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Ophthalmology Viva & Practical - Complete Exam Notes

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1. Bones Forming the Orbit (7 Bones)

• Maxilla (floor + medial wall)
• Zygomatic (lateral wall + floor)
• Ethmoid (medial wall - "paper plate"/lamina papyracea - thinnest part)
• Lacrimal (medial wall)
• Sphenoid (lateral wall, apex)
• Frontal (roof)
• Palatine (small contribution to floor)

The medial wall is thinnest (ethmoid/lamina papyracea) - most vulnerable to blowout fractures. Average orbital volume = 30 mL.

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2. Layers of the Cornea (5 Layers)

1. Epithelium - stratified squamous non-keratinized, 5-6 cell layers thick; regenerates rapidly (24-48 hrs). Innervated by ophthalmic branch of CN V1.
2. Bowman's layer - acellular condensed stroma; does NOT regenerate if damaged (scars form).
3. Stroma - thickest layer (~90% of corneal thickness); collagen lamellae (type I) arranged in highly regular orthogonal pattern - key to transparency.
4. Descemet's membrane - basement membrane of endothelium; regenerates if damaged.
5. Endothelium - single layer of cells that pump fluid out of stroma (maintains dehydration = transparency). Does NOT regenerate.

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3. Factors Affecting Corneal Transparency

1. Avascularity - no blood vessels in normal cornea
2. Regular collagen arrangement - stroma collagen fibrils of uniform diameter and spacing (destructive interference of scattered light)
3. Relative dehydration - maintained by endothelial pump; cornea is kept at ~78% water content (vs ~100% hydration = opaque)
4. Smooth surface - covered by tear film for uniform refracting surface
5. No myelination of nerve fibers within cornea

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4. Nutrition/Derivation of Cornea

• Aqueous humor (primary source - glucose, amino acids via diffusion from anterior chamber)
• Tear film (oxygen from atmosphere)
• Limbal capillaries (peripheral cornea only)

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5. Power of the Eye / Eyeball

• Cornea contributes ~70% of total refracting power
• Lens contributes ~30% (but can change with accommodation - the cornea cannot)
• The lens is a biconvex structure - anterior surface less curved (~10 mm radius), posterior surface more curved (~6 mm radius)

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6. Visual Pathway (Step by Step)

Photoreceptors (rods & cones) in retina
        ↓
Bipolar cells (1st order neuron)
        ↓
Ganglion cells (2nd order neuron) → axons form optic nerve (CN II)
        ↓
Optic chiasm (nasal fibers decussate; temporal fibers stay ipsilateral)
        ↓
Optic tract → lateral geniculate nucleus (LGN) of thalamus
        ↓
Optic radiations (3rd order neuron)
  - Upper fibers → superior lip of calcarine cortex
  - Lower fibers (Meyer's loop, temporal lobe) → inferior lip
        ↓
Primary visual cortex (V1), occipital lobe, area 17 (calcarine cortex)

In many exam contexts: 1st = photoreceptor/bipolar, 2nd = ganglion cell (optic nerve/tract), 3rd = LGN to cortex.

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7. Pupillary Reflex Pathway (Light Reflex)

Afferent limb:

Efferent limb:

• Light in one eye → both pupils constrict
• Direct response = ipsilateral constriction
• Consensual response = contralateral constriction

RAPD (Relative Afferent Pupillary Defect) / Marcus Gunn Pupil:

• Tested with swinging flashlight test
• In optic nerve lesion on one side: when light swings TO the affected eye, both pupils dilate (paradoxical dilation)
• Indicates defective afferent limb (asymmetric optic nerve disease)

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8. Layers of the Retina (10 Layers)

1. Retinal Pigment Epithelium (RPE)
2. Photoreceptor layer (outer segments of rods & cones)
3. External limiting membrane (tight junctions between Müller cells & photoreceptors)
4. Outer nuclear layer (cell bodies of photoreceptors)
5. Outer plexiform layer (synapses between photoreceptors & bipolar cells)
6. Inner nuclear layer (cell bodies of bipolar, horizontal, amacrine, Müller cells)
7. Inner plexiform layer (synapses between bipolar & ganglion cells)
8. Ganglion cell layer (cell bodies of ganglion cells)
9. Nerve fiber layer (axons of ganglion cells forming optic nerve)
10. Internal limiting membrane (inner boundary, Müller cell footplates)

Fovea: Central pit in macula, ~1.5 mm from optic disc; contains only cones; no blood vessels (foveal avascular zone); thinnest retina; highest visual acuity. Inner layers are displaced peripherally.

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9. Tear Film (3 Layers)

1. Lipid layer (outermost) - secreted by Meibomian glands (tarsal glands); prevents evaporation
2. Aqueous layer (middle, thickest ~98% of tear film) - secreted by lacrimal gland (main) and accessory lacrimal glands (Krause, Wolfring); contains antibodies (IgA), lysozyme, lactoferrin
3. Mucin layer (innermost) - secreted by goblet cells of conjunctiva; allows tear film to spread over hydrophobic corneal epithelium

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10. Lacrimal Gland and Sac - Location

• Located in the lacrimal fossa, in the superolateral angle of the orbit (frontal bone)
• Divided by levator aponeurosis into orbital (larger, upper) and palpebral (smaller, lower) lobes
• Nerve supply: Parasympathetic from CN VII (facial) → greater petrosal nerve → pterygopalatine ganglion → zygomatic nerve → lacrimal gland

• Lies in the lacrimal groove (between anterior and posterior lacrimal crests) of the medial orbital wall
• Extends slightly above medial canthal tendon (upper part is the fundus)

