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MBBS Professional Examination - Ophthalmology

Complete Model Answers

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SECTION A (50 Marks)

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Q.1 - A 45-year-old farmer with pain, redness, watering, photophobia, and diminution of vision in the right eye following trauma with vegetative matter (20 Marks)

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a) Diagnosis and Clinical Presentation (6 Marks)

• Pain - moderate to severe (less severe than bacterial ulcer)
• Redness and congestion
• Watering (lacrimation) and discharge
• Photophobia
• Diminution of vision (due to corneal opacity over the visual axis)
• Symptoms usually appear 24-72 hours after injury and progress slowly

• Lid edema and spasm (blepharospasm)
• Mucopurulent discharge
• Conjunctival congestion and circumcorneal (ciliary) flush

• Corneal ulcer with characteristic features:
  • Dry, rough, elevated, "heaped-up" or "feathery" edges
  • Satellite lesions (small white infiltrates surrounding the main ulcer) - pathognomonic
  • Immune ring (Wessely ring) - an immunological reaction around the ulcer
  • Hypopyon (sterile, white, fluffy, mobile) - seen in anterior chamber
  • Endothelial plaque - white deposits on corneal endothelium
  • In severe cases: corneal perforation and endophthalmitis

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b) Investigations and Diagnosis (6 Marks)

• Detailed examination of the ulcer characteristics
• Assessment of anterior chamber reaction, hypopyon

• Scraping from the floor and edges of the ulcer under slit-lamp guidance
• Collected on glass slides for:
  • KOH (10%) wet mount - shows fungal hyphae (branching septate hyphae for Fusarium/Aspergillus)
  • Gram stain - to rule out bacteria
  • Giemsa stain - fungal elements
  • Calcofluor white stain - fluorescent staining of fungal cell wall (very sensitive)
  • PAS (Periodic Acid-Schiff) stain - highlights fungal elements

• Media used: Sabouraud's Dextrose Agar (primary for fungi), Blood agar, Chocolate agar
• Incubate at 25-30°C for up to 4-6 weeks
• Identifies species and guides antifungal therapy

• Non-invasive, in-vivo detection of fungal hyphae in corneal stroma
• Very sensitive and specific, gives real-time results

• Rapid, sensitive molecular identification of fungal species

• Assesses depth of ulcer, status of Descemet's membrane

• If media is hazy, to rule out endophthalmitis or posterior segment involvement

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c) Management (8 Marks)

• Hospitalization in severe cases
• Avoid patching (creates warm, moist environment favoring fungal growth)
• Stop any prior corticosteroid use (worsens fungal infection)

• Natamycin 5% eye drops - drug of choice for filamentous fungi (Fusarium, Aspergillus); hourly during day, 2-hourly at night initially
• Voriconazole 1% eye drops - excellent for Fusarium and Aspergillus; used when natamycin fails
• Amphotericin B 0.15% eye drops - for Candida and Aspergillus
• Fluconazole 0.3% eye drops - for Candida

• Voriconazole 200 mg BD orally
• Itraconazole 100-200 mg daily
• Fluconazole for Candida

• Cycloplegic drops (Atropine 1%) - to reduce ciliary spasm and pain, prevents posterior synechiae
• Antiglaucoma medications if IOP raised (timolol, dorzolamide)
• Lubricating drops - to prevent dryness
• Oral analgesics - for pain relief
• Systemic NSAIDs - to reduce inflammation

1. Therapeutic Penetrating Keratoplasty (TPK)
   • Indicated when: ulcer not responding to medical therapy, impending/actual perforation, extensive stromal involvement
   • Emergency procedure to save the eye
2. Corneal Debridement
   • Removes epithelium and necrotic tissue; enhances drug penetration
3. Conjunctival Flap
   • For perforated ulcers as a temporary measure to seal the perforation
4. Tissue Adhesive (Cyanoacrylate glue)
   • For small perforations (<2 mm)
5. Intrastromal/Intracameral Antifungal Injection
   • Voriconazole injected directly into corneal stroma or anterior chamber for refractory cases
6. Evisceration/Enucleation
   • Last resort if the eye is destroyed and panophthalmitis occurs

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Q.2 - Neat Labelled Diagram: Passage of Lacrimal Apparatus (6 Marks)

Lacrimal Lake (medial canthus)
        ↓
Lacrimal Puncta (superior & inferior, on medial lid margin)
        ↓
Lacrimal Canaliculi
  • Ampulla (dilated portion near punctum)
  • Vertical part (~2 mm)
  • Horizontal part (~8 mm)
        ↓
Common Canaliculus (junction of superior & inferior canaliculi)
        ↓
Lacrimal Sac (sits in lacrimal fossa, between anterior & posterior lacrimal crests)
  • Fundus (upper blind end, above medial canthal tendon)
  • Body
        ↓
Nasolacrimal Duct (~18 mm long; runs in bony nasolacrimal canal)
        ↓
Inferior Meatus of Nose (opens beneath inferior turbinate)
  • Valve of Hasner (mucosal fold at opening)

