DISEASES OF THE UVEAL TRACT 2017 (SN) - Keratic --------- 2015 (SN) - Keratic ------------ 2012 (LQ) - Discuss the etiology, clinical features and management of Anterior Uveitis. 2012 (SN) - Iris bomble 2011 (SN) - Complication of Anterior Uveitis 2011 (SN) - Management of Endopthalmitis 2010 (LQ) - Discuss the symptoms, signs and management of Acute Iridocyclitis (Anterior Uveitis). 2008 (LQ) - Describe the aetiopathology of Acute Anterior Uveitis, its complications and management. 2007 (SN) - Occlusio papillae 2005 (LQ) - What is the clinical features and management of Acute Anterior Uveitis. 2003 (LQ) - Describe the clinical features, complications & management of Acute Anterior Uveitis. 2001 (SN) - Difference between ciliary congestion & Superciliary congestion.DISEASES F THE CORNEA 2016 (SN) - Hypopyon 2014 (LQ) - Clinical Features, Complication & Management of Fungal Corenal Ulcer. 2013 (LQ) - Clinical features, Complication & Management of Bacterial Corenal ulcers. 2013 (SN) - Keratoconus 2009 (LQ) - What is Hypopyon Corenal Ulcer ? What are the signs, symptoms and complications ? 2007 (LQ) - Describe the clinical features and management of Mycotic Corneal Ulcer. 2006 (LQ) - Discuss the aetiology, predisposing factors of Corneal ulcer. How will you diagnose fungal corneal ulcer ? 2005 (SN) - Keratoconus 2005 (LQ) - Complication and management of Herpes Zoster Opthalmicus.DISEASES F THE CORNEA 2016 (SN) - Hypopyon 2014 (LQ) - Clinical Features, Complication & Management of Fungal Corenal Ulcer. 2013 (LQ) - Clinical features, Complication & Management of Bacterial Corenal ulcers. 2013 (SN) - Keratoconus 2009 (LQ) - What is Hypopyon Corenal Ulcer ? What are the signs, symptoms and complications ? 2007 (LQ) - Describe the clinical features and management of Mycotic Corneal Ulcer. 2006 (LQ) - Discuss the aetiology, predisposing factors of Corneal ulcer. How will you diagnose fungal corneal ulcer ? 2005 (SN) - Keratoconus 2005 (LQ) - Complication and management of Herpes Zoster Opthalmicus.2003 (LQ) - Draw a lebel vertical section of cornea. Write its nerve supply and source of nutritiDISEAES OF THE CONJUNCTIVA 2017 (LQ) - Describe the etiology, clinical features and treatment of Vernal Conjuctivitis. 2017 (SN) - Pserysium2016 (LQ) - Aetiology, clinical feature & management of Ophthalmic Neonatoxum. 2012 (LQ) - Name the diseases causing acute follicular conjunctivitis. Give the management of any one of them. 2011 (LQ) - Discuss the etiology, clinical features and management of Spring Cattrah. 2010 (SN) - Opthalmia nodosa 2007 (LQ) - Describe the etiology, clinical features and treatment of Vernal Conjuctivitis. 2005 (LQ) - Describe the etiology, clinical features and treatment of Phyctenular Conjuctivitis. 2004 (SN) - Pannus 2001 (SN) - Vernal ConjuctivitisOPTICS & REFRACTION 2017 (LQ) - Describe optical changes of aphakia, clinical picture & disadvantages of aphakic glasses. 2016 (LQ) - Clinical ----- of myopia and clinical picture & management of pathological myopia. 2013 (LQ) - Accommodation. Pathophysiology & Management of Presbyopia. 2012 (LQ) - Describe the types of Myopia, its degenerative features and management. 2011 (LQ) - Describe the classification and management of Hypermetropia. 2011 (SN) - Strum conoid 2010 (LQ) - Describe mechanism of Accommodation. How will you manage a patient aged 45 years who finds difficulty in reading. 2010 (SN) - Aphakia 2009 (LQ) - What is the optical principle involved in Myopia ? What is the pathological Myopia ? Write the management in Myopia. 2008 (SN) - Accommodation 2005 (LQ) - Describe a normal fundus. What are the changes that occurs in these eyes suffering from pathogocial Myopia. 2004 (LQ) - What are common refractive errors and its management ? 2003 (LQ) - What is the pathological Myopia and its symptoms, signs and treatment ? 2001 (SN) - Difference between phakic eye & aphkic eye. 2001 (SN) - Myopia

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OPHTHALMOLOGY EXAM ANSWERS - Complete Study Guide


PART 1: DISEASES OF THE UVEAL TRACT


Keratic Precipitates (KPs) (2017 SN, 2015 SN)

Definition: Keratic precipitates are inflammatory cellular deposits on the posterior surface of the corneal endothelium, seen in uveitis.
Types:
TypeDescriptionAssociated Conditions
Fine/Stellate KPSmall, dusty depositsHSV, VZV, CMV, Fuchs Heterochromic Iridocyclitis (FHI)
Small non-granulomatous KP (NGKP)Small, roundHLA-B27 disorders, trauma, JIA, Posner-Schlossman syndrome
Granulomatous KP ("Mutton-fat" KP)Large, greasy, whitish; mainly inferior corneaSarcoidosis, TB, syphilis, VKH syndrome, sympathetic ophthalmia
Coin-shaped KPCharacteristic circular shapeCMV uveitis
Crenated KPTranslucent, discrete, medium-largeRegressed granulomatous anterior uveitis
Distribution:
  • Arlt's triangle: KPs in an inferior triangle (apex near corneal centre, base at inferior limbus) - non-specific
  • Diffuse KP: Characteristic of FHI and herpetic uveitides
  • KP beneath areas of stromal opacification: Suggests HSV or VZV keratouveitis
Pathophysiology: Breakdown of the blood-aqueous barrier allows macrophages, lymphocytes, and fibrin to enter the anterior chamber. These cells deposit on the cooler, inferior corneal endothelium (due to convection currents in aqueous humor).

Anterior Uveitis (Iridocyclitis / Acute Iritis) - LQ (2012, 2010, 2008, 2005, 2003)

Definition

Uveitis is inflammation of the uveal tract (iris, ciliary body, choroid). Anterior uveitis (iritis/iridocyclitis) involves the iris alone (iritis) or iris + ciliary body (iridocyclitis) and is the most common form (~75% of all uveitis).

Etiology / Aetiopathology

Idiopathic - most common (~50%)
Infective:
  • Viral: HSV, VZV, CMV, rubella
  • Bacterial: TB, syphilis, Lyme disease, brucellosis
  • Parasitic: Toxoplasmosis
Immune-mediated / Systemic disease:
  • HLA-B27-associated: Ankylosing spondylitis (most common systemic cause), reactive arthritis (Reiter's), psoriatic arthritis, inflammatory bowel disease
  • Sarcoidosis
  • Juvenile idiopathic arthritis (JIA) - especially ANA-positive girls
  • Vogt-Koyanagi-Harada (VKH) syndrome
  • Behcet's disease
Traumatic: After blunt/penetrating injury
Drug-induced: Rifabutin, cidofovir, fluoroquinolones, cancer immunotherapy
Pathophysiology: HLA-B27-mediated autoimmune cross-reactivity (molecular mimicry) is the best-understood mechanism. Microbial antigens sharing epitopes with uveal proteins trigger T-cell attack on uveal tissue. Breakdown of the blood-aqueous barrier leads to protein leakage (flare) and cellular influx into the anterior chamber.

