Visual Anatomy and Ophthalmic Disease Guide

Contents
Anatomy .................................................................................................................................................. 5
1. General data of the visual analyser/phylogenetic and ontogenetic development ........................ 5
2. Blood supply and innervations of the visual analyser .................................................................... 7
3. Applied anatomy of the orbit.......................................................................................................... 8
4. Applied anatomy of the lids .......................................................................................................... 10
5. Applied anatomy of the lacrimal apparatus ................................................................................. 12
6. Applied anatomy of the conjunctiva ............................................................................................. 14
7. Applied anatomy of the cornea and sclera ................................................................................... 15
8. Applied anatomy of the anterior chamber angle and ocular hydrodynamics .............................. 16
9. Applied anatomy of the lens and vitreous body ........................................................................... 18
10. Applied anatomy of the uvea.................................................................................................... 20
11. Applied anatomy of the retina .................................................................................................. 22
12. Applied anatomy of the visual pathway and cortical centres................................................... 23
13. Perception of light, adaptation. Disorders of adaptation ......................................................... 24
14. Perception of colour. Theory of colour vision. Disorders of colour vision ............................... 25
15. Central and peripheral vision.Visual acuity. Examination methods ......................................... 26
16. Visual field. Examination methods. Pathological changes of visual field. ................................ 27
Refraction and refractive errors ........................................................................................................... 30
17. Refraction. Emmetropia and ametropia ................................................................................... 30
18. Methods of examination of refraction. Objective and subjective methods ............................. 31
19. Myopia. Definition, clinical findings, treatment (glasses, contact lenses, surgery).................. 32
20. Hypermetropia. Definition, clinical findings, Treatment (glasses, contact lenses, surgery)..... 34
21. Astigmatism- definition, clinical findings, treatment................................................................ 35
22. Accomodation. Disorders of accommodation (insufficiency, paralysis, spasm), Presbyopia.
Treatment of presbyopia ...................................................................................................................... 37
23. Binocular vision ......................................................................................................................... 39
24. Types of correction for ametropia- glasses, contact lenses, surgery ....................................... 40
25. Examination methods in Opthalmology: Examination of the conjunctiva, Lacrimal system,
Cornea, Sclera, Anterior chamber, Iris, Pupil, lens, Posterior segment of eye, Intraocular pressure .. 42
26. Diagnostics with ultrasonography, Fluorescein angiography, electrophysiological tests. ....... 46
Orbital diseases: .................................................................................................................................... 47
27. Clinical findings of orbital diseases ........................................................................................... 47
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28. Inflammatory and vascular orbital diseases ............................................................................. 47
29. Endocrine diseases and tumours of the orbit ........................................................................... 50
Eyelid diseases ...................................................................................................................................... 52
30. Clinical findings in eyelid diseases ............................................................................................ 52
31. Congenital anomalies of the eyelids ......................................................................................... 53
32. Diseases due to Various eyelid positions .................................................................................. 54
33. Inflammatory diseases of the eyelids ....................................................................................... 57
Lacrimal gland diseases......................................................................................................................... 59
34. Diseases of the lacrimal gland- acute and chronic dacryoadenitis, Mikulicz syndrome,
tumours of the lacrimal gland. .............................................................................................................. 59
35. Lacrimal drainage system diseases- Stenosis (atresia of the lacrimal punctum, Canalicular
stenosis, Dacryocystitis (acute, chronic, neonatal))- clinical findings and treatment .......................... 60
36. Dry eye syndrome- types, clinical findings, treatment ............................................................. 63
Diseases of the conjunctiva .................................................................................................................. 64
37. Diseases of the conjunctiva- clinical findings ............................................................................ 64
38. Inflammatory diseases of the conjunctiva- acute conjunctivitis .............................................. 64
39. Allergic Conjunctivitis and Kertoconjunctivitis ......................................................................... 66
40. Chronic infectious conjunctivitis. Chronic non-infectious conjunctivitis. Trachoma. ............... 67
41. Degenerations of the conjunctiva ............................................................................................. 71
42. Tumours of the eyelids and conjunctiva ................................................................................... 72
Cornea- diseases ................................................................................................................................... 74
43. Clinical findings in corneal diseases .......................................................................................... 74
44. Inflammation of the cornea due to Bacterial infections ........................................................... 74
45. Inflammation of the cornea due to viral infections .................................................................. 75
46. Parenchymatous Keratitis ......................................................................................................... 76
47. Corneal dystrophies .................................................................................................................. 77
48. Corneal surgery ......................................................................................................................... 78
49. Diseases of the sclera ................................................................................................................ 78
50. Normal and pathological pupillary responses .......................................................................... 79
Lens disorders ....................................................................................................................................... 81
51. Congenital lens anomalies ........................................................................................................ 81
52. Cataract. Cataract surgery ........................................................................................................ 81
53. Symptamology of vitreous body disorders. Vitreous body diseases ........................................ 84
Diseases of the uveal tract: ................................................................................................................... 88
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54. Uveitis. Etiology, pathogenesis and treatment ......................................................................... 88
55. Inflammatory diseases of the anterior uvea ............................................................................. 89
56. Intermediate and posterior uveitis ........................................................................................... 89
57. Uveitis due to syndrome diseases ............................................................................................ 91
58. Uveal tumours........................................................................................................................... 91
Retina- diseases .................................................................................................................................... 92
59. Clinical findings in retinal diseases: .......................................................................................... 92
60. Macular degeneration............................................................................................................... 92
61. Pigment degeneration of the retina. ........................................................................................ 93
62. Peripheral degeneration of the Retina ..................................................................................... 94
63. Acute vascular disorders of the retina ...................................................................................... 95
64. Diabetic retinopathy ................................................................................................................. 97
65. Vascular changes of the retina due to arterial hypertension, renal diseases and toxemic
retinopathy of pregnancy ..................................................................................................................... 99
66. Inflammations of the retina (Central serous retinopathy and periphlebitis) ......................... 100
67. Drug, professional and other intoxications of the Retina and optic nerve............................. 102
68. Retinal detachment- Types, clinical findings and Treatment ................................................. 102
69. Tumours of the Retina ............................................................................................................ 104
70. Retinopathy of prematurity- diagnosis, clinical findings, treatment ...................................... 105
Optic nerve disorders.......................................................................................................................... 106
71. Optic neuritis........................................................................................................................... 106
72. Ischeamic optic neuropathy .................................................................................................... 108
73. Edema of the optic disk........................................................................................................... 109
74. Atrophy of the optic disk......................................................................................................... 110
75. Diseases of the chiasm and central part of the visual analyzer. Localization of visual disorders
of visual pathways according to the visual field defects .................................................................... 111
76. Glaucoma- Definition, types, etiology and pathogenesis ....................................................... 113
77. Glaucoma- diagnosis methods ................................................................................................ 115
78. Clinical findings in primary open angle glaucoma- etiology, risk factors, clinical findings,
treatment, prophylaxis ....................................................................................................................... 116
79. Clinical findings in closed angle glaucoma. Acute glaucoma- Risk factors, Clinical findings,
Treatment and prophylaxis ................................................................................................................. 117
80. Congenital glaucoma............................................................................................................... 119
81. Secondary glaucoma ............................................................................................................... 120
82. Concomitant strabismus- types, treatment, prophylaxis ....................................................... 121
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83. Paralytic strabismus- DDx with concomitant strabismus ....................................................... 122
84. Amblyopia. Treatment ............................................................................................................ 124
85. Trauma of the orbit,eyelids and conjunctiva .......................................................................... 125
86. Mechanical eye injuries. Non-penetrating injuries of the eye globe- contusion, lamellar
laceration, superficial foreign bodies. Diagnosis management. ......................................................... 126
87. Penetrating injuries of the eye globe- intraocular FBs, penetrating and perforating ocular
trauma127
88. Chemical and thermal burns of the eye. First aid ................................................................... 128
89. Eye injuries due to phycial agents/ electric ophthalmopathy ................................................ 128
90. Causes and prevention of blindness ....................................................................................... 129
91. Sympathetic opthalmia ........................................................................................................... 130
92. Pharmacological agents in ophthalmology ............................................................................. 130
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Anatomy
1. General data of the visual analyser/phylogenetic and ontogenetic

development
General data of the visual analyser

 Eye= organ of sight
 Situated in orbital cavity, spherical
Structure of the eye: 3 layers
1) Fibrous outer layer
 Sclera= white of the eye, maintains shape of eye and for
attachment of extraocular muscles. Where the optic nerve pierces
it= lamina cribrosa
 Cornea= anterior 6th of eye, transparent, refracting surface
 Limbus= join of the cornea and sclera
2) Middle vascular layer

 Iris: coloured, aperture in the centre= pupil. Sphincter papillae and dilator
papillae muscles.
 Ciliary body: attached to the iris, ciliary muscles
 Choroid: highly vascular, between the sclera and retina
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3) Inner nervous tissue layer
 Retina: composed of 10 layers of nerve cells and fibres. Lines ¾ of eyeball.
Maclea lutea= yellow area situated posteriorly with central depression
fovea centralis= most sensitive part of retina
 Optic disc: only nerve fibre layer thus no visual response here aka Blind spot
 Optic nerve: from lamina cribrosa to optic chiasm
Interior the eyeball:

1. Aqueous humour: ciliary epithelium secrete clear fluid into anterior and posterior chambers
of eye.
2. Lens: transparent, biconvex immediately behind the pupil
3. Vitreous: transparent, colourless, inert gel in the posterior eyeball.
Accessory structures of the eye:

1. Eyebrows: supraorbital margins of frontal bones. Protect from sweat, dust and FBs
2. Eyelashes and eyelids:
- eyelids= movable folds of tissue above and below the front of the eye. They have thin
covering skin, muscles (orbilaris oculi, levator palpebrae superiors and Muller muscles),
tarsal plate (sheet of dense CT), a lining of conjunctiva
- Eyelashes= short curved hair
3. Lacrimal apparatus:
Tears secreted by lacrimal gland and accessory glands drains into conjunctival
sac lacrimal sac (via canaliculi) nasolacrimal duct nasal cavity (inferior
meatus)
4. Extraocular muscles: Six intrinsic muscles; 4 straight and 2 oblique

1) Straight muscles-
- Medial rectus rotates eyeball inwards, adducts
- Lateral rectus rotates eye outwards , abducts
- Superior rectus upwards (elevates eye), adducts and rotates eye medially
- Inferior rectus downwards , adducts and rotates eye medially
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2) Oblique-
- Superior oblique it depresses, abducts and rotates eye laterally (look to your shoulder!)
- Inferior oblique elevates, abducts and rotates eye laterally
Phylogenic and ontogenic development:

Ectoderm and mesoderm where the eyes develop
The CNS develops from the neural tube. The anterior part of the neural tube thickens optic plate,
grows optic vesicles
Optic vesicles invaginates to form an optic cup; hyaloids artery provides nutrition for developing
structures. Inner layer forms the retina and the outer layer develops into pigment epithelium. Neural
ectoderm secretes vitreous which fills the cavity.
Mesoderm and anterior optic cup ciliary body and iris
Surface ectoderm forms the lens.
2. Blood supply and innervations of the visual analyser

Blood supply:
Internal carotid ophthalmic artery branch ciliary (short and long) arteries and central retinal
artery
Innervations:
1) Motor nerves:
CN III (oculomotor)
Just remember, all extra-ocular muscles are supplied by occulomotor (CN III), except:
- Lateral rectus (LR) abducens (CN VI)... LR6
- Sup. Oblique (SO) trochlear (CN IV)... SO4
CN IV (trochlear) superior oblique
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CN VI (abducens) lateral rectus
CN VII (facial)  orbicularis oculi
NOTE: insertions of rectus muscles= front of equator, oblique= behind the equator
2) Sensory nerve: CN V (trigeminal) ophthalmic branch supplies whole eye

3) Autonomic nerves:
- Sympathetic iris (dilator pupillae muscle), ciliary body, muller’s muscles, lacrimal gland
- Parasympathetic iris (sphincter pupillae muscle, ciliary body and lacrimal gland
NOTE: orbital veins have no valves infection of eyelids, facial skin and nose can lead to cavernous
sinus thrombosis
3. Applied anatomy of the orbit
Remember the bones: frontal,

sphenoid, zygomatic, maxilla,
lacrimal, ethmoid
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The orbit is pyramidal shaped space in the frontal bone. It has a base, apex and 4 walls
Roof lesser wing of sphenoid and orbital plate of frontal bone
Floor orbital surface of maxilla, and maxillary process of zygomatic bone
Lateral wall frontal process of zygomatic bone, greater wing of sphenoid
Medial wall frontal process of maxilla, lacrimal bone and orbital plate of ethmoid
Base opens out into the face, bounded by eyelids. AKA orbital rim
Apex @ opening of optic canal
Foramina and fissures of the orbit:
Foramen Position Structures passing
Optic canal apex of orbit - Optic nerve
- Ophthalmic artery
Sup. Orbital fissure Between roof and lat. Wall - Oculomotor
- Trochlear
- Abducens
- Opthalmic n.
- Opthalmic veins
Inf. Orbital fissure Between lat. Wall and floor - Infraorbital n. & a
- Zygomatic n.
- Orbital br. Of
shpenopalatine ganglion
Ant. Ethmoidal f. Medial wall - Ant. Ehtmoidal nerves
and vessels
Post. Ethmoidal f. “ - Post ethmoidal n and v
Intra-orbital groove and Floor - Intra-orbital n & v
foramen
Surgical spaces of the orbit:

