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OPHTHALMOLOGY CLASS TEST — MS LEVEL ANSWERS

Based on Kanski's Clinical Ophthalmology (10th Ed.) — closest to AK Khurana's standard

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SECTION A: EXPLAIN WHY (4×5 = 20) — Answer Any 4

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Q1. Corneal Graft Has Lower Risk of Rejection Compared to Other Grafts

Basis of Immunological Privilege:

What Breaks This Privilege?

• Host stromal vascularization — the single most important risk factor; new blood and lymphatic vessels establish afferent and efferent arms of immune response
• Larger grafts (>8 mm), eccentric grafts, herpetic infection, previous failed grafts, glaucoma

Types of Rejection (if it occurs):

1. Epithelial rejection — elevated rejection line, 3 months post-op
2. Subepithelial rejection — Krachmer spots (subepithelial infiltrates)
3. Stromal rejection — diffuse haze
4. Endothelial rejection — Khodadoust line (linear KP moving from host-graft junction)

Comparison with Other Grafts:

Conclusion: The cornea is immunologically privileged due to avascularity, alymphaticity, immune deviation, and local immunosuppressive factors — hence it has the lowest rejection rate among all transplants. — Kanski's Clinical Ophthalmology, 10th Ed., p. 294

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Q2. Dacryocystectomy Is Preferred in Chronic Dacryocystitis

Pathology in Chronic Dacryocystitis:

• Chronic obstruction of the nasolacrimal duct → stagnation of tears → secondary infection
• Sac is dilated, fibrosed, and filled with mucopurulent material
• Active chronic infection with Gram-positive cocci (Staphylococcus, Streptococcus) or fungi (Candida, Aspergillus)
• Sac wall is thickened, scarred, non-functional

Why DCT, Not DCR (Dacryocystorhinostomy)?

Key Points:

• DCR creates a surgical fistula between lacrimal sac and nasal mucosa — bypasses obstruction but preserves the sac
• DCT removes the entire sac — eliminates the reservoir of infection permanently
• In elderly patients with dry eyes, even epiphora may not be a major concern
• Sac excision must always be sent for histopathology to rule out sac tumors (transitional cell carcinoma)

Conclusion: In chronic dacryocystitis, the sac is irreversibly damaged and serves as a focus of infection. DCT removes this focus permanently and is the definitive treatment of choice.

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Q3. Proliferative Diabetic Retinopathy Is More Vision-Threatening Than Non-Proliferative

NPDR (Non-Proliferative Diabetic Retinopathy):

• Mechanism: Basement membrane thickening, pericyte loss, increased vascular permeability, microaneurysm formation
• Features: Microaneurysms, dot-blot hemorrhages, hard exudates, cotton-wool spots, venous beading, IRMA
• Vision threat: Diabetic Macular Edema (DME) → slow, insidious vision loss (central)
• No neovascularization — confined within retina

PDR (Proliferative Diabetic Retinopathy):

• Mechanism: Severe retinal ischemia → hypoxia → upregulation of VEGF (Vascular Endothelial Growth Factor) → neovascularization
• Features: New vessels on disc (NVD), new vessels elsewhere (NVE), new vessels on iris (NVI — rubeosis iridis)

Why PDR Is MORE Vision-Threatening:

High-Risk Characteristics for PDR (ETDRS criteria):

• NVD ≥ 1/4–1/3 disc area
• Any NVD with vitreous/preretinal hemorrhage
• NVE ≥ 1/2 disc area with vitreous/preretinal hemorrhage

Management of PDR:

• Pan-retinal photocoagulation (PRP) — ablates ischemic retina, reduces VEGF stimulus
• Anti-VEGF injections (ranibizumab, bevacizumab, aflibercept)
• Vitrectomy for non-clearing vitreous hemorrhage or tractional RD

Conclusion: NPDR causes slow macular edema; PDR causes sudden, severe, often irreversible vision loss through vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma — making PDR far more vision-threatening.