Clinical Features

Symptoms:
  • Pain (deep, aching orbital pain, worsened by light)
  • Redness (ciliary/circumcorneal flush - brick-red zone around limbus)
  • Photophobia (consensual photophobia is characteristic - pain in the affected eye when light is shone in the other eye)
  • Lacrimation (watering)
  • Blurred vision
  • Onset: usually acute, but may be chronic/recurrent
Signs:
  1. Ciliary flush (circumcorneal injection) - deep, brick-red injection around the limbus (dilated deep ciliary vessels, does NOT blanch with topical adrenaline)
  2. Keratic precipitates (KP) - deposits on corneal endothelium (see above)
  3. Aqueous flare - Tyndall effect (beam of light visible in anterior chamber due to protein) - graded 0 to 4+
  4. Cells in anterior chamber - white cells visible with slit-lamp - graded 0 to 4+
  5. Hypopyon - layering of pus cells in inferior anterior chamber (especially HLA-B27, Behcet's, endophthalmitis)
  6. Posterior synechiae - adhesions of iris to anterior lens capsule; cause irregular pupil, poor dilation
  7. Iris changes: Iris nodules (Koeppe - at pupil margin; Busacca - in iris stroma), iris atrophy, heterochromia
  8. Pupil changes: Small (miosis due to iris sphincter spasm), irregular (from synechiae)
  9. Reduced IOP (from ciliary body hyposecretion) - though elevated IOP may occur in herpetic or trabeculitis-related uveitis
  10. Band keratopathy - calcium deposition in chronic/JIA uveitis

Grading (Wills Eye Manual)

AC Cells:
  • 0: <1 cell | 0.5+: 1-5 | 1+: 6-15 | 2+: 16-25 | 3+: 26-50 | 4+: >50
AC Flare:
  • 0: None | 1+: Faint | 2+: Moderate (iris details clear) | 3+: Marked (iris details hazy) | 4+: Intense (fibrin/plastic aqueous)

Investigation

  • Slit-lamp examination (gold standard)
  • HLA-B27 (acute unilateral/alternating uveitis with hypopyon)
  • FBC, ESR, CRP
  • CXR / CT chest (sarcoidosis, TB)
  • ACE level (sarcoidosis)
  • VDRL/TPHA (syphilis)
  • Mantoux / IGRA (TB)
  • ANA, RF (JIA)
  • Aqueous tap for PCR (HSV, VZV, CMV)

Complications (2011 SN)

  1. Posterior synechiae → irregular pupil, seclusio pupillae
  2. Occlusio pupillae / Iris bombe - see below
  3. Secondary glaucoma (trabecular block, pupil block, peripheral anterior synechiae)
  4. Complicated cataract (posterior subcapsular lens opacity - "snowflake" or "rosette")
  5. Cystoid macular edema (CME) - most common cause of visual loss in chronic uveitis
  6. Band keratopathy (calcium deposition in Bowman's layer)
  7. Phthisis bulbi (end-stage shrunken eye from chronic inflammation)
  8. Vitreous opacities / Cyclitic membrane
  9. Hypotony (ciliary body shutdown)
  10. Retinal detachment (tractional)
  11. Epiretinal membrane

Management

General:
  • Treat underlying cause if identified
Mydriatic/Cycloplegic agents (most important - given immediately):
  • Purpose: (1) Relieves ciliary spasm (pain), (2) Prevents/breaks posterior synechiae, (3) Rests the ciliary body
  • Mild-moderate: Cyclopentolate 1% TDS
  • Severe: Atropine 1% BD-QID
  • Additional: Phenylephrine 10% (mydriatic) to dilate pupil fully and break synechiae
Corticosteroids (anti-inflammatory):
  • Topical: Prednisolone acetate 1% q1-6h (most cases); Difluprednate 0.05%
    • Severe: loading dose - 1 drop/minute for 5 minutes at bedtime
  • Periocular: Sub-Tenon triamcinolone 40 mg/mL (0.5-1 mL) for severe unilateral disease
  • Systemic: Oral prednisolone if bilateral severe, posterior segment involvement
NSAIDs: Topical ketorolac / systemic ibuprofen as adjunct
IOP management: Topical beta-blockers or carbonic anhydrase inhibitors if elevated (avoid prostaglandin analogues - may worsen uveitis)
Steroid-sparing immunosuppressants (chronic/recurrent): Methotrexate, mycophenolate mofetil, azathioprine, cyclosporine; biologics (adalimumab - FDA-approved for non-infectious uveitis)
Treatment of synechiae: Intensive mydriatics; if seclusio pupillae with iris bombe - surgical iridectomy/laser PI

Iris Bombe (2012 SN)

Definition: Iris bombe is a condition where the entire posterior surface of the iris is adherent to the anterior lens capsule (360° posterior synechiae = seclusio pupillae), completely blocking aqueous flow from the posterior to the anterior chamber.
Mechanism:
  • 360° posterior synechiae form in severe/untreated anterior uveitis
  • Aqueous produced by ciliary body accumulates in the posterior chamber
  • Pressure from trapped aqueous pushes the peripheral iris forward
  • Iris takes a characteristic "tent-like" or "bombé" configuration (forward bowing of the peripheral iris with deepened posterior chamber centrally)
  • This causes secondary angle-closure glaucoma (high IOP, shallow anterior chamber peripherally)
Clinical Features:
  • Deep central AC, very shallow peripheral AC
  • Forward-bowing iris (visible on slit-lamp)
  • High IOP
  • History of recurrent/chronic uveitis
  • Shallow AC peripherally with closed angle on gonioscopy
Complications: Secondary angle-closure glaucoma with acute IOP rise
Treatment:
  • Urgent laser peripheral iridotomy (PI) or surgical iridectomy to create a new passage for aqueous
  • Intensive topical steroids and cycloplegics
  • IOP-lowering agents (topical beta-blockers, IV acetazolamide, mannitol)

Occlusio Pupillae (2007 SN)

Definition: Occlusio pupillae is the condition where a fibrous exudative membrane (cyclitic membrane) covers the entire pupillary opening, blocking the pupil completely.
Cause: Severe fibrinous exudate in uveitis organizes into a membrane over the pupil (different from seclusio pupillae which is iris-lens adhesion - here the pupil itself is obstructed by a membrane).
Effects:
  • Blocks light entry → severe visual impairment
  • Can cause secondary glaucoma (pupil block)
  • Can lead to iris bombe if aqueous is also blocked
Treatment:
  • Surgical membranectomy / Nd:YAG laser membrane disruption
  • Treatment of underlying uveitis

Difference: Ciliary Congestion vs. Conjunctival (Subconjunctival/Superficial) Congestion (2001 SN)

FeatureCiliary Congestion (Deep)Conjunctival Congestion (Superficial)
Also calledCircumcorneal flush / Perilimbal flushConjunctival hyperemia / Superciliary congestion
Vessels involvedDeep episcleral/anterior ciliary vesselsSuperficial conjunctival vessels
DistributionAround the limbus (circumcorneal), 3-5mm zonePeripheral conjunctiva, away from limbus
ColorDeep brick-red / violet-redBright red
MovementVessels do NOT move with conjunctivaVessels move freely with conjunctiva
Response to adrenalineDoes NOT blanch with topical 1:1000 adrenalineBlanches with topical adrenaline
CausesKeratitis, Iridocyclitis, Acute glaucomaConjunctivitis, foreign body, allergy
SignificanceIndicates deep ocular pathologyIndicates superficial pathology

Management of Endophthalmitis (2011 SN)