• Valve of Rosenmuller - mucosal fold at junction of canaliculus and lacrimal sac; prevents reflux
• Valve of Krause - at the junction of lacrimal sac and nasolacrimal duct
• Valve of Hasner - at the lower end of nasolacrimal duct; failure to canalize = congenital nasolacrimal duct obstruction (CNLDO)
• Medial canthal tendon - superficial head passes anterior to lacrimal sac; deep head passes posterior

• Blinking compresses the lacrimal sac → tears are pumped inferiorly
• Orbicularis oculi muscle (preseptal and pretarsal parts) is responsible

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Q.3 - Factors Responsible for Corneal Transparency (6 Marks)

• Normal cornea has no blood vessels; neovasularization causes opacity
• Nutrients supplied by aqueous humor, tear film, and limbal vessels

• Corneal stroma has a tendency to absorb water (hydrophilic GAGs: keratan sulfate, chondroitin sulfate); fully hydrated cornea becomes opaque
• Normal hydration maintained at ~78% water content
• Maintained by:
  • Epithelial barrier - tight junctions prevent tear water entry
  • Endothelial pump (Na-K ATPase) - actively pumps water out of stroma into aqueous
  • Endothelial barrier - tight junctions prevent aqueous entry

• Type I collagen fibrils are uniformly small in diameter (~25-30 nm) and arranged in a precise lattice pattern
• This regularity causes destructive interference of scattered light (Bragg diffraction), allowing light to pass straight through
• In scarring, collagen arrangement is disrupted → opacity

• Keratocytes are flattened, with minimal organelles in the cytoplasm
• Their refractive index closely matches the surrounding stroma

• Regular epithelium + precorneal tear film provides a smooth optical surface
• Any irregularity causes light scattering

• Corneal nerves lose their myelin sheath at the limbus; myelin would scatter light

• No melanin or other pigments that absorb light

• These layers lack cells and are structurally homogeneous

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Q.4 - Differential Diagnosis of Red Eye (6 Marks)

Painful Red Eye with Visual Disturbance:

Painful Red Eye without Visual Disturbance:

Other Causes:

• Dry eye syndrome - burning, foreign body sensation, intermittent blurring
• Blepharitis - lid margin inflammation
• Pterygium - fibrovascular growth
• Allergic conjunctivitis - itching, ropy discharge, papillae

• Discharge: purulent = bacterial; watery = viral; ropy/mucoid = allergic
• Pain: deep/boring = scleritis, glaucoma, uveitis; gritty/superficial = conjunctivitis
• Vision: reduced = corneal/uveal/glaucoma; normal = conjunctivitis, episcleritis
• Pupil: mid-dilated fixed = AACG; small/irregular = uveitis; normal = conjunctivitis

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Q.5 - Optics of Myopia and Management (6 Marks)

Optics of Myopia:

• In an emmetropic eye, parallel rays focus exactly on the retina
• In myopia, the image falls anterior to the retina
• This occurs due to:
  1. Axial myopia (most common) - eyeball is too long (axial length >24 mm)
  2. Refractive myopia - refractive power of the eye is too high, due to:
     • Increased corneal curvature (curvature myopia)
     • Increased lens power (index myopia) - seen in nuclear sclerosis
     • Increased index of refraction

• Concave (diverging, minus power) lens is used
• The lens diverges parallel rays so that after refraction by the eye, they converge on the retina
• The correcting lens is placed at the anterior focal plane of the eye

Management of Myopia:

• Spectacles with concave (minus) lenses
• Contact lenses (soft or rigid gas-permeable)
• Orthokeratology - specially designed rigid contact lenses worn at night to temporarily reshape cornea

• LASIK (Laser-Assisted In-Situ Keratomileusis): Most popular; flap created, underlying stroma ablated with excimer laser; suitable for up to -12D; rapid recovery
• PRK (Photorefractive Keratectomy): Epithelium removed, surface ablation; suitable for thin corneas; slower recovery
• LASEK (Laser Epithelial Keratomileusis): Modified PRK with epithelial flap
• SMILE (Small Incision Lenticule Extraction): Femtosecond laser creates and extracts a stromal lenticule; flapless; fewer dry eye complications

• Phakic IOL (Implantable Collamer Lens/ICL): Lens implanted in front of natural lens; for high myopia (> -8D to -18D) where laser surgery is not suitable
• Clear Lens Extraction (Refractive Lens Exchange): Natural lens removed and replaced with IOL; for very high myopia >-20D

• Atropine eye drops (0.01%) - most evidence for slowing myopia progression
• Multifocal/bifocal spectacles/contact lenses
• Outdoor activity (>2 hours/day) - reduces progression

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Q.6 - Neat Labelled Diagram: Sturm's Conoid (6 Marks)

