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Here are complete model answers for all questions in the paper:

ASMC-ABVMU Ophthalmology Exam - Model Answers

PART A - Long Question (20 Marks)

Case: 60-year-old female, gradual bilateral vision loss over 3 years. IOP: RE 28 mmHg, LE 34 mmHg; circumciliary congestion in LE.

(a) Differential Diagnosis (2 marks)

The two most likely diagnoses are:

Primary Open Angle Glaucoma (POAG) - bilateral, asymmetric, elevated IOP (28 & 34 mmHg), gradual progressive vision loss
Primary Angle Closure Glaucoma (PACG) - especially for the LE which has circumciliary congestion, very high IOP (34 mmHg), suggesting acute or subacute angle closure

The right eye presents more as POAG (no congestion, moderately elevated IOP), while the left eye presentation with circumciliary congestion favors PACG or acute exacerbation.

(b) Define Glaucoma and List Risk Factors (3 marks)

Definition: Glaucoma is a chronic, progressive optic neuropathy characterized by:

Characteristic structural damage to the optic nerve head (cupping)
Corresponding visual field defects
In most cases, raised IOP (though IOP may not always be elevated in normal-tension glaucoma)

Risk Factors for Glaucoma:

Risk Factor	Detail
Raised IOP	Most important modifiable risk factor; >21 mmHg
Age	Risk increases after age 40; significantly higher >60
Family history	First-degree relative increases risk 4-9x
Race	African-Americans: higher risk of POAG; Asians: higher risk of PACG
Myopia	High myopia predisposes to POAG
Hypermetropia	Shallow AC - predisposes to angle closure
Thin central corneal thickness (CCT)	<555 µm - risk factor for POAG
Diabetes mellitus	Increased risk of POAG
Systemic hypertension	Associated with vascular optic neuropathy
Corticosteroid use	Topical or systemic steroids can raise IOP
Previous ocular trauma	Secondary glaucoma

(c) Classify Glaucoma (4 marks)

A. By Mechanism of IOP Elevation

1. Primary Glaucoma (no identifiable cause)

Primary Open Angle Glaucoma (POAG)
- Most common type worldwide
- Angle is anatomically open
- Trabecular meshwork dysfunction - aqueous outflow resistance increased
- Chronic, asymptomatic, bilateral
- Also: Normal Tension Glaucoma (NTG) - IOP consistently ≤21 mmHg
Primary Angle Closure Glaucoma (PACG)
- Anatomical obstruction at angle by iris
- Subtypes:
  - Acute PACG (symptomatic: pain, redness, halos, nausea)
  - Subacute (intermittent)
  - Chronic PACG
  - Primary angle closure suspect (PACS) - narrow angle, no damage
  - Primary angle closure (PAC) - narrow angle, raised IOP, no disc damage

2. Secondary Glaucoma (identifiable cause)

Open angle: Pseudoexfoliation glaucoma, pigmentary glaucoma, uveitic glaucoma, traumatic, steroid-induced
Angle closure: Neovascular glaucoma (rubeosis iridis), phacolytic, lens-induced, iris bombe in uveitis

3. Developmental / Congenital Glaucoma

Primary congenital glaucoma (trabeculodysgenesis)
Sturge-Weber syndrome, Axenfeld-Rieger syndrome

B. By Age of Onset

Congenital (birth - 3 years): Buphthalmos
Infantile (3 months - 3 years)
Juvenile (3 - 35 years)
Adult (>35 years)

(d) Disc Changes and Visual Field Changes (6 marks)

Optic Disc Changes in Glaucoma

Normal disc: Cup-to-disc (C:D) ratio ≤0.4, pink neuroretinal rim (NRR) with ISNT rule (Inferior > Superior > Nasal > Temporal rim width)

Glaucomatous changes (in order of progression):

Increased C:D ratio:
- C:D >0.6 is suspicious
- C:D >0.7 or asymmetry between eyes >0.2 is significant
- Vertical elongation of cup (vertical C:D > horizontal)
Neuroretinal rim thinning / notching:
- Inferior pole first → then superior → then nasal/temporal
- Notching: focal loss of NRR, most commonly inferotemporal or superotemporal
Disc haemorrhages (Drance haemorrhages):
- Splinter/flame-shaped haemorrhages at disc margin
- Early marker, more common in NTG
- Predict future field loss
RNFL (Retinal Nerve Fiber Layer) defects:
- Wedge-shaped RNFL defects visible on red-free photography
- Superotemporal and inferotemporal most common
Bayoneting of vessels:
- Blood vessels appear to double-back at disc margin due to deep excavation
Bean-pot cupping:
- Severe stage - cup extends under disc rim (overhanging edges)
Nasal shift of vessels / Nasalization:
- Central retinal vessels shift nasally
Peripapillary atrophy (PPA):
- Beta zone (direct surrounds disc) more significant than alpha zone

