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III-MBBS Ophthalmology — January 2023 (RUHS) — Full Answers

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SECTION-A

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Q1. Fill in the Blanks (6 × 1 = 6)

Note on (e): The Kayser-Fleischer ring is a golden-to-greenish-brown band in the peripheral cornea (Descemet's membrane), seen in ~95% of Wilson's disease patients with neurological signs. (Harrison's 21st Ed., p. 11784)

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Q2. Answer the Following (4 × 1 = 4)

• Colored halos: In ACG, corneal edema causes prismatic splitting of light → rainbow-colored halos. (Cataract may cause halos but they are not colored/rainbow.)
• Munson's sign: Bulging of the lower lid on downward gaze due to the conical protrusion of the cornea in keratoconus.
• Episcleritis: Presents as a tender, localized, lentil-shaped raised reddish nodule (nodular episcleritis); non-itchy and painful.
• Atropine contraindication: Atropine causes pupillary dilation, which pushes the peripheral iris into the angle, precipitating/worsening acute angle-closure (congestive) glaucoma. It is not contraindicated in acute iridocyclitis — in fact, it is used therapeutically.

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Q3. Case — 51-year-old woman, severe R brow/cheek/eye pain, blurry vision, rainbow halos, IOP = 48 RE & 22 LE

a) Most Likely Etiology

b) Treatment

1. Systemic: IV/oral Acetazolamide (500 mg IV stat, then 250 mg PO QID)
2. Hyperosmotic agents: IV Mannitol 20% (1–1.5 g/kg) if needed
3. Topical: β-blocker (Timolol 0.5%), α₂-agonist (Brimonidine), Pilocarpine 2–4% (to break the pupillary block — given after IOP starts to fall), Prostaglandin analogue
4. Definitive treatment: Nd:YAG Laser Peripheral Iridotomy (LPI) — creates a hole in peripheral iris to bypass pupillary block; performed in both eyes (fellow eye prophylactically)
5. Treat pain and nausea; position patient supine

c) Differential Diagnosis of RED EYE in Adults

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Q4. Write Briefly on Any Five (5 × 2 = 10)

a) ARMD (Age-Related Macular Degeneration)

• Degenerative disease of the macula in patients >50 years
• Dry (atrophic): Drusen deposits, geographic atrophy of RPE; gradual central vision loss
• Wet (exudative/neovascular): Choroidal neovascularization (CNV), subretinal fluid/hemorrhage, rapid severe vision loss; Amsler grid distortion (metamorphopsia)
• Treatment: Dry — AREDS2 supplements (vitamins C, E, zinc, lutein, zeaxanthin); Wet — intravitreal anti-VEGF injections (Bevacizumab, Ranibizumab, Aflibercept)

b) Color Blindness

• Deficiency in cone photoreceptors (especially M or L cones)
• Protanopia: Red deficiency; Deuteranopia: Green deficiency (most common, X-linked recessive)
• Tritanopia: Blue deficiency (rare, autosomal dominant)
• Achromatopsia: Complete absence of color vision (rod monochromatism)
• Diagnosed with Ishihara pseudoisochromatic plates; also Farnsworth-Munsell 100-hue test
• Significance: Disqualifies from certain professions (pilot, armed forces, railway, etc.)

c) Astigmatism

• Refractive error due to unequal curvature of the cornea (or lens) in different meridians → light not focused at a single point
• Regular: Two principal meridians perpendicular to each other — corrected with cylindrical lenses
• Irregular: No uniform meridians — corrected with rigid contact lenses (RGP)
• Types: With-the-rule (vertical meridian steeper), Against-the-rule, Oblique
• Symptoms: Blurred vision at all distances, asthenopia, squinting

d) Blepharitis

• Chronic inflammatory condition of the eyelid margins
• Anterior: Staphylococcal (squamous/ulcerative scales at base of lashes) or seborrhoeic
• Posterior: Meibomian gland dysfunction (MGD) — thickened/capped meibomian orifices, frothy tear film
• Symptoms: Lid margin redness, crusting, burning, foreign body sensation, mild photophobia
• Complications: Recurrent stye/chalazion, dry eye, inferior corneal PEE
• Treatment: Warm compresses, lid hygiene (scrubs), topical antibiotics (chloramphenicol), artificial tears; oral doxycycline for MGD