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11. Anterior Chamber

• Bounded anteriorly by cornea, posteriorly by iris and pupil (and lens in the pupil area)
• Filled with aqueous humor
• Angle (iridocorneal angle) contains trabecular meshwork → Canal of Schlemm → aqueous drainage
• Depth: ~3 mm centrally
• Aqueous humor is produced by ciliary body (ciliary processes) by active secretion + ultrafiltration; drains via trabecular meshwork (conventional, 90%) and uveoscleral route (unconventional, 10%)

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12. Visual Acuity Testing

Snellen Chart (standard):

• Tested at 6 metres (or 20 feet)
• Normal vision = 6/6 (20/20)
• Format: 6/X means patient reads at 6 m what a normal eye can read at X metres
• Each letter subtends 5 minutes of arc at designated distance

Procedure:

1. Test each eye separately (cover the other)
2. Use pinhole to differentiate refractive error from pathology (pinhole improves acuity if refractive)
3. Note best-corrected visual acuity

Near vision: Jaeger's chart or N-notation tested at 33 cm

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13. Confrontation Test

1. Examiner sits ~1 metre facing patient, at same level
2. Patient covers one eye; examiner covers opposite eye
3. Patient fixes on examiner's eye/nose
4. Examiner moves finger/target from periphery inward in all quadrants
5. Patient reports when they first see the target; compared to examiner's own field (assumed normal)

• Not quantitative / cannot map precise field defects
• Depends on examiner having normal visual fields (inherent flaw)
• Cannot detect subtle field losses (e.g., early glaucoma)
• Poor at detecting small central scotomas
• Inter-examiner variability
• Not sensitive for small defects

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14. Functions of Vitreous Humor

• Maintains shape of the posterior eyeball (fills vitreous chamber)
• Optical clarity - allows light transmission to retina (99% water, gel-like collagen/hyaluronic acid matrix)
• Metabolic support - slight nutritive function for lens and retina
• Shock absorption - protects retina and lens from trauma
• Holds retina in place against RPE
• Supports lens (anteriorly)

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15. Optic Nerve

• Formed by axons of retinal ganglion cells
• Has 4 parts: intraocular (optic disc, 1 mm), intraorbital (25-30 mm), intracanalicular (6-10 mm in optic canal), intracranial (10 mm to chiasm)
• Covered by dural, arachnoid, and pial sheaths (continuous with brain meninges) - hence raised ICP causes papilloedema
• Exits orbit via optic canal (in lesser wing of sphenoid)
• Blood supply: Posterior ciliary arteries + ophthalmic artery branches

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16. Cross-Section of Eyeball (Drawing Points)

1. Fibrous coat - Sclera (posterior 5/6) + Cornea (anterior 1/6)
2. Vascular coat (Uvea) - Choroid + Ciliary body + Iris
3. Neural coat - Retina

• Cornea, lens (biconvex), iris, pupil
• Anterior chamber (between cornea and iris/lens)
• Posterior chamber (between iris and lens)
• Vitreous chamber (posterior to lens)
• Ciliary body, suspensory ligaments (zonules) of lens
• Optic disc, optic nerve
• Fovea/macula
• Retina, choroid, sclera

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Quick Summary Table for Viva

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👁️ OPHTHALMOLOGY VIVA - Complete Q&A Guide

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SECTION 1: ANATOMY Q&A

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1. Epithelium (stratified squamous non-keratinized)
2. Bowman's layer
3. Stroma (~90% of thickness)
4. Descemet's membrane
5. Endothelium

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• Aqueous humor (main - glucose, amino acids)
• Tear film (oxygen from atmosphere)
• Limbal capillaries (peripheral cornea only)

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1. Avascularity
2. Regular collagen arrangement in stroma - uniform fibril diameter and spacing (destructive interference of scattered light)
3. Relative dehydration - endothelial pump keeps cornea at ~78% hydration
4. Smooth anterior surface - maintained by tear film
5. No myelinated nerve fibers within cornea

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• Horizontal diameter: ~12 mm
• Vertical diameter: ~11 mm
• Central thickness: ~0.5 mm
• Peripheral thickness: ~0.7 mm

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1. Retinal Pigment Epithelium (RPE)
2. Photoreceptor layer (rods & cones - outer segments)
3. External Limiting Membrane (ELM)
4. Outer Nuclear Layer (ONL) - photoreceptor nuclei
5. Outer Plexiform Layer (OPL) - photoreceptor-bipolar synapses
6. Inner Nuclear Layer (INL) - bipolar, horizontal, amacrine, Müller cells
7. Inner Plexiform Layer (IPL) - bipolar-ganglion synapses
8. Ganglion Cell Layer (GCL)
9. Nerve Fiber Layer (NFL)
10. Internal Limiting Membrane (ILM)

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• Contains only cones (no rods)
• Highest visual acuity
• Avascular (foveal avascular zone - FAZ)
• Thinnest part of retina (inner layers displaced peripherally - Henle's layer)
• No blood vessels, so relies on choroidal circulation for nutrition

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• Macula lutea: Area ~5.5 mm diameter temporal to optic disc; contains yellow pigment (xanthophyll); contains the fovea; has 2+ layers of ganglion cells
• Fovea: Central pit within the macula; ~0.35 mm depression (foveola); only cones; highest acuity

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• ~1.5 mm in diameter
• Has no photoreceptors (hence physiological blind spot)
• Cup-to-disc ratio normally ≤0.5
• Raised disc = papilloedema (raised ICP); Pale disc = optic atrophy; Increased cup = glaucoma

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• Fibrous coat: Sclera (posterior 5/6, white, opaque) + Cornea (anterior 1/6, transparent)
• Vascular coat (Uvea): Choroid (posterior) + Ciliary body + Iris (anterior)
• Neural coat: Retina