1) Subperiosteal space: between periosteum and bone
2) Peripheral orbital space: between periosteum and extraocular muscles. Continous
3) Central space: cone shaped enclosed by extraocular muscles
4) Tenon’s space: under Tenon’s capsule
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4. Applied anatomy of the lids
 2 folds of tissue above and below the eyes, covers the eyeball.
Functions:
- eyelids and eyelashes protect from injury reflex closure of lids when conjunctiva, cornea or
eyelashes are touched (conjunctival or corneal reflex).
- Regular blinking spreads tears from meibomian gland’s secretions over cornea prevent
drying
- Orbicularis oculi contracts closed eyelids. Levator palpebrae contracts eyelids open
 Split into upper and lower portions meet at the medial and lateral canthi of the eye
 Opening between the 2 eyelids palpebral aperture/opening
1) Skin: thin, loose and easily distendible by edema or blood  sweat glands and sebaceous
glands
2) Superficial fascia: no fat, palpebral part of orbicularis oculi muscle
The eyelashes are attached here with ciliary glands of Moll (modified sweat glands which
open in hair follicles or directly in the lid margin). Also there are Glands of Zeis (sebaceous
gland) in the vicinity of the yelashes
3) Orbicularis oculi muscle has 3 parts: innervated by Facial nerve (CN VII- temporal and
zygomatic branches)
- Palpebral  close eyelids
- Lacrimal  tear drainage
- Orbital  close eyelids
4) Tarsus: thin plate of dense fibrous tissue found deep to the palpebral region of the
orbicularis oculi muscles.
- Superior tarsus= upper eyelid
- Inferior tarsus= lower eyelid
- Broad in the middle and narrows as it ends
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- Lateral ends of both tarsi are attached to the lateral orbital margin by lateral palpebral
ligament
- Medial ends connected to med. Orbital margin by medial palpebral ligament
- Tarsal glands (Meibomian glands) within the tarsal plates which secrete oil into the tear film
that keeps tears from evaporating too quickly and prevent eyelids from sticking together when
they’re closed
5) Levator apparatus:
- Levator palpebrae superioris
- Superior tarsal muscles
Both open the eyelids- only present in upper eyelids
Blood supply lacrimal arteries
Venous drainage ophthalmic vein
Nerve supply: CN VII (orbicularis oris), CN III (lev. Palp. Sup). Sensory ophthalmic division of CN V
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5. Applied anatomy of the lacrimal apparatus
Main parts:
1) Lacrimal gland has 2 parts:

a) Main part= lies in the lacrimal fossa in the anterolateral part of the roof of orbit
b) Palpebral part: embedded in the lat. Part of upper eye lid
Lacrimal gland gives about 12 ducts which open into the superior fornix of the conjunctiva. Carries
secreted tears to the conjunctival sac
Blood supply: lacrimal branch of ophthalmic artery
Nerve supply: lacrimal brach of ophthalmic nerve
2) Conjunctival sac: membrane that lines the eye

lids, covers anterior part of the eye ball except
cornea
- Superior and inferior fornix
- Eyes closed= space between the fornix and
eyeball= conjunctival sac
- Most tears reaching the conjunctival sac
evaporates and the remaining passes into the
lacrimal puncti
3) Lacrimal puncti, canaliculi, lacrimal sac

- Lacrimal puncti= minute openings in the medial
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ends of the margins of upper and lower lids which lead to 2 canaliculi opening in the lacrimal
sac
- Nasolacrimal duct- arises from the sac and passes into the nasolacrimal canal to open into the
inferior meatus of the nose
Tear= secretion from the lacrimal gland. Slightly alkaline and mainly consist of water and NaCl, sugar,
urea, protein, lysozyme and bactericidal enzymes. pH is 7.5.
Functions: surface of the eyeball needs to be hydrated well. The tear film (fluid which fills the
conjunctival sac) spreads over the surface of corneal epithelium:
- It washes away dust and contains lysozymes, immunoglobulins
- Murmidase= bacterial lysozyme
- Oiliness of the tear film delays evaporation and prevents drying of cornea and conjunctiva
NOTE: normally rate of tear secretion balanced out by rate of drainage. If anything irritant to the
eye tear secretion increased and conjunctival vessels dilate.
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6. Applied anatomy of the conjunctiva
The conjunctiva is a thin, translucent, vascular membrane
It covers the under surface of the lid and reflected over the anterior eyeball up to the limbus
Prone to infection exposed to dust, wind, heat , irritation
Parts:
1) Palpebral-
covers under upper and
lower eyelids. Adherent
to the tarsus. Very thin
2) Bulbar- covers
anterior eyeball
3) Fornices- folds
of the conjunctiva
formed by the reflection
of mucous membrane
from the lids
4) Plica
semilunaris- crescent
fold at inner canthus
Functions of the conjunctival sac:

- Motility of the eyeball
- Articulating layer= surface conjunctiva is smooth and moist so the mucous membrane glides
easily and painlessly across each other. The tear film is a lubricant
- Protective function= lymphocytes and plasma cells beneath the palpebral conjunctiva and
fonices. Immunoglobluins, prostaglandins etc. Protect the eye
2 layers: epithelium (2-5 layers) & stroma (BVs, Ct, glands e.g. glands of Krause and glands of
wolfring)
Blood supply anterior and posterior conjunctival arteries and veins
Nerve supply sensory (branhes of ophthalmic and maxillary division of CN V), sympathetic
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7. Applied anatomy of the cornea and sclera
The cornea is a clear transparent structure. It contains of 5 layers:
1) Epithelium- stratified squamous,

replaced within 7 days after damage
2) Bowman’s membrane- collagen fibrils, doesn’t regenerate when damaged permanent corneal
opacity
3) Stroma- 90% of corneal thickness. Keratocytes, collagen fibrils and ground substance
4) Descemet’s membrane- can regenerate
5) Endothelium- flattened hexagonal cells in single layer- role of dehydration, no regeneration
It is transparent due to:

- No blood vessels
- No myelin around nerves
- Dehydration
- Regular arrangement of corneal lamellas (lattic theory of cornea)
Nutrition: avascular structure, so it gets its nutrition from:
- Perilimbal blood vessels at the periphery of the cornea (limbus)
- Aqueous humour- supplies glucose
- Oxygen from atmosphere directly through tear film
Nerve supply= purely sensory, ophthalmic division of CN V
Functions=
- Major refracting medium
- Protects intraocular contents
Sclera: white, fibrous composed of collagen and is continuous with the cornea anteriorly.
 The sclera and cornea form the rigid outer covering of the eye
 All 6 intraocular muscles insert into the sclera
 Relatively avascular rarely get infections
 Blue/thin in childhood and where uvea shines through it pathologically
 Yellow in old age fat deposition
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Functions= overcome stress and strain due to deposition of fibrous bands, retina and choroid
maintain their optical shape by sclera, insertion of extraocular muscles
8. Applied anatomy of the anterior chamber angle and ocular hydrodynamics

Anterior chamber is an angular space. Anterior of it is the inner surface of the cornea and posteriorly
by the lens within the papillary aperture, anterior surface of the iris
and part of the ciliary body
 It is approx 3mm in depth and contains 0.35ml of aqeous humour

 More shallow in elderly and children
 The chamber depth is slightly diminished during accommodation (increased lens curvature
and forward translocation of lens)
The anterior chamber

angle is an anatomical
angle created by the root
of the iris and the inner
surface of the cornea.
Within it lie the
structures involved in the
outflow passage of
aqueous, namely the
trabecular meshwork
and Schlemm’s canal.
Depth in healthy eye
is 30 degrees.
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 Schwalbe’s line: anterior border of the angle and represents the termination of descemet’s
membrane. Schwalbe’s line cells produce phospholipids to facilitate drainage of aq. Humour
 Schlemms canal: underlies trabecular meshwork, lymphatic like vessels that collects aq.
Humour in the anterior chamber and delivers it to episcleral blood vessels via aqueous veins.
It
It is connected to episcleral and conjunctival veins by channels; 2 types:
1) Indirect system channels form intrascleral plexus and drains into episcleral venous
system
2) Direct system  lots of large vessels that drain directly into the episcleral venous system
(aqueous veins)
Episcleral veins drain into the cavernous sinus via anterior ciliary and superior ophthalmic veins,
conjunctival veins drain into superior ophthalmic or facial veins
 Trabecular meshwork: sieve like structure lined by trabeculocytes (phagocytic), drainage of
aqueous humour, roughly triangular and the apex is Schwalbe’s line. Base is sclera spur and
ciliary body
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 Scleral spur: wedge-shaped, pale, translucent,posterior to the trabecular meshwork
Just remember, this is where aqueous is drained and blockage of this pathway/angle glaucoma
9. Applied anatomy of the lens and vitreous body

Lens:
Shape: biconcave, transparent structure. Placed between the iris and vitreous.
 Suspensory ligament suspends it
 Zonule of zinn is attached to the ciliary body and equator of the lens
 Anterior surface is less convex/flat (10mm) and posterior surface is more convex (6mm)
 It is a purely epithelial structure with no nerves or BVs
Functions:
 Transmits 80% of light
 Refractive media of the eye (45% refractive power of the eye)
 Accomodation for near vision
 Absorbs UV light
Structure: lenticular capsule (acellular envelope), lenticular epithelium (single layer of cuboidal cells
only on the anterior capsule, lenticular fibres, suspensory ligament of Zonule of Zinn (transparent,
straight fibres)
Parts:
1) Lens capsule: thin, transparent membrane,
thicker anteriorly and thinnest in posterior pole
2) Nucleus: different depending on stages of life
- Embryonic nucleus= 1-3 months of gestation
- Fetal nucleus = 3 months of gestation until
birth
- Infantile nucleus = birth puberty
- Adult nucleus= early adult life
3) Cortex: between capsule and nucleus. Lens
fibres.
Vitreous body:
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 Stabilizes globe and prevents retinal detachment, refractive media of the eye
 Inert, avascular (derives nutrition from choroid and ciliary body), transparent, jelly like
structure
 Collagen and hyaluronic acid
 Advancing age, myopia and chemical/mechanical trauma makes the vitreous become like
‘fluid’ due to coagulation of proteins
Attachments:
1. Hyaloid capsular ligament of Wieger and ciliary epithelium attaches it anteriorly to the lens.
Vitreous base= strongest attachment
2. Attached posteriorly to the edge of the optic dist and fovea forming a ring-shaped structure
around them
Age changes in vitreous:
 At birth= Cloquet’s canal runs straight from the lens to optic disc and contains primary
vitreous
 In young persons= homogenous gel but fibres become coarse with age
 Old age and high myopes= secondary vitreous liquefies (syneresis) and shrinks vitreous
detachment, retinal hemorrage and break
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10. Applied anatomy of the uvea
Uveal tract (Vascular pigmented layer), takes its name from uva (grape) because it is the dark
pigmentation and shape of it is like a grape.
Following structures: iris, ciliary body, choroid
Anatomically, they are continuous with so disease from one part may spread to the other
Iris:
 Coloured, central aperture is the pupil (4mm).

 It divides the space between the cornea and lens into the anterior and posterior chambers
of the eye
 Regulates the amount of light rays reaching the retina
 At the periphery, iris attaches to the middle of the anterior surface via the ciliary body
Parts:
 Ciliary zone= series of radial

streaks (underlying BVs) and crypts
(depression where endothelium layer
is missing)
 Papillary zone
 Collarette= zig zag line that
divides the 2 zones
Structure: 3 layers
1) Endothelium- contains crypt which communicate with anterior chamber
2) Stroma- loosely arranged CT, BVs, Nerves and muscles:
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- Sphincter pupillae circular band surrounding the pupil. Constricts pupil (CNIII-
parasympathetic )
- Dilator pupillae  radial fibres extending from ciliary body. Pupil dilation (sympathetic)
3) Pigment epithelium- 2 layers on posterior surface of the body
NOTE: colour of iris varies according to melanin content of melanocytes (pigment cells) in stromal
and epithelial layer.
Ciliary body: attaches to iris.

Parts:
 Pars plicata= anterior 1/3 of ciliary body (2mm) secrete aqeous humour
 Pars plana= posterior 2/3 (4mm). Relatively avascular
Structure:
 Ciliary muscles= non-striated accomodation of lens
 Stroma= loose CT, pigments and BVs
 Ciliary process= suspensory ligament/ zonule of zinn attaches to these cilia and equator of
the lens. Site of aqeous production
 Epithelium= 2 layers of pigmented and non-pigmented cells
Choroid:
Middle tunic of the eyeball (between sclera and retina). Extends from ora serrate up to the optic
nerve aperture.
Outer layers of the retina need nutrition from the choroid. So, inflammation of choroid always
involves the retina.
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Structure: from sclera retina
1. Suprachoroidal lamina- thin membrane of collagen fibres, melanocytes. Suprachoroidal
space= space between membrane and sclera
2. Stroma- loose CT, pigment cells, macrophages, mast cells, blasma cells. BVs in 3 layers
3. Bruchs membrane- close to pigment epithelium of retina
NOTE: Choriocapillaris in stroma nourishes the outer layers of the retina. They are fenestrated
capillaries that lead to slow blood flow, maximal utilization of oxygen and nutrition and precipitation
of allergic substances
Function: regulates temperature, supplies nourishment to outer layers of the retina

Blood supply posterior and anterior ciliary arteries
NOTE: the blood flow through the choroid is the highest in the entire body
11. Applied anatomy of the retina

The retina= inner layer of eye. Derived from neuroectoderm. It extends from the optic disc to the ora
serrate in front.
 Ora serrata: anterior termination of the

retina where it is continuous with the
epithelium of the ciliary body (look at the
picture in the previous question)
 Macula Lutea (yellow spot): in the
posterior pole
 Fovea centralis- small depression in the
centre of the macula. Cones here. Most
sensitive part of the retina
Structure: 2 main layers: I)outer retinal pigment epithelium II) inner neural layer
10 layers namely : just remember pigment epithelium and photoreceptors (rods and cones)
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Blood supply:
1) Choriocapillaries (of choroid) supplies pigment epithelium, layer of rodss and cones and
outer nuclear layer
2) Branch of ophthalmic artery central retinal artery supplies rest of layers
3) Muller cells spans nearly the whole thickness of the retina nutrition
Venous drainage:
- Central vein, vortex veins
Functions:
- Photosensitive part of the eye
- Rods and cones
- More sensitive to rods than cones which are stimulated by dim light. Rods contain Rhodopsin
(photosensitive pigment)
- Cones are sensitive to bright light and colour
- Macula lutea cones day and colour vision
- Peripheral retina contains mainly rods night vision
12. Applied anatomy of the visual pathway and cortical centres

Visual pathway:
Optic nerves optic chiasm optic tracts lateral geniculate bodies optic radiation occipital
cortex
1) Optic nerve: optic nerve fibres leave the retina. Retina is then divided into temporal and
nasal halves at level of fovea centralis. Optic nerve join the optic chiasm
2) Optic chiasm: above pituitary fossa.
- Decussation of nerve fibres (nerve fibres from nasal side cross over to the opposite side, and
nerve fibres from temporal side do not cross but pass into optic tracts of the same side)
3) Optic tract: run backwards to lateral geniculate body
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4) Lateral geniculate bodies: oval structures. Fibres from the optic tract ends here and new
fibres of optic radiations originate from them
5) Optic radiations: go back and medially to terminate in the occipital lobes
6) Occipital cortex: in occipital lobe
Cortical centres:
1. First order neurons- bipolar cells of retina
2. Second order neurons- ganglion of the retina, optic nerve lateral geniculate body
3. Third order neurons- takes impulses via optic radiations to the occipital lobe (visual
centre- Brodmann area 17)
13. Perception of light, adaptation. Disorders of adaptation