          Rays in vertical meridian
              |  |
              |  |
─────────────────────────────────────────────── Light rays (parallel)
              |  |
              |  |
              
    Focal Line 1 (horizontal focus)
    ━━━━━━━━━━━━ ← rays in one meridian focus here first
    
         Circle of Least Confusion
              ● ← smallest cross-section, midpoint of conoid
              
    Focal Line 2 (vertical focus)
         |
         | ← rays in the other meridian focus here
         |

• An astigmatic eye has two focal lines at right angles to each other, not a single point focus
• First focal line (anterior): formed by rays in the more powerful meridian (shorter focal length)
• Second focal line (posterior): formed by rays in the less powerful meridian
• Circle of Least Confusion (CLC): the point midway between the two focal lines where the cross-section of the conoid is a circle (smallest blur circle); the equivalent sphere of the astigmatism
• Interval of Sturm: the distance between the two focal lines; greater interval = greater degree of astigmatism
• The conoid is named after the German physicist J.C. Sturm

• When correcting astigmatism with a cylindrical lens, we aim to collapse the Sturm's conoid to a single point focus on the retina
• The spherical equivalent places the CLC on the retina (minimum blur)

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SECTION B (50 Marks)

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Q.7 - A 68-year-old patient with gradually progressive painless diminution of vision in both eyes over 3 years (20 Marks)

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a) Differential Diagnosis of Gradual Painless Diminution of Vision (8 Marks)

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b) Surgical Techniques for Cataract Management (12 Marks)

• Mechanism: Uses ultrasonic energy (40,000 Hz) to emulsify and aspirate the lens nucleus through a small incision (2.2-2.8 mm)
• Steps:
  1. Topical or peribulbar anesthesia
  2. Clear corneal or scleral tunnel incision (2.2-2.8 mm main port + side port)
  3. Capsulorhexis (CCC - continuous curvilinear capsulorhexis) - circular opening in anterior capsule
  4. Hydrodissection - BSS injected to separate nucleus from capsule
  5. Phacoemulsification of nucleus using phaco tip (various techniques: divide and conquer, stop and chop, phaco chop)
  6. Irrigation and Aspiration (I/A) of cortical material
  7. IOL implantation into the capsular bag (foldable IOL through small incision)
  8. Wound hydration/closure
• Advantages: Small incision, rapid visual recovery, minimal astigmatism, sutureless

• Incision: 5-7 mm scleral tunnel incision (self-sealing)
• Nucleus delivered manually (phacosandwich or fishhook technique) without phacoemulsification
• Advantages: Cheaper, safe in hard nuclei, no phaco machine needed, good for developing countries
• Suitable for very hard (Grade IV/V) nuclei

• Large limbal incision (10-12 mm)
• Anterior capsule opened with can-opener capsulotomy
• Nucleus expressed manually, cortex aspirated, rigid PMMA IOL inserted
• Requires multiple sutures; induces significant astigmatism
• Now largely obsolete, reserved for very hard nuclei or when phaco unavailable

• Entire lens (including capsule) removed
• Cryoprobe used to freeze and extract the lens
• No posterior capsule left for IOL support → anterior chamber IOL or scleral-fixated IOL needed
• High complication rate (vitreous disturbance, retinal detachment, CME)
• Now obsolete, used only in subluxated/dislocated lenses

• Laser performs capsulorhexis, corneal incisions, and lens fragmentation
• More precise, reproducible capsulotomy
• Reduces phaco energy needed
• Expensive; outcomes similar to conventional phaco in experienced hands

• Monofocal IOL - corrects for one distance (usually distance); reading glasses needed
• Multifocal IOL - corrects for near and distance; reduces spectacle dependence
• Toric IOL - corrects pre-existing corneal astigmatism
• Extended Depth of Focus (EDOF) IOL - extended range of vision

• Posterior capsule rupture (most common intraoperative complication)
• Vitreous loss
• Dropped nucleus
• Endophthalmitis (0.1%)
• Cystoid macular edema (CME / Irvine-Gass syndrome)
• Posterior Capsular Opacification (PCO) / "After-Cataract" (see Q.12)

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Q.8 - Neat Labelled Diagram: Anterior Chamber Angle and Aqueous Humour Drainage Pathway (6 Marks)

• Produced by the ciliary body (non-pigmented ciliary epithelium) at ~2.5 μL/min
• Mechanisms: active secretion (Na-K ATPase), ultrafiltration, diffusion

Conventional (Trabecular) Pathway - 90% of outflow:

Posterior Chamber
        ↓
Through Pupil
        ↓
Anterior Chamber
        ↓
Anterior Chamber Angle
        ↓
Trabecular Meshwork (uveal → corneoscleral → juxtacanalicular layers)
        ↓
Schlemm's Canal (inner wall endothelium)
        ↓
Collector Channels (25-35 channels)
        ↓
Aqueous Veins (of Ascher)
        ↓
Episcleral Veins
        ↓
Systemic Venous Circulation