Visual Field Changes in Glaucoma (Sequence)

Stage	Field Defect
Early	Enlargement of blind spot; isopter contraction
Early-moderate	Bjerrum's scotoma / arcuate scotoma (follows RNFL arc from blind spot, between 10-20° from fixation)
Moderate	Seidel scotoma (comma-shaped extension from blind spot)
Moderate-advanced	Arcuate or ring scotoma (double arcuate = annular scotoma)
Advanced	Nasal step (Ronne's nasal step) - asymmetric field loss at horizontal midline nasally
Late	Altitudinal defect (half the field - superior or inferior)
End-stage	Tunnel vision (only central island remains) → eventual loss of central vision

(e) Investigations and Management of POAG (5 marks)

Investigations

To confirm diagnosis:

Tonometry - Goldmann applanation tonometry (gold standard for IOP)
Gonioscopy - to assess angle; confirms open angle in POAG
Optic disc assessment - Slit lamp with +90D lens / direct ophthalmoscope; fundus photography
Visual fields - Humphrey automated perimetry (24-2 or 30-2 program); Frequency Doubling Technology (FDT)
OCT (Optical Coherence Tomography) - RNFL thickness, ganglion cell complex analysis; detects structural loss before field loss
HRT (Heidelberg Retinal Tomograph) - 3D disc topography

Other: 7. Central Corneal Thickness (CCT) - thin CCT underestimates IOP; adjust target IOP accordingly 8. Diurnal IOP curve - 4-hourly IOP over a day to detect peak IOP 9. Blood pressure measurement - calculate ocular perfusion pressure 10. Systemic evaluation - rule out secondary causes (blood sugar, thyroid)

Management of POAG

Goal: Reduce IOP to a "target pressure" at which optic nerve damage progression is halted or slowed.

Step 1 - Medical Management (First-line)

Drug Class	Drug	Mechanism	Dose
Prostaglandin analogues (first choice)	Latanoprost, Travoprost, Bimatoprost	Increase uveoscleral outflow	Once daily at night
Beta-blockers	Timolol 0.5%	Reduce aqueous production	BD
Alpha-2 agonists	Brimonidine 0.2%	Reduce production + increase outflow	BD/TDS
Carbonic anhydrase inhibitors (topical)	Dorzolamide, Brinzolamide	Reduce aqueous production	BD/TDS
CAI (systemic)	Acetazolamide 250mg	Reduce production	TDS-QID (short term)
Miotic (rarely)	Pilocarpine 2-4%	Increase trabecular outflow	QID

Combination drops (e.g., Cosopt - Timolol + Dorzolamide; Combigan - Timolol + Brimonidine) improve compliance.

Step 2 - Laser Treatment

Selective Laser Trabeculoplasty (SLT): Laser applied to trabecular meshwork; improves drainage; can be used as primary or adjunct therapy; repeatable
Argon Laser Trabeculoplasty (ALT): Similar but less repeatable

Step 3 - Surgical Management

Trabeculectomy (Filtration surgery): Creates a new drainage pathway from AC to subconjunctival space (filtering bleb). Antifibrotics (Mitomycin C, 5-FU) enhance success. Gold standard surgical option.
Tube/Shunt surgery (Glaucoma Drainage Device - GDD): Ahmed, Baerveldt, Molteno implants - for cases where trabeculectomy has failed or is likely to fail
Minimally Invasive Glaucoma Surgery (MIGS): iStent, Hydrus - for mild-moderate POAG combined with cataract surgery
Cycloablation: Diode laser cycloablation - for refractory end-stage glaucoma

Follow-up: Regular monitoring of IOP, RNFL on OCT, and visual fields every 6-12 months to assess progression.

PART A - Short Notes (5 marks each)

1. Types of Intraocular Lens (IOL)

An IOL is an artificial lens implanted in the eye, most commonly after cataract extraction, to replace the natural crystalline lens.