Definition: Endophthalmitis is infection of the intraocular contents (vitreous and aqueous humor). It is an ophthalmic emergency.
Classification:
  • Exogenous: Post-surgical (most common - especially post-cataract, 0.05-0.1%), post-traumatic, bleb-related
  • Endogenous: Hematogenous spread (Candida, Klebsiella, endocarditis-related)
Clinical Features:
  • Marked pain, redness, photophobia
  • Severe loss of vision
  • Lid edema
  • Conjunctival chemosis and injection
  • Corneal haze/edema
  • Hypopyon (large, often with fibrin)
  • Loss of/reduced red reflex
  • Vitritis (cells in vitreous - "white/grey reflex")
  • Bleb with white milky appearance (bleb-related)
Investigations:
  • Aqueous and vitreous tap for Gram stain and culture
  • B-scan ultrasound (to assess vitreous and posterior segment)
Management (EVS - Endophthalmitis Vitrectomy Study guidelines):
1. Vitreous/Aqueous sampling - IMMEDIATELY on presentation (before starting antibiotics)
2. Intravitreal antibiotics (cornerstone of treatment):
  • Vancomycin 1 mg/0.1 mL (covers Gram-positive organisms including Staphylococcus)
  • Ceftazidime 2 mg/0.1 mL (covers Gram-negative organisms)
  • Injected into vitreous cavity
3. Pars plana vitrectomy (PPV):
  • Indicated if: (a) Light perception (LP) only vision or worse, (b) Bleb-related endophthalmitis, (c) Fungal endophthalmitis, (d) No improvement 48h after intravitreal antibiotics
  • EVS showed: In hand-motion (HM) or better vision - intravitreal antibiotics alone as effective as immediate vitrectomy; in LP or worse - vitrectomy significantly better
4. Systemic antibiotics:
  • Oral fluoroquinolones (ciprofloxacin/moxifloxacin) 10-14 days
  • Systemic vancomycin + ceftazidime for severe/bleb-related
5. Topical treatment:
  • Intensive topical fortified antibiotics: Vancomycin + Ceftazidime/Tobramycin
  • Topical steroids (after 48h, once infection is controlled)
  • Cycloplegics (atropine 1%)
6. Antifungal (Voriconazole intravitreal 100 mcg/0.1 mL) if fungal endophthalmitis suspected (Candida, Aspergillus - especially in immunocompromised, IV drug users, post-trauma)
Repeat intravitreal injections at 48h if inadequate response

PART 2: DISEASES OF THE CORNEA


Hypopyon (2016 SN)

Definition: Hypopyon is a collection of white cells (leukocytes/pus) that settle by gravity to form a visible horizontal fluid level in the inferior anterior chamber.
Characteristics:
  • Sterile or infected
  • Appears as a cream/white layer at the bottom of AC
  • Level shifts with change of head position (gravitational)
  • Indicates severe anterior segment inflammation
Causes:
  • Corneal ulcer (bacterial, fungal, amoebic) - pus from adjacent ulcer spills into AC
  • Uveitis: HLA-B27 disease (most common cause of sterile hypopyon), Behcet's disease
  • Infectious endophthalmitis
  • Masquerade syndromes: Retinoblastoma, leukemia (tumor cells mimicking hypopyon)
  • Drug-induced: Rifabutin
  • Severe keratitis (Hypopyon corneal ulcer)
Significance: Indicates serious ocular infection or inflammation requiring urgent treatment

Hypopyon Corneal Ulcer (2009 LQ)

Definition: A corneal ulcer associated with hypopyon in the anterior chamber, indicating severe infection with extension of inflammation into the anterior segment.
Etiology: Most commonly caused by Pseudomonas aeruginosa (rapidly progressing), Pneumococcus/Streptococcus, Staphylococcus, Moraxella; also fungal organisms.
Signs:
  • Corneal ulcer with stromal infiltrate and excavation
  • Mucopurulent/purulent discharge
  • Severe ciliary injection
  • Corneal edema
  • Hypopyon (sterile collection - toxins from bacteria diffuse into AC, attract WBCs)
  • Chemosis of conjunctiva
  • Reduced/absent corneal sensation
Symptoms:
  • Severe pain
  • Photophobia
  • Marked lacrimation
  • Marked visual impairment
  • Lid edema
Complications:
  • Perforation of cornea
  • Iris prolapse
  • Descemetocele (bulging of Descemet's membrane through thinned stroma)
  • Corneal scarring / leucoma
  • Secondary glaucoma
  • Endophthalmitis
  • Panophthalmitis
  • Phthisis bulbi

Bacterial Corneal Ulcer (2013 LQ)

Etiology

  • Contact lens wearers: Pseudomonas aeruginosa (most virulent, produces proteases causing rapid corneal "melting")
  • Non-contact lens: Staphylococcus aureus, Streptococcus pneumoniae, Moraxella lacunata (chronic alcoholics), Enterobacteriaceae

Predisposing Factors

  • Contact lens use (especially extended wear)
  • Corneal trauma (especially vegetable matter)
  • Ocular surface disease (dry eye, blepharitis)
  • Immunosuppression
  • Topical steroid use
  • Previous corneal disease (herpes, bullous keratopathy)
  • Malnutrition / Vitamin A deficiency

Clinical Features

Symptoms: Acute onset pain, redness, photophobia, discharge (mucopurulent), reduced vision
Signs:
  • Eyelid edema, conjunctival injection and chemosis
  • Mucopurulent discharge
  • Corneal infiltrate (grey/white opacity) with surrounding epithelial defect
  • Stromal thinning/ulceration (excavation)
  • Stromal edema
  • Satellite lesions (fungal), feathery edges (fungal); well-defined edges (bacterial)
  • Hypopyon (in severe cases)
  • Reduced/absent corneal sensation
  • Anterior uveitis
Microorganism-specific features:
  • Pseudomonas: Rapid progression, liquefactive necrosis ("melting"), blue-green mucopurulent discharge, central ulcer, ring infiltrate
  • Pneumococcal: Serpiginous/creeping corneal ulcer with hypopyon
  • Staphylococcal: Peripheral ulcer with slight purulent infiltrate

Investigations

  • Corneal scraping (gold standard): Gram stain, KOH mount, culture on Blood agar, Chocolate agar, Sabouraud's agar
  • Slit-lamp examination
  • B-scan USG if posterior segment not visible

Complications

  • Corneal perforation
  • Descemetocele
  • Iris prolapse / adherent leucoma
  • Secondary glaucoma
  • Endophthalmitis
  • Panophthalmitis
  • Corneal scarring (leucoma / macula / nebula)
  • Anterior staphyloma (if large perforation heals with iris)
  • Phthisis bulbi

Management

First line - Topical Antibiotics (based on culture; empiric broad-spectrum initially):
  • Fluoroquinolones (ciprofloxacin 0.3% or moxifloxacin 0.5%) Q1-2h (drug of choice for most bacterial ulcers)
  • Fortified antibiotics (for severe/culture-directed):
    • Fortified Vancomycin (25 mg/mL) - Gram-positive cover
    • Fortified Ceftazidime (50 mg/mL) or Tobramycin (13.6 mg/mL) - Gram-negative cover
    • Alternating Q30-60 min
Cycloplegic: Atropine 1% or cyclopentolate 1% BD-TDS (reduces pain and prevents synechiae)
IOP control: If elevated, topical beta-blocker or CAI
Steroids: Controversial; some use weak topical steroids after 48h of antibiotics only if culture-directed and organism is sensitive
Systemic antibiotics: For severe, large ulcers with scleral extension or impending perforation; fluoroquinolone orally
Surgical:
  • Tectonic bandage contact lens or corneal glue (tissue adhesive) for impending perforation
  • Tectonic lamellar/penetrating keratoplasty (PKP) for perforated ulcers

Fungal (Mycotic) Corneal Ulcer (2014 LQ, 2007 LQ, 2006 LQ)

Etiology

Filamentous fungi (tropical/agricultural settings):
  • Fusarium species (most common worldwide, contact lens-associated)
  • Aspergillus species (most common in South/Southeast Asia)
Yeast:
  • Candida albicans (immunocompromised patients, chronic corneal disease)