• Anterior chamber: Between cornea and iris; filled with aqueous humor
• Posterior chamber: Between iris and lens; filled with aqueous humor
• Vitreous chamber: Behind lens; filled with vitreous humor

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1. Maintains shape of posterior segment of eyeball
2. Optical clarity for light transmission to retina
3. Metabolic support for lens and retina
4. Shock absorption (protective cushion)
5. Helps keep retina in apposition with RPE
6. Supports the lens anteriorly

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• Location: Superolateral angle of orbit in lacrimal fossa (frontal bone)
• Divided by levator aponeurosis into orbital (larger) and palpebral (smaller) lobes
• Nerve supply:
  • Sensory: CN V1 (lacrimal nerve)
  • Sympathetic: from superior cervical ganglion
  • Parasympathetic (secretomotor): CN VII → greater petrosal nerve → pterygopalatine ganglion → zygomatic nerve (CN V2) → lacrimal nerve → lacrimal gland

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• Lacrimal sac: lies between anterior and posterior lacrimal crests
• Nasolacrimal duct opens at inferior meatus (valve of Hasner)

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• Boundaries: Anteriorly - posterior surface of cornea; Posteriorly - anterior surface of iris and pupil/lens
• Contents: Aqueous humor
• Depth: ~3 mm centrally
• Angle (iridocorneal angle): Contains trabecular meshwork → Canal of Schlemm → aqueous drainage
• Aqueous humor production: Ciliary processes (active secretion + diffusion + ultrafiltration), ~2 µL/min
• Drainage: 90% via trabecular meshwork/Canal of Schlemm; 10% uveoscleral route

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SECTION 2: PHYSIOLOGY Q&A

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• Total power = ~60 Dioptres

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• 1st order: Photoreceptor → Bipolar cell
• 2nd order: Bipolar cell → Ganglion cell (axons form optic nerve)
• 3rd order: LGN → Visual cortex (via optic radiations)

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• Before chiasm (optic nerve): Monocular blindness (ipsilateral eye)
• At chiasm (central): Bitemporal hemianopia (pituitary tumor - most common cause)
• Optic tract: Contralateral homonymous hemianopia
• Optic radiation (temporal): Contralateral superior quadrantanopia (Meyer's loop)
• Occipital cortex: Contralateral homonymous hemianopia with macular sparing

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• Light in one eye → both pupils constrict
• Direct reflex = same eye constricts
• Consensual reflex = other eye constricts

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• Tested with swinging flashlight test
• Indicates unilateral/asymmetric optic nerve or severe retinal disease
• When light swings TO the affected eye, both pupils paradoxically dilate (because the afferent signal is weaker on that side)
• Efferent pathway is intact (both eyes still respond to light in the normal eye)

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1. Accommodation - ciliary muscle contracts → zonules relax → lens becomes more convex → increased power
2. Convergence - both eyes converge (medial recti contract)
3. Pupillary constriction - miosis

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• Small, irregular, bilateral pupils
• Light reflex absent; near reflex intact
• Classic cause: Neurosyphilis
• Lesion: Pretectal area (destroys light reflex fibers but spares near reflex fibers)

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SECTION 3: INSTRUMENTS

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• A hand-held instrument to examine the fundus (optic disc, retina, vessels, macula)
• Light illuminates the fundus; reflected light returns through the pupil to the examiner's eye
• Magnification: ~15x (erect, virtual image)
• Field of view: Small (~5°)
• Examines: optic disc, retinal vessels, macula, vitreous, red reflex
• Used in undilated or dilated pupil (better view when dilated)

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• Examination of anterior segment: cornea, anterior chamber (cells/flare), iris, lens
• With special lenses (+78D, +90D): posterior segment/fundus
• Uses: diagnose corneal disease, cataracts, anterior uveitis, foreign bodies, glaucoma angle (with goniolens)

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1. Goldmann applanation tonometer - gold standard; measures force needed to flatten 3.14 mm² of cornea; requires slit lamp
2. Schiotz tonometer - indentation tonometer; portable; measures depth of indentation
3. Tono-Pen - electronic, portable applanation tonometer
4. Non-contact tonometer (NCT/air-puff) - uses puff of air; no contact; screening tool

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1. Goldmann perimeter - kinetic perimetry; manual; bowl-shaped; maps entire field using moving targets of varying size/intensity
2. Humphrey automated perimeter - static perimetry; computer-controlled; most widely used; produces detailed field printout
3. Confrontation test - bedside clinical test (not an instrument per se)

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• Contact lens fitting
• Pre-operative assessment for cataract/refractive surgery
• Diagnosing keratoconus (irregular astigmatism)

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• Classify glaucoma (open vs. closed angle)
• Assess angle anatomy
• Laser treatment planning

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• A-scan (axial length): One-dimensional; measures axial length of the eyeball (used for IOL power calculation before cataract surgery; normal axial length = ~23-24 mm)
• B-scan (brightness scan): Two-dimensional cross-sectional image; used when fundus cannot be visualized (dense cataract, vitreous hemorrhage); can detect retinal detachment, vitreous opacities, tumors

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• Documentation of optic disc, retina, macula
• Monitoring diabetic retinopathy, glaucoma, macular degeneration
• Fluorescein angiography (with fluorescein dye to study retinal vasculature)

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• Axial length (more accurate than A-scan ultrasound)
• Corneal curvature
• Anterior chamber depth Used to calculate intraocular lens (IOL) power before cataract surgery.

