I now have enough from the medical library to answer everything. Here is the complete answer:
Ophthalmology Exam - Section B: Complete Answers
Q.4 - Fill in the Blanks
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Haab striae are seen in - Infantile (congenital) glaucoma (horizontal breaks/tears in Descemet's membrane caused by raised IOP stretching the cornea in buphthalmos)
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Munson sign is seen in - Keratoconus (also keratoglobus) - it is the bulging of the lower eyelid when the patient looks downward, caused by the conical protrusion of the cornea
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Arlt's line is seen in - Trachoma (a horizontal scar on the superior tarsal conjunctiva in cicatricial/late-stage trachoma)
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Cherry red spot is seen in - Central Retinal Artery Occlusion (CRAO) - the fovea retains its red color from the choroidal supply while the surrounding ischemic retina turns white/opaque (also seen in storage disorders like Tay-Sachs, Niemann-Pick)
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Gunn's Sign is seen in - Hypertensive retinopathy (arteriovenous (A-V) nipping/nicking where the thickened arterial wall compresses the underlying vein at crossings)
Q.5 - MCQs
1. Marcus Gunn Pupil is NOT seen in? - Answer: (c) Papilloedema
Marcus Gunn pupil (Relative Afferent Pupillary Defect / RAPD) is a sign of unilateral optic nerve or retinal disease. It is seen in:
- Optic neuritis (a)
- Traumatic optic neuropathy (b)
- Optic nerve compression (d)
In papilloedema, both optic nerves are usually affected equally (bilateral disc swelling from raised intracranial pressure), so there is no relative afferent defect. RAPD is absent in symmetric bilateral disease.
2. Which is NOT associated with Glaucoma? - Answer: (b) Reversible damage
Glaucoma is characterized by:
- Raised IOP (a) - a major risk factor
- Visual field defects (c) - characteristic arcuate scotomas, nasal step, etc.
- Optic disc cupping (d) - increased cup-to-disc ratio
Reversible damage is NOT a feature. Glaucomatous optic neuropathy causes irreversible loss of retinal ganglion cells. This is one of the key points in glaucoma - vision loss once established cannot be recovered, only further loss can be prevented.
3. Which is NOT seen in High Myopia? - Answer: (c) Shallow anterior chamber
High myopia (>6D) is associated with an elongated eyeball and features:
- Foster Fuchs spots (a) - pigmented macular lesions from choroidal neovascularization
- Risk of retinal detachment (b) - due to vitreous degeneration and peripheral retinal lattice degeneration
- Concave (diverging) lens used for correction (d)
Shallow anterior chamber is NOT a feature of high myopia. In fact, myopic eyes tend to have a deeper anterior chamber due to the elongated axial length. Shallow anterior chamber is classically associated with hypermetropia (far-sightedness) and predisposes to angle-closure glaucoma.
4. Which is NOT found in Anterior Uveitis? - Answer: (c) Steroids are contraindicated
Anterior uveitis (iritis/iridocyclitis) features include:
- Keratic precipitates (a) - inflammatory cells depositing on corneal endothelium
- Aqueous flare (b) - protein leakage making the aqueous beam visible on slit lamp
- Recurrent episodes (d) - classically it is a relapsing-remitting condition
Steroids are NOT contraindicated - they are the mainstay of treatment (topical steroids are the first-line therapy for anterior uveitis, along with mydriatics/cycloplegics). So option (c) is the WRONG/FALSE statement.
5. Kayser-Fleischer Ring is found in... - Answer: (b) Chalcosis
This is a tricky question. The Kayser-Fleischer ring is classically associated with Wilson's disease (copper deposition in Descemet's membrane). However, among the options given, the mechanism is copper deposition in the cornea, which also occurs in chalcosis (copper foreign body in the eye).