e) Optic Neuritis

• Inflammation of the optic nerve; most commonly demyelinating (associated with Multiple Sclerosis)
• Clinical features: Acute unilateral vision loss, pain on eye movement (90%), color desaturation (red), RAPD (swinging flashlight test positive), central scotoma
• Papillitis (anterior): Disc swelling visible; Retrobulbar neuritis (posterior): Disc appears normal initially ("patient sees nothing, doctor sees nothing")
• Diagnosis: MRI brain/orbit (periventricular plaques), VEPs (delayed P100)
• Treatment: IV methylprednisolone 1g/day × 3 days (speeds recovery but does not alter final visual outcome)

f) Xerophthalmia

• Ocular manifestations of Vitamin A deficiency
• WHO Classification:
  • XN: Night blindness
  • X1A: Conjunctival xerosis
  • X1B: Bitot's spots (foamy white patches on bulbar conjunctiva, temporal)
  • X2: Corneal xerosis
  • X3A: Corneal ulceration <1/3 cornea
  • X3B: Keratomalacia (>1/3 cornea — emergency, leads to blindness)
  • XS: Corneal scarring
  • XF: Xerophthalmic fundus
• Treatment: Vitamin A supplementation (200,000 IU orally on days 1, 2, 14 for children >1 year)

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Q5. Explain Briefly on Any Three (3 × 5 = 15)

a) Congenital Glaucoma (Buphthalmos)

• Caused by maldevelopment of the trabecular meshwork/anterior chamber angle → obstructed aqueous outflow → raised IOP
• Triad: Epiphora (watering), photophobia, blepharospasm in a neonate
• Signs: Enlarged cornea (>12 mm in neonate = abnormal), Haab's striae (horizontal breaks in Descemet's membrane), corneal edema/haze, increased cup:disc ratio
• Diagnosis: Examination under anesthesia (EUA) — IOP, corneal diameter, gonioscopy
• Treatment: Surgical (medical therapy is temporizing only) — Goniotomy or Trabeculotomy (if cornea is clear); Trabeculectomy or tube surgery for failures

b) Retinopathy of Prematurity (ROP)

• Proliferative retinal vasculopathy in premature infants due to incomplete retinal vascularization
• Risk factors: Prematurity (<32 weeks / <1500g birth weight), supplemental oxygen therapy
• Classification (ICROP): 3 zones (I–III), 5 stages (1=demarcation line → 5=total retinal detachment), Plus disease (vascular dilation/tortuosity)
• Treatment threshold: Type 1 ROP (Zone I any stage with plus, Zone I stage 3, Zone II stage 2 or 3 with plus) → treatment within 48–72 hours
• Treatment: Intravitreal anti-VEGF (Bevacizumab — preferred for Zone I) or Laser photocoagulation (ablation of avascular retina)
• Screening: All infants <32 weeks or <1500g; begin at 4 weeks chronological age or 31 weeks PMA, whichever is later

c) Myopia (Short-Sightedness)

• Refractive error where parallel light rays focus anterior to the retina
• Axial myopia (most common): Increased axial length; Refractive myopia: Increased refractive power of lens/cornea
• Symptoms: Blurred distance vision, clear near vision, squinting
• Simple myopia: <6D; High/Pathological myopia: >6D — associated with posterior staphyloma, lattice degeneration, retinal detachment, CNVM, glaucoma, cataract
• Correction: Concave (diverging) lenses; contact lenses; refractive surgery (LASIK, PRK, SMILE)
• Myopia control: Atropine 0.01%, orthokeratology, multifocal contact lenses

d) Differentiating Incomitant vs. Comitant Squint

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SECTION-B

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Q6. 65-year-old Type 2 DM × 15 years, diminished vision, no cataract

a) What Retinal Condition Should Be Tested For?