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SECTION 4: DEMONSTRATIONS

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• Sit facing the patient at ~1 metre, at the same level
• Both at eye level

1. Ask patient to cover their LEFT eye; you cover your own RIGHT eye (mirror image)
2. Both fix on each other's uncovered eye (patient fixates on YOUR uncovered eye)
3. Bring a finger/white-headed pin from outside (periphery) toward the center in all 4 quadrants (superior, inferior, temporal, nasal) and diagonally
4. Ask patient to say when they first see the target; compare with when YOU see it (your field = reference normal)
5. Repeat for the other eye

• Not quantitative - cannot precisely map or document field defects
• Depends on examiner having normal visual fields (inherent assumption error)
• Cannot detect subtle/early field losses (e.g., early glaucoma)
• Poor sensitivity for small central scotomas
• Relies on patient cooperation and understanding
• Inter-examiner variability
• Only rough estimate of peripheral field

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1. Position patient 6 metres from chart (well-illuminated)
2. Test one eye at a time - cover the OTHER eye with an occluder (ask patient not to press on the eye)
3. Ask patient to read the smallest line they can see clearly, from top to bottom
4. Record as 6/X (6 = testing distance; X = smallest line read)
5. If patient cannot read the top letter (6/60): test at closer distances (record as CF, HM, PL, NPL)
6. Pinhole test: Place pinhole in front of eye - if acuity improves, refractive error is the cause; if no improvement, organic pathology is likely
7. Repeat for second eye

• CF (Counting Fingers) - count fingers at specified distance
• HM (Hand Movements) - can perceive hand movements
• PL (Perception of Light) - can detect light only
• NPL (No Perception of Light) - no light perception = total blindness

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1. Dim the room
2. Ask patient to fix gaze on a distant object (prevents accommodation reflex)
3. Shine pen torch from the side into one eye
4. Observe SAME eye for pupillary constriction (direct reflex)

1. Shine torch into one eye
2. Observe the OTHER eye - it should also constrict (consensual reflex)

1. Swing light alternately from one eye to the other (2-3 seconds per eye)
2. Normal: both pupils constrict as light enters each eye
3. RAPD: affected eye shows paradoxical dilation when light swings to it

1. Ask patient to look at a distant object (pupils dilate)
2. Then look at a near object (finger ~33 cm)
3. Observe: convergence, accommodation, and miosis (pupillary constriction)

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1. Ask patient to look up (and slightly lateral)
2. Press firmly with index finger over the lacrimal sac area (just below the medial canthal tendon, medial to inner canthus)
3. Observe the punctum (lower and/or upper)
4. Positive test: Mucopurulent or mucoid material regurgitates from the punctum = nasolacrimal duct obstruction/dacryocystitis

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1. Ask patient to fixate on a distant target
2. Cover one eye with an occluder
3. Observe the uncovered eye for any movement to take up fixation
4. If uncovered eye moves → it had a manifest squint (tropia)
5. Uncover the eye; observe for any refixation movement
6. Repeat for other eye

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• "What is the afferent pathway?" - Retina → CN II → pretectal nucleus
• "What is the efferent pathway?" - EW nucleus → CN III → ciliary ganglion → short ciliary nerves → sphincter pupillae
• "Why does the other eye also constrict?" - Because each pretectal nucleus projects bilaterally to both EW nuclei
• "Where is the lesion if direct reflex is lost but consensual is preserved?" - Efferent limb (CN III or ciliary ganglion)
• "Where is the lesion if both direct and consensual are lost in one eye?" - Afferent limb (optic nerve of that eye) = RAPD/Marcus Gunn
• "What is Horner's syndrome?" - Ptosis, miosis, anhidrosis due to sympathetic chain lesion
• "What dilates the pupil?" - Dilator pupillae (radial) - sympathetic (CN T1 sympathetic chain → superior cervical ganglion → long ciliary nerve)
• "What constricts the pupil?" - Sphincter pupillae (circular) - parasympathetic (CN III)

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QUICK REVISION CHEAT SHEET

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👁️ OPHTHALMOLOGY VIVA - Additional Topics

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1. MENACE REFLEX (Threatening Reflex / Visual Threat Response)

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Threatening object approaching (visual stimulus)
        ↓
Retina → Optic nerve (CN II) → Optic chiasm → Optic tract
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Visual cortex (occipital lobe, area 17/18) → Association areas
        ↓
Corticobulbar fibers → Facial nerve nucleus (CN VII, pons)
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CN VII (orbicularis oculi) → Eye blink / lid closure

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• Absent menace reflex with intact corneal reflex → cortical visual impairment or severe visual loss (retinal/optic nerve pathology)
• Used in infants to grossly assess presence of vision before they can respond to Snellen charts
• Absent in: cortical blindness, severe amblyopia, malingering (but malingerers sometimes blink anyway)
• Can be abolished by unilateral occipital lobe lesion (for the contralateral visual field)
• Important: Do NOT touch the lashes or create air current when testing - this would test the corneal reflex, not the menace reflex

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1. Cover one eye
2. Make a sudden threatening hand gesture toward the uncovered eye without creating an air draught and without touching the eyelashes
3. Move hand rapidly toward the eye from 50 cm to ~5 cm
4. Normal: patient blinks/closes eye
5. Note: bring the hand from the lateral/peripheral side first so you're not just triggering an accommodation response
6. Repeat for other eye

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2. HFA - HUMPHREY FIELD ANALYZER

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• Patient sits with head on chin rest in front of a hemispherical white bowl
• One eye is occluded; near refractive error corrected with a trial lens
• Patient fixates on a central target
• The instrument projects brief light stimuli (static, non-moving) at defined locations within the visual field
• Patient presses a handheld button when they see the stimulus
• Computer uses the SITA (Swedish Interactive Thresholding Algorithm) to determine the threshold light intensity at each location
• Results compared with age-matched controls → generates:
  • Total deviation map (comparison with normals)
  • Pattern deviation map (focal losses)
  • Mean Deviation (MD) and Pattern Standard Deviation (PSD) indices