Classification:

A. By Position in Eye:

Type	Position	Details
Posterior chamber IOL (PCIOL)	In the capsular bag (most common)	Placed behind iris, in the capsular bag after ECCE/phaco
Anterior chamber IOL (ACIOL)	Anterior to iris	Used when posterior capsule is ruptured; less preferred
Iris-fixated IOL	Clipped to iris	E.g., Artisan lens
Sulcus IOL	Ciliary sulcus	When capsular bag is inadequate

B. By Material:

PMMA (Polymethylmethacrylate): Rigid, non-foldable; older lenses; requires larger incision (~6mm)
Acrylic (hydrophobic/hydrophilic): Most commonly used today; foldable; injected through 2.2-2.8mm incision
Silicone: Foldable; not suitable if silicone oil is likely to be used
Collamer (HEMA): Used in phakic IOLs (e.g., ICL - Implantable Collamer Lens)

C. By Optical Design:

Type	Feature	Indication
Monofocal	Single focal point (distance)	Standard; patient needs reading glasses
Multifocal (MIOL)	Multiple focal points (distance + near)	Reduced spectacle dependence; risk of halos/glare
Extended Depth of Focus (EDOF)	Elongated focal range	Better intermediate vision; fewer dysphotopsias
Toric IOL	Corrects astigmatism	Patients with corneal astigmatism ≥1.5D
Accommodating IOL	Shifts position to mimic accommodation	Limited effectiveness

D. Special Types:

Phakic IOL: Implanted with the natural lens still in situ; for refractive correction of high myopia (e.g., Visian ICL, Artisan)
Scleral-fixated IOL: Fixated to sclera with prolene sutures when no capsular support exists
Blue-light filtering IOL: Contains yellow chromophore to filter blue light and protect macula

Power Calculation: A-scan biometry + IOL Master; formulae: SRK/T, Hoffer Q, Holladay, Barrett Universal II

2. Superior Orbital Fissure - Draw and Structures Passing Through It

Superior Orbital Fissure (SOF): A cleft between the greater and lesser wings of the sphenoid bone, connecting the middle cranial fossa to the orbit.

Shape: Comma-shaped / laterally wider, medially narrowed

Structures passing through (Divided by Annulus of Zinn / Common Tendinous Ring):

WITHIN the Annulus of Zinn (inside the muscle cone):

Oculomotor nerve (CN III) - superior & inferior divisions
Nasociliary nerve (branch of CN V1)
Abducens nerve (CN VI)
Mnemonic: "LOAN" - Lacrimal, Oculomotor, Abducens, Nasociliary (inside ring)

OUTSIDE the Annulus of Zinn (outside muscle cone):

Lacrimal nerve (branch of CN V1)
Frontal nerve (branch of CN V1)
Trochlear nerve (CN IV)
Superior ophthalmic vein
Inferior ophthalmic vein (joins/passes near)
Sympathetic fibers (from plexus)

Mnemonic for structures outside ring: "Lazy French Tarts Sit Naked In Anticipation" - Lacrimal, Frontal, Trochlear, Superior ophthalmic vein

Summary Table:

Structure	Division of CN	Location
CN III superior division	Oculomotor	Inside ring
CN III inferior division	Oculomotor	Inside ring
CN VI (Abducens)	-	Inside ring
Nasociliary nerve	CN V1	Inside ring
CN IV (Trochlear)	-	Outside ring
Lacrimal nerve	CN V1	Outside ring
Frontal nerve	CN V1	Outside ring
Superior ophthalmic vein	-	Outside ring

Note: The optic nerve (CN II) passes through the Optic Canal, NOT the superior orbital fissure.

Clinical: SOF syndrome (Rochon-Duvigneaud syndrome) - involvement of CN III, IV, V1, VI causing ophthalmoplegia + V1 sensory loss + ptosis + proptosis (due to tumour, thrombosis, fracture, aneurysm in region).

3. Hypermetropia - Definition, Signs, Symptoms & Management

Definition: A refractive error in which parallel rays of light coming from infinity are focused behind the retina, when accommodation is relaxed. The eyeball is too short (axial hypermetropia) or the refracting power of the eye is too weak (refractive hypermetropia).

Types:

Axial: Short AP diameter (most common)
Refractive: Reduced corneal/lens curvature, or reduced refractive index
Positional: Posterior displacement of lens

Degrees: Low (<+2D), Moderate (+2 to +5D), High (>+5D)

Classification by Accommodation:

Latent: Corrected by inherent tone of ciliary muscle; not detected without cycloplegic refraction
Manifest:
- Facultative: Can be corrected by accommodation
- Absolute: Cannot be corrected by accommodation (exhausted)
Total: Latent + Manifest (measured under cycloplegia)

Signs:

Small eyeball / short axial length on A-scan
Small corneal diameter
Shallow anterior chamber
Fundoscopy: Small disc, crowded disc appearance (pseudopapilledema), reduced cup-to-disc ratio
Cross-eyes in children (accommodative esotropia)

