iridotomy — for angle-closure glaucoma (pupillary block)
  7. Deep sclerectomy / viscocanalostomy — non-penetrating filtering surgeries

4D. Clinical Features of Acute Angle Closure

Symptoms:
  • Sudden onset severe unilateral eye pain
  • Decreased/blurred vision with coloured halos around lights (corneal oedema)
  • Nausea and vomiting (vagal response)
  • Headache (same side)
Signs:
  • Marked conjunctival injection (circumcorneal/ciliary flush)
  • Corneal haziness/oedema (cloudy cornea)
  • Fixed, mid-dilated pupil (~4–6 mm; oval; non-reactive to light)
  • Shallow anterior chamber
  • Very high IOP (50–80 mmHg)
  • Rock-hard eyeball on palpation
  • Closed angle on gonioscopy
  • Fundus: rarely visible due to corneal haze

4E. Neuroprotection in Glaucoma

Definition: Strategies aimed at protecting retinal ganglion cells (RGCs) from death independently of IOP lowering, targeting the neurodegenerative pathway directly.
Rationale: Visual field loss can progress despite normal IOP — suggesting IOP-independent mechanisms (glutamate excitotoxicity, oxidative stress, mitochondrial dysfunction, neurotrophin deprivation).
Approaches under study/use:
Agent/StrategyMechanism
Brimonidine (alpha-2 agonist)Neuroprotective in addition to IOP reduction (animal studies); upregulates BDNF
Memantine (NMDA antagonist)Blocks glutamate excitotoxicity (trials in humans inconclusive)
Citicoline (CDP-choline)Supports neuronal membrane integrity; some clinical evidence
Calcium channel blockersImproved optic nerve blood flow (e.g., nilvadipine — ongoing research)
Neurotrophins (BDNF)Support RGC survival; gene therapy delivery being studied
Stem cell therapyReplacing lost RGCs — experimental
Mitochondria-targeted agentsReducing oxidative stress in RGCs
Current clinical reality: No agent is currently FDA-approved specifically for neuroprotection in glaucoma. IOP lowering remains the only proven neuroprotective strategy. However, brimonidine and citicoline have the most supportive clinical data of the purely neuroprotective agents.
Sources: Kanski's Clinical Ophthalmology 10th Edition; Tintinalli's Emergency Medicine; Goldman-Cecil Medicine
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