Uveoscleral (Non-Conventional) Pathway - 10% of outflow:

Anterior Chamber Angle
        ↓
Ciliary Muscle Interstices
        ↓
Supraciliary / Suprachoroidal Space
        ↓
Sclera → Systemic circulation (via scleral vessels)

1. Schwalbe's line - anterior termination of Descemet's membrane; junction of cornea and trabeculum
2. Trabecular meshwork - sieve-like tissue; main site of outflow resistance
3. Scleral spur - posterior attachment of trabecular meshwork; landmark for gonioscopy
4. Ciliary band - anterior face of ciliary body
5. Iris root

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Q.9 - Lens-Induced Glaucomas: Classification, Clinical Features and Management (6 Marks)

Classification:

• Mechanism: Hypermature (Morgagnian) cataract → lens capsule becomes permeable → high molecular weight lens proteins leak into AC → macrophages engulf proteins → macrophages clog trabecular meshwork → raised IOP
• Clinical features: Middle-aged/elderly; extreme pain; very high IOP; white intumescent lens; cells and flare (white fluffy), no keratic precipitates; open angle on gonioscopy; hypopyon may be present
• Treatment: Lower IOP medically (acetazolamide, timolol, mannitol) → cataract surgery (ECCE/phaco)

• Mechanism: Intumescent (swelling) lens (immature/mature cataract) → pushes iris forward → pupillary block → angle closure → raised IOP
• Clinical features: Sudden onset, painful; red eye; shallow AC; lens-induced angle closure; fellow eye may have deep AC
• Treatment: Lower IOP medically → Nd:YAG laser iridotomy (relieves pupillary block) → cataract surgery

• Mechanism: Trauma or surgery causes lens material to enter AC → clogs trabecular meshwork
• Clinical features: History of trauma/surgery; white lens particles in AC; moderate IOP elevation; open angle
• Treatment: Topical steroids + IOP-lowering drugs; surgical washout of lens material if uncontrolled

• Mechanism: Sensitization to lens protein → immune reaction → inflammation + trabecular blockage
• Clinical features: After extracapsular surgery or trauma; intense granulomatous uveitis; mutton-fat KPs; raised IOP

• Subluxated or dislocated lens → pupillary block (anterior dislocation) → angle closure

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Q.10 - Primary Angle Closure Glaucoma (PACG): Diagnosis and Management (6 Marks)

Pathophysiology:

Diagnosis:

• Sudden severe headache and eye pain
• Nausea and vomiting
• Halos around lights (corneal edema)
• Profound visual loss
• Abdominal pain (may mimic GI emergency)

• Circumcorneal flush (ciliary injection)
• Corneal edema (steamy, hazy)
• Shallow anterior chamber
• Mid-dilated, vertically oval, fixed pupil (ischemic sphincter)
• High IOP (40-80 mmHg)
• Congested episcleral vessels
• Tender globe

• Slit-lamp biomicroscopy - shallow AC, corneal edema
• Gonioscopy (after clearing corneal edema) - confirms angle closure
• Tonometry - elevated IOP
• Optic disc assessment - cupping if chronic
• Visual field testing - Humphrey automated perimetry
• Van Herick test - peripheral AC depth estimation
• Pachymetry - corneal thickness
• UBM (Ultrasound Biomicroscopy) - plateau iris configuration

Management:

1. Systemic: IV Acetazolamide 500 mg (carbonic anhydrase inhibitor) + oral glycerol 50% or IV mannitol 20% (hyperosmotic agent)
2. Topical IOP-lowering: Timolol 0.5%, Brimonidine 0.2%, Dorzolamide 2%
3. Pilocarpine 2-4% - miotic; constricts pupil, pulls peripheral iris away from angle (use only after IOP starts falling, not when IOP very high as iris is ischemic)
4. Topical steroids - reduce inflammation
5. Analgesics and antiemetics - for pain/nausea

1. Nd:YAG Laser Peripheral Iridotomy (LPI) - creates a hole in peripheral iris → bypasses pupillary block → equalizes pressure between posterior and anterior chambers → opens angle. Treatment of choice.
2. Surgical Peripheral Iridectomy - if laser fails or not available
3. Fellow Eye: Prophylactic LPI in the other eye (high risk of developing acute attack)

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Q.11 - Visual Field Defects in Primary Open Angle Glaucoma (POAG) (6 Marks)

• Enlarged blind spot (due to nerve fiber loss around optic disc)
• Isolated paracentral scotoma - small absolute/relative scotoma within 10-20° of fixation (Bjerrum area)
• Nasal step (Ronne's nasal step) - asymmetric loss across horizontal meridian in the nasal field