Symptoms:

Asthenopia (eyestrain, headache - frontal/brow ache after near work)
Blurring of near vision (absolute hypermetropia)
Blurring of distance vision (high degrees)
In children: Crossed eyes (accommodative convergent squint)
Predisposition to acute angle closure glaucoma (shallow AC)
Reading fatigue, difficulty concentrating

Management:

Optical correction:
- Spectacles with convex (+) lenses (full correction under cycloplegia in children; in adults, prescribe the maximum plus accepted)
- Contact lenses (daily soft lenses or toric for astigmatism)
Refractive surgery:
- LASIK / LASEK / PRK: For low to moderate hypermetropia (<+4-5D); treats up to +6D in some centers
- SMILE: Available for myopia primarily; not for hypermetropia
- Phakic IOL (ICL): For high hypermetropia not amenable to corneal surgery
- Clear Lens Extraction (Refractive Lens Exchange): For high hypermetropia in older patients; with multifocal/EDOF IOL
Treat amblyopia (in children): Patching of the better eye; penalization

4. Viral Keratitis - Signs, Symptoms & Management

The most common cause of viral keratitis is Herpes Simplex Virus (HSV-1). Other causes include Herpes Zoster Ophthalmicus (HZV), Adenovirus, Acanthamoeba (not viral but often grouped).

A. Herpes Simplex Keratitis (HSK)

Subtypes:

Type	Features
Epithelial keratitis	Most common; dendritic ulcer (branching with terminal bulbs); rose bengal/fluorescein stains
Geographic (amoeboid) ulcer	Large irregular epithelial ulcer (usually post-steroid use)
Stromal keratitis	Interstitial keratitis; disc keratitis; necrotizing keratitis
Endothelial keratitis	Keratouveitis; linear endotheliitis
Metaherpetic keratitis	Healed/scarred; not active virus - trophic ulcer

Symptoms:

Foreign body sensation, photophobia, lacrimation
Blurred vision (if involving visual axis)
Pain (usually mild in epithelial type; more severe in stromal/uveitis type)
Herpetic vesicles on lid/perioral skin (in primary infection)
Reduced corneal sensation (hypoesthesia - hallmark of repeated HSV infection)

Signs:

Dendritic ulcer: Branching linear lesion with terminal bulbs - pathognomonic of HSV epithelial keratitis
Staining with rose bengal (stains devitalized cells) and fluorescein
Reduced corneal sensation (cotton wisp test)
Stromal haze / ghost vessels / lipid deposits (in chronic stromal keratitis)
Corneal vascularization in chronic disease
Disciform oedema (Wessely immune ring) in stromal disease
Iritis/uveitis with keratic precipitates (KPs) in keratouveitis

Management:

Stage	Treatment
Epithelial HSK	Topical antiviral: Acyclovir 3% ointment 5x/day for 14 days OR Ganciclovir 0.15% gel 5x/day; Debridement; NO steroids
Stromal HSK	Topical steroids (Prednisolone) + topical antiviral (cover); oral acyclovir 400mg 3-5x/day
Prophylaxis for recurrence	Oral acyclovir 400mg BD or valacyclovir 500mg OD for 1 year (HEDS trial)
Keratoplasty	For severe corneal scarring with reduced vision - penetrating keratoplasty

B. Herpes Zoster Ophthalmicus (HZO)

Reactivation of VZV in trigeminal nerve, ophthalmic division (V1)
Hutchinson's sign (vesicles on tip of nose = nasociliary branch involved = high risk of ocular involvement)
Keratitis: Pseudodendrites (mucus plaques - no terminal bulbs - different from HSV dendrites)
Treatment: Oral acyclovir 800mg 5x/day for 7-10 days within 72 hours; topical lubricants; steroids for stromal inflammation

5. Vernal Keratoconjunctivitis (VKC)

Pathophysiology

VKC is a chronic, recurrent, bilateral allergic conjunctivitis with both IgE-mediated (Type I hypersensitivity) and cell-mediated (Type IV) immune mechanisms playing important roles.