Remember the spectrum of light. The visible spectrum of light is from about 400- 700nm
 In order to get clear vision, light reflected from objects is focused onto the retina of both
eyes.
 We need:
a) refraction of light rays (question 17) and
b) accommodation of the eyes to light (covered in question 23)
 Absolute perception of light= ability to perceive light in full darkness at complete adapation
to it
 Distinguishing light perception= eye to distinguish the smallest difference in intensity of 2
light stimuli
 Light perception of rods is about 300x higher than cones
Light perception depends on:
- Visual adaptation
- Spectral composition of light i.e. rods are stimulated by dim light (scotopic vision), in bright
light the rays are focused on the macula lutea (photopic vision)
- Place of stimulation
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- Duration of light stimulation
- Pupil width
- Condition of the transparent eye mediums, photoreceptors and optical paths
- Physiological factors- age, vitamin deficiency etc.
Adaptation:
- The alteration of the level of light perception according to illumination of surrounding objects
- Light adaptation
- dark adaptation (ability to adapt to decreasing illumination e.g. going from bright light to dimly
lit room need time to perceive object in the room time elapsed dark adaptation
Disorders of adaptation:
1) Hemeralopia: disturbance of dark adaptation. Day blindness and night sight. Defective vision
in bright light- seen in patients with impaired cone function
Etiology:
a) Functional- heavy diet, liver diseases, lack of Vit A, B, C
b) Organic- degeneration retinae pigmentosa, myopia, retinal ablation, glaucoma, Grave’s
disease
2) Nyctalopia: can’t see in dim light or at night
Etiology:
a) Congenital or acquired macular degenerations- combined with disturbance of colour
vision, central vision; nystamus
b) Chronic alcohol and nicotine poisoning- damage cones and macula sheath
14. Perception of colour. Theory of colour vision. Disorders of colour vision

Perception of colour: ability to distinguish between colours by stimulations of rays with different
wavelengths
3 important factors influence colour vision
1) Wavelength (colour tone)
2) Brightness/luminosity  depends on intensity of light source
3) Saturation
Primary colours are Red, green, blue
Cones photopigments Wavelength
Erythrolabe- red sensitive 575nm
Chlorolabe- Green sensitive 540nm
Cyanolabe- blue sensitive 430nm
Theory of colour vision:

- Normal colour vision is called ‘trichomatric’ (red, green, blue) young-Helmholtz theory. If
you mix the 3 colours together produce white colour, thus red, green and blue are the
primary colours
Disorders of colour vision: ‘Dischromatopsia’
1) Abnormal Trichromacy : will be colour blind to some extent, type of cone affected perceives
light slightly out of alignment i.e. ‘faulty’ cone
- Protanomaly red sensation is defective/ reduced sensitivity to red
- Deuteranomaly green sensation is defective
- Tritanomaly  absence of blue sensation (v rare)
2) Dichromacy: people with dichromatic colour vision have only 2 types of cones which are
able to perceive colour i.e. they have total absence of function of one cone type
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- Protanopia unable to perceive any ‘red’ light
- Deuteranopia unable to perceive green light
- Tritanopia unable to see blue light
3) Monochromacy (achromatopsia): colour blindness
Etiology:
- Congenital: absence of red,green or blue pigments of cones. Partial or complete. Transmitted
via females (autosomal recessive)
i) Partial colour blindness cannot recognize the primary colours. Green is the
most common. Absence of one or 2 photopigments in foveal ones
ii) Total colour blindness everything is grey. Rare, assoc with nystagmus and
central scotoma
- Acquired: diseases of macula and optic nerve e.g. macular degenerations. E.g. blue blindness in
sclerosing black cataracts
4) Chromatopsia: visual defect in which coloured objects appear unnaturally coloured and
colourless objects appear tinged with colour i.e. imperfect perception of various colours.
- Cyanopsia= blue vision
- Erythropsia= red vision
- Chloropsia= green vision
- Xanthopsia= yellow vision
15. Central and peripheral vision.Visual acuity. Examination methods

Definition- visual acuity is a measurement of central vision only assessment of total visual system
from cornea to occipital cortex. It is a measure of the smallest retinal image which can be
appreciated. It is the sharpness of near and distant vision.
Normal vision relies on the following:
 Both eyes in alignment (extraocular muscles functioning)
 Clear cornea
 Clear lens of the eye
 Clear ocular media (aqueous and vitreous)
 Intact retina, optic nerve,visual pathway
Examination methods:
Tested separately for each eye.
 One eye is covered (palm, paper, glasses), don’t use fingers as the patient will be able to see
between them.
 The patient is asked to identify certain visual symbols optotypes at a metre of 5 or 20
feet test for distant vision. Sharpness of vision is measured as a fraction:
Actual distance/ Standard distance= visual acuity
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Normal visual acuity is 20/20 or as 1.0 (actual distance equals the standard distance)
 E.g. of diminished visual acuity- the patient will only see the ‘4’ at a distance of 50 metres.
Visual acuity is 5/50 0.1
 The ophthalmologist tests visual acuity after determining objective refraction using integral
lens system (a box of individual lenses and an image projector that projects visual symbols at
a defined distance in front of the eye)
 Plus lenses (convex) farsighted/ hyperopia
 Minus lenses (concave) shortsighted/myopia
 Astigmatism cylindrical lenses
 If the patient cannot see at a distance of 5 metres we shorten the distance and if they still
cannot see the optotypes the examiner has the patient to count fingers, and discern the
direction of a point light source; in a dark room, light is concentrated on the eyes. The
patient is asked when the light is on the eyes and off, if he tells correctly= visual acuity PL
(perception of light). Also if the patient gives correct indication of the direction from where
the light is coming the visual acuity is also PL
16. Visual field. Examination methods. Pathological changes of visual field.

Visual field entire area that can be seen when the eye is directed forward, including peripheral
vision seen i.e. the portion of the subject’s surroundings that can be seen at any one time
 Central area of the retina is the most sensitive to light. We see best what is directly in front
of us
 More peripheral areas of the retina are less sensitive to light, but we can still see, though
less clearly, objects off to the side or below the head
 Just how much we can see the world around us visual field
Normal field of vision:
- Upwards= 60°
- Inwards= 60°
- Downwards= 70°
- Outwards= >90°
Boundary- the peripheral limits

the visual field
Point of fixation- area of
maximum visual acuity in the normal visual field. Corresponds to the fovea of the retina
Blind spot- area of absolute scotoma (non-seeing area) within the boundaries of normal visual field.
Responds to a region of no cones or rods on the retina.
Perimetry- techniques used to evaluate peripheral and central visual fields using targets of various
sizes and colours.
Monocular visual filed= amount of outside world visible to each eye

Bincoular vision= when both eyes opened, larger field
1) Kinetic perimetry:
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- A target is moved across the field to map out 2D extent of the field.
- You move the stimulus from periphery towards the centre until you can see it
- Point of perception is recorded along different meridians
- Join the isoper and plot it
-
NOTE: left is nasal side, right is temporal
side. Normal blind spot is the blue dot,
centre of the circle is the macular area
(sharpest vision)
Normal field of vision= 160-170°
2) Static perimetry:
- Glaucoma assessment
a) Suprathreshold perimetry visual stimuli are presented above expected normal
threshold values in various location in the visual field. Loss of sensitivity stimulus
not seen
b) Threshold perimetry target of different and increasing intensities are presented at
designated points in the visual field until just visible to find out the patient’s
threshold for that point.
Pathological changes of visual field:
Visual fields assess the potential presence of blind spots (scotomas), which could indicate eye
diseases.
Visual field defect= a portion of the visual field is missing, can be central (optic disc or nerve
problem) or peripheral (any defect up to the optic chiasm)
 Optic nerve damage caused by glaucoma creates a specific visual field defect
 Optic neuropathy due to optic nerve damage can damage the retina
 Strokes, tumours can affect the visual field.
Central field loss Peripheral field loss

- Optic neuropathy - Retinitis pigmentosa
- Macular degeneration - Glaucoma
- Cone dystrophies - Retinal detachment
- Best’s disease
- Achromatopsia
Scotoma- defect surrounded by normal visual field. It is an area of depressed visual function (non-
seeing area.)
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i) Absolute scotoma- all vision is lost, no perception of light (PL)
ii) Relative scotoma- variable amount of vision remains. Objects of low luminescence
cannot be seen but larger or brighter ones can be seen
Hemianopia: loss of half the field of vision of both eyes

Etiology:
i) Trauma to head
ii) Tumour e.g. cerebral or pituitary
iii) Vascular lesions e..g aneurysms, cerebral thrombosis
iv) Inflammation e.g. meningitis, encephalitis
v) Degerenation e.g. MS
Types:
1) Homonymous hemianopia: loss of right or left binocular field of vision. Usually lesions on
the occipital lobe, optic tract, optic radiations
2) Bitermporal heminaopia: loss of both temporal fields. Site of lesion= optic chiasm
3) Binasal hemianopia: loss of both nasal fields. Rare. Site of lesion is on either side of optic
chiasm.
4) Altitiduinal hemianopia: defect in upper or lower horizontal half of the visual field. Can be
unilateral or bilateral (unilateral= defect is before the chiasm)
5) Quadrantanopia: incomplete hemianopia, ‘pie’ of visual field loss
6) Sectoral defect: incomplete hemianopia
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Refraction and refractive errors
17. Refraction. Emmetropia and ametropia

Refraction: when light rays pass from a medium of one density to a medium of different density they
are refracted (bent). This is the principle used in the eye to focus light onto the retina.
 Light rays pass through the conjunctiva cornea aqeous fluid lens vitreous retina
 They are all more dense than air (except the lens), they have a constant refractory power
Remember, the normal eye is like a camera. Light hits the retina and picture is perceived. The retinal
image is inverted but is re-inverted physiologically by the brain. One medium to another medium
refraction of light; how light focuses onto the retina.
Lens:
 Biconcave elastic transparent structure suspended behind the iris from the ciliary body by
the suspensory ligament.
 It’s the only structure in the eye that changes its refractory power
 Light from a distant object needs least refraction. As the object moves closer we need
increased refraction power
 Increase refractive power for near vision ciliary contracts anterior lens bulges forward
(convex)
 Ciliary muscle relax increase pull on suspensory ligament lens thinner  distant vision
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Emmetropia:
- The normal optical condition of the eye i.e. normal sight
- Rays of light focus onto the retina (fovea centralis) with accommodation at rest
- No error of refraction
- An emmetropic eye will have a clear image of a distant object without any internal adjustment
of optics.
- Average power of the normal emmetropic eye is +58 to +60 D i.e. 6/6 or 20/20 vision
- Most emmetropic eyes are about 24mm in length
Ametropia:
- Light rays do not come to focus on the retina properly, with accommodation at rest. Focus is in
front (myopia)or behind (hypermetropia)the retina
Etiology:
1) Axial ametropia= abnormal length of eyeball (too long myopia, too short
hypermetropia)
2) Curvature ametropia= abnormal curvature of refracting surface of cornea or lens (too
strong myopia, too weak hypoermetropia)
3) Index ametropia= abnormal refractive index (too high myopia, too low hypermetropia)
4) Abnormal position of lens (forward displacement myopia, backward displacement
hypermetropia)
18. Methods of examination of refraction. Objective and subjective methods

Examination of refraction: measuring the additional refractive power needed to produce a sharp
image on the retina.
1) Subjective refraction testing:

- Placing various combinations before the patient’s eye until the maximum visual acuity is
reached.
- Need info from the patient
2) Objective refraction testing:
- E.g. for infants when the patient cannot give subjective info or when the info is unreliable
(retinoscopy)
Retinoscopy (shadow testing)
- The retina is illuminated through the pupil
- The examiner observes the optical phenomena in the patient’s pupil whilst moving the light
source
Refractometry: principle based on opthalmoscopic observation of a test image projected onto the
patient’s retina. Distance between test figure and eye is changed until the image appears in focus on
the retina. Refraction then calculated from measured values.
Automated refractometry: measures refraction automatically with the aid of light-sensitive

detectors and computer until a focused image appears on the retina.
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With the retinoscope, the examiner moves the
light source across the pupil at a distance of 50cm
from the patient. Produces a light reflex (red spot)
in the patient’s eye. We need to be able to note
how the red spot behaves as the light source of
the retinoscope is moved:
a) Top picture ‘with motion’: red spot moves
in same direction as light source i.e the far
point of the eye is behind the light source.
Need (+) lenses
b) ‘against’ motion: light reflex of the pupil
moves in opposite directions (red arrows)
to the light source (yellow arrows). Far
point of the eye lies between the eye and
light source. Need (-) lenses
19. Myopia. Definition, clinical findings, treatment (glasses, contact lenses,

surgery)
Myopia short sightedness. Parallel rays of light come
to focus in front of the retina. Distant vision is blurred
Etiology: increase in axial length affects the posterior

pole and surrounding areas
1) Axial increased anteroposterior diameter of
globe- most common cause
2) Curvature increased curvature
i) Cornea conical cornea, ectasia
ii) Lens lenticonus
3) Index increased refractive index of nucleus e.g. senile nuclear cataract
4) Forward displacement of lens anterior dislocation of lens
Types:
1) Congenital (developmental myopia)- present at birth, unilateral or bilateral
2) Simple myopia- most common type, doesn’t progress after adolescence
3) Pathological myopia- degenerative and progressive. Hereditary. Associated with excess
accommodation.
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Clinical findings:
- Indistinct distant vision e.g. young children cannot see blackboard clearly
- Black spots floating
- Prominent eyes, large pupil, deep anterior chamber
- May be divergent squint
- Fundus examination
Treatment:
1. Glasses: spherical concave lenses minus lenses diverging lenses. No need to wear them
all the time if it is not severe myopia.
2. Contact lenses minus lenses
NOTE: the closer the ‘minus’ lens is to the eye, the weaker its refractive power minus
lenses used to correct myopia should be no stronger than necessary. Accommodation can
compensate for an over correction however. Accomodative astehnopia (rapid ocular fatigue)
and result due to excess contraction of ciliary muscles
Also, most patients have ‘lazy’ accommodation due to atropy of ciliary muscles. Slight
undercorrection usually better tolerated than overcorrection.
3. Hygiene- proper position, good illumination ad correct distance from the book (25cm) while
reading is essential
4. Surgery-
I) Radial keratotomy peripheral cuts of the cornea to flatten the increased curvature
of cornea
II) Excimer laser reshapes and flattens central cornea
III) Epikeratophakia alter surface topography of cornea by using donor tissue
IV) Keratomileusis freeze disc of cornea and ad grinding it to alter shape of cornea
(flattens cornea)
V) LASIK (laser- assisted in situ keratomileusis) corrects myopia of -8 -16
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20. Hypermetropia. Definition, clinical findings, Treatment (glasses, contact
lenses, surgery)
Hypermetropia- far sightedness. Aka hyperopia. Light focuses behind the retina. The eyes are small
and short.
Etiology:
1) Axial eyeball too short
2) Curvature flat cornea
3) Index increase in refractive index e.g. in diabetic and sine cortical cataracts
4) Backward displacement of lens posterior dislocation
5) Absence of lens/ aphakia acquired high hypermetropia
Types:
1) Latent hypermetropia- overcome by normal tone of ciliary muscles. Detected only when
ciliary muscles are paralysed by atropine
2) Manifest hypermetropia- detected without paralysing ciliary muscle
i) Facultative overcome by accommodation
ii) Absolute can’t be overcome by accommodation
Clinical findings: accommodation can compensate for slight to moderate hyperopia in young
people chronic overuse of ciliary muscles.
a) Symptoms:
- Blurring of vision near work ,Frontal headache and eye strain,Burning and dryness in eyes 
asthenopic symptoms
- Presbyopia occurs prematurely
in adults
b) Signs:
- Small eye prone to closed angle
glaucoma
- Bright reflex
- Psueodpapillitis i.e. hyperaemic
disc with blurred margin
(similar to papillitis- inflamed
optic nerve head)
Treatment:
Spherical convex lensesconverging
lenses plus lenses .
Refractive power (D) in plus lenses
are positive.
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NOTE: before correcting hyperopia, need to do refraction testing after giving some cycloplegics. The correction is then
made with the strongest plus lens that patient can tolerate without compromising visual acuity
Correcting aphakia doesn’t need cycloplegia.
21. Astigmatism- definition, clinical findings, treatment