• Arcuate (Bjerrum) scotoma - arcuate-shaped scotoma following the nerve fiber layer from blind spot, arching above/below fixation to the nasal field
• Double arcuate scotoma - both superior and inferior arcuate scotomas present
• Seidel scotoma - comma-shaped extension of the blind spot along the arcuate path

• Ring (annular) scotoma - superior and inferior arcuate scotomas meet nasally
• Island of vision (temporal island + central island) - only central and temporal vision remain

• Tunnel vision - only a small central island of vision remains
• Total blindness (final stage)

• Defects respect the horizontal midline (follow nerve fiber layer anatomy)
• Central vision preserved until late (hence "silent thief of sight")
• Defects are more pronounced in superior field (inferior retinal fibers more vulnerable)
• Detected by: Humphrey Visual Field Analyzer (HVFA, 24-2 or 30-2 program), Goldmann perimetry

• Mean Deviation (MD): global field loss index
• Pattern Standard Deviation (PSD): localized field loss
• GHT (Glaucoma Hemifield Test): superior vs inferior field asymmetry
• VFI (Visual Field Index): percentage of normal visual field remaining

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Q.12 - After-Cataract (Posterior Capsular Opacification) and Management (6 Marks)

Definition:

Pathogenesis:

• Proliferation and migration onto the posterior capsule
• Fibrosis (anterior subcapsular type - myofibroblastic transformation of LECs → fibrosis, capsular wrinkling/contraction)
• Elschnig pearl formation (large bladder cells / posterior subcapsular type) - swollen epithelial cells form characteristic "Elschnig pearls"

Types:

1. Fibrotic type - fibrous plaques, capsular wrinkling; occurs earlier
2. Pearl type (Elschnig pearls) - rows of large bladder cells; more visually significant
3. Mixed type - both components

Clinical Features:

• Gradual, progressive, painless blurring of vision (months to years post-surgery)
• Glare, halos, reduced contrast sensitivity
• On slit-lamp: wrinkling/opacification of posterior capsule behind IOL
• Red reflex is reduced or irregular

Management:

• Mechanism: Nd:YAG laser (1064 nm, pulsed) delivers focused photodisruptive energy to posterior capsule → creates a clear central opening (capsulotomy)
• Procedure:
  • Dilate pupil
  • Contact lens (Abraham capsulotomy lens) placed on eye
  • Laser focused on posterior capsule behind IOL
  • Circular or cruciate opening created (~3-4 mm)
  • Typically 1-3 pulses of 1-3 mJ each
• Advantages: Outpatient, quick, painless, highly effective
• Complications:
  • IOL pitting (most common)
  • Transient IOP spike (use apraclonidine prophylactically)
  • Floaters from capsular debris
  • CME
  • Retinal detachment (rare, 0.5-1%)
  • Dislocation of IOL

• If laser not available
• Mechanically open posterior capsule using a needle or vitrector
• Done under operating microscope

• Thorough cortical clean-up during surgery
• In-the-bag IOL implantation
• Square-edge IOL design (sharp optic edge creates a mechanical barrier to LEC migration)
• Hydrophobic acrylic IOLs have lower PCO rates than PMMA
• Pharmacological prevention (investigational): anti-proliferative agents, anti-VEGF

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SECTION B - Complete Model Answers (50 Marks)

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Q.7 - 68-year-old with Gradually Progressive Painless Diminution of Vision (Both Eyes, 3 Years) (20 Marks)

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a) Differential Diagnosis of Gradual Painless Diminution of Vision (8 Marks)

Corneal Causes:

Lens Causes:

Vitreous Causes:

Retinal Causes:

Optic Nerve / CNS Causes:

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b) Surgical Techniques for Cataract Management (12 Marks)

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1. Phacoemulsification ("Phaco") - Current Gold Standard

• Divide and Conquer: Nucleus grooved into quadrants, each emulsified
• Stop and Chop: Initial central groove, then mechanical chop into fragments
• Phaco Chop: Horizontal or vertical chopper used to split nucleus into pieces with minimal ultrasound energy

• Monofocal IOL - corrects distance; reading glasses needed
• Multifocal IOL - near + far; spectacle independence
• Extended Depth of Focus (EDOF) - range of vision
• Toric IOL - corrects astigmatism
• Accommodating IOL - mimics natural accommodation

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2. Manual Small Incision Cataract Surgery (MSICS)

1. Conjunctival peritomy
2. Scleral groove 2 mm from limbus
3. Scleral tunnel into clear cornea (biplanar, self-sealing)
4. CCC (continuous capsulorhexis) or can-opener capsulotomy
5. Hydrodissection
6. Nucleus delivery techniques:
   • Phacosandwich (irrigating vectis + sinskey hook)
   • Fishhook technique (bent 26G needle)
   • Wire vectis delivery
7. Cortex aspiration with Simcoe cannula
8. Rigid PMMA IOL or foldable IOL implanted
9. Conjunctiva repositioned (no sutures for wound)