• Non-Proliferative DR (NPDR): Mild → Moderate → Severe (4-2-1 rule: >20 hemorrhages in 4 quadrants / venous beading in 2 quadrants / IRMA in 1 quadrant)
• Proliferative DR (PDR): Neovascularization of disc (NVD) or elsewhere (NVE)
• Diabetic Macular Edema (DME): Most common cause of visual loss; center-involving vs. non-center-involving

b) Clinical Features of Diabetic Retinopathy

1. Microaneurysms — earliest sign (dot hemorrhages)
2. Flame/blot hemorrhages
3. Hard exudates (lipid deposits — yellow, well-defined, near macula)
4. Cotton wool spots (soft exudates — nerve fiber layer infarcts)
5. IRMA (Intraretinal microvascular abnormalities)
6. Venous beading/looping
7. Neovascularization (NVD/NVE) — proliferative stage
8. Vitreous hemorrhage, Traction retinal detachment, Rubeosis iridis — advanced

c) Management of Diabetic Retinopathy

d) Screening for Diabetic Retinopathy

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Q7. Write Briefly on Any Five (5 × 2 = 10)

a) Graves Ophthalmopathy (Thyroid Eye Disease)

• Autoimmune orbital inflammation in hyperthyroidism (Graves disease); mediated by TSH-receptor antibodies stimulating orbital fibroblasts → glycosaminoglycan deposition → extraocular muscle and orbital fat expansion
• NOSPECS classification: No signs → Only signs → Soft tissue → Proptosis → Extraocular muscle → Corneal → Sight loss
• Features: Lid retraction (Dalrymple's sign), lid lag (von Graefe's), proptosis/exophthalmos, periorbital edema, chemosis, restrictive myopathy (inferior rectus first → hypotropia, diplopia), corneal exposure keratopathy, compressive optic neuropathy (most serious)
• Treatment: Treat thyroid; selenium (mild); IV methylprednisolone (moderate-severe); orbital decompression; radiotherapy; teprotumumab (anti-IGF-1R); strabismus/lid surgery

b) Complications of Cataract Surgery

c) Routes of Ocular Drug Administration

d) Visual Field Changes in Glaucoma

• Glaucoma causes characteristic nerve fiber bundle defects (corresponding to RGC axon loss at the disc):

1. Earliest: Paracentral scotoma, nasal step (Ronne's nasal step)
2. Arcuate (Bjerrum) scotoma: Arcs from blind spot — superior or inferior arcuate
3. Ring scotoma: Superior + inferior arcuate scotomas meeting
4. Advanced: Temporal island + central island of vision
5. End-stage: Total blindness

• Assessed by: Humphrey Visual Field Analyzer (automated perimetry), Goldmann perimetry
• Normal blind spot at 15° temporal; cup:disc ratio >0.6 suspicious

e) Hyphaema

• Blood in the anterior chamber (between cornea and iris)
• Causes: Blunt trauma (most common), post-surgical, spontaneous (sickle cell, rubeosis iridis, bleeding disorders)
• Grading: Grade 0 (microhyphaema) → Grade 1 (<1/3 AC) → Grade 2 (1/3–1/2) → Grade 3 (>1/2) → Grade 4 (total/8-ball hyphaema)
• Complications: Raised IOP, corneal blood staining, secondary haemorrhage (day 2–5, worse than primary), anterior synechiae
• Treatment: Bed rest, head elevation 30–45°, shield, cycloplegics (atropine), topical steroids, IOP lowering drops; avoid aspirin/NSAIDs; surgical washout if IOP uncontrolled or corneal staining risk

f) Allergic Conjunctivitis

• Types:
  • Seasonal/Perennial allergic conjunctivitis (SAC/PAC): IgE-mediated, mast cell degranulation; bilateral itching, watering, mild papillae, chemosis
  • Vernal keratoconjunctivitis (VKC): Young males, warm climates; giant cobblestone papillae (upper tarsal), Horner-Trantas dots (limbal), shield ulcer; eosinophil-rich
  • Atopic keratoconjunctivitis (AKC): Adults with atopic dermatitis; lower lid predominantly, corneal involvement, risk of keratoconus
  • Giant papillary conjunctivitis (GPC): Contact lens/prosthesis related
• Treatment: Avoid allergen; topical antihistamines (Azelastine); mast cell stabilizers (Sodium cromoglycate, Lodoxamide); dual-action drops (Olopatadine — first-line); cold compresses; topical steroids (short-term for severe); systemic antihistamines