Definition: derived from the Greek word stigma (point) and literally means a lack of a focal point. It
is characterized by a curvature anomaly of the refractive media parallel incident rays do not
converge at a point but drawn apart. There is more than one focal point
Astygmatism occurs when the cornea or lens has slightly different surface curvature in one direction
from the other
1) Strum’s conoid: Regular astigmatism (2 principle meridian- the parallel rays are focused
onto 2 focal points)
Etiology: corneal astigmatism, lenticular astigmatism
With the rule astigmatism- vertical meridian is more curved e.g. normal cornea
Against the rule astigmatism- horizontal meridian is more curved
- Toric curvature i.e. has 2 different focal lengths, and the optical power in orientations are
perpendicular to each other.
- One principal meridian is more curved than the second principle meridian. The one with
minimum curvature has the minimum power
- The configuration of the rays refracted through the toric surface is called Strum’s conoid.
- It is basically a condition where the refractive power of the cornea and lens is not the same in
all meridians, therefore instead of a single focal point there are 2 focal points
- If parallel rays fall upon such a surface, the vertical rays will come to focus sooner than
horizontal
- Both rays after refraction are perfectly symmetrical but they have 2 foci
- Whole bundle of rays= Strum’s conoid
- Distance between 2 foci= foci interval of strum
- If the retina is situated at A to E, the image will be blurred as rays never come to focus in a
single point
- The shape of bundle of light rays at different levels in strum’s conoid is as follows:
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1) At point A i.e. retinal plane at A :
- Compound hypermetropic astigmatism.
- Vertical meridian is converging more than
horizontal rays
- Both foci are behind the retina
2) At point B:
- Simple hypermetropic astigmatism
- Vertical meridian is emmetropic (vertical rays are
diverging)
- Horizontal meridian is hypermetropic
i.e. rays in one meridian focus on the retina and the
other focus lies behind the retina
3) At point C and D
- Mixed astigmatism (circle of least diffusion)
- Vertical meridian is myopic
- Horizontal meridian is hypermetropic
i.e. one focus in front of retina, the other behind the
retina
4) At point E
- Simple myopic astigmatism
- Vertical meridian is myopic
- Horizontal meridian is emmetropic i.e. the
horizontal rays have come into focus while
the vertical rays are divergent and lies in
front of the retina
5) At point F
- Compound myopic astigmatism
- Both foci are in front of the retina
- Both horizontal and vertical rays are diverging
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2) Irregular astigmatism
Present when the corneal surface is irregular. There are multiple focal points which produces a
completely blurred image on the retina.
- Can be caused by: corneal ulcerations and scarring of cornea, penetrating corneal trauma,
cataracts, lenticonus
Symptoms:
- Diminished visual acuity everything is distorted
- Asthenopic symptoms (eye attempts to compensate for the refractive error) burning
sensation in eyes or headache
Treatment: only regular astigmatism can be corrected
a) Regular astigmatism: purpose is to bring the ‘focal lines’ of the 2 main meridians together at
one focal point.
- Need a lens that refracts in only one plane
- Cylindrical lenses
- Once the 2 ‘focal lines’ have converged into a focal point, additional spherical lenses can be
used to shift this focal point onto the retina if needed
b) Irregular astigmatism:
- Cannot be corrected with eye glasses
- Keratoplasty or surgical correction of the refractive error
22. Accomodation. Disorders of accommodation (insufficiency, paralysis, spasm),

Presbyopia. Treatment of presbyopia
Accomodation= ability of clear vision from different distances
3 main factors are involved in accommodation
1) Pupil
- Influences accommodation by controlling amount of light entering the eye
- Bright light constricted parasympathetic stimulation
- Dim light dilated  sympathetic stimulation
- If pupils constrict in dim light insufficient light enters the eyes and thus not enough
photosensitive pigments in rods and cones are stimulated
2) Movements of the eyeballs- convergence
- Extraocular muscles move the eyes to obtain clear image i.e. they rotate the eyes so they
converge on the object viewed
- Autonomic control
- Convergence incomplete double vision i.e. diplopia
3) Lens  refer to question 17 on refraction
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Disorders of accommodation:
a) Accommodation spasm= inadequate contraction of ciliary muscles

Etiology: rare, functional impairment or can be iatrogenic (parasympathetic agents- miotic agents).
Rarely it is organic.
Symptoms: patient complains of deep eye pain and blurred distance vision (lenticular myopia)
Diagnosis: refraction testing and measuring range of accommodation
Treatment: treat the underlying cause, can use cycloplegics
Prognosis: completely reversible by discontinuing the parasympathomimetic agents. Also good for
patients with functional causes
b) Accomodation palsy= failure of accommodation due to paralysis of ciliary muscle

Etiology:
- Iatrogenic drug induced parasympatholytic agents e.g. atropine, scopolamine
- Peripheral causes oculomotor palsy, lesions of ciliary ganglion or ciliary muscle
- Systemic DM, diphtheria, syphilis, MS, tumours
Symptoms:
- Blurred near vision and may be associated with mydriasis where the sphincter pupillae muscle
is also involved.
Presbyopia:
- Insufficiency of accommodation due to advancing age (usually 40 years). Not an error of
refraction. Begins when the range of accommodation falls below 3 diopters.
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Etiology: physiological failure of accommodation due to
- Hardening of lens with age
- Weakness of ciliary muscle and suspensory ligament
- Excessive close work
- Prodromal stage of close angle glaucoma
Symptoms:
- Blurring of vision when reading and improved when book is helf furgher away
- Hypermetropia- earliest onset of presbyopia (as accommodation decreases with advancing
age, near vision becomes increasingly difficult)
- Myopia- delayed onset of presbyopia
Treatment:
- Prescribing convex spherical lenses for near work
- Bifocal contact lenses
23. Binocular vision

 Binocular or stereoscopic vision is when both eyes are used together- it is the ability to maintain
visual focus on an object with both eyes and creating a single visual image
 Comes from the latin roots ‘bini’= double, ‘oculus’= eye
 The left eye sees more on the left than can be seen by the other eye and vice versa
 Usually the brain gets images from both (bi) eyes (ocular) simultaneously.
 Images from both eyes are fused in the brain so only one image is perceived- the brain uses the
slight difference of both images to work out how far away an object is depth perception
 Movement perception how the brain can work out how quickly an object is moving towards
or away from a person
 Humans have a maximum horizontal field of view of about 200° with the 2 eyes. Approximately
120° of this makes up the binocular field of view (seen by both eyes)
 Binocular vision provides a much more accurate assessment of an object relative to another due
to:
- Simultaneous macular perception- both eyes
function simultaneously and normally
- Stereopsisperception of depth by the brain of
visual stimuli from both eyes in combination
- Fusion  the 2 slightly dissimilar images in each
eye are converted into a single image by fusion,
which results in stereopsis or 3D vision
- Parallax position or direction of an object differs
when viewed from different positions
Without binocular vision distortions in depth
perception and visual measurement of distance
- Remember the position of the eyes are controlled

by extraocular muscles. Every eye movement of the
eyball is a ‘synkinesis’ thus:
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o Abduction of one eye accompanied by adduction of the other
o Elevation or depression of one eye is accompanied by the same movement of the
other eye
o Only exception bilateral abduction of the eye in convergence where both medial
rectus contract together
What causes loss of binocular vision:
- Reduced vision in one eye
- Loss of coordination of movement between the 2 eyes (refer to end of the syllabus for
Strabismus)
- Problem with the brain comparing images from both eyes
Disorders of binocular vision:
 Orthophoria muscular balance with parallel visual axes i.e. normal condition of balance of
ocular muscles of 2 eyes (normal)
 Heterophoria Type of squint in which one eye tends to deviate medially or laterally.
Fusion is broken.
 Esophoria latent inward deviation
 Exophoria latent outward deviation
 Hyperphoria latent upward deviation of one eye
 Hypophoria latent downward deviation of one eye
 Cyclophoria latent rotation of one eye
 Diplopia Seeing double objects.
24. Types of correction for ametropia- glasses, contact lenses, surgery

Ametropia abnormal refractive condition (myopia, hyperopia, astigmatism) image fails to focus
on the retina
I) Glasses- lenses
Types:
Monofocal lenses
1) Spherical lens- They refract light equally along every axis
- Convex=hypermetropia, presbyopia, magnifying lens
o When the lens is moved in front of the eye, the object
moves in the opposite direction
o If an object is close to the lens, it appears magnified
- Concave= myopia
o When the lens is moved in front of the eye, the object
moves in the same direction
o An object seen through the lens appears to be diminished
in size
2) Cylindrical lens (toric)- convex or concave. They refract light only along one axis
- Convex= object moves in opposite direction
- Concave= object moves in the same direction
Use for regular astigmatism
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Prism: 2 plain refractive surfaces are at an angle to each other.
To treat heterophoria (latent strabismus), convergence insufficiency, ocular muscle paralysis,
preparation for surgery to correct strabismus
Multifocal lenses
Bifocal lenses:
- Upper and middle portion of lens for distance correction
- Lower portion is for near-field correction- gaze is lowered and converged to read
- Patients can see distant objects in focus and read using one pair of eyeglasses eliminates
need to change glasses.
Trifocal lenses:
- Lens contains a third refractive correction between distance and near-field portions.
- This intermediate portion sharply images the intermediate field between distance vision and
reading range without any need for accommodation
II) Contact lenses

Contact lenses alter the vergence power of the anterior surface of the eye. They rest on the corneal
surface
NOTE: contact lenses differ to eyeglasses because the contacts correct the refractive error closer to
the location of its origin the quality of the optical image viewed through contacts is higher than
viewed via eyeglasses.
Types:
1) Hard lens- contains a plastic which is non-toxic (PMMA- polymethyl methacrylate)
- Durable, firm, inert stable and nearly unchanging shape
- Can get corneal edema due to hypoxia of cornea, FB sensation
- Spherical astigmatism of less than 2.5 diopters
- Toric severe astigmatism
2) Soft lens- HEMA (hydroxyethyl methacrylate)= hydrophilic
- Comfortable and stable
- Delicate and short life span
3) Gas permeable lens- mixture of hard and soft material
- Minimum corneal hypoxia
- Can scratch and break
NOTE: the cornea needs oxygen. So contact lens materials should be oxygen-permeable
Complications: conjunctivitis, corneal epithelial edema results due to corneal hypoxia
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III) Surgery
1) Radial keratotomy (RK): low myopias (-1 -6 D). Decreases myopia
by flattening the corneal curvature the central zone (3-4mm) is
marked out and use a diamond knife to make deep radial incisions up
to the Descemet’s membrane between the limbus and optical zone.
Uneven healing can lead to irregular astigmatism
2) Photorefractive keratectomy (PRK): for myopia (-

1-8D). The central part of the cornea (optical zone)
is reshaped by the laser after corneal epithelial
debridement. Use computer for precision of laser to
sculpt surface of cornea. For hypermetropia, myopia
and astigmatism. Only very thin layers are
removed doesn’t weaken the eye
3) LASIK= laser-assisted in situ keratomileusis

It is a modification of PKK. We cut the cornea and get a flap of it flap is folded to the side and we
use a laser to remove tissue from the exposed surface, then the flat is replaced back. For myopia nad
astigmatism
25. Examination methods in Opthalmology: Examination of the conjunctiva,

Lacrimal system, Cornea, Sclera, Anterior chamber, Iris, Pupil, lens, Posterior
segment of eye, Intraocular pressure
Examination of the conjunctiva:
 Direct inspection
 Bulbar conjunctiva is visible between the eyelids
 Palpebral conjunctiva- averting the upper or lower eyelids
 Normal smooth, shiny and moist
Look for any reddening, secretion, thickening, scars of FBs. Both upper and lower eyelids examined
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for congestion in conjunctivitis, scarring (chemical burn), symblepharon (adhesion of lids to globe)
e.g. chemical burn
Examination of the lacrimal system:

Schirmer tear testing: for info of quantity of watery component in tear secretion
Swelling and redness (mucocele), regurgitation test- there is watery, mucoid or purulent discharge
through the puncta on pressure over the sac, fistula may be present due to repeated rupture or
leakage from the infected ac with epitheliazation
Patency of the nasolacrimal duct is tested by instilling fluorescein solution into the conjunctival sace
of the eye dye is present in nasal mumous expelled into paper tissue after 2 mins lacrimal duct
is open
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Examination of the cornea:
use a light source and a loupe. The cornea is smooth, clear and refractive. Reflection is distorted in
any corneal defects.
Epithelial defects intense green colour after application of fluorescein dye, corneal scars and
infiltrates are grayish white.
We need to evaluate the corneal sensitivity too examined bilaterally to detect any differences
between both eyes  patient looks straight ahead and the examiner holds the upper eyelids and
touches the corena anteriorly
Examination of the Sclera:

I. Curvature and colour thinning and pigmentation in myopia
II. Vessles ciliary injection and nodule is seen in scleritis
Anterior portion examined directly by a slit lamp. Sclera posterior to the equator ultrasound
Examination of the anterior chamber:

The anterior chamber is filled with clear
aqeous humour. Cellular infiltration and
collection of pus is known as hypopyon.
Bleeding in anterior chamber (hyphema)
- It is important to evaluate the depth
of the anterior chamber (normal
depth= 2.5mm iris will be well
illuminated by a lateral light source)
- Shallow anterior chamber medial
shadow on the iris
NOTE: dilation of pupil with a mydriatic is

contraindicated in patients with shallow
anterior chamber due to risk of angle
closure glaucoma
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Examination of the iris:
I) Colour= heterochromia iridum parts of the same iris are of different colour
- Muddy= iritis
- White atrophic patches (glaucoma)
II) Pattern= ill-defined or lost pattern (chronic iridocyclitis)
III) Position= anterior synechia (adhesion of iris to posterior surface of cornea), posterior
synechia (adhesion to lens capsule)
Examination of the pupil

Size= 2-4mm
Anisocoria= unequal size of both pupils
Miosis= pupil is small and constricted (spincter pupillae muscle)
Mydriasis= pupil is dilated
 Direct light reflex examiner first covers both eye of patient, then uncovers one eye
pupil will constrict after latency period of 0.2s. other eye tested in same manner.
 Indirect light reflex examiner places hand on the bridge of patient’s nose to ‘separate’ the
patients eyes prevents incident light from directly striking the eye being examined (direct
light reflex). The examiner illuminates one eye while observing the other non-illuminated
eye both pupils constrict
 Evaluating near reflex/ accommodation relfex: patient focus on a distant object then on an
object in the near field (10cm from eyes e.g. patient’s finger) normal near reflex if both
eyes converge with accommodation and miosis (contraction)

Examination of the Lens:
Use slit lamp. Can also use focused light
Direct illumination red reflex of fundus.
Grey shadows lens opacities cataracts
Examination of the posterior segment of the eye?? I think this is the subjective examination of
retinal functions e.g. visual acuity (snellens test), visual field etc
Examination of intraocular pressure:

With the patient’s eyes closed, the examiner places hand on the patients head and palpates the eye
through the upper eyelid with both index fingers. Repeat on other eye.
‘rock hard’ eyeball acute angle closure glaucoma. Slight increases in intraocular pressure e.g.
chronic glaucoma will not be palpable
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26. Diagnostics with ultrasonography, Fluorescein angiography,
electrophysiological tests.
Fluroescein angiography (FA)
 Diagnostic procedure that uses a special camera to record the blood flow in the retina
 Fluorescein dye is injected into a vein
(antecubital vein) dye passes through BVs of
eye photographs taken to record the blood
flow in the retina.
 Can reveal abnormal BVs or damage to the
lining underneath the retina.
 Images captured in black and white
 Dye will fluoresce the BVs
 Detect hypofluorescence (darkness- vascular
filling defect e.g. corneal scar, cataract) or
hyperfluorescence (brightness- leaking
fluorescein from incompetent BVs e.g. diabetic
neovascularization)
Ultrasonography:
The eye is a superficial fluid filled structure thus an
ultrasound is a good modality to view ocular pathology and anatomy. Sound waves generated
>20kHz are reflected back to the transducer by tissues. When sound waves return, the piezo-electric
crystal in the transducer vibrates electrical impulse translated to an image.
Indications obtain globe length, tumours, visualize lens dislocation, detect retinal detachment.
B- mode scan (B= brightness) 2D image of orbital structures
A mode scan (A= amplitude) precise measurement of optic nerve and muscle thickness
Can combine with Doppler scans to evaluate blood flow.
Electrophysiological tests:
 Electroretinaogram (ERG)
Diagnostic test that measures the electrical activity generated by neural and non-neuronal cells in
the retina in response to a light stimulus.
The electrical response is due to retinal potential generated by light flux of sodium of K+
i. Negative ‘a’ wave activity of rods and cones reflects hyperpolarization of
photoreceptors due to closure of Na+ channels.
ii. Positive ‘b’ wave derived from inner retinal layers  hyperpolarization of
photoreceptor cells result in decrease neurotransmitter released depolarization
follows (increased extracellular K+)
iii. Positive ‘c’ wave from retinal pigment epithelium and photoreceptors
 Electro-oculogram
The changes in the resting current when the eyes are moved laterally and picked up by the
electrodes placed at the inner and outer canthi. Absent in retinal dystrophies and degenerations
46 | P a g e
Orbital diseases:
27. Clinical findings of orbital diseases

Change in position of the globe with respect to the orbital rim is a cardinal symptom of many
orbital diseases
Cardinal symptoms: unilateral or bilateral

 enophthalmos (recession of the eyeball within the orbital cavity) or
 exophthalmos (protrusion of the eyeball) are characteristic of many orbital disorders.
 DDx with pseudoexophthalmos= due to a very long eyeball in severe myopia and
pseudoenophthalmos= small eyeball e.g. microphthalmos
28. Inflammatory and vascular orbital diseases

NOTE:
- Proptosis= passive or mechanical protrusion of the eyeball
- Exophthalmos= active protrusion of the eyeball forwards
1. Inflammatory orbital diseases

The orbital cavity is in close proximity to the paranasal sinuses  susceptible to inflammation
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Second most frequent group of orbital disorders after Graves’ disease
a) Orbital cellulitis
Most frequent cause of exophthalmos in children
Definition:
 Purulent inflammation of cellular tissues of orbit. Cardinal symptoms of limited motility and
general malaise
Etiology:
 Extension of infection from
neighbouring parts e.g. sinuses, teeth,
face, lips etc
Symptoms & signs:
 Exophthalmos
 Severe pain in moving the eyeball
 Chemosis (conjunctival swelling) and
swelling of lids inability to open eyes
 Impaired eye movement ‘cemented’
globe
 Mild proptosis and impaired motility can cause diplopia
DDx:
 Preseptal cellulitis (inflammation is anterior to orbital septum)
Treatment:
 High IV Abs
 Analgesics and anti-inflammatories
 Treatment of underlying sinusitis
 Hot compress relieves the pain and prevents stasis
Complications:
 Optic neuritis  subsequent atrophy and loss of vision
 Abscess
 Thrombophlebitis of orbital veins can result in cavernous sinus thrombosis with meinigitis,
cerebral abscess or sepsis
b) Cavernous sinus thrombosis:
 Superior and inferior ophthalmic veins enters the sinus anteriorly
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 Superior and inferior petrosal sinus leaves the sinus posteriorly
 Sinus communicates with pterygoid plexus, cerebrum and middle ear directly and indirectly
Definition:
 Rare but severe acute clinical syndrome in which the spaces of the cavernous sinus posterior
to the orbital cavity become thrombosed. Not an orbital disorder in a strict sense
Etiology:
 Purulent inflammation has spread from middle ear, petrous bone, orbital cavities or from
facial skin via the angular vein
Symptoms:
 Headache, stupor, fever and vomiting
Signs:
 Edema over mastoid process of temporal bone of affected side
 Paralysis of opposite lateral rectus muscle (bilateral involvement)
 Paralysis of extraocular muscles  total opththalmoplegia , if optic nerve also involved
orbital apex syndrome
 Proptosis and exophthalmos
 Fundus retinal veins dilated, papillitis, papilledema
The limited motility of the globe is neurogenic due to damage to the nerves in the cavernous sinus
rather than mechanical limitation of motility (orbital cellulitis)
Treatment:
 High dose systemic ABs
 Anticoagulation therapy
c) Orbital Pseudotumour
Definition: lymphocytic tumour of unknown origin
 Eye swelling, chemosis, exophthalmos (unilateral or bilateral). Limited motility with diplopia.
 CT and MRI shows diffuse soft tissue swelling and need biopsy to confirm diagnosis. High
systemic cortisone, orbital radiation therapy or surgical intervention
DDx:
 Graves
 Orbital cellulitis
d) Myositis: special form of pseudotumour but lymphatic infiltration involves one or more
ocular muscles
e) Orbital periostitis: inflammation of periosteum lining of orbital cavity (TB, syphyllis)
f) Mucocele: mucous filled cysts invade the orbital cavity in chronic sinusitis.
Vascular orbital diseases: rare. Pulsating exophthalmos

a) Pulsating Exophthalmos
Definition: acute exophthalmos with palpable and audible pulsations
Etiology: abnormal communication between cavernous sinus and ICA (direct shunt) or its branches
(indirect shunt) arteriovenous aneurysm
Symptoms and signs:
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 Unpleasant sound in the head like a machine and synchronous with their pulse
 Dilated episcleral and conjunctival vessels
 Increased intraocular pressure
b) Intermittent Exophthalmos varicose dilation of orbital veins  uni-/bilateral

exophthalmos
c) Orbital hematoma orbital bleeding usually post-traumatic (can be due to

coagulopathy e.g. Vit C (-), anticoagulants. Exophthalmos accompanied by hematoma,
eyelid swelling, subconjunctival hemorrage
29. Endocrine diseases and tumours of the orbit

1) Endocrine diseases- endocrine exophthalmos
Etiology:
- Generalized disturbance of endocrine system
- Increased secretion of thyrotropic hormone from pituitary due to low thyroxin levels
- Increased secretion of exophthalmos producing substances (EPS) and long acting thyroid
stimulators (LATS)
Types:
- Hyperthyroidism- Grave’s disease, exophthalmic goitre, thyrotoxicosis mild exophthalmus
- Hypothyroidism- thyrotropic exophthalmos  extreme exophthalmus (after thyroid gland is
removed usually)
Symptoms:
- Anterior protrusion of eyeball with inability to close lids
Grave’s disease:
Definition: autoimmune disorder thyroid dysfunction inflammatory lymphocytic infiltration of
orbital cavity  affects ocular muscles fibrosis later
Most common cause of both bilateral and unilateral exophthalmos
Symptoms:
 Red, dry eyes with sensation of pressure. Limited ocular motility double vision
Signs: exophthalmos is a cardinal sign.
Eyelid signs are as follows:
Dalrymple’s sign Upper eyelid is retracted giving a peculiar stare
Von Graefe’s sign Upper lid lags on downward movement of eye
Gifford’s sign Upper eyelid is difficult to evert (eyelid edema)
Stellwag’s sign Infrequent and incomplete blinking
Kocher’s sign Fixed gaze
Clinical diagnosis:
 Thickened extraocular muscles (US or
CT)
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 Signs and symptoms
DDx: orbital tumour or pseudotumour
Treatment:
- Manage thyroid dysfunction systemic iodine and antithryoid drugs
- Prednisone (corticosteroid) helps with edema and infiltration
- Radiation therapy of orbital cavity
- Surgical decompression of orbital cavity recurrent cases that don’t respond to treatment to
avoid compressive optic neuropathy
2) Tumours of the orbit:

All orbital tumours displace the globe causing exopthlamos (causing limited ocular motility).
Hemangioma:
 Most common benign orbital tumour of adults and children
 Nasal superior location
 Capillary hemangiomas in children and cavernous hemangiomas in adults.
 Can use cortisone and low RT
Dermoid and epidermoid cyst:
 Most common orbital tumours in children
 Dermal or epidermal structures displaced in deeper layers
 Usually located anterior to the orbital septum (not the orbit itself)
 Complete removal- T
Meningioma:
 Can be from the optic nerve (menangioma of optic nerve sheath) or from within the cranium
(sphenoid menangioma)
 Exopthalmus, limited movitily, compressive optic neuropathy
 Associated with Neruofibromatosis
Burkitt’s lymphoma
Rhabdomyosarcoma- most common primary tumour in children. Grows rapidly, DDx with orbital
cellulitis.
Most common orbital metastasis originate from nueroblastomas.