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• 24-2 program: Tests 54 points within 24° of fixation (most common for glaucoma)
• 30-2 program: Tests 76 points within 30°
• 10-2 program: Macular/central 10° (for advanced glaucoma or macular disease)

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• Cannot effectively assess far peripheral vision
• Patient needs to understand and cooperate (poor in cognitive impairment, inattention, slow response)
• Limited in patients with severe central visual loss
• Can show false positives/negatives if patient is fatigued or anxious
• Learning effect (first test often less reliable)

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• Fixation losses: >20% = unreliable (patient not fixing on central target)
• False positive rate: >15% = trigger-happy patient
• False negative rate: >33% = inattentive patient or advanced disease

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3. OCULAR MOVEMENTS

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• Primary position (straight ahead)
• Right gaze, Left gaze
• Up-right, Up-left
• Down-right, Down-left
• Up (elevation), Down (depression)

1. Right (Right LR + Left MR)
2. Left (Left LR + Right MR)
3. Up-right (Right SR + Left IO)
4. Down-right (Right IR + Left SO)
5. Up-left (Left SR + Right IO)
6. Down-left (Left IR + Right SO)

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1. Saccades - fast, voluntary, conjugate movements to a new target (frontal eye fields)
2. Smooth pursuit - slow, involuntary tracking of a moving target (parieto-occipital cortex)
3. Vergence - disconjugate movements (convergence/divergence) for near/far objects
4. Vestibulo-ocular reflex (VOR) - stabilizes gaze during head movement (semicircular canals)
5. Optokinetic nystagmus - rhythmic response to moving field of images
6. Fixation - maintaining gaze on a stationary target

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1. Hold a pen/finger torch as the target
2. Ask patient to follow the target with both eyes, keeping head still
3. Move target to the 6 cardinal positions in an "H" or star pattern
4. Look for:
   • Limitation of movement (palsy)
   • Nystagmus
   • Diplopia (ask patient if they see double in any position)
   • Abnormal head posture
5. Test ductions (monocular) and versions (binocular) separately if needed

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• Loss of: adduction, elevation, depression (by superior and inferior rectus), elevation (inferior oblique)
• Lateral rectus and superior oblique intact → eye deviated down and out
• Ptosis (levator palpebrae superioris = CN III)
• Pupil dilation (loss of parasympathetic via CN III)

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• Weakness of superior oblique → cannot depress eye in adduction
• Patient complains of vertical diplopia, worse on looking down and inward (e.g., reading, going down stairs)
• Head tilt to opposite side (compensatory)
• Most common cause of isolated vertical diplopia

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• Weakness of lateral rectus → failure of abduction
• Eye deviated medially (esotropia)
• Diplopia on lateral gaze to the side of palsy
• Head turned toward side of palsy (compensatory)

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4. ROPLAS TEST (Syringing of Nasolacrimal Duct)

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1. Instill topical anaesthetic drops (proparacaine/tetracaine) in the eye
2. Dilate the lower punctum with a punctum dilator
3. Insert lacrimal cannula into the lower punctum, advance horizontally along the canaliculus, then turn vertically downward into the lacrimal sac
4. Gently inject normal saline

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5. DEMONSTRATION: IRRIGATION vs. INSTILLATION

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A. INSTILLATION OF EYE DROPS

1. Wash hands thoroughly
2. Ask patient to sit or lie back, tilt head back
3. Ask patient to look UP
4. Gently pull down the lower eyelid with your index finger to form a conjunctival fornix/pouch
5. Hold the dropper bottle 1-2 cm above the eye (do NOT touch the eye or lashes - risk of contamination)
6. Instil 1 drop into the lower conjunctival fornix (not directly onto cornea)
7. Ask patient to gently close the eye (do NOT blink vigorously - squeezing pushes drug out)
8. Apply gentle pressure at the medial canthus (nasolacrimal pressure/punctal occlusion) for 1-2 minutes to reduce systemic absorption
9. Wipe excess with tissue

• Only 1 drop needed - conjunctival sac holds max 7 µL; a drop = 30-40 µL; excess drains away
• If 2 drops of different medications needed: wait at least 5 minutes between drops
• Suspensions should be shaken before use
• Ointments applied last (after drops) as they blur vision

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B. IRRIGATION OF THE EYE

• Chemical burns (acids/alkalis) - most urgent; must be done immediately
• Foreign bodies
• Before surgical procedures
• Copious discharge

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1. Instil topical anaesthetic drops (proparacaine) - reduces blepharospasm
2. Position patient with head tilted slightly toward the affected side
3. Place a kidney dish against the cheek to collect fluid
4. Evert both lids to expose fornices
5. Irrigate with a continuous, gentle stream of normal saline directed at the inner canthus across the cornea toward the outer canthus
6. Ensure fornices are irrigated (use a cotton swab to sweep fornices for particulate matter)
7. Check pH with litmus paper before and after irrigation (target pH 7.0-7.4 for chemical burns)
8. Continue irrigation for at least 30 minutes for chemical burns (especially alkali - penetrate deeper)
9. After irrigation, check under both lids for retained particles

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6. HIRSCHBERG REFLEX (Hirschberg Corneal Light Reflex Test)

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1. Shine a pen torch or light source at the patient's eyes from ~33 cm at midline
2. Ask patient to look at the light
3. Observe the position of the corneal light reflex (Purkinje image) in each eye
4. Normally: the reflection is seen at the centre of the pupil or just slightly nasal (due to positive angle kappa)

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• Reflex displaced NASALLY (medially) → eye is deviated outward (exotropia)
• Reflex displaced TEMPORALLY (laterally) → eye is deviated inward (esotropia)

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• Only a rough estimate of deviation; not precise
• Cannot detect small angles of squint
• Affected by angle kappa (angle between visual axis and pupillary axis)
• Does not differentiate between manifest and latent squint
• Formal prism cover test needed for accurate measurement