Predisposing Factors

  • Trauma with vegetable/plant material (thorns, paddy husk) - classic history
  • Agricultural workers
  • Topical steroid overuse
  • Immunosuppression (HIV, diabetes)
  • Antibiotic overuse altering flora
  • Chronic corneal disease
  • Contact lens wear (Fusarium)

Clinical Features

Symptoms: Pain (less severe than bacterial), photophobia, reduced vision, discharge (mucopurulent)
Signs (characteristic):
  1. Dry, rough, raised surface of the ulcer (vs. wet in bacterial)
  2. Feathery/fluffy/filamentous margins (hyphae extending beyond visible margin)
  3. Satellite lesions - small infiltrates surrounding the main ulcer
  4. Immune ring (Wessely ring) - antigen-antibody reaction at edge of ulcer
  5. Hypopyon (viscous, not shifting readily, immobile - unlike bacterial)
  6. Endothelial plaques (inflammatory deposits on posterior cornea)
  7. Deep stromal involvement with minimal epithelial defect
  8. Less vascularization than bacterial

Diagnosis

  • KOH (10-20%) wet mount of corneal scraping - shows hyphae (filamentous) or pseudohyphae (Candida)
  • Gram stain / Giemsa stain
  • Culture on Sabouraud's dextrose agar with chloramphenicol (gold standard, slow - takes 5-7 days)
  • Confocal microscopy (noninvasive, rapid - shows hyphae in vivo)
  • PCR (rapid, sensitive)
  • Lactophenol cotton blue (differentiates species)

Complications

Same as bacterial: perforation, endophthalmitis, scarring

Management

Topical antifungals (mainstay):
  • Natamycin 5% drops Q1-2h - drug of choice for filamentous fungi (Fusarium, Aspergillus); poorly penetrates stroma
  • Voriconazole 1% drops Q1-2h - excellent for Aspergillus, penetrates stroma well; emerging as first-line alternative
  • Amphotericin B 0.15-0.3% - drug of choice for Candida
  • Econazole 1% - alternative azole
Systemic antifungals:
  • Oral voriconazole (200 mg BD) for deep/stromal infection
  • Oral fluconazole for Candida
Cycloplegic: Atropine 1% BD-TDS
Debridement: Corneal epithelial debridement to improve drug penetration
AVOID: Topical steroids (worsen fungal infection)
Duration: Minimum 6 weeks (fungi grow slowly)
Surgical:
  • Penetrating keratoplasty (PKP) for non-responsive or perforated cases
  • Corneal glue for impending perforation

Keratoconus (2013 SN, 2005 SN)

Definition: A non-inflammatory, progressive ectatic (thinning) disorder of the cornea in which the cornea assumes an irregular conical shape due to axial thinning and protrusion.
Epidemiology: Onset: teens to early 20s. More common in atopic individuals. Bilateral (though asymmetric).
Etiology/Associations:
  • Idiopathic (most cases)
  • Atopic disease (eczema, asthma, hay fever) - repeated eye rubbing
  • Down's syndrome (trisomy 21)
  • Marfan's syndrome, Ehlers-Danlos syndrome
  • Leber's congenital amaurosis
  • Vernal keratoconjunctivitis
Pathology: Loss of collagen fibrils and lamellae in Bowman's layer and stroma; anterior stroma thinning at apex; iron deposition in epithelium (Fleischer ring).
Clinical Features:
  • Progressive myopia and irregular astigmatism (which cannot be corrected with spectacles)
  • Blurred, distorted vision (diplopia, ghosting)
  • Frequent change of spectacle prescription
Signs:
  1. Munson's sign: V-shaped deformity of lower lid on downgaze
  2. Scissor reflex on retinoscopy (irregular reflex)
  3. Fleischer ring: Iron (hemosiderin) deposits in epithelium at base of cone (seen with cobalt blue filter)
  4. Vogt's striae: Fine, vertical, deep stromal stress lines (disappear with pressure on globe)
  5. Corneal thinning at apex (visible on slit-lamp, pachymetry)
  6. Irregular mires on keratometry/corneal topography (irregular astigmatism)
  7. Rizzuti's sign: Focal illumination of nasal cornea when light shone from temporal side
  8. Korb sign: Light reflected from the apex of the cone
Acute Hydrops: Sudden rupture of Descemet's membrane allowing aqueous humor to enter stroma; causes sudden pain, marked corneal opacification, reduced vision.
Investigations:
  • Corneal topography (Placido disc / Scheimpflug - Pentacam): Shows irregular inferior steepening, bow-tie pattern
  • Pachymetry: Reduced corneal thickness at apex
  • Slit-lamp: Vogt's striae, Fleischer ring, thinning
Management:
  1. Spectacles / Rigid gas-permeable (RGP) contact lenses - first-line for mild/moderate
  2. Custom soft lenses / Scleral lenses - better tolerance for advanced
  3. Corneal collagen cross-linking (CXL) - riboflavin (B2) drops + UV-A irradiation; halts progression by strengthening collagen cross-links (currently most important treatment)
  4. Intrastromal corneal ring segments (ICRS/Intacs) - reduce irregularity, improve BCVA
  5. Penetrating keratoplasty (PKP) or DALK (deep anterior lamellar keratoplasty) - for advanced keratoconus not amenable to contact lenses; excellent outcomes

Herpes Zoster Ophthalmicus (HZO) - Complications & Management (2005 LQ)

Definition: Reactivation of Varicella-Zoster Virus (VZV) in the ophthalmic division (V1) of the trigeminal nerve.
Hutchinson's Sign: Vesicular rash on tip or side of nose (nasociliary nerve branch) - strongly predicts ocular involvement (up to 76%)

Ocular Complications

Anterior Segment:
  • Conjunctivitis (papillary or follicular)
  • Episcleritis / Scleritis
  • Keratitis: Punctate epithelial keratitis (PEK), pseudodendrites (raised, mucous plaques - without terminal bulbs, unlike HSV), anterior stromal infiltrates, nummular keratitis (coin-shaped infiltrates)
  • Neurotrophic keratitis (loss of corneal sensation - high risk of exposure keratopathy)
  • Iritis / Uveitis (sectoral iris atrophy, KP, cells/flare)
  • Acute retinal necrosis (ARN)
  • Trabeculitis / secondary glaucoma
Posterior Segment:
  • Acute retinal necrosis (ARN)
  • Progressive outer retinal necrosis (PORN) in immunocompromised
  • Optic neuritis
Other:
  • Postherpetic neuralgia (most distressing long-term complication - burning pain persisting after rash heals)
  • Ptosis (third nerve palsy)
  • Cranial nerve palsies (III, IV, VI)
  • VZV-related encephalitis

Management

  1. Systemic antivirals (essential - given within 72h of rash onset):
    • Acyclovir 800 mg 5x/day x 7-10 days, OR
    • Valacyclovir 1 g TDS x 7 days (better bioavailability), OR
    • Famciclovir 500 mg TDS x 7 days
    • Intravenous acyclovir for immunocompromised / CNS involvement
  2. Analgesics: NSAIDs, gabapentin/pregabalin, amitriptyline (for postherpetic neuralgia)
  3. Skin care: Calamine lotion; keep lesions clean and dry
  4. Topical antivirals: NOT routinely indicated for HZO (unlike HSV)
  5. Eye-specific treatment:
    • Cycloplegic (atropine 1%) for uveitis
    • Topical steroids for keratitis/uveitis (with antiviral cover)
    • Lubricating drops/ointment for neurotrophic/exposure keratopathy
    • IOP-lowering agents for secondary glaucoma
    • Tarsorrhaphy if severe neurotrophic keratitis
  6. Vaccination: Shingrix (recombinant) vaccine - recommended for >50 years to prevent HZO