- Keratoconus (a) - has Fleischer ring (iron deposits at cone base), NOT Kayser-Fleischer
- Chalcosis (b) - copper deposition causes a Kayser-Fleischer-like ring in the cornea
- Argyrosis (c) - silver deposition causes a grey/slate-colored discoloration, NOT KF ring
- Buphthalmos (d) - enlarged eye from infantile glaucoma, no KF ring
Note: If Wilson's disease were an option, it would be the classic answer. But among these four options, chalcosis (copper foreign body) is correct because the KF ring is specifically a copper deposition phenomenon.
Q.6 - Clinical Case: 65-year-old with Bilateral, Gradual, Painless, Progressive Dimness of Vision (3 years), Greyish-white opacity in pupillary area
Part 1: Differential Diagnoses (5 marks)
- Senile Cataract (most likely) - Nuclear/posterior subcapsular cataract is the most common cause; greyish-white opacity in pupillary area, bilateral, progressive, does not improve with glasses
- Posterior Capsular Opacification (PCO) - in patients with prior cataract surgery
- Corneal Opacity/Leucoma - corneal scarring from old keratitis, dystrophies
- Vitreous Opacity - vitreous degeneration or hemorrhage (less likely to be greyish-white in pupillary area)
- Lens-induced conditions - e.g., hypermature cataract (Morgagnian)
Primary diagnosis: Senile Cataract - the classic triad is present: age >60, bilateral gradual painless visual loss, not correctable with spectacles, visible opacity in pupillary area.
Part 2: Management (15 marks)
A. Evaluation / Workup:
- History: Duration, rate of progression, previous ocular surgery, systemic diseases (DM, HTN), medications (steroids), family history
- Visual Acuity (Snellen chart) - both distance and near; with and without correction
- Slit-lamp examination - type of cataract (nuclear, cortical, posterior subcapsular), grading (LOCS system)
- Pupillary reflexes - rule out RAPD (suggests posterior segment disease)
- Fundus examination - assess posterior segment through the opacity; if not possible, use:
- B-scan ultrasonography - rule out vitreous hemorrhage, retinal detachment, posterior staphyloma
- ERG (Electroretinogram) - assess retinal function if fundus not visible
- IOP measurement - rule out glaucoma
- Biometry (A-scan) - axial length + keratometry for IOL power calculation (pre-surgical)
- Corneal endothelial count - specular microscopy (pre-surgical)
- Systemic work-up - Blood glucose (DM), BP, CBC, ECG (pre-anesthesia fitness)
B. Indications for Surgery:
- Visual acuity <6/18 in the better eye (affecting daily activities)
- Patient's subjective complaint of significant visual disability
- Complications: lens-induced glaucoma, uveitis
C. Surgical Treatment: Cataract Extraction
The definitive treatment is surgical removal of the cataract:
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Phacoemulsification (Phaco) with foldable IOL implantation - gold standard
- Small incision (2.2-2.8 mm), self-sealing
- Ultrasonic fragmentation of nucleus
- Implant foldable IOL (acrylic) in the capsular bag
- Faster recovery, minimal astigmatism
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MSICS (Manual Small Incision Cataract Surgery) - if hard nucleus or resource-limited setting
- Effective, cost-efficient alternative used widely in developing countries
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ECCE (Extra-capsular Cataract Extraction) - older technique, reserved for very hard cataracts
IOL choices:
- Monofocal IOL (standard)
- Multifocal/EDOF IOL (reduces spectacle dependence)
- Toric IOL (if significant astigmatism present)
D. Post-operative Care:
- Topical antibiotic + steroid eye drops (e.g., moxifloxacin + prednisolone)
- NSAIDs drops (prevent cystoid macular edema)
- Eye shield at night for first week
- Review at day 1, week 1, month 1
- Spectacle prescription at 4-6 weeks post-op
- Watch for complications: endophthalmitis, PCO, cystoid macular edema, corneal decompensation
E. If PCO develops post-operatively:
- Nd:YAG laser posterior capsulotomy - quick outpatient procedure to restore vision
Sources: Kanski's Clinical Ophthalmology 10th Ed.; The Wills Eye Manual; Robbins & Cotran Pathologic Basis of Disease; Harrison's Principles of Internal Medicine 22E; Bradley & Daroff's Neurology in Clinical Practice