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QUICK SUMMARY TABLE

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👁️ OPHTHALMOLOGY VIVA - Lens Proteins, Optic Nerve Parts, Pigments of Retina

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1. LENS PROTEINS

A. Crystallins (~90% of total lens protein)

B. Albuminoid / Water-Insoluble Proteins (~10%)

• Formed when crystallins denature and aggregate over time
• Increases with age - this progressive aggregation + oxidation is the basis of age-related cataract
• Also includes cytoskeletal proteins: connexins (gap junctions - important for lens nutrition), vimentin, actin, filensin

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• Aqueous humor (anterior surface) - glucose, amino acids
• Vitreous humor (posterior surface)
• Internal circulation via gap junctions (connexins) between lens fibers - solutes move from the periphery (cortex) to the nucleus by this "microcirculation"

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POSTERIOR ──── Posterior capsule
                 Posterior subcapsular cortex
    NUCLEUS ──── Adult nucleus (hardest)
                 Fetal nucleus
                 Embryonic nucleus  (Y-sutures)
                 Infantile nucleus
                 Cortex
                 Anterior subcapsular epithelium (only on anterior surface)
ANTERIOR ──── Anterior capsule (thickest part of capsule)

• Lens capsule: Thickest basement membrane in the body; type IV collagen + laminin; thickest anteriorly near the pre-equatorial zone
• Lens epithelium: Single layer of cuboidal cells; present only on the anterior surface; mitotically active cells at the equator (germinative zone) → differentiate into lens fibers
• Lens fibers: Primary (form embryonic nucleus) and secondary (form all subsequent layers); packed hexagonally; lose nuclei and organelles when mature → transparency
• Lens sutures: Y-shaped sutures at anterior (erect Y) and posterior (inverted Y) poles where lens fibers interdigitate

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1. UV radiation, oxidative stress, aging, diabetes → oxidation of crystallins
2. α-crystallin chaperone system is overwhelmed
3. Crystallins denature and aggregate into high-molecular-weight complexes
4. These aggregates scatter light → opacity (cataract)
5. In diabetic cataract: excess glucose → sorbitol (aldose reductase pathway) → osmotic swelling of lens fibers → "snowflake/Christmas tree" cataract
6. In nuclear sclerosis: hardening and yellowing of nucleus with aging due to crystallin cross-linking

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• All lens fiber cells present from birth are retained throughout life (no cell turnover - lens fibers lose nucleus and organelles)
• Highest protein concentration of any tissue (~35%)
• Avascular throughout life
• Only the anterior epithelium can divide
• Proteins synthesized in utero remain in the nucleus forever → highly susceptible to oxidative damage over decades

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2. PARTS OF THE OPTIC NERVE

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1. Intraocular Segment (Optic Disc)

• Length: ~1 mm
• From ganglion cell axons converging at the optic disc to the posterior sclera (lamina cribrosa)
• Optic disc diameter: ~1.5 mm
• Lamina cribrosa: Sieve-like portion of sclera through which axons pass; point of vulnerability in glaucoma (raised IOP deforms lamina → damages axons)
• No myelin within the eye (myelination begins just behind the lamina cribrosa - hence optic disc appears pale/white)
• No photoreceptors at optic disc → physiological blind spot

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2. Intraorbital Segment

• Length: ~25-30 mm
• Runs from the posterior sclera to the optic canal
• Slightly longer than the orbital depth (~20 mm) - this slack allows free eye movement without tension on the nerve
• Surrounded by: Meningeal sheaths (dura, arachnoid, pia) continuous with brain - hence subarachnoid space surrounds it
• Blood supply: Central retinal artery enters the nerve ~10-15 mm posterior to the globe (intrinsic supply); also pial vessels from ophthalmic artery
• Axons become myelinated here (Schwann cells → oligodendrocytes)

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3. Intracanalicular Segment

• Length: ~6-10 mm
• Passes through the optic canal in the lesser wing of the sphenoid bone
• The ophthalmic artery (branch of internal carotid) enters the canal here and travels inferolateral to the nerve
• This is the most vulnerable segment to injury in head trauma (canal is rigid, no room for swelling)
• Optic canal dimensions: ~5 mm long, ~5-6 mm diameter

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4. Intracranial Segment

• Length: ~10 mm
• From the optic canal to the optic chiasm
• Lies above the cavernous sinus, internal carotid artery, and pituitary gland
• At the chiasm: nasal (medial) fibers decussate; temporal (lateral) fibers stay ipsilateral

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• Subarachnoid space surrounds the intraorbital optic nerve → raised intracranial pressure (ICP) is transmitted to the nerve sheath → compresses the central retinal vein → venous stasis → papilloedema
• Optic nerve sheath meningioma can grow along the nerve
• CSF can accumulate around the nerve in idiopathic intracranial hypertension

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3. PIGMENTS IN THE RETINA

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1. Melanin (in Retinal Pigment Epithelium - RPE)

• Location: Retinal Pigment Epithelium (outermost layer of retina, resting on Bruch's membrane/choroid)
• Type: Elongated melanin granules (distinct from melanin elsewhere in the body - uniquely elongated shape in RPE)
• Structure: RPE = single layer of cuboidal cells ~14 µm wide, 10-14 µm tall; tallest in the fovea
• Melanin granules aggregate toward the apical surface (toward rods and cones)

1. Absorbs scattered light passing through the neural retina → prevents reflection and glare
2. Thermal regulation - absorbs light energy and dissipates as heat
3. Contributes to the dark adaptation mechanism
4. Also present in the choroidal stroma (separate from RPE melanin)

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2. Rhodopsin (in Rods) - Visual Purple