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Q8. Short Notes (4 × 5 = 20)

a) Counselling Parents of a 5-month-old with CNLDO (AETCOM)

1. Explain the condition: The tear drainage system (nasolacrimal duct) is blocked at birth due to an imperforate valve (Hasner's valve). Very common (~6% of neonates). Often resolves spontaneously.
2. Natural history: ~90% resolve by 12 months of age with conservative management
3. Conservative treatment: Teach Crigler massage (Lacrimal sac massage) — 2–3 times daily, firm downward pressure over the lacrimal sac with a clean fingertip to build hydrostatic pressure and rupture the membrane
4. Topical antibiotics: For secondary conjunctivitis (mucopurulent discharge) — brief courses only; not curative
5. Warning signs: Acute dacryocystitis (swelling/redness over lacrimal sac = urgent referral), orbital cellulitis
6. Definitive treatment if no resolution by 12–13 months: Probing and syringing under brief general anesthesia (>90% success); intubation or DCR (dacryocystorhinostomy) for failures
7. Reassure parents: Good prognosis, simple procedure if needed; no long-term harm if managed appropriately

b) Management of Acute Uveitis (Anterior Uveitis/Iridocyclitis)

• Aims: Relieve pain, reduce inflammation, prevent complications (posterior synechiae, secondary glaucoma, cataract, CME)

1. Cycloplegics: Atropine 1% (3–4 weeks) — relieves ciliary spasm (photophobia, pain), prevents/breaks posterior synechiae, puts the eye at rest; Homatropine or Cyclopentolate for shorter-term use
2. Topical corticosteroids: Prednisolone acetate 1% — initially hourly, tapered over weeks; reduces inflammation
3. Systemic NSAIDs/steroids: For severe cases; oral prednisolone for bilateral/recurrent/non-infectious
4. IOP monitoring: Steroid-induced glaucoma vs. inflammatory glaucoma; add IOP-lowering drops if needed
5. Treat underlying cause: HLA-B27 associated (AS, Reiters) — rheumatology; TB uveitis — ATT; herpetic — antivirals
6. Immunosuppressants: Methotrexate, Mycophenolate, Azathioprine for recurrent/chronic/systemic disease

c) Pathology of Retinoblastoma

• Most common primary intraocular malignancy in children (<5 years); arising from primitive retinal cells (retinoblasts)
• Genetics: Loss of both alleles of RB1 tumor suppressor gene (chromosome 13q14) — "two-hit hypothesis" (Knudson)
  • Hereditary (40%): Germline mutation — bilateral, multifocal, earlier onset; AD inheritance; risk of second malignancies (osteosarcoma)
  • Non-hereditary (60%): Somatic — unilateral, unifocal

• Small blue round cells with scant cytoplasm, hyperchromatic nuclei, high mitotic activity
• Flexner-Wintersteiner rosettes (pathognomonic): Columnar cells around central lumen
• Homer-Wright rosettes: No central lumen
• Fleurettes: Most differentiated — photoreceptor-like cells
• Areas of necrosis and calcification (key feature — seen on CT as "cottage cheese" calcification)
• Growth patterns: Endophytic (into vitreous — vitreous seeds), Exophytic (under retina — RD), Diffuse infiltrating

d) Refractive Surgery

• Surgical correction of refractive errors by reshaping the cornea or replacing the natural lens

• Phakic IOL (ICL — Implantable Collamer Lens): For high myopia/thin corneas; preserves accommodation
• RLE (Refractive Lens Exchange): Clear lens extraction + IOL; eliminates future cataract risk; loss of accommodation

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