Labeled Vertical Section of Cornea / Nerve Supply / Nutrition (2003 LQ)

Layers of Cornea (from anterior to posterior):
1. Epithelium (Non-keratinized stratified squamous, 5-6 layers thick)
        ↓
2. Bowman's Layer (Acellular, condensed anterior stroma - NOT regenerated if damaged)
        ↓
3. Stroma (90% of corneal thickness; collagen lamellae, keratocytes, glycosaminoglycans)
        ↓
4. Descemet's Membrane (Basement membrane of endothelium - thickens with age)
        ↓
5. Endothelium (Single layer of hexagonal cells - pumps fluid out, NOT regenerated)
Nerve Supply:
  • Ophthalmic division (V1) of trigeminal nerve (CN V) via the long ciliary nerves and anterior ciliary nerves (nasociliary branches)
  • Cornea is the most densely innervated tissue in the body (~300-600 nerve endings/mm²)
  • Supplies: Pain, touch, temperature sensation
  • Important: Corneal reflex (afferent = trigeminal V1, efferent = facial CN VII - orbicularis)
  • Cornea has NO sympathetic nerve supply to vessels (it's avascular)
Sources of Nutrition:
  1. Aqueous humor (from ciliary body) - primary source for endothelium and stroma; provides glucose, amino acids, O2
  2. Limbal capillaries (peripheral 1-2 mm of cornea gets nutrients from limbal vessels)
  3. Atmospheric oxygen (O2 via tear film) - primary source of O2 for epithelium
  4. Tear film - lubricates epithelium, provides growth factors (EGF), O2

PART 3: DISEASES OF THE CONJUNCTIVA


Vernal Keratoconjunctivitis (VKC) / Spring Catarrh (2017 LQ, 2011 LQ, 2007 LQ, 2001 SN)

Definition

A bilateral, recurrent, chronic allergic inflammation of the conjunctiva primarily affecting young males in warm/tropical climates. Predominantly a Type I (IgE-mediated) and Type IV (cell-mediated) hypersensitivity reaction.

Etiology

  • Allergens: Pollens, dust mites, animal dander (unknown specific allergen often)
  • Age: 5-25 years; uncommon after puberty (hormonal influence - more common in males)
  • Season: Worse in spring/summer (hence "spring catarrh"), may be perennial in tropics
  • Atopic association: 50% have personal/family history of atopy (asthma, eczema, hay fever)
  • Immune mechanism: Mast cell degranulation (IgE) + eosinophil and T-cell infiltration

Types

  1. Palpebral (Tarsal) type - most common
  2. Limbal type - more common in Africans/dark-skinned
  3. Mixed type

Clinical Features

Symptoms:
  • Intense itching (hallmark - worst on rubbing)
  • Burning sensation
  • Photophobia
  • Lacrimation
  • Stringy/ropy mucous discharge (ropy - characteristic mucus from goblet cells + eosinophils)
  • Foreign body sensation
  • Worse in hot weather
Signs:
Palpebral type:
  • Giant papillae (cobblestone/cauliflower appearance) on upper tarsal conjunctiva - pathognomonic (papillae >1mm = giant papillae)
  • Papillae have flat tops, separated by furrows
  • Horner-Trantas dots: absent in tarsal type
Limbal type:
  • Limbal papillae (gelatinous, thickened limbus - especially superior)
  • Horner-Trantas dots: White chalky dots at limbus (accumulations of degenerated eosinophils) - pathognomonic of limbal VKC
  • More common in African/pigmented patients
Mixed type: Both present
Corneal changes (most important for vision):
  • Punctate epithelial erosions (PEE) superiorly
  • Shield ulcer (Vernal corneal ulcer / Vernal plaque) - oval shallow ulcer in upper cornea from large papillae abrading epithelium + eosinophil toxic proteins
  • Calcific plaque formation
  • Superficial corneal vascularization (pannus)
  • Pseudogerontoxon (arcus-like change at limbus)

Management

1. General / Avoidance:
  • Cold compresses (vasoconstriction, symptomatic relief)
  • Wearing sunglasses
  • Moving to cooler climate (curative)
  • Avoid allergens
2. Medical:
  • Mast cell stabilizers (first-line, prophylactic): Sodium cromoglycate (2%) QID, Lodoxamide (0.1%) QID - prevent mast cell degranulation
  • Antihistamines (symptomatic): Topical olopatadine (dual action - antihistamine + mast cell stabilizer), emedastine; systemic antihistamines
  • Topical NSAIDs: Ketorolac (adjunct)
  • Topical corticosteroids (for acute flares only - short courses): Fluorometholone, loteprednol (preferred in children - less IOP risk); prednisolone for severe flares. Avoid long-term due to steroid cataract, glaucoma risk.
  • Topical cyclosporine A (0.05-1%): For refractory cases not responding to steroids; steroid-sparing agent of choice
  • Topical tacrolimus: Alternative to cyclosporine
3. Treatment of Shield Ulcer:
  • Superficial keratectomy (surgical debridement of calcific plaque)
  • Amniotic membrane transplant for refractory cases
4. Supratarsal injection of corticosteroid (triamcinolone): For refractory cases with giant papillae; injected under upper lid into conjunctival fornix

Ophthalmia Neonatorum (2016 LQ)

Definition

Conjunctivitis occurring in a newborn within the first 28 days (4 weeks) of life. Also called neonatal conjunctivitis or conjunctivitis of the newborn.

Etiology (Aetiology) - by time of onset

OrganismOnset After BirthKey Features
Chemical (Silver nitrate - Crede's prophylaxis)Within 24-48 hoursMild, self-limiting; rare now with newer prophylaxis
Neisseria gonorrhoeae2-5 daysMOST SEVERE - hyperacute purulent conjunctivitis, risk of corneal perforation
Chlamydia trachomatis5-14 daysMost common bacterial cause currently; mucopurulent, chronic
Staphylococcus aureusVariable (2-5 days)Common; moderate purulent discharge
Herpes simplex virus (HSV-2)5-14 daysVesicular lid lesions, dendrites; rare but vision-threatening
Other bacteriaVariableHaemophilus, Streptococcus pneumoniae
Source of infection: Mainly from infected maternal birth canal during delivery (vertical transmission)

Clinical Features

General:
  • Eyelid swelling (edema)
  • Conjunctival injection
  • Discharge (varies by organism)
Gonococcal (most severe - vision emergency):
  • Onset 2-5 days
  • Hyperacute, profuse purulent (green-yellow pus) discharge
  • Marked eyelid edema
  • Chemosis
  • Risk of corneal ulceration and perforation if untreated
  • Gram stain: Gram-negative intracellular diplococci
Chlamydial (most common currently):
  • Onset 5-14 days
  • Mucopurulent discharge (moderate)
  • Follicles ABSENT (follicles require mature lymphoid tissue - not present in neonates)
  • Pseudomembranes
  • Papillary hypertrophy
  • If untreated: Scarring, chronic infection; can cause Chlamydial pneumonia
Herpetic:
  • Vesicular lesions on lids
  • Serous/serosanguinous discharge
  • Dendritic corneal ulcer
  • Systemic HSV (encephalitis) risk

Investigations

  • Conjunctival swab for Gram stain, culture (chocolate agar for gonorrhoea)
  • Giemsa stain (Chlamydial inclusions - basophilic intracytoplasmic inclusions)
  • PCR/NAAT (Chlamydia)