Mast cell degranulation releases histamine, tryptase, prostaglandins, leukotrienes
Eosinophils are recruited → release major basic protein (MBP) causing epithelial toxicity
Th2 lymphocytes release IL-4, IL-5, IL-13 (IgE class switching, eosinophil recruitment)
Giant papillae form due to fibroblast activation by TGF-β and substance P

Signs and Symptoms

Symptoms:

Intense itching (cardinal symptom)
Lacrimation, photophobia
Foreign body sensation, burning
Thick ropy/stringy mucoid discharge
Increased blinking
Seasonal exacerbation (late spring/summer)

Signs - Palpebral VKC (Upper tarsal plate):

Cobblestone papillae (<1mm): flat-topped polygonal papillae
Giant papillae (>1mm): formed when septa rupture
Whitish inflammatory infiltrates in severe disease

Signs - Limbal VKC (common in dark-skinned patients):

Gelatinous limbal papillae
Horner-Trantas dots: White chalky dots at limbus = eosinophil aggregates; pathognomonic of VKC
Maxwell-Lyons sign: Fine superficial keratitis

Corneal involvement:

Superior punctate epithelial erosions
Epithelial macroerosions (shield ulcer) - sterile; upper 1/3 of cornea
Plaques (white calcium deposits in shield ulcer)
Pseudogerontoxon: Lipid arc at limbus

Types of VKC

Palpebral type: Upper tarsal plate involvement predominates
Limbal type: Limbal involvement predominates (more common in Africans and Asians)
Mixed type: Features of both

Management

Approach	Drug/Intervention
Mast cell stabilizers (first-line, chronic)	Sodium cromoglicate 2%, Lodoxamide 0.1% (more potent)
Antihistamines (topical)	Olopatadine, Ketotifen, Azelastine - dual action (antihistamine + mast cell stabilizer)
Steroids (short course for acute exacerbation)	Fluorometholone, Loteprednol (safer); Prednisolone 1% (short courses only) - monitor IOP
Cyclosporine 0.05-1% (steroid-sparing)	Immunomodulation; reduces papillary hypertrophy; for moderate-severe/steroid-dependent VKC
Tacrolimus 0.03% (alternative to cyclosporine)	FK506; effective for severe/refractory VKC
Oral antihistamines	Loratadine (non-sedating); Diphenhydramine (sedating - useful for sleep)
Supratarsal steroid injection	Triamcinolone acetonide - for refractory palpebral VKC with giant papillae
Cold compresses	Symptomatic relief
Avoidance of triggers	Sun, dust, pollen
Surgical	Debridement of plaques, excision of giant papillae (rarely needed)

6. Factors Responsible for Transparency of Cornea

The cornea is normally transparent, allowing 90% of light to pass through. Several structural and biochemical factors maintain this transparency:

1. Avascularity

Cornea has NO blood vessels; vascularization causes opacity
Nutrition via aqueous humor (anteriorly), tears, and diffusion from limbal vessels (periphery)

2. Absence of Myelination

Corneal nerves lose their myelin sheaths at the limbus (Dohlman)
Myelin is opaque; absence ensures transparency

3. Regular Arrangement of Collagen Fibrils (Maurice's Lattice Theory)

Collagen fibrils in the stroma are of uniform diameter (~25nm) and regularly spaced (spacing < half wavelength of visible light ~200nm)
Regular spacing leads to destructive interference of scattered light waves → no net scatter → transparency
Type I and V collagen fibrils maintained in regular array by proteoglycans (keratan sulphate and chondroitin sulphate-containing proteoglycans - lumican, mimecan, keratocan, decorin)

4. Relative Dehydration of Stroma (Deturgescence)

Stroma has a natural tendency to imbibe water (hydrophilic proteoglycans)
Maintained in a relatively dehydrated state (78% water) by two active pumping mechanisms:
- Corneal endothelium (most important): Na+/K+-ATPase pump; bicarbonate pump; actively transports fluid from stroma into AC
- Corneal epithelium: Barrier function preventing excess water entry from tears
Loss of endothelial function (Fuchs dystrophy, surgical trauma, endothelial cell count <500/mm²) → corneal oedema → clouding

5. Smooth Anterior Surface

Maintained by the pre-corneal tear film (mucin, aqueous, lipid layers)
Irregular surface (dry eye, scarring) → scattering → reduced clarity

6. Absence of Pigment

No melanin or other pigment in corneal layers (unlike iris/retina)

7. Uniform Epithelium

Epithelium must be smooth and intact; disruption causes scattering

8. Bowman's Layer and Descemet's Membrane

These acellular collagenous layers are also transparent by virtue of regular structure

Summary (Mnemonic - "CARDSAP"):

Collagen regular arrangement (Maurice's theory)
Avascularity
Relative dehydration (endothelial pump)
Deturgescence
Smooth tear film surface
Absence of pigment / myelination
Proteoglycans maintaining fibril spacing

Source: Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition; standard ophthalmic textbooks.

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