Optic nerve gliomas: second most common malignant orbital tumour in children. Associated with
neurofibromatosis.
Neurofibromatosis: genetic disorder that causes tumours to form on nerve tissue
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Eyelid diseases
30. Clinical findings in eyelid diseases
I) Position- drooping of upper lid below its normal position
occurs in ptosis
- Outrolling of lid margin ectropion
- Inrolling of lid margin entropion
II) Palpebral aperture- may be narrow e.g. ptosis
- It may be wide e.g. exopthlmos, Bell’s palsy
III) Movement
- Restricted in symblepharon i.e. adhesion of the lids to the globe as
in acid burn cases
IV) Margins- crusts seen in blepharitis i.e. inflammation of the lid margin
- may be thickened (tylosis)
V) lashes
- misdirected backwards and rub against the cornea (trichiasis)
- scanty (madarosis)
- white colour (poliosis)
- multiple rows of eyelashes present which rub against the cornea (distichiasis)
VI) Glands
- Stye situated at or near the lid margin
- Chalazion away from lid margin
VII) Lacrimal puncta
- Eversion ectropion
- Occlusion due to scarring or eyelash
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31. Congenital anomalies of the eyelids
Coloboma:
Definition
- Triangular notch in the upper lid margin near the nasal side
usually. The base of it is at the eyelid margin
Etiology
- Defective closure of optic cup
Symptoms
- Depending on the extent drying of conjunctivae and cornea can
lead to ulceration
Treatment
- Plastic surgery close the defect or skin flap
Epicanthal folds:
Crescent fold of skin usually extending bilaterally between
upper and lower eyelids and covering the medial angle of the
eye. Rare and harmless. Typical in eastern Asians.
Pronounced fold will cause esotropia (eye turns inwards i.e.
strabismus)
Blepharophimosis
- Shortening of the horizontal palpebral fissure without
pathologic changes of the eyelids.
- As long as the centre of the pupil remains unobstructed despite the decreased size of palpebral
fissure no need for surgical enlargement of palpebral fissure (plastic surgery)
Ankyloblepharon:
- Horizontal shortening of the palpebral
fissure with fusion of eyelids at the lateral
and medial angles of the eye
- Partial or total fusion can occur between
upper and lower lids is bilateral
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32. Diseases due to Various eyelid positions
Trichiasis eyelids misdirected backwards and rub against cornea due to
entropion (discussed in this question), Blepharitis (next question), recurrent stye
(next question) or scars of lid e.g burn, operation. FB sensation and photophobia.
Irritation, lacrimation. Corneal ulcer is a complication
Entropion
Definition:
 lid margins rolled inwards. Margin of eyelid and eyelashes in contact with the globe not the
conjunctiva only.
Etiology:
 congenital entropion- skin and orbicularis oris thickened. Usually lower eyelids
 Spastic entropion – only lower eyelid.
- Palpebral ligaments, eyelid retractor become lax with age and tarsus tilts
inwards
- Blepharospasm- abnormal contraction of eyelid muscles
- Senile enophthalmus due to atrophy of orbital fat tissue unstable lower
eyelid
 Cicatricial entropion- contraction of palpebral conjunctiva due to
infection or trauma e.g. burns, chemical injuries.
Signs and symptoms:
- Constant rubbing of eyelashes against eyeball (trichiasis) FB irritation Blepharospasm
exacerbates entropion
- Conjunctiva red and eye fills with tears
Treatment:
- Congenital semicircular resection of skin and orbicularis oculi
- Spastic surgery.
- Cicatricial
o resection of skin and muscle remove the strip of skin and muscle 3mm away from
lid margin
o resect tarsus, skin and muscle
o burow’s operation eyelid everted with a spatula, horizontal incision through
conjunctiva and tarsal plate along the whole lid margin
Complications:
- damage corneal epithelium with superinfection corneal ulcer and scarring
Ectropion:
Definition:
 lid margin rolls outwards i.e. turned away from eyeball. Almost exclusively affects lower
eyelids.
Etiology:
 Congenital ectropion
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 Senile ectropion palpebral ligaments and tarsus
become lax with age- tarsus sags outwards
 Paralytic ectropion parlysis of orbicularis oculi muscle
that closes the eyelid
 Cicatrical ectropion infection or injury
 Mechanical ectropion thickening of conjunctiva
Symptoms
- Epiphora i.e. constant eye watering (eversion of the punctum= tears flow down the cheek
instead of draining in nose)
Signs:
- Conjunctive dries and appears thicker in texture
- Chronic conjunctivitis
- Corneal ulcer
- Eyelid inflammation- blepharitis
Treamtent:
Usually surgery tighten the lower eyelid followed by horizontal tightening of the skin. Or plastic
surgery to correct eyelid deformity
Ptosis:
Definition: drooping of upper lid below its normal position.
Unilateral or bilateral. Greek ptosis= falling.
Etiology:
1) Congenital- most cases. Hereditary. AD.
- Maldevelopment of levator palpebrae muscle (myogenic)
- Congenital weakness of rectus muscle
- Aplasia of oculomotor nerve (neurogenic)
Upper lid droops over the centre of the pupil involves increased risk of amblyopia. Also link
epicanthal folds and blepharophimosis. Usually unilateral ptosis
2) Acquired
- Neurogenic ptosis=
o Partial or complete paralysis of CN III (paralytic ptosis) usually unilateral and covers
whole eye.
o lesions in sympathetic nerve (sympathetic ptosis- Horner’s palsy)
- Myogenic ptosis- MG (bilateral, assymetrical and progresses) or MD
- Traumatic ptosis= after injuries
Symptoms:
- No symptom if pupil not covered by the lid (pupil covered visual disturbance)
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- Cosmetic disfigurement
- Wrinkling of forehead(contract frontalis
muscle to increase the palpebral fissure),
tilting head backward, elevate eyebrow
Signs:
- Narrow palpebral fissure
- No skin folds of upper eyelids
- ‘lid lag’ upper lid doesn’t move when the
patient glances down (for congenital ptosis-
DDx with acquired ptosis)
Treatment:
- Congenital surgical retraction of upper lid
- Acquired depends on cause.
Complications:
- Amblyopia if congenital untreated
- Surgical overcorrection can lead to ulceration
as a result of incomplete closure of the lids
Blepharospasm:
Definition: involuntary spasmodic contraction of
orbicularis oculi muscle (facial nerve supplies it).
The palpebral fissure appears contracted and
narrowed or closed at the outer canthus. Eyebrows are
lowered
 Etiology: prolonged bleopharospasm or epiphora
 Symptoms: triad= photosensitivity, epiphora,
blepharospasm
 Treatment: mild muscle relaxants. Severe
trasnsect the fibres of the facial nerve supplying
the muscle.
Lagophthalmos:
Incomplete closure of palpebral aperture when eyes are
shut
 Etiology: congenital, ectropion, ptosis, paralysis
of OO muscle
 Complication: keratitis
 Treatment: AB eye ointment
Ankyloblepharon:
Partial or incomplete adhesion of margins of the 2
eyelids e.g. due to chemical burn
Symbelapharon:
Adhesion of the lids to the globe due to ulcers, diphtheria or burns
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Symptoms: lagophthalmos, diplopia, cosmetic disfigurement.
33. Inflammatory diseases of the eyelids

Blepharitis:
Definition: chronic inflammation fo lid margins
Etiology:
 Follows chronic conjunctivitis due to Staphylococcus
 Parasites, head louse
Types:
1) Squamous blepharitis: due to dandruff on scalp and
eyebrows  more mild
- Numerous white coloured small scales accumulate among
eyelashes
- Eyelashes fall out easily
- Hyperaemic underlying skin
2) Ulcerative Blepharitis: infective condition  more
progressive
- Yellow crusts glue lashes together
- Removal of crusts shows small ulcers that bleed easily
- Eyelashes fall and replaced by misdirected lashes
Symptoms:
 Itching, redness, sore, lacrimation, photophobia
Sequelae:
 Trichiasis, tylosis (hypertrophy of lid margin), madarosis (scanty eyelashes- destroyed roots),
ectropion, epiphora
Treatment:
 Bathe lid margins with sodium bicarbonate solution to remove scales and crusts
 Epilation of eyelashes
 AB ointment and drops
Hordeolum (Stye)
Definition, etiology and types:
 acute suppurative inflammation of Zeis’s gland or gland of Moll (external hordeolum)  S.
Aureus.
 Internal hordeolum is due to infection of meibomian glands more
violent because the gland is larger and is embedded deeply in dense
fibrous tissue
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 Hordeolum is often associated with acne and diabetes.
Symptoms: painful nodules with central core of pus
 External hordeolum= appears at margin of eyelids where sweat glands are located
 Internal= only revealed by everting the eyelid and is accompanied by conjunctivitis.
Signs:
 External= painful and hard swelling in lid margin. Red and edematous lid margin. Yellow
discolouration i.e. abscess can form pointing near the base of the lash
 Internal= everting lid shows yellow spot (pus)
Treatment:
 Antibiotic ointment and application of dry heat (red heat lamp) will rapidly heal the lesion.
Incision and drainage of abscess.
Chalazion (tarsal or meibomian cyst)

Definition:
 Chronic granulomatous inflammation of
the meibomian gland or tarus
 It’s a firm nodular bulb
Etiology:
 Chronic inflammation glandular tissue
replaced by granulation tissue containing
giant cells
 Multiple in number
 More common in adults
Symptoms:
 Pain if chalazion is superinfected
 Swelling of lid
 Single or multiple in number
Signs:
 Small non-tender hard swelling in the lid, slightly away from the lid margin
 Everting the lid shows red or purple lining over the swelling becomes grey later. Yellow
pyogenic organisms infect it
Treament:
 Chalazion clamp lesion incised and fatty contents removed with a curette.
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Lacrimal gland diseases
34. Diseases of the lacrimal gland- acute and chronic dacryoadenitis, Mikulicz
syndrome, tumours of the lacrimal gland.
Acute dacryoadenitis:
Definition: acute inflammation of the lacrimal gland. Rare. Intense inflammation and extreme
tenderness on palpation
Etiology: associated with mumps, influenza, infectious mononucleosis

etc. Pneumococci and staphylococci
Symptoms:
 Marked pain, redness and swelling in upper and outer angle of
orbit. Excessive eye watering. Usually unilateral
Signs:
 Congestion and chemosis of conjunctiva
 Enlargement & tenderness (maybe) of preauricalr glands
Complications:
 Suppuration leads to abscess and fistula formation
 Drying of eye can cause degeneration and atrophy of the gland
Treatment:
 Depends on underlying cause. moist heat, disinfectant compresses and local ABs
DDx:
 Internal hordeolum (smaller and circumscribed)
 Eyelid abscess (fluctuation)
 Orbital cellulitis (assoc. with reduced motility of eyeball)
Chronic dacyroadenitis:
Etiology: chronic inflammation of the lacrimal gland due to incomplete healing of acute
dacryoadenitis. Can be due to TB, leukemia, sarcoidosis.
Symptoms: usually no pain. S-curve deformity of palpebral fissure resulting from welling of the gland
is apparent (same as in acute)
DDx: periostitis
Treatment: depend on underlying cause.Systemic corticosteroids.
Mikulicz’s syndrome:
Definition: symmetrical enlargement of the lacrimal and salivary glands (parotid) usually with
lymphoid tissue hyperplasia. Etiology is unknown, may be autoimmune. Occurs in association with
underlying disorders e.g. TB, sylphilis, leukemia.
Symptoms:
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 Xerostomia difficult swallowing
 Enlarged lacrimal glands absent or decreased tears
 Enlarged parotid gland
Treatment:
 Biopsy is key to diagnose.
 Treat underlying cause
 Can use artificial tears to maintain eye moisture
Tumours of the lacrimal gland:
Accounts for only about 7% of orbital neoplasms. Much rarer in children
 Benign pleomorphic adenoma slowly progressive painless swelling in upper lid. Can be
due to mechanical ptosis and should be excised
 Malignant: adenoid cystic carcinoma and pleomorphic adenocarcinoma.
Symptoms:
 Grow very slowly
 After awhile, they displace the eyeball inferiorly and medially double vision
Diagnose: CT, US, MRI, biopsy.
Treatment: entire tumour should be removed. Removal of the entire contents of the orbit may be
required. Systemic administration of corticosteroids indicated for unspecific tumours.
35. Lacrimal drainage system diseases- Stenosis (atresia of the lacrimal punctum,
Canalicular stenosis, Dacryocystitis (acute, chronic, neonatal))- clinical
findings and treatment
Atresia of the lacrimal punctum i.e. punctal stenosis
Can be congenital or acquired. Acquired is a condition in which the external opening of the lacrimal
canaliculus (located in the nasal part of the palpebral margin) is narrowed or occluded. Rare cause of
epiphora (persistent tearing)
So, what and where is the lacrimal punctum?
 In the medial part of the eyelid margins near the medial cathus
 It opens into the tear layer. Tears are collected through the puncti into the canaliculi
Etiology:
 Chronic lid inflammation (chronic blepharitis)
 Dry eye syndrome
 Infections of eyelids e.g. trachoma, herpes simplex
 Long-term treatment of antiglaucoma agnets e.g. timolol
Treatment:
 Punctum dilator inserted in the punctum
Canalicular stenosis:
Can be;
 congenital (congenital anophthalmos or severe microphthalmos) or
 acquired e.g. Blepharitis, canaliculitits, infections, trauma (burns), drug induced (Docetaxel,
pilocarpine)
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pathophysiology:
 inflammatory conditions cause the lacrimal mucosa to swell fibrotic narrowing or
obstruction
Symptoms:
 excess moisture of eyes, overflow of tears on the cheek and mildly blurred vision
signs:
 increased tear lake, epiphora, sentosis of punctum and difficulty in passing lacrimal dilator or
probe
treatment: treat the underlying cause. Use topical steroid drops and artificial tears.
- Surgery if incomplete stenosis (canalicular stenting and intubation), removal of the
canaliculus and directly anastomosing
the lacrimal sac mucosa.
NOTE: we can locate stenosis by probing and
irrigation. Use of a topical anaesthetic then a
conical probe is used to dilate the punctum. The
lower lacrimal system is flushed with physiologic
slaine. If the passage is unobstructed, the solution
will drain freely in the nose
!! canalicular stenosis will result in reflux through

the irrigated punctum
Dacryocystitis: inflammation of the lacrimal sac (usually due to obstruction of the nasolacrimal
duct). Unilateral in most cases
a) Acute dacryocystitis:
Definition: acute suppurative inflammation of the lacrimal sac
Etiology: usually a stenosis within the lacrimal sac. Retention of tear fluid
leads to infection from Staph, pneumococci, Strep etc.
Symptoms:
 Highly inflamed, painful swelling in the vicinity of the lacrimal sac
 Malaise, fever
 Conjunctival congestion
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 An abscess in the lacrimal sac can forom can rupture skin and from a draining fistula
Complication:
 acute inflammation that has spread to the surrounding tissue of the lids and cheek entails a
risk of sepsis and cavernous sinus thrombosis
DDx:
 hordeolum (small, circumscribed, nonmobile inflamed swelling)
 orbital cellulitis (Assoc. with reduced motility of eyeball)
Treatment:
 hot compress, systemic ABs, analgesics, anti-inflammatories
 pus from fluctuating abscess needs to be drained via an incision
 after the acute symptoms have subsided dacryocystorhinostomy (create a new drainage
route for the tear fluid to bypass the nasolacrimal duct- direct connection between
lacrimal sac and nasal mucosa)
b) Chronic Dacryocystitis:
Definition: common chronic suppurative inflammation of the lacrimal sac due to obstruction of the
nasolacrimal duct (secondary to inflammation of CT or nasal mucosa, pressure by nasal polyp,
hypertrophy of inferior turbinate)
Symptoms: increased lacrimation. Applying pressure on the inflamed lacrimal sac causes large
amount of transparent mucoid pus to regurgitate through the punctum.
Complication: corneal ulcer
Treatment: surgery – dacryocystorhinostomy or removal of lacrimal sac
c) Neonatal dacryocystitis
Etiology:
Failure of canalization of the nasolacrimal duct, the lumen is blocked by epithelial debris. Can be
bilateral. The retention of tear fluid provides ideal growth conditions for bacteria.
Symptoms: 2-4 wks after birth pus secreted from puncta. Pus can collect into the palpabral fissure.
Conjunctiva not usually involved. Epiphora evident in 2nd week of life (usually tears secreted 3-4
weeks after birth)
DDx: conjunctivitis
Treatment:
a) Conservative massage over the lacrimal sac area and clean the
discharge multiple times a day. Broad spectrum antibiotics- eyedrops
and nose drops
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36. Dry eye syndrome- types, clinical findings, treatment
Types:
- keratoconjunctivitis sicca (dry eyes affecting cornea and conjunctiva)
- Keratitis sicca (dryness and inflammation of cornea)
- Dysfunctional tear syndrome (inadequate quality of tears)
Symptoms of dry eye:

- Burning, itching, aching, heavy and fatigued eyes, dry sensation, red eyes, photophobia,
blurred vision.
I’ll mainly talk about Keratoconjunctivitis Sicca;
Definition: non-infectious, characterised by reduced moistening of conjunctiva and cornea (Dry eyes)
Tear film:
1) Oily component (outer lipid layer- secretes meibum) produced by meibomian glands in the
lids prevents tear film from evaporating too quickly and increase lubrication 
pathology= ‘evaporative dry eye’
2) The watery component (middle aqueous layer) is produced by lacrimal and accessory
lacrimal glands supplies oxygen to the cornea, antibacterial function to wash away debris
3) Mucin component produced by goblet cells in the conjunctiva , glands of Henle and Manz
helps anchor and spread the tears across the surface of the eyes i.e. it makes the corneal
surface hydrophilic so tear film sticks to the cornea
Etiology: can represent a disorder in and of itself