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3. Extracapsular Cataract Extraction (ECCE) - Conventional

1. Large superior limbal incision
2. Can-opener capsulotomy (multiple punctures around anterior capsule)
3. Expression of nucleus using lens loop/pressure on posterior lip
4. Irrigation/aspiration of cortex (Simcoe cannula)
5. Rigid PMMA IOL placed in capsular bag
6. Multiple 10-0 nylon sutures to close incision

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4. Intracapsular Cataract Extraction (ICCE) - Historical

• Zonules weakened with alpha-chymotrypsin (enzymatic zonulolysis)
• Cryoprobe applied to anterior lens surface
• Entire lens delivered in one piece

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5. Femtosecond Laser-Assisted Cataract Surgery (FLACS)

• Corneal incisions (precise, repeatable)
• Capsulotomy (perfectly circular, more reproducible than manual CCC)
• Lens fragmentation (pre-softens nucleus, reduces phaco energy)

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Complications of Cataract Surgery:

• Posterior capsule rupture (PCR) - most common serious intraoperative complication
• Vitreous loss
• Nucleus drop into vitreous
• Suprachoroidal hemorrhage (expulsive)

• Corneal edema
• Raised IOP
• Uveitis
• Wound leak

• Posterior Capsular Opacification (PCO) - see Q.12
• Cystoid Macular Edema (CME / Irvine-Gass)
• Retinal detachment
• Endophthalmitis (0.05-0.1%)

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Q.8 - Anterior Chamber Angle and Aqueous Humour Drainage Pathway (6 Marks)

Aqueous Humour Production:

• Produced by the non-pigmented ciliary epithelium of the ciliary body
• Rate: ~2.0-2.5 μL/min
• Mechanisms:
  • Active secretion (main - Na/K ATPase driven) ~80%
  • Ultrafiltration ~15%
  • Simple diffusion ~5%

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Structures of the Anterior Chamber Angle (Gonioscopic Landmarks, Anterior to Posterior):

━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
1. SCHWALBE'S LINE
   (anterior limit of Descemet's membrane;
    junction of cornea and trabeculum)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
2. TRABECULAR MESHWORK
   • Anterior (non-functional) pigmented band
   • Posterior (functional) band: aqueous filtration
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
3. SCHLEMM'S CANAL
   (lies behind posterior trabecular meshwork)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
4. SCLERAL SPUR
   (white line; posterior attachment of TM;
    anterior attachment of ciliary muscle)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
5. CILIARY BAND
   (grey/brown band = anterior face of ciliary body)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
6. IRIS ROOT
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

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Aqueous Drainage Pathways:

Conventional (Trabecular) Route - 80-90% of total outflow:

Posterior Chamber
        ↓  (through pupil)
Anterior Chamber
        ↓
Trabecular Meshwork
  [3 layers: uveal → corneoscleral → juxtacanalicular (JCT)]
  [JCT = main site of resistance]
        ↓
Schlemm's Canal
  [circumferential channel; inner wall has giant vacuoles]
        ↓
25-30 Collector Channels
        ↓
Aqueous Veins (of Ascher)
        ↓
Deep Episcleral Venous Plexus
        ↓
Episcleral Veins
        ↓
Superior Ophthalmic Vein → Cavernous Sinus → Systemic Circulation

Uveoscleral (Non-Conventional) Route - 10-20% of outflow:

Anterior Chamber Angle (between iris root & ciliary body)
        ↓
Ciliary Muscle Interstices (spaces between ciliary muscle bundles)
        ↓
Supraciliary / Suprachoroidal Space
        ↓
Through Sclera → Vortex veins / Scleral pores → Systemic circulation

• Prostaglandin analogues (e.g., latanoprost) - primary mechanism
• Cycloplegics (atropine)
• Uveitis

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Q.9 - Lens-Induced Glaucomas: Classification, Clinical Features and Management (6 Marks)

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Classification and Clinical Features:

1. Phacolytic Glaucoma (Lens Protein Glaucoma)

• Elderly patient with neglected mature/hypermature cataract
• Sudden onset severe pain and redness
• Very high IOP (50-80 mmHg)
• Corneal edema
• Deep anterior chamber (open angle)
• Milky-white or "pea soup" cells and flare in AC (no KPs - sterile)
• White fluffy deposits on lens surface (macrophages)
• Gonioscopy: open angle with white material in angle

1. Reduce IOP: IV Acetazolamide 500 mg + IV Mannitol 20%
2. Topical: Timolol + Brimonidine + Dorzolamide
3. Anti-inflammatory: Topical steroids
4. Definitive: Cataract surgery (ECCE/Phaco) - removes source of protein
5. Miotics (pilocarpine) and laser iridotomy are NOT helpful (open angle)

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2. Phacomorphic Glaucoma

• Sudden onset pain, redness, visual loss
• Shallow AC (shallower than fellow eye)
• Intumescent white/grey lens
• High IOP
• Closed angle on gonioscopy
• Fellow eye has open angle (distinguishes from primary AACG)