Management

General measures:
  • Regular saline irrigation (wash away discharge)
  • Topical antibiotics (based on organism)
Gonococcal:
  • Systemic: Single dose IV/IM Ceftriaxone 25-50 mg/kg (max 125 mg)
  • Topical: Saline irrigation + topical fluoroquinolone or chloramphenicol
Chlamydial:
  • Systemic: Oral Erythromycin syrup 12.5 mg/kg QID x 14 days (topical alone is insufficient)
  • Topical: Tetracycline 1% or erythromycin ointment QID (adjunct)
  • Treat parents simultaneously (for chlamydial STI)
Herpetic:
  • Systemic: IV Acyclovir (20 mg/kg TDS x 14-21 days)
  • Topical: Acyclovir 3% ointment or ganciclovir gel 5x/day
Chemical (silver nitrate): No treatment needed; self-limiting in 24-48h

Prophylaxis (Crede's Method)

  • 0.5% Erythromycin ointment instilled in both eyes at birth (WHO recommendation)
  • 1% Tetracycline ointment (alternative)
  • Povidone-iodine 2.5% solution (effective against gonorrhoea, chlamydia, and herpes)
  • Silver nitrate 1% (historical Crede's method - largely replaced)

Acute Follicular Conjunctivitis (2012 LQ) - Diseases & Management

Follicles = lymphoid germinal centers in conjunctival substantia propria, appear as round, avascular, slightly raised lesions with clear centers
Diseases causing Acute Follicular Conjunctivitis:
  1. Adenoviral keratoconjunctivitis (most common overall):
    • Epidemic Keratoconjunctivitis (EKC) - Adenovirus serotypes 8, 19, 37
    • Pharyngoconjunctival Fever (PCF) - Adenovirus 3, 4, 7
  2. Herpes simplex virus (HSV)
  3. Newcastle disease (Rare, from poultry workers)
  4. Molluscum contagiosum (umbilicated lid lesions → follicular reaction)
  5. Inclusion conjunctivitis (Chlamydia trachomatis serotypes D-K)
  6. Trachoma (early) - Chlamydia trachomatis serotypes A-C
  7. Toxic follicular conjunctivitis (prolonged topical drug use)
Management of Adenoviral Conjunctivitis (most common):
  • No specific antiviral approved (self-limiting in 2-3 weeks)
  • Cold compresses, lubricating drops for comfort
  • Topical antihistamines for itch
  • Topical broad-spectrum antibiotics (chloramphenicol/moxifloxacin) to prevent secondary bacterial infection
  • Topical steroids (short course for pseudomembranes, subepithelial infiltrates - with caution)
  • Strict hygiene to prevent spread (highly contagious)

Phlyctenular Conjunctivitis (2005 LQ)

Definition

A delayed-type (Type IV) hypersensitivity reaction to microbial antigens (most commonly TB protein - old tuberculin), presenting as a nodular inflammation at the limbus.

Etiology

  • Mycobacterium tuberculosis (most common historically) - reaction to tuberculoprotein (purified protein derivative - PPD)
  • Staphylococcal exotoxins (most common in developed countries)
  • Moraxella species
  • Candida
  • NOT an active infection - it is a hypersensitivity reaction in sensitized individuals

Clinical Features

  • Phlycten: Small (1-3mm), elevated, yellowish-white nodule at limbus (conjunctival phlycten) or cornea (corneal phlycten)
  • Surrounded by dilated vessels
  • Intense photophobia, pain, lacrimation (especially when cornea involved)
  • Conjunctival phlycten: Less severe symptoms, resolves without scarring
  • Corneal phlycten: Migrates across cornea (wandering phlycten), leaving a triangular scar (vascularized fascia)
  • Fascicular ulcer: A leash of blood vessels follows the migrating corneal phlycten

Management

  1. Treat underlying cause: Anti-TB therapy if TB is the etiology (INH, rifampicin, etc.)
  2. Topical steroids: Prednisolone acetate or fluorometholone QID (reduces hypersensitivity reaction)
  3. Cycloplegic: If corneal involvement
  4. Systemic tetracycline: For Staphylococcal phlyctenulosis
  5. Nutrition: Vitamin A supplementation (associated deficiency)
  6. Systemic NSAIDs as adjunct

Pterygium (2017 SN)

Definition: A triangular, wing-shaped fibrovascular growth of bulbar conjunctiva that encroaches onto the cornea, always from the interpalpebral area (typically nasal side).
Etiology: Chronic UV radiation exposure (outdoor workers), dusty/dry environment, low latitude; role of HPV debated.
Zones:
  • Cap (ahead of advancing edge on cornea)
  • Head (limbal portion)
  • Body (over sclera)
  • Apex (nasal/temporal toward canthus)
Clinical Features:
  • Asymptomatic in early stages
  • Redness, irritation, foreign body sensation
  • If approaches visual axis: Reduced vision, induced astigmatism
  • Stocker's line: Iron deposit at leading edge
Management:
  • Medical (early/small): Lubricants, UV protection (sunglasses), topical vasoconstrictors for redness
  • Surgical (approaching visual axis, rapidly growing, cosmetic):
    • Surgical excision + conjunctival autograft (superior conjunctiva - gold standard; prevents recurrence)
    • Beta-irradiation (post-op) / Mitomycin-C (MMC) topical (anti-mitotic to prevent recurrence)
    • Bare sclera technique (high recurrence - not preferred)

Pannus (2004 SN)

Definition: A fibrovascular membrane growing between the corneal epithelium and Bowman's membrane from the superior limbus, associated with conjunctival or corneal inflammation.
Types:
  • Trachomatous pannus: In trachoma (Chlamydial infection) - grows from superior limbus downward; a late sequelae of trachoma (Stage II-IV)
  • Degenerative pannus: Associated with bullous keratopathy, interstitial keratitis
  • Other: VKC, phlyctenulosis
In Trachoma: Pannus is the most important corneal complication - formed from inflamed limbal tissue and causes corneal opacification, vascularization, and visual impairment.
Management: Treat underlying cause; surgical (superficial keratectomy, keratoplasty for opacity).

Ophthalmia Nodosa (2010 SN)

Definition: A chronic granulomatous conjunctivitis/uveitis caused by caterpillar/moth hairs (setae or spicules) penetrating the conjunctiva or cornea.
Cause: Contact with caterpillar hairs (especially processionary caterpillar), tarantula hairs
Mechanism: Hairs penetrate and migrate through tissues, causing a foreign body granulomatous inflammatory reaction; hairs may migrate to cornea, AC, vitreous, or retina.
Clinical Features:
  • Chronic recurrent conjunctivitis
  • Nodular conjunctival granulomas (Zeis glands/conjunctiva)
  • Corneal opacification (if hair penetrates cornea)
  • Uveitis (if AC)
  • Retinitis (if vitreous/retina)
Management: Removal of hairs (with slit-lamp forceps if visible); topical steroids; surgical removal if deep.

PART 4: OPTICS & REFRACTION


Myopia (2012 LQ, 2009 LQ, 2005 LQ, 2003 LQ, 2001 SN)

Definition

A refractive error in which parallel rays of light from infinity are focused in front of the retina when accommodation is at rest. Near objects are seen clearly; distant objects are blurred ("near-sightedness").