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Q4. Visual Field Testing Is Done in Glaucoma Patients

Anatomical Basis:

• RNFL fibres run in arcuate patterns around the fovea (Henle's fibre layer)
• The horizontal raphe separates superior and inferior arcuate bundles
• Damage to specific bundles → corresponding field defects respecting the horizontal midline

Progression of Glaucomatous Visual Field Defects:

Why VF Testing Is Essential:

1. Detect functional damage early — structural damage precedes functional loss; VF confirms functional impact
2. Monitor progression — mean deviation (MD) worsens by ~1 dB/year in untreated POAG
3. Guide treatment — severity of field loss guides target IOP
4. Assess treatment efficacy — stable VF = controlled disease
5. Legal/driving fitness — bilateral advanced VF loss disqualifies patients from driving

Standard Automated Perimetry (SAP) — Humphrey Field Analyzer:

• 24-2 program — tests 52 points within 24° of fixation (standard)
• 10-2 program — monitors residual central field in advanced disease
• Outputs: Grayscale, Total Deviation, Pattern Deviation, MD, PSD, GHT (Glaucoma Hemifield Test)

Humphrey Criteria for Glaucomatous Damage (Hodapp-Parrish-Anderson):

• GHT outside normal limits on ≥2 consecutive tests, OR
• Cluster of ≥3 non-edge points depressed at P<5% (one at P<1%), OR
• Corrected PSD occurring in <5% of normals

Other Perimetric Tests:

• FDT (Frequency Doubling Technology) — detects early RNFL loss
• SWAP (Short Wavelength Automated Perimetry) — blue-on-yellow, tests M ganglion cells early
• Goldmann kinetic perimetry — for advanced disease, driving assessments

Conclusion: Visual field testing maps functional damage corresponding to RNFL loss, detects glaucoma early, guides treatment decisions, and monitors progression — it is indispensable in glaucoma management. — Kanski's Clinical Ophthalmology, 10th Ed., p. 381

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Q5. White Pupillary Reflex in a Child Should Not Be Ignored

Normal Red Reflex vs Leukocoria:

• Normal fundal reflex is red-orange (light reflected from vascular choroid through clear media)
• Any opacity or abnormality in the visual axis causes leukocoria

Causes of Leukocoria (Mnemonic: CCRPPTV):

Why It Must NEVER Be Ignored — Retinoblastoma:

• Most common intraocular malignancy of childhood (1:15,000–20,000 live births)
• Caused by mutation in RB1 gene (chromosome 13q14) — classic tumor suppressor "two-hit" model
• If untreated: extends along optic nerve → intracranial → meningeal seeding → 100% fatal
• 5-year survival if diagnosed early (intraocular stage): >95%
• 5-year survival if diagnosed late (extraocular): <10%

Consequences of Ignoring Leukocoria:

1. Delayed diagnosis of retinoblastoma → metastatic spread → death
2. Delayed treatment of congenital cataract → irreversible amblyopia (deprivation amblyopia — critical period ends by 7–8 years)
3. Untreated Coats' disease → tractional/exudative RD → phthisis bulbi
4. Untreated ROP → bilateral blindness

Investigation Protocol:

• Fundoscopy under anaesthesia (EUA) — mandatory
• B-scan ultrasound — calcification confirms retinoblastoma
• CT/MRI orbit — extraocular extension, optic nerve involvement
• Systemic workup if retinoblastoma confirmed (bone marrow, LP for bilateral/hereditary cases)

Conclusion: Leukocoria in a child represents a sight- and life-threatening condition until proven otherwise. Retinoblastoma must be excluded urgently. Any delay in diagnosis risks metastatic spread and death, while vision-threatening conditions like congenital cataract cause irreversible amblyopia if not treated within the critical period.

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SECTION B: SHORT NOTES (2×5 = 10) — Answer Any 2

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SN1. Presbyopia

Physiology of Accommodation (Normal):

• Ciliary muscle contracts → zonular fibres relax → lens becomes more convex (rounded) → increased refractive power → near focus
• This is mediated by the parasympathetic innervation (oculomotor nerve via ciliary ganglion)

Pathophysiology of Presbyopia (Helmholtz Theory):

• With age, the crystalline lens loses elasticity (nuclear sclerosis → lens becomes rigid)
• Aged lens cannot change shape even when ciliary muscle contracts
• Lens fibres lose their ability to slide and deform
• Zonules remain intact; ciliary muscle may remain functional — the fault lies with the lens itself

Age of Onset:

• Amplitude of accommodation: 14D at birth → 7D at 25 yrs → 4D at 40 yrs → <1D at 60 yrs
• Clinical symptoms appear when amplitude falls below 4–5 dioptres
• Emmetropes and hypermetropes are affected earlier; myopes may compensate with their existing near focus

Clinical Features:

• Difficulty reading fine print, need to hold objects further away ("arm's length reading")
• Asthenopia (eye strain), headache after near work
• Need for better lighting
• Reading addition (near addition) required — typically +1.0D at 40 yrs, increasing to +3.0D by 60 yrs

Management:

1. Spectacle correction:
   • Reading glasses (single vision near)
   • Bifocals (distance + near)
   • Progressive addition lenses (PALs) — no visible demarcation line
2. Contact lenses: Monovision or multifocal CLs
3. Surgical correction (Kanski 10th Ed., p. 294–295):
   • Refractive lens exchange (RLE/CLE): Removal of clear lens + multifocal IOL implantation
   • Multifocal/EDOF IOL: Restores near-intermediate-distance vision
   • Monovision LASIK: One eye for distance, other for near
   • Presbyopic LASIK (presbyLASIK): Multifocal corneal profile
   • Intracorneal inlays: Small-aperture (Kamra) or refractive inlays
   • Conductive keratoplasty (CK): Radiofrequency shrinks peripheral stroma → steepens cornea for near

— Kanski's Clinical Ophthalmology, 10th Ed., p. 5494–5525

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SN2. Biometry

Goal:

Parameters Measured:

Methods of Axial Length Measurement:

• Contact method: probe directly on cornea (may compress and underestimate AL by 0.1–0.3 mm)
• Immersion method (Prager shell) — more accurate, no corneal compression
• Sound velocity: 1532 m/s through aqueous/vitreous; 1641 m/s through lens

• Uses partial coherence interferometry (PCI) or swept-source OCT
• Non-contact, highly reproducible (±0.02 mm)
• Cannot be used in dense cataracts (posterior subcapsular) or vitreous hemorrhage → revert to immersion A-scan

IOL Power Calculation Formulae:

Special Situations:

• Post-LASIK/PRK eyes: Standard keratometry gives erroneous K → use adjusted keratometry methods (Masket, True-K, etc.)
• Silicone oil-filled eyes: AL measurement requires correction factor (oil velocity = 980 m/s)
• Dense cataracts: Optical biometry fails → immersion A-scan

Formula: SRK II (simplified):

P = A − 0.9K − 2.5L Where P = IOL power, A = A-constant (lens-specific), K = average keratometry (D), L = axial length (mm)

Conclusion: Accurate biometry is the cornerstone of modern cataract surgery outcomes. The shift from contact A-scan to optical biometry has reduced post-operative refractive surprises significantly.

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SN3. Anti-Glaucoma Medications

Classification:

1. Prostaglandin Analogues (First-line monotherapy)

• IOP reduction: 25–35%
• Side effects: Conjunctival hyperaemia, iris pigmentation, periorbital fat atrophy, hypertrichosis, Prostaglandin-Associated Periorbitopathy (PAP)
• Contraindicated: Active uveitis, pregnancy

2. Beta-Adrenergic Blockers

• IOP reduction: 20–30%
• Side effects: Bradycardia, bronchospasm, depression, masking hypoglycaemia
• Contraindicated: Asthma, COPD, heart block, bradycardia

3. Carbonic Anhydrase Inhibitors (CAI)

• Side effects (oral): Metabolic acidosis, hypokalemia, renal stones, aplastic anaemia, Stevens-Johnson syndrome
• Contraindicated: Sulfa allergy, renal stones, sickle cell

4. Alpha-2 Adrenergic Agonists

• Side effects: Allergic follicular conjunctivitis (20–25%), dry mouth, fatigue, CNS depression in children
• Contraindicated: MAO inhibitor use, infants/children (respiratory depression)

5. Miotics (Cholinergic Agonists)

• Side effects: Miosis (dim vision), brow ache, induced myopia, risk of RD in high myopes, ciliary spasm
• Now largely replaced by prostaglandins

6. Hyperosmotic Agents (Acute Angle Closure Emergency)

7. Combination Preparations:

• Dorzolamide + Timolol (Cosopt)
• Brimonidine + Timolol
• Latanoprost + Timolol (Xalacom)

Treatment Stepladder (POAG):

Monotherapy (PGA) → Add β-blocker or CAI → Triple therapy → 
Laser (SLT/ALT) → Surgery (trabeculectomy / tube-shunt)

Conclusion: Anti-glaucoma drugs form the primary medical management of glaucoma. Prostaglandin analogues are the preferred first-line agents; combination therapy is used when monotherapy fails to achieve target IOP. — Kanski's Clinical Ophthalmology, 10th Ed.

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