1. Reduce IOP medically (same as above: IV Acetazolamide, Mannitol)
2. Nd:YAG laser peripheral iridotomy (LPI) - relieves pupillary block
3. Topical pilocarpine (use after LPI)
4. Definitive: Cataract surgery (removes the causative intumescent lens)

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3. Lens Particle Glaucoma

• History of trauma or previous cataract surgery
• White fluffy lens particles visible in AC
• Mild to moderate IOP elevation
• Mild flare and cells
• No hypermature cataract

1. Topical steroids (reduce inflammation)
2. IOP-lowering drops
3. Surgical washout (anterior vitrectomy/I/A) if uncontrolled

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4. Phakoanaphylactic (Phaco-anaphylactic) Uveitis with Glaucoma

• History of penetrating trauma or extracapsular surgery
• Intense granulomatous uveitis
• Mutton-fat keratic precipitates (KPs)
• Raised IOP + inflammation

• Intense topical and systemic steroids
• IOP-lowering medications
• Surgical removal of residual lens material

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5. Lens Dislocation-Induced Glaucoma

• Supine position (for anterior dislocation - allows lens to fall back)
• Mydriatics (to dilate pupil, break pupillary block)
• IOP lowering
• Surgical lens removal if needed

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Q.10 - Primary Angle Closure Glaucoma (PACG): Diagnosis and Management (6 Marks)

Pathogenesis:

• Resistance to aqueous flow from posterior to anterior chamber at the pupillary margin
• Increased pressure in posterior chamber → pushes iris forward (iris bombe) → peripheral iris apposes trabecular meshwork

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Clinical Stages:

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Diagnosis - Acute Attack:

• Sudden severe unilateral headache and eye pain
• Nausea and vomiting (may mimic GI emergency)
• Halos around lights (corneal edema causing prismatic dispersion)
• Profound rapid visual loss
• Ciliary pain (photophobia)

• Circumcorneal (ciliary) flush - deep red/violet injection
• Steamy (edematous) cornea - hazy, "ground glass" appearance
• Shallow anterior chamber
• Mid-dilated, vertically oval, FIXED pupil (sphincter ischemia from high IOP)
• Congested episcleral vessels
• IOP: 40-80 mmHg (severely elevated)
• Fundus: optic disc may appear hyperemic (or cupped if chronic)

1. Tonometry (Goldmann applanation) - confirms very high IOP
2. Slit-lamp biomicroscopy - corneal edema, shallow AC, mid-dilated fixed pupil
3. Gonioscopy (after cornea clears) - confirms angle closure; identifies peripheral anterior synechiae (PAS)
4. Van Herick test - peripheral AC depth < 1/4 corneal thickness = high risk
5. Visual field testing (Humphrey perimetry) - after acute episode resolves
6. Optic disc assessment - OCT RNFL, stereo disc photography
7. Pachymetry - corneal thickness
8. A-scan biometry - short axial length, anterior lens position
9. UBM (Ultrasound Biomicroscopy) - plateau iris configuration diagnosis

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Management:

Step 1: Immediate Medical Treatment (Emergency):

Step 2: Definitive Treatment (After IOP controlled):

• Creates a small hole in the peripheral iris
• Allows aqueous to flow directly from posterior to anterior chamber, bypassing the pupillary block
• Equalizes pressure across iris → iris flattens → angle opens
• Done in both eyes (prophylactic LPI in fellow eye)
• Energy: 3-10 mJ, usually 1-3 pulses; site: superotemporal position (under upper lid)
• Complications of LPI: Hemorrhage (minor, self-limiting), IOP spike (use apraclonidine prophylactically), dysphotopsia (streaks/shadows), closure of iridotomy, uveitis

• If laser iridotomy fails or cornea too edematous for laser
• Full-thickness excision of peripheral iris through limbal incision

Step 3: If Angle Does Not Open After Iridotomy:

• Trabeculectomy (filtration surgery) - creates a drainage bleb under conjunctiva
• Aqueous shunt surgery (Ahmed/Baerveldt valve)
• Cataract extraction - increasingly recommended as primary treatment for PACG with cataract; removing the thick lens deepens the AC and opens the angle dramatically
• Laser peripheral iridoplasty (ALPI) - for plateau iris syndrome
• Goniosynechialysis - surgical separation of PAS

Fellow Eye Management:

• Prophylactic laser peripheral iridotomy in the fellow eye is mandatory (60% chance of developing AACG within 5 years without treatment)

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Q.11 - Visual Field Defects in Primary Open Angle Glaucoma (POAG) (6 Marks)

• RNFL fibers from the macula pass directly to the temporal optic disc (papillomacular bundle)
• Superior and inferior arcuate fibers sweep around the macula to the disc
• These arcuate fibers are most vulnerable to glaucomatous damage
• Field defects respect the horizontal midline (nerve fibers above and below horizontal raphe do not cross)