Types / Classification (2012 LQ)

By degree:
  • Mild: Up to -3D
  • Moderate: -3D to -6D
  • High: -6D to -10D
  • Pathological/Degenerative: >-6D (some say >-10D)
By etiology:
  1. Axial myopia: Increased antero-posterior diameter of the eyeball (most common)
  2. Curvature myopia: Increased curvature of cornea or lens
  3. Index myopia: Increased refractive index of lens (nuclear sclerosis - "second sight" in elderly)
  4. Positional myopia: Anterior displacement of crystalline lens
  5. Accommodative excess: Spasm of accommodation

Pathological (Degenerative) Myopia (2012 LQ, 2009 LQ, 2003 LQ)

Definition: High myopia (>-6D or >-10D) associated with progressive axial elongation and degenerative changes at the posterior pole.
Etiology/Mechanism: Excessive axial elongation causes mechanical stretching of sclera, choroid, and retina, leading to degenerative changes.
Fundus Changes / Degenerative Features (2005 LQ):
  1. Tessellated (tigroid) fundus: Visible choroidal vessels through thin/atrophied RPE
  2. Myopic crescent (conus): White/yellowish crescent at temporal disc margin (stretched RPE/choroid)
  3. Foster-Fuchs spot (Fuchs' spot): Dark pigmented area at macula - subretinal neovascularization with RPE proliferation
  4. Posterior staphyloma: Outward bulging of posterior sclera (visible on fundoscopy / ultrasound)
  5. Lattice degeneration: Peripheral retinal thinning with "fence-post" pattern - risk of retinal breaks
  6. Retinal breaks and holes: Risk of retinal detachment
  7. Disc changes: Large, tilted disc, larger optic cup (peripapillary atrophy)
  8. Vitreous degeneration / liquefaction: Floaters, syneresis (premature)
  9. Peripheral retinal degeneration: Snail-track, white-with/without-pressure
  10. Chorioretinal atrophy: Lacquer cracks (ruptures in Bruch's membrane) → CNV (choroidal neovascularization)
Normal Fundus (for comparison - 2005 LQ):
  • Optic disc: Oval/round, pink, distinct margins; cup:disc ratio 0.3-0.4; vessels emerge centrally
  • Macula: Oval darker area temporal to disc; foveal reflex visible (bright center)
  • Vessels: Arteries: bright red, narrow (2/3 vein width); veins: dark red, wider; A:V ratio = 2:3

Symptoms of Myopia

  • Blurred distant vision (clear near vision)
  • Squinting to improve distance vision
  • Asthenopia (eye strain) at distance
  • Floaters (vitreous degeneration)
  • Night blindness (degenerative myopia)
  • Photopsia (flashing lights - retinal traction)

Management of Myopia

Optical correction:
  • Concave (diverging, minus) lenses (spectacles or contact lenses)
  • Full correction for high myopia; under-correction may worsen progression in children (controversial)
Myopia control (slowing progression in children):
  • Atropine 0.01% drops (most effective - reduces axial elongation)
  • Orthokeratology (Ortho-K): Rigid gas-permeable lenses worn overnight
  • Multifocal soft contact lenses: Peripheral defocus lenses
  • Outdoor activity (2+ hours/day protective)
Refractive surgery (permanent correction):
  • LASIK (Laser-assisted in-situ keratomileusis): Most popular; reshapes corneal stroma with excimer laser (suitable up to ~-12D)
  • PRK/LASEK: Surface ablation (no flap)
  • SMILE (Small-incision lenticule extraction): Latest - no flap
  • Phakic IOL (Implantable collamer lens - ICL): For high myopia/thin cornea
  • Clear lens extraction with IOL: For very high myopia in older patients
Complications of Pathological Myopia:
  • Retinal detachment (most serious)
  • Choroidal neovascularization (CNV) → anti-VEGF treatment
  • Macular holes
  • Posterior staphyloma
  • Complicated cataract
  • Glaucoma (higher risk)
  • Amblyopia (if anisometropia in childhood)

Hypermetropia (2011 LQ, 2004 LQ)

Definition

A refractive error in which parallel rays of light from infinity are focused behind the retina when accommodation is at rest ("far-sightedness").

Classification

By Degree:
  • Low: Up to +2D
  • Moderate: +2D to +5D
  • High: >+5D
By Manifest vs. Latent:
  • Latent hypermetropia: Corrected by continuous (tonic) accommodation - not detectable on routine refraction without cycloplegia; revealed only after cycloplegic refraction
  • Manifest hypermetropia: Not corrected by accommodation; detectable without cycloplegia
    • Facultative: Can be overcome by accommodation (younger patients)
    • Absolute: Cannot be overcome by accommodation (older patients)
By Etiology:
  • Axial (most common - short antero-posterior diameter)
  • Curvature (flat cornea or lens)
  • Index (decreased refractive index)
  • Positional (posterior lens subluxation)
  • Absence of lens (aphakia - extreme hypermetropia)

Clinical Features / Symptoms

  • Blurred near vision (far vision better, though may also blur in high +)
  • Asthenopia (eye strain, headache) after close work (excessive accommodation)
  • Convergent squint (esotropia) in children (excess accommodation drives excess convergence)
  • Amblyopia (in children - from uncorrected high hypermetropia)
Signs:
  • Small eye, crowded anterior segment
  • Shallow anterior chamber (risk of angle-closure glaucoma)
  • Flat cornea
  • Cycloplegic refraction reveals true (total) hypermetropia

Management

  • Convex (converging, plus) lenses (spectacles or contact lenses)
  • Refractive surgery: LASIK, PRK (limited correction range)
  • Clear lens extraction (CLE) with IOL: For high hypermetropia
Indications for glasses in children:
  • All cases of accommodative esotropia (full correction)
  • High hypermetropia (>+3D)
  • Anisometropia (to prevent amblyopia)

Presbyopia (2013 LQ, 2010 LQ)

Mechanism of Accommodation

Accommodation is the increase in refracting power of the eye to focus near objects, achieved by increasing the curvature of the crystalline lens.
Mechanism (Helmholtz theory):
  1. Ciliary muscle contracts (sphincter-like contraction)
  2. Zonular fibers relax (become slack)
  3. Elastic lens substance rounds up (becomes more convex, especially anterior surface)
  4. Lens refracting power increases (e.g., from 60D to 70D)
  5. Near objects come to focus on retina
Near reflex triad: Accommodation + Convergence + Pupillary constriction (miosis)

Pathophysiology of Presbyopia

  • With increasing age (usually starts becoming symptomatic ~40-45 years), the crystalline lens becomes harder (nuclear sclerosis) and less elastic
  • The ciliary muscle also weakens with age
  • Result: Loss of accommodation - reduced amplitude of accommodation
  • Amplitude of accommodation:
    • At 10 years: ~14D
    • At 40 years: ~6D
    • At 50 years: ~2D
    • At 60 years: ~1D (essentially nil clinically)
  • When amplitude falls to 4-5D or less → reading difficulty becomes apparent

Symptoms

  • Difficulty reading fine print (needs to hold book at arm's length - "short-armed reader")
  • Need for more light for near work
  • Onset usually 40-45 years
  • Worse in dim light (larger pupil reduces depth of focus)

Management of Presbyopia / Patient aged 45 with reading difficulty (2010 LQ)

Assessment:
  • History: Reading difficulty, near vision, occupation
  • Cycloplegic refraction (to determine full refractive error including latent hypermetropia)
  • Amplitude of accommodation test (near point measurement)
Optical Correction:
  1. Reading glasses (near addition): Plus lenses added to the distance correction; typical Add for 45 years = +1.00 to +1.50D; for 60 years = +2.50 to +3.00D
  2. Bifocal glasses: Distance correction above, near addition below (suitable for those needing both)
  3. Progressive/Varifocal lenses: Gradual progression from distance to near power (cosmetically preferred)
  4. Contact lenses: Monovision (one eye for distance, one for near) or multifocal contacts
Surgical options:
  • Monovision LASIK
  • Refractive lens exchange with multifocal/EDOF (extended depth of focus) IOL
  • Conductive keratoplasty (CK) - radiofrequency to shrink peripheral corneal stroma
  • Presbyopia-correcting intraocular lenses

Aphakia (2010 SN, 2017 LQ)

Definition

Absence of the crystalline lens from its normal position, resulting in extreme hypermetropia.