• Location: Membranous discs in the outer segments of rod cells
• Structure: 39 kDa protein = Opsin (scotopsin) + Chromophore (11-cis-retinal, a vitamin A derivative)
• Rhodopsin is embedded in the lipid bilayer of disc membranes on the cytoplasmic (outer) surface

11-cis-retinal + scotopsin → Rhodopsin (dark)
         ↓  LIGHT
Rhodopsin → all-trans-retinal + opsin (bleaching)
         ↓  
Nerve impulse generated (via transducin/cGMP cascade)
         ↓
all-trans-retinal → converted back to 11-cis-retinal in RPE cells
(RPE65 enzyme essential for this conversion)
         ↓
11-cis-retinal returns to rods → rhodopsin resynthesis

• Deficiency of Vitamin A → insufficient retinal → night blindness (nyctalopia)
• Rods shed old discs from the tip → phagocytosed by RPE cells daily
• New discs formed continuously at the base of the outer segment

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3. Iodopsin (in Cones) - Cone Pigment

• Location: Membranous discs in the outer segments of cone cells
• Structure: Opsin (photopsin, of 3 types) + 11-cis-retinal (same chromophore as rhodopsin)
• The 3 types of cone opsins (photopsins) determine color sensitivity:

• Color blindness: Deficiency/abnormality of one or more cone opsins (usually red-green, X-linked recessive)
• Unlike rods, cone discs retain continuity with the plasma membrane (not shed as freely)

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4. Lipofuscin (in RPE cells)

• Location: Basal cytoplasm of RPE cells
• Origin: Accumulates from incompletely digested photoreceptor disc material (residual bodies/phagosomes)
• Fluorescent under UV light - used in fundus autofluorescence (FAF) imaging
• Increases with age
• Clinical: Excessive lipofuscin accumulation in RPE → RPE cell death → Age-related macular degeneration (AMD) and Best's disease (vitelliform macular dystrophy)

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BONUS: Macular Pigment (Xanthophyll)

• Location: Inner and outer plexiform layers of the macula/fovea (Henle's fiber layer)
• Composition: Lutein and Zeaxanthin (yellow carotenoid pigments)
• This is what gives the macula lutea its yellow colour ("lutea" = yellow)
• Functions:
  1. Filters short-wavelength (blue) light before it reaches the photoreceptors → reduces phototoxicity
  2. Acts as an antioxidant
  3. Improves contrast sensitivity
• Obtained from diet (green leafy vegetables, eggs)
• Clinical: Low macular pigment = increased risk of AMD

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SUMMARY TABLE

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QUICK VIVA EXTRAS

Visual Acuity - Definition

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The Formal Definition

• Normal eye can resolve two points separated by a minimum angle of 1 minute of arc
• Each letter on the Snellen chart subtends 5 minutes of arc at the designated distance
• Each limb/stroke of the letter subtends 1 minute of arc (the critical detail)

• Normal VA = 1/1 = 1.0 (or expressed as 6/6 or 20/20)

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Types of Visual Acuity

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Expression of Visual Acuity

• Snellen notation: 6/6 (metric) or 20/20 (feet)
  • Numerator = testing distance
  • Denominator = distance at which a normal eye reads the same letter
• Decimal notation: 6/6 = 1.0, 6/12 = 0.5, 6/60 = 0.1
• LogMAR notation: Used in research; 6/6 = LogMAR 0.0; better acuity = negative values

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Normal Visual Acuity

• Distance VA: 6/6 (tested at 6 metres on Snellen chart)
• Near VA: N6 or Jaeger 1 (tested at 33 cm)
• The fovea (with its dense cone packing) provides the highest visual acuity in the entire retina

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Key Anatomical Basis

1. Highest density of cones (no rods)
2. Each cone connects to its own bipolar and ganglion cell (1:1:1 ratio - no convergence)
3. Foveal avascular zone - no blood vessels overlying the photoreceptors
4. Inner retinal layers are displaced peripherally (nothing obstructs light reaching cones)

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Clinical Case: Acute Angle-Closure Glaucoma (AACG)

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A. MOST PROBABLE DIAGNOSIS

Clue-by-Clue Analysis:

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B. CLINICAL FEATURES

Symptoms

• Colored halos around lights (due to diffraction of light by edematous cornea)
• Transient blurring/obscuration of vision
• Mild headache and eye ache

• Severe, agonising ocular pain (may radiate to head, temple, brow)
• Gross sudden diminution of vision - "almost blind in that eye"
• Redness of the eye
• Nausea and vomiting (due to severe pain and vagal stimulation - can mislead diagnosis toward a GI or neurological cause)
• Coloured halos around lights (rainbow rings)
• Headache

Signs (Examination findings)

• Circumcorneal (ciliary) congestion - brick-red injection around the limbus
• Lids may be edematous

• Hazy/steamy cornea - epithelial edema due to raised IOP
• Loss of corneal luster

• Very shallow (both eyes - anatomical predisposition)
• Flare and cells possible

• Mid-dilated, fixed, oval pupil (sphincter ischaemia from elevated IOP)
• Pupil non-reactive to light
• Iris bombe - forward bowing due to aqueous pressure behind iris

• Glaukomflecken (small, white anterior subcapsular opacities) - pathognomonic of previous acute attack; represent focal lens ischaemia

• Markedly elevated - typically >40 mmHg, may reach 60-80 mmHg
• Normal IOP = 10-21 mmHg

• Optic disc hyperaemia or pallor in prolonged attacks
• Cupping in long-standing disease

• Shallow anterior chamber (as in this case) - anatomically predisposed

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C. PREDISPOSING FACTORS

Anatomical Factors (most important)