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Sequence of Visual Field Loss (Early to Late):

Stage 1 - Pre-perimetric / Very Early:

• Enlarged blind spot - due to periparafoveal RNFL loss
• Changes visible on OCT before perimetry detects them
• RNFL thinning on OCT (especially superotemporal/inferotemporal sectors)

Stage 2 - Early Glaucoma:

• Isolated paracentral scotoma - small absolute or relative scotoma within 10-20° of fixation in the Bjerrum area (arcuate zone, 10-20° from fixation)
• Nasal step (Ronne's step) - asymmetric loss across the horizontal meridian in the nasal field; one of the earliest detectable field defects; caused by unequal loss in superior vs inferior arcuate fibers

Stage 3 - Moderate Glaucoma:

• Seidel scotoma - paracentral scotoma that enlarges and connects to the blind spot in a comma or comet shape; early extension of blind spot along arcuate path
• Arcuate (Bjerrum) scotoma - arcuate-shaped field loss connecting the blind spot and curving around fixation to the nasal horizontal midline (follows the arcuate fiber bundle); can be superior, inferior, or both
• Double arcuate scotoma - both superior and inferior arcuate scotomas present simultaneously

Stage 4 - Advanced Glaucoma:

• Ring (annular) scotoma - superior and inferior arcuate scotomas join nasally, forming a complete ring around fixation (central and temporal island remain)
• Peripheral constriction with temporal island preserved

Stage 5 - End-Stage / Severe Glaucoma:

• Tunnel vision - only a small central island of vision remains (5-10° around fixation)
• Temporal island - isolated island of temporal vision may persist even after central vision lost (temporal fibers most resistant)
• Total blindness - final stage

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Characteristics of Glaucomatous Field Defects:

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Visual Field Testing Methods:

1. Automated (Static) Perimetry - Humphrey Visual Field Analyzer (HVFA):
   • 24-2 or 30-2 program - tests 54 or 76 points within central 24° or 30°
   • 10-2 program - for central field assessment in advanced glaucoma
2. Key Indices on HVFA printout:
   • MD (Mean Deviation): Global field sensitivity loss vs age-matched normal; -2 to -6 dB = mild; -6 to -12 dB = moderate; < -12 dB = severe
   • PSD (Pattern Standard Deviation): Localized field loss; elevated in early/moderate glaucoma
   • GHT (Glaucoma Hemifield Test): Compares corresponding superior and inferior sectors; "Outside Normal Limits" = significant
   • VFI (Visual Field Index): Percentage of normal visual field remaining; 100% = normal; 0% = total loss
   • Reliability indices: Fixation losses, false positive/negative responses
3. Goldmann (Manual Kinetic) Perimetry:
   • Useful in advanced glaucoma to map residual visual field
4. Frequency Doubling Perimetry (FDT):
   • Detects early glaucomatous changes; portable screening tool

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Q.12 - After-Cataract (Posterior Capsular Opacification - PCO) and Management (6 Marks)

Definition:

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Pathogenesis (Elschnig's Theory):

1. The equatorial lens capsule (germinative zone)
2. The anterior capsule periphery

• Fibrotic metaplasia (anterior-type): LECs transform into myofibroblasts → capsular wrinkling, fibrosis, contraction of capsule
• Bladder cell (Elschnig pearl) formation (equatorial-type): LECs become large swollen "bladder cells" → migrate posteriorly

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Types of After-Cataract:

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Clinical Features:

• Progressive, painless blurring of vision (weeks to years after surgery)
• Glare and halos (especially in bright light or at night)
• Reduced contrast sensitivity
• Monocular diplopia or ghost images
• On slit-lamp: wrinkling or opacity of posterior capsule visible behind the IOL
• Reduced or irregular red reflex on ophthalmoscopy
• BCVA may drop from 6/6 to 6/60 or worse

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Management:

1. Nd:YAG Laser Posterior Capsulotomy - Gold Standard

• Outpatient, non-invasive
• Immediate visual improvement
• Quick (5-10 minutes)
• Highly effective (>95% success)

• IOP spike (most common; transient; use apraclonidine prophylaxis)
• IOL pitting (small pits on posterior IOL surface; more with PMMA, less with acrylic)
• Anterior uveitis
• Floaters (capsular debris in vitreous)
• Cystoid Macular Edema (CME)
• Retinal detachment (0.5-1%; risk higher in myopes, history of RD)
• IOL dislocation (rare, if IOL not well-seated)

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2. Surgical Posterior Capsulotomy

• Manual opening of posterior capsule using needle or vitrector
• Done when laser not available or capsule too fibrotic/thickened for laser
• Can be done at time of primary cataract surgery in children (mandatory in pediatric cases as PCO develops rapidly)

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3. Prevention of PCO:

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