Causes

  • Post-surgical aphakia (post-cataract extraction without IOL) - most common
  • Trauma (dislocation out of eye, traumatic cataract extraction)
  • Congenital (rare)
  • Spontaneous dislocation (Marfan's, homocystinuria)

Optical Changes of Aphakia (2017 LQ)

  1. Extreme hypermetropia (+10D to +14D) - lens contributed ~15-20D of total refracting power
  2. Loss of accommodation - completely lost without lens
  3. Increased depth of field - due to larger aperture effects
  4. Increased visual field - Roving ring scotoma with aphakic glasses (see below)
  5. Image magnification - ~30% increase in image size with aphakic glasses (due to high plus lens away from nodal point)

Clinical Picture of Aphakia

  • Deep anterior chamber
  • Iridodonesis (trembling of iris - loss of lens support)
  • Dark pupillary reflex (no lens)
  • Absence of lens shadow on oblique illumination
  • Loss of Purkinje image III (normally formed by anterior lens surface)
  • High hypermetropia on refraction

Disadvantages of Aphakic Glasses (2017 LQ)

  1. Jack-in-the-box phenomenon (Roving ring scotoma): Objects appear and disappear as they move in and out of the peripheral field (due to prismatic effect of thick lens edges); creates a distorted visual field
  2. Magnification (~30%): Objects appear much larger - incompatible with binocular vision if other eye is phakic (aniseikonia)
  3. Pincushion distortion: Straight lines appear curved inward
  4. Chromatic aberration: Color fringing
  5. Restricted field of view: The thick lens + frame restricts peripheral vision
  6. Heavy/cosmetically unacceptable: Very thick, heavy lenses
  7. Monocular aphakia: Cannot wear aphakic glasses if other eye is normal (>25% aniseikonia - not tolerable)
  8. Spatial disorientation: Poor depth perception, difficulty with stairs/pouring liquids
Modern alternatives to aphakic glasses:
  • Intraocular lens (IOL) implantation (best - eliminates all optical disadvantages)
  • Contact lenses (less magnification ~7%, better than glasses but no accommodation)

Accommodation (2008 SN, 2010 LQ)

(Covered above under Presbyopia - see Mechanism of Accommodation)
Additional points:
  • Amplitude of accommodation = difference between far point (most distant point seen clearly) and near point (closest point seen clearly), expressed in Diopters = 1/far point(m) subtracted from 1/near point(m)
  • Range of accommodation = distance between far point and near point
  • Near point of accommodation: In emmetrope - ~10cm at age 10; recedes with age
  • Stimulus to accommodation: Blurred image on fovea, chromatic aberration, convergence, proximal cues

Astigmatism and Strum's Conoid (2011 SN)

Definition of Astigmatism: A refractive error in which the refracting power of the eye is not the same in all meridians, so parallel rays cannot be brought to a single focus.
Sturm's Conoid (Conoid of Sturm): In astigmatism (not corrected by a spherical lens), the refracted rays do not converge to a single point, but form two focal lines (the principal foci) at different distances, connected by a conoid-shaped beam called the Conoid of Sturm.
Components:
  1. Anterior focal line (focal line closest to the lens - corresponding to the steeper/more powerful meridian)
  2. Circle of least confusion (CLC) - midpoint between the two focal lines where the blur is most symmetrical/round; this is where vision is best with a spherical lens
  3. Posterior focal line - corresponding to the flatter/less powerful meridian
Sturm's interval = the distance between the two focal lines = degree of astigmatism
Clinical significance: CLC is the point to which spherical equivalent correction brings a patient. Cylindrical lenses are needed to collapse the conoid to a single point focus. Understanding Sturm's conoid is fundamental to understanding astigmatic correction.

Phakic vs. Aphakic Eye (2001 SN)

FeaturePhakic EyeAphakic Eye
LensPresentAbsent
Anterior chamber depthNormal (~3mm)Deep (increased)
IrisStable, supported by lensIridodonesis (trembling iris)
Refractive status (emmetrope)Emmetropic/normalExtreme hypermetropia (+10 to +14D)
AccommodationPresentAbsent
Purkinje image IIIPresent (anterior lens)Absent
Lens shadow on oblique illuminationPresentAbsent
Fundal reflexNormalAppears brighter/clear
PupilNormalDark, reflex unobstructed

HIGH-YIELD SUMMARY: Frequently Repeated Topics

TopicYears AskedType
Anterior Uveitis / Iridocyclitis2003, 2005, 2008, 2010, 2012LQ (5x)
Pathological Myopia2003, 2005, 2009, 2012LQ (4x)
Vernal Conjunctivitis / Spring Catarrh2001, 2007, 2011, 2017LQ/SN (4x)
Fungal Corneal Ulcer2006, 2007, 2014LQ (3x)
Keratic Precipitates2015, 2017SN (2x)
Keratoconus2005, 2013SN (2x)
Presbyopia/Accommodation2008, 2010, 2013LQ/SN (3x)
Aphakia2001, 2010, 2017SN/LQ (3x)

*Sources: Wills Eye Manual (9781975160753), Kanski's Clinical Ophthalmology 10th Ed (9780443110993), supplemented by standard ophthalmology principles.*Here is your complete ophthalmology exam answer guide covering all four topics. Here's a quick orientation:

What's Covered

Part 1 - Diseases of the Uveal Tract

  • Keratic Precipitates (2017, 2015 SN) - full classification, types, associations
  • Anterior Uveitis/Iridocyclitis (5 LQ years) - etiology, pathophysiology, clinical features, grading tables, investigations, complications, management
  • Iris Bombe (2012 SN) - mechanism, signs, treatment
  • Occlusio Pupillae (2007 SN)
  • Ciliary vs. Conjunctival Congestion comparison table (2001 SN)
  • Endophthalmitis management (2011 SN) - intravitreal antibiotics, vitrectomy indications (EVS trial)

Part 2 - Diseases of the Cornea

  • Hypopyon (2016 SN) and Hypopyon Corneal Ulcer (2009 LQ)
  • Bacterial Corneal Ulcer (2013 LQ) - full management including fortified antibiotic regimens
  • Fungal/Mycotic Corneal Ulcer (2014, 2007, 2006 LQ) - KOH mount diagnosis, natamycin/voriconazole treatment
  • Keratoconus (2013, 2005 SN) - all signs (Munson's, Vogt's striae, Fleischer ring), CXL
  • Herpes Zoster Ophthalmicus (2005 LQ) - complications by site, acyclovir dosing
  • Cornea layers, nerve supply, nutrition (2003 LQ)

Part 3 - Diseases of the Conjunctiva

  • Vernal Keratoconjunctivitis (4 appearances) - cobblestone papillae, Horner-Trantas dots, shield ulcer, mast cell stabilizers, cyclosporine
  • Ophthalmia Neonatorum (2016 LQ) - timing table, gonococcal vs. chlamydial management
  • Acute Follicular Conjunctivitis (2012 LQ) - causes + adenoviral management
  • Phlyctenular Conjunctivitis (2005 LQ) - TB hypersensitivity mechanism
  • Pterygium (2017 SN), Pannus (2004 SN), Ophthalmia Nodosa (2010 SN)

Part 4 - Optics & Refraction

  • Myopia - classification, pathological changes (Fuchs' spot, staphyloma, lattice), management including LASIK/ICL/atropine
  • Hypermetropia - latent vs. manifest classification, esotropia link
  • Presbyopia - Helmholtz mechanism, amplitude by age, near addition guide
  • Aphakia (2017 LQ) - optical disadvantages of aphakic glasses (jack-in-the-box, 30% magnification, aniseikonia)
  • Sturm's Conoid (2011 SN)
  • Phakic vs. Aphakic comparison table
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