1. Hypermetropia (far-sightedness) - most significant predisposing factor
   • Hypermetropic eye is anatomically smaller (shorter axial length)
   • Has a smaller corneal diameter, shallower anterior chamber, and forward-placed lens
   • The patient wearing glasses for both distance AND near confirms this
2. Shallow anterior chamber - depth <2.5 mm (normal ~3 mm)
3. Narrow iridocorneal angle - angle <20°
4. Thick or anteriorly positioned lens - enlarges with age, pushing iris forward
5. Small corneal diameter (microcornea)
6. Short axial length of the eyeball

Age-related Factors

1. Increasing age (>40 years) - lens grows throughout life (~0.02 mm/year); displaces iris anteriorly, progressively shallowing the angle

Sex

1. Female sex - women have shorter axial lengths and shallower anterior chambers (3:1 female predominance in AACG)

Racial Factors

1. East Asian/Inuit populations - higher prevalence due to anatomical predisposition

Precipitating Factors (trigger the acute attack)

1. Emotional stress/excitement - sympathetic stimulation → mydriasis → angle crowding (as in this case)
2. Dim illumination - pupil dilates in dark room → crowding of angle
3. Mydriatic drugs - anticholinergics (atropine, tropicamide), adrenergics (phenylephrine), antihistamines
4. Systemic drugs - topiramate, sulfonamides, tricyclic antidepressants, SSRIs
5. Prolonged reading/close work - miosis (accommodative) → relative pupillary block worsens
6. Supine posture - lens falls forward

Other

1. Family history - first-degree relatives have ~6x increased risk
2. Fellow eye with shallow AC (bilateral anatomy) - as in this case

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D. MANAGEMENT

AACG is an ophthalmic emergency. Aim: rapidly lower IOP, break the attack, then treat definitively to prevent recurrence.

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STEP 1: Immediate Medical Management (Lower IOP)

A. Reduce Aqueous Production

• Timolol 0.5% eye drops - 1 drop to affected eye immediately
• Reduces aqueous secretion by ciliary body

• Apraclonidine 1% or Brimonidine 0.2% - 1 drop
• Reduces aqueous production + increases uveoscleral outflow

• Acetazolamide (Diamox) 500 mg IV immediately (or 250 mg orally if IV not available), then 250 mg 4 times daily orally
• Reduces aqueous production by ~50%
• Contraindicated in sulfa allergy, renal stones, sickle cell disease

B. Osmotic Agents (Vitreous Dehydration - Emergency)

• Mannitol 20% 1-2 g/kg IV over 1 hour (most rapid, most effective)
• OR Glycerol 50% 1 g/kg oral (avoid in diabetics)
• Contraindicated in cardiac failure, renal failure

C. Constrict the Pupil (Pull Iris Away from Angle)

• Constricts sphincter pupillae → pulls iris away from angle → opens drainage
• Do NOT use if IOP >40 mmHg - ischaemic sphincter cannot respond; may worsen forward vector
• Once IOP is reduced below 40 mmHg, pilocarpine becomes effective

D. Reduce Inflammation

• Prednisolone 1% or Dexamethasone 0.1% eye drops
• Reduces secondary inflammation and iritis

E. Symptomatic Relief

• Analgesia (oral/parenteral) for severe pain
• Antiemetic (metoclopramide) for nausea/vomiting

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STEP 2: If Attack is Resistant / IOP Not Falling

• Central corneal indentation with a squint hook - forces aqueous into the angle mechanically
• Clear corneal edema first with topical 50% glycerol (improves visualization for gonioscopy/laser)
• Early laser iridotomy once corneal edema partially clears
• Paracentesis (AC tap) - quick, immediate IOP reduction; small risk of lens damage

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STEP 3: Definitive/Surgical Treatment

Laser Peripheral Iridotomy (LPI) - Treatment of Choice

• Performed bilaterally once attack is broken (clear cornea, IOP normalised)
• Creates a small hole in the peripheral iris → allows aqueous to bypass pupil → equalizes pressure between posterior and anterior chambers → iris falls back → angle opens
• Done prophylactically in the fellow eye (bilateral anatomical predisposition - high risk of attack in fellow eye)

Other Surgical Options (if LPI fails or angle remains closed):

• Lens extraction (phacoemulsification) - EAGLE trial shows clear lens extraction may be superior to LPI in some patients; removes the lens that is causing pupillary block
• Peripheral iridectomy (surgical, if laser unavailable)
• Goniosynechialysis - breaks peripheral anterior synechiae
• Trabeculectomy - if IOP remains elevated despite patent iridotomy
• Cyclodiode laser - in refractory cases

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STEP 4: Long-term Follow-up

• Continue pilocarpine 2% 4 times daily in affected eye; 1% in fellow eye until LPI done
• Continue topical steroids for at least 1 week post-attack
• Repeat gonioscopy after LPI to confirm angle is open
• Monitor IOP at each visit
• If any phacomorphic element (large lens contributing to closure) → cataract surgery considered

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SUMMARY FLOW CHART

ACUTE AACG
     |
Immediate: Timolol + Apraclonidine + Acetazolamide IV + Mannitol IV
     |
IOP drops below 40 mmHg → Add Pilocarpine 2%
     |
Corneal clears → Laser Peripheral Iridotomy (BOTH eyes)
     |
Persistent elevation → Lens extraction / Trabeculectomy
     |
Long-term: IOP monitoring + Fellow eye prophylaxis

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• The fellow eye MUST be treated - 50% chance of AACG in the other eye within 5 years if left untreated
• Glaukomflecken = pathognomonic of previous acute attack
• Colored halos = corneal edema from raised IOP (NOT optic nerve damage)
• Hypermetropia + shallow AC + female + age >40 = classic AACG patient profile
• Pilocarpine is ineffective when IOP >40 mmHg - reduce IOP first