1) Reduced tear production: due to systemic disorders e.g. RA, or atrophy/destruction of
lacrimal gland
2) Altered composition of tear film: Vit. A deficiency, some oral contraceptives, environment
e.g. air conditioning. The tear film breaks up too quickly  corneal drying
Symptoms:
- Burning, red eyes
- Reflex lacrimation from wind, cold, low humidity
- FB sensation
Diagnose:
- Schirmer tear testing shows recution of water content of tears, tear break-up time (for mucin
content of tear film) is reduced (<5 sec).
Treatment:
- Artificial tear solutions
- Punctual plugs to temporarily close the puncta
- Severe= surgical obliteration of the puncta
NOTE: dry eyes is the opposite to illacrimation (epiphora), which is due to
hypersecretion of the lacrimal gland  emotional distress, increased eye irritation
or caused by obstructed drainage stenosis of lacrimal system, eyelid deformity (ectropion,
entropion)
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Diseases of the conjunctiva
37. Diseases of the conjunctiva- clinical findings
i. Bulbar:
- Congestion
- Secretion, chemosis or edema
- Growths or spots or cysts
ii. Palpebral
- Congestion conjunctivitis
- Follicles, papillae, FB
- Scarring e.g. burn, trachoma
- Symblepharon (adhesion of lids to globe)
iii. Plica semilunaris- can be displaced
iv. Caruncle- inflammation or growth
38. Inflammatory diseases of the conjunctiva- acute conjunctivitis

Okay, first let’s just do conjunctivitis as a whole
Definition: inflammatory process involving the surface of the eye and is characterized by vascular
dilation, cellular inflammation and exudation.
- Acute abrupt onset, initially unilateral then bilaterally within one week. <4 weeks
- Chronic >3-4 weeks
Symptoms:
- Reddened eyes
- Sticky eyelids in morning due to increased secretion
- Swelling of the lids
- FB sensation, sensation of pressure, burning sensation
- Photophobia and alcrimation
Conjunctival reactions include:
o Hyperemia- congestion of conjunctival vessels reddened eyes= typical sign. Usually in
fornix
o Discharge mucoid, purulent, watery (allergic and viral), bloody, mucopurulent
o Chemosis white glassy edema and swelling of the conjunctiva projecting from the
palpebral fissure.
o Epiphora – reflex lacrimation
o Follicle  lymphocytes in the palpebral and bulbar conjunctiva accumulate in masses with
granular appearance
o Papillae cobblestone projection with a central network of finely branching vessels.
o Membranes and pseudomembranes- form from necrotic epithelial tissue. Bleeds on
removal (true membrane), doesn’t bleed (pseudomembrane)
o Swollen LNs (viral conjunctivitis)
Acute conjunctivitis:
1) Acute mucopurulent conjunctivitis
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Etiology: Staph, Strep, pneumococcus, Haemophilis aegyptus, adenovirus etc. Often assoc. with
measles and scarlet fever. Usually bilateral
Symptoms: redness, grittiness, feeling of FB, mucopurulent discharge and crusting in fornices and lid
margins, sticking of lids in the morning
Signs: congestion, fiery red eye, chemosis
Treatment: frequent washing of the eye with warm saline/H20, control infection e.g. AB eyedrops
and eye ointment.
2) Purulent conjunctivitis (Acute Blenorrhoea)
2 types:
a) Adults acute purulent conjunctivitis
b) Babies opthalmia neonatorum
Acute purulent conjunctivitis:
o Etiology: gonococcus infection mainly. But the same clinical picture can be seen in Staph,
strep.
o Diphteriae, Chlamydia oculogenitalis.
o Symptoms: swelling of lids and conjunctiva, purulent discharge at lid borders, canthi and
fornices
o Signs: congestion, red and velvety palpebral conjunctiva, severe chemosis and pus,
preauricular lymphadeopathy
o Complications: corenal ulcer, iritis diminished vision
o Treatment: same as above
Opthalmia neonatorum:
o Etiology: mostly Chlamydia and gonococcus. Can be S.aureus,
Strep. Pneumonia. Usually bilateral and occurs due to maternal
infection
o Symptoms: any discharge from the baby’s eye during 1st week of
life is alarming (tears secreted 3-4wks after birth).
- Bright red conjunctiva with pouring of thick yellow pus
o DDx: neonatal dacryocystitisonly symptomatic 2-4 weeks after
birth with reddening and swelling of the region of the lacrimal
sac and purulent discharge from the puncta.
o Complications: corneal ulcer and opacity
o Treatment: broad spectrum ABs. If gonococcal (gentamicin eyedrops), if chlamydial
(erythromycin), if herpes simplex (acyclovir)
3) Membranous conjunctivitis (Diptheric conjunctivitis)

The conjunctival surface is covered by a fibrinous membrane, usually in children
o Etiology: Corynebacterium Diptheriae. Can be gonococcus, pneumococcus, Strep can also
produce a membrane
o Symptoms: serous or mucopurulent discharge
o Signs: everting the eyelids shows a white membrane covering the palpebral conjunctiva
which peels without too much bleeding.
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o DDx: pseudomembrane caused by gonococcus, Staph, pneumococcus, strep, E. coli often
associated with measles, whooping cough and influenza. Membrane peels off easily and the
underlying epithelium is intact
39. Allergic Conjunctivitis and Kertoconjunctivitis

Allergic conjunctivitis
1) Acute or subacute Catarrhal conjunctivitis- urticarial reaction to the allergen
Etiology:
1. Bacterial protein of endogenous nature e.g. staph in nose or URT
2. Exogenous protein e.g. hay fever, contact with animals
3. Chemicals, cosmetics, drugs e.g. atropine, hair dye
Symptoms: itching, watery secretion, redness of conjunctiva, skin of the lid is red and swollen
DDx: from acute bacterial infection (in allergic conjunctivitis there’s marked hyperemia and itching,
watery secretion)
Treatment: remove the allergen, antihistamines, vasoconstrictors (adrenaline- reduce congestion)
2) Phlyctenular conjunctivitis (Eczematous conjunctivitis)

Definition: allergic reaction of the conjunctiva due to endogenous proteins.
Characterized by formation of a bleb or nodule near the limbus (phlycten= bleb
compact mass of mononuclear cells, lymphocytes and polymorphs under the
epithelium)
Etiology:
1. Allergic reaction to endogenous bacterial protein e.g. TB
2. Staph infections of tonsils and adenoids
Symptoms: discomfort, itching, irritation, reflex lacrimation. Small, round, grey-yellow nodules on on
bulbar conjunctiva or near the limbus
Clinical types:
1. Conjunctiva alone is involved phlyctenular conjunctivitis
2. Bleb is at the limbus involving conjunctiva and cornea phlyctenular kerato-conjunctivitis
3. Cornea alone involved phlyctenular keratitis (can be ulcerative or diffuse infiltrative)
Course:
1. Vesicular stage bleb.
2. Stage of ulceration surface epithelium becomes necrotic and ulcers form on the
conjunctiva
3. Healing stage ulcers heal without scar
3) Spring Catarrh (Vernal conjunctivitis)

- Definition: recurrent, bilateral/seasonal (occurs with onset of hot weather)
- Etiology: IgE mediated- hypersensitivity to exogenous allergen e.g. pollen, dust
Types:
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a) Palpebral form everting upper lid shows palpebral conjunctiva looking like cobblestones
i.e. hard nodules (diffuse papillary hypertrophy)- milky white colour due to thickened
epithelium of the conjunctiva
b) Bulbar form small nodules at the limbus
Symptoms:
o Itching
o Thick, white, ropy
mucous discharge
o Burning and FB sensation
o Photophobia
o Lacrimation
DDx: trachoma
Treatment: symptomatic- topical corticosteroids
Keratoconjunctivitis: refer to question 36.
40. Chronic infectious conjunctivitis. Chronic non-infectious conjunctivitis.

Trachoma.
Chronic infectious conjunctivitis:
a) Angular conjunctivitis (Diplobacillary conjunctivitis)
The reddening of the conjunctiva is confined exclusively to the intermarginal strip of the bulbar
conjunctiva
Etiology:
 Morax-Axenfield diplobacillus- proteolytic enzymes wastes away the conjunctival epithelium
Symptoms:
 Red eye
 Frequent blinking
 Mild mucopurulent discharge (maybe)
 Excoriation of skin at outer and inner canthi i.e. skin scrapes away
Complication:
 Blepharitis if untreated
Treatment:
 Oxytetracycline ointment
b) Follicular conjunctivitis- development of follicles. Infants- only after 3

months it can develop
Etiology:
 Exposure to chemicals and toxins e.g. pilocarpine
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 Viruses- herpes and adenovirus
 Any conjunctivitis of long duration can cause this
Multiple follicles are present in the lower fornix- they are rounded 1-2mm in size. No
scarring (DDx with trachoma)
Types:
 Inclusion conjunctivitis= Chlamydial infection. Production of inclusion bodies similar to
trachoma.
 Epidemic Keratoconjunctivitis= adenovirus.
 Pharyngoconjunctival fever= pharyngitis and fever. Adenovirus
 Acute herpetic conjunctivitis= young children. Corneal ulcers
Chronic non-infectious conjunctivitis

Simple chronic conjunctivitis- continuation of acute conjunctivitis
Etiology:
 Irritation by smoke, dust, heat, allere,
 Concretions, misplaced eyelashes, dacryocystitis, chronic rhinitis
 FB in fornix
 Intranasal infection and dandruff of scalp
Symptoms and signs:
 Burning discomfort
 Hot and dry edges of lids
 Sticky looking conjunctival surface
 Congestion
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Trachoma: (Egyptian opthalmia)
Trachoma means ‘rough’ in Greek.
Etiology:
 Chlamydia trachomatis serotypes A-C
 Rare in temperate countries but edemic in warm climates
 It is a common cause of blindness
Stages:
I. Hyperplasia of lymph follicles on upper tarsus
II. Papillary hypertrophy of upper tarsus, subepithelial infiltrates, pannus formation,
follicles on the limbus
III. Increasing scarring and symptoms of keratoconjunctivitis sicca.
IV. Progression to
- Entropion= rolling of lid margin results from scarring
- Trichiasis= misdirected eyelashes due to conjunctival scarring
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- Keratitis
- Superinfection
- Ulceration= due to dry and misdirected eyelashes
- Xerosis= destruction of goblet cells due to conjunctival scarring
- perforation of corneal ulcer and finally loss of the eye.
Symptoms:
 Mild irritation and FB sensation
 Frequent blinking
 Mild itching
 In chronic stage, cornea is involved pain, lacrimation, photophobia
Signs:
a) Conjunctival
- Congestion- red, velvety, jelly-like thickening of palpebral conjunctiva
- Papillae- may be in palpebral conjunctiva
- Follicles- seen in upper and lower fornix, palpebral conjunctiva, plica and bulbar conjunctiva
- Star-shaped scarring at centre of follicle in late stages
b) Corneal
- Superficial karatitis
- Herbert’s pits follicle like infiltration near the limbus of the upper part.
- Pannus lymphoid infiltration with vascularisation seen in upper cornea
a) Progressive panus superficial BVs are parallel and directed downwards and extend
beyond a zone of infiltration and haze is present
b) Regressive pannus infiltration is short and BVs extend beyond haze.
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Treatment: topical erythromycin or tetracycline for 2-3 weeks. Systemic: erythromycin or tetra for at
least 3 weeks.
41. Degenerations of the conjunctiva

Pingueculum (pinguis= fat)
Definition: harmless yellow-grey triangular thickening (hyaline infiltration) of the conjunctival
epithelim near the limbus in the palpebral fissure
Etiology:
 Occurs in elderly people exposed to strong sunlight, wind, dust etc.
No symptoms
Signs- the triangular yellow apth is near the limbus in the palpebral aperture.
The base is always towards the limbus and apex away from the cornea.
No treatment is needed.
Pterygium (from Greek word- butterfly)

Definition:
- Triangular sheet of fibrovascular tissue that invades the cornea. It has 3 parts: head/apex
(rests on cornea), neck (narrow- near limbus) and body (remaining fleshy part)
- Subconjunctival tissue proliferates as granulation tissue
which invades the cornea and destroys the superficial layers
of stroma and bowman’s membrane
Etiology: usually follows a pingueculum, UV rays
Course:
a) Progressive stage= early stage. Increases in size and invades centre of the cornea and can
cover the whole pupil
b) Atrophic stage= stops growing but never disappears completely
Symptoms:
- Only produces symptoms if the papillary area is covered by the pterygium impaired
vision astigmatism.
- Double vision in abduction can occur due to scarring of conjunctival tissue which can gradually
impair ocular motility (rectus medius)
Signs:
- Deposits of iron (Stocker’s line) may lie in front of the apex
Treatment:
- Only needed when symptoms happen surgical removal of head and body, and the sclera is
left open at the site. Cornea is then smoothed with an excimer laser.
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Pseuopterygium: differs from pterygium because the adhesion is between the scarred conjunctiva
and the cornea and sclera. It is dues to chemical injuries and burns. Pain and double vision. Treated
by excision of the scarred conjunctival tissue and covering the defect e.g. graft.
Lithiasis (concretions)
Etiology: accumulation of epithelial cells and thick mucous secretions from
Henle’s glands, but they never become calcified
FB sensation and irritation. Minute hard yellow spots in palpebral
conjunctiva which project and rub against the lid or cornea. Removed by a
sharp needle.
Subconjunctival hemorrhage (ecchymosis)

Extensive bleeding under the conjunctiva due to rupture of the vessels bright red, sharply
delineated area around normal conjunctiva.
Etiology:
- Injury to eyeball and orbit
- Spontaneous in elderly (compromised vascularisation in arteriosclerosis)
- Severe conjunctivitis
- Bleeding disorders e.g. scurvy
Harmless, spontaneously resolve within 2 weeks.
Course: bright red (oxyhemoglobin) blackish-red-orange-yellow
(oxyhemoglobin breaks down) absorbed within 2 weeks
42. Tumours of the eyelids and conjunctiva

Cysts: harmless and benign. Usually post-operative, post-traumatic or spontaneous. Fluid-filled
inclusions of conjunctival epithelium whose goblet cells secrete into the cyst, not on the surface. FB
sensation. Removed surgically.
Congenital:
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a) Dermoid – yellow-gray colour. Smooth solid round lesions usually on the outer limbus.
Usually stationary in growth. Can cause astigmatism. Dissected off and replaced by graft
b) Dermolipoma- only on outer canthus only
Papilloma:
In inner canthus, fornices and limbus. Link HPV. Benign
and do not turn malignant. Permanent FB sensation,
surgical removal.
Squamous cell carcinoma:

Occurs at limbus or lid margin (transition zone). Spreads over the
surface into the fornices and may penetrate the eyeball. Whitish,
raised thickened area of epithelial tissues. Precancerous lesion can
progress to carcinoma in situ. Operation and postoperative RT
Pigmented tumours:
i. Nevi or congenital mole  benign, slightly raised
epithelial or subepithelial tumours. Some contain a pseudocyst. Can be pigmented or
unpigmented. Can degenerate into conjunctival melanosis 50% of cases. Need complete
excision.
ii. Acquired Conjunctival melanosis= pigmented thickening of conjunctival epithelium. DDx
from congenital melanosis- acquired is mobile.
iii. Malignant melanoma = typically at the limbus in elderly. It spreads over the surface of
the eyeball. Mestases in the body is common. Enucleation of the globe is needed.
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Cornea- diseases
43. Clinical findings in corneal diseases

 Pain rich innervations from I branch of trigeminal nerve
 Lowering of visual acuity
 Halo diffraction of light to due epithelial edema
 Photophobia
 Tearing reflex stimulation of nerve endings
44. Inflammation of the cornea due to Bacterial infections

Firstly, let’s talk about the predisposing factors and pathogenesis of corneal infections
a) Predisposing factors:
 Blepharitis
 Dry eyes
 Contact lenses
 Lagophthalmos
 Trauma
b) Pathogenesis: (pathogens= virus, bacteria, fungi- invade cornea through superficial lesion)
Corneal lesion pathogens colonize corneal stroma (red eye) antibodies infiltrate at the
site (corneal opacity and point of entry expands irritation of the anterior chamber with
hypopyon (pus accumulates) pathogens infest the entire corneastroma melts down to
Descemet’s membrane remains intact (descemetocele), descemet’s membrane protrudes
anteriorly Descemet’s membrane perforates aqueous humour leaks (perforated
corneal ulcer)- immediate surgery e.g. keratoplasty  prolapsed iris adhesions of the iris
will produce a white corneal scar.
NOTE: rapidly progressing corneal ulcer (bacteria) is referred to a serpiginous corneal

ulcer most dangerouspenetrates corena and leads to intraocular involvements.
Over 90% of all corneal inflammations are caused by bacteria.
NOTE: most bacteria are unable to penetrate the cornea as long as the epithelium remains intact.
Only Gonococci and diphtheria can penetrate the intact corneal epithelium
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Symptoms: moderate to severe pain (except moraxella), photophobia, impaired vision, tearing,
purulent discharge. (NOTE: viral forms produce watery discharge)
Remember- serpiginous corneal ulcers are associated with hypopyon (pus in anterior chamber) and
posterior adhesion of the iris and lens (posterior synechia)
Treatment: conservative= topical ABs with broad spectrum Abs (ofloxacin). Surgery for perforated
corenal ulcer emergency keratoplasty
45. Inflammation of the cornea due to viral infections

Viral keratitis caused by:
 Herpes Simplex virus
 Varicella-zoster virus
 Adenovirus
 Rarely- measles or rubella virus
Viral keratitis is non-purulent type of keratitis
Herpes Simplex Keratitis:
Caused by HSV-I. Usually young adults and children affected. Recurrence occurs due to febrile cold,
pneumonia, physical exhaustion or exposure to sunlight.
Symptoms: very painful, photophobia, lacrimation, swelling of lids.
Types: according to the specific layer of the cornea in which the lesion is located. Mostly occurs in
stroma and endothelium
a) Dendritic keratitis/ulcer- necrotic and swollen epithelial cells. Decreased corneal sensitivity
and can progress to stromal keratitis. Visible after fluorescein dye applied.
b) Stromal keratitis- intact epithelium, no defects shown with fluorescein dye. Slit-lamp shows
diskiform corneal infiltrates (diskiform keratitis)
c) Endothelitis: HSV is in the aqueous humour. Swelling of epithelial cells and opacification of
the corenal stroma. Endothelial cells involved in anterior chamber can cause secondary
glaucoma.
Treatment: trifluride (virostatic agent) if infection involves epithelium. Stromal and intraocular
types can be treated with acyclovir
NOTE: corticosteroids contraindicated in epithelial herpes simplex infections but can be used to treat
stromal keratitis where the epithelium is intact
Herpes Zoster keratitis:

Caused by varicella-zoster virus. Due to endogenous recurrence of
chickenpox. The eye is only infected when the ophthalmic division of
the trigeminal nerve is involved, thus the nasociliary nerve supplying
the interior of the eye will also be affected. It occurs with the elderly
with decreased immunity (diabetes, AIDs, cancer). Unilateral
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Symptoms: rows of vesicular eruption take place along the branches of the
ophthalmic division of the 5th CN suppuration, bleeding and pitting scars.
Neuritis. Fever and malaise. Skin of lid and face is red and edematous
Signs: Hutchinson’s sign- vesicular lesions on the tip of the nose (eruption
of nasociliary branch)
 Decreased or absent corneal sensitivity
Treat: acyclovir ointment or systemic.
46. Parenchymatous Keratitis

AKA intersitital keratitis
 Defintion: non ulcerative inflammation affecting the stroma of the cornea without primary
involvement of epithelium and endothelium
 Etiology: infectious or autoimmune
- Infectious: syphilis, M. Leprae, TB, EBV, lyme, sarcoidosis
- Majority is due to congenital syphilis (bilateral in 80% of cases). Acquired adult syphilis
produces IK much less frequently and is unilateral
Pathogenesis of congenital syphilis:
T. pallidum invades & sensitizes cornea during fetal stage exposure to toxin inflammation of
cornea due to Ag-Ab reaction
Stages:
1) Progressive stage= Hazy patches appear in deep layers of stroma. Associated with uveitis.
Ground glass appearance of cornea
2) Florid stage (2 months)= salmon patches due to haziness of cornea. Superficial
vascularisation. Vessels and conjunctiva appears heaped at limbus
3) Stage of regression= corneal haze resolves slowly (from periphery towards centre),
cloudiness disappears and vessels become obliterated and remain as fine opaque lines
(ghost vessels)
 Clinical features:
- Pain, photophobia, blepharospasm
- Diffuse corneal haze (nonulcerative stromal keratitis) and neovascularisation, uveitis
- Edema
- Deep opacities and ghost vessels
- Hearing impairment
Treatment: topical corticosteroids, high dose systemic steroids or penicillin
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47. Corneal dystrophies
Definition: a group of corneal metabolic dysfunctions that always lead to bilateral opacification of
various layers of the cornea. They are rare.
Types:
a) Epithelial corneal dystrophies
- Reis-Buckler’s dystrophy= bilateral. Corneal erosions and later scarring on Bowman’s
membrane. Typical ring opacity- subepithelial grey opacities arranged in fish net
- Cogan’s microcystic dystrophy= dot opacities characterized by recurrent attacks of pain,
watering, photophobia and blepharospasm. Microcysts form under the epithelium increased
hydration of cornea
- Messman’s Juvenile epithelial dystrophy= small vesicles
between epithelium and bowman’s membrane. Bilateral.
Minimal symptoms
b) Stromal corneal dystrophies:
- Granular dystrophy= hyaline deposits in anterior stroma.
Fragmented opacities surrounded by areas of clear
cornea between the deposits.
- Macular dystrophy= mucopolysaccharide

deposits severe loss of visual acuity in second
decade of life
- Lattice dystrophy= amyloid deposits. Spider like
opacities in cornea.
c) Endothelial dystrophy:
- Fuch’s endothelial dystrophy (most common corneal dystrophy). Atrophy of endothelial cells
(leads to bullous keratopathy- hydration of cornea with stromal edema and epithelial
bullae),along with edema and formation of vesicles. Grey punctuate opacities seen in stroma.
Treatment: corneal transplant (penetrating keratoplasty) may be needed (treatment of choice in

Fuchs’s)
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48. Corneal surgery
Keratoplasty= corneal transplant or graft. The patient’s opaque corneal tissue is replaced by the
donor’s clear cornea. Goal= to obtain normal visual acuity
Indications= corneal diseases affecting the stroma (scars, dystrophy, degeneration, post-
inflammatory opacities)
Types: a) full thickness= penetrating keratoplasty i.e. the full thickness of the cornea is replaced
b) Partial thickness= lamellar keratoplasty i.e. NOTE: the corneal epithelium,
superficial layers of stroma replaced.  Descemet’s membrane and deep layers
of the cornea need to be intact and
healthy and is only suitable for removing
superficial opacifications down to about
the middle of the cornea
49. Diseases of the sclera

Inflammations:
1) Episcleritis (superficial)
Definition: circumscribed, nodular inflammation of the episclera
(CT b/w sclera and conjunctiva). Women usually affected.
Bilateral mostly. There is a lymphocytic infiltration.
Etiology:
 Allergic reaction to endogenous protein or toxin
 Collagen disease e.g. history of RA
 Can be associated with prior episodes of herpes zoster
and gout
Types:
1) Simple diffuse epislceritis
2) Nodular episcleritis
Symptoms:
 Localized redness over sclera
 Mild to moderate pain
Signs:
 Circumscribed nodule 2-3mm away from limbus, hard, immovable and tender
 Episcleral vessels arranged radially become hyperaemic
DDx: conjunctivitis and scleritis
NOTE: conjunctival vessles are the most superficial. Episcleral vessels lie within Tenon’s capsule and
arranged radially. Addition of vasoconstrictive eyedrops  conjunctival but not the episcleral
injection will disappear DDx conjunctivitis with episcleritis
Treatment: usually resolves within 1-2 weeks. If severe topical steroids or NSAIDs
2)Scleritis (Deep)
Definition: diffuse or localized inflammation of the deep slceral tissues. Occurs as anterior scleritis
(95%- anterior to the equator of globe) and posterior scleritis(5%)
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Etiology:
 Systemic autoimmune or rheumatoid disease. E.g. RA, herpes zoster, SLE. Can occasionally
be due to bacterial or viral inflammation (as with episcleritis)
Types:
1) Diffuse  multiple, hard whitish nodules (pin head size) in inflamed area of sclera
2) Nodular one or more nodules, less circumscribed than episcleritis, welling dark red-blue
and later becomes purple like (semitransparent)
3) Necrotizing  large areas of avascular sclera leads to necrosis. Serious condition. Uveitis
present usually. Uveal pigment visible through the really thin sclera.
Treatment: corticosteroids and NSAIDs, analgesics. Extreme sclera thinning or perforation needs
surgery e.g. donor sclera or cornea used.
Staphyloma- bulging of sclera in which underlying uveal tissue in the bulge is also thinned or
degenerated. Often associated with increased intraocular pressure. Most common is the posterior
staphyloma bulging of entire posterior pole of the eyeball
Ectasia- thinning and bulging of sclera without uveal involvement.
No treatment for both.
Colour changes:
inflammation red,
very thin and blue due to underlying choroid e.g. newborns, OI.
Juandice yellow,
alkaptonuira brownish
50. Normal and pathological pupillary responses

Normal papillary response question 25, just remember;
 miosis= constriction sphincter pupillae muscle (PSNS).
- Physiological in babies, old age, glue eyes.
- Pharmacological= pilocarpine.
- Pathological= unilateral e.g. iritis, horners syndrome. Bilateral= pontine hemorrage
 mydriasis= dilation dilator pupillae muscle (SNS)
- physiological= myopia
- pharmacological= mydriatics e.g. atropine, tropicamide, phenylephrine
- pathological=
a) retina and optic nerve diseases:optic nerve atrophy, absolute glaucoma, acute
congestive lesions
b) central lesion (above geniculate body): meningitis, hemorhage
c) CN III palsy
Normal size of the pupil= 2-4mm
Pathological papillary responses:
Anisocoria with dilated pupil in affected eye
 Anisocoria= unequal sized pupils
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a) complete oculomotor palsy (loss of motor and parasympathetic function) tumours,
aneurysms, inflammation, bleeding. Direct light reflex without constriction in affected side
(fixed pupil), near reflex miosis is absent, impaired motility and double vision.
b) Tonic pupil (ciliary ganglion affected- link DM, virus, trauma). Direct and delayed light
reflexes absent or delayed. Dilation is also delayed. Near reflex is slow but present. Motility
unimpaired. Harmless cause of unilateral mydriasis.
c) Iris defect: trauma, acute angle closure glaucoma
 Anisocoria with Constricted pupil in the affected eye

= horner’s syndrome:
Etiology: damage to sympathetic pathway
a) 1st neuron- tumours, encephalitis
b) 2nd neuron- trauma, goitre, aneurysm
c) 3rd neuron- internal carotid aneurysm
Clincialpicture: misosis due to failure of dilator pupillae muscle, ptosis (Muller muscle fails),
enophthalmus (failure of lower eyelid retractors lower lid projects and eye looks smaller),
decreased sweat gland secretion
Diagnosis: pupil dilates more slowly in direct and indirect light reflexes (dilation deficit), normal near
reflex.
 Isocoria with constricted pupils (isocoria= equal sized

pupils)
Argyll-Robertson pupil
Etiology:
- proposed that the disorder is due to a lection in the pretectal region and Edinger-Westphal
nucleus, encephalitis, trauma, bleeding, tumours, alcoholism
signs:
- light reflex lost
- accommodation reflex retained
- small pupil, not round, constriction not always symmetrical
pharmacological agents- morphine, pilocarpine cause bilateral papillary constriction
adie pupil= unilateral dilated pupil usually in young women. Unknown etiology.
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Lens disorders
51. Congenital lens anomalies
Lenticonus= conical protrusion of the anterior pole (anterior lenticonus) or
posterior pole (posterior lenticocus)
- Myopia
- Decreased visual acuity
- Post. Type can be associated with lens opacity
Leniglobus= hemispherical protrusion
Microphakia= lens has an abnormally small diameter due to disruption of eye
development.
52. Cataract. Cataract surgery

Definition: opacity of the lens or its capsule and vision is impaired. Comes from the Greek word
katarrakteas (waterfall), because it was thought that cataract was fluid from the brain flowing in
front of the lens. Can be acquired or congenital
General symptoms: seeing only shades of grey, visual impairment, blurred vision, distorted vision,
glare or star bursts, monocular diplopia, altered colour perception etc.
1) Acquired cataract
 Senile Cataract: 90% of all cataracts. ‘age related cataract’
Etiology: occurrence usually familial.
Classification: according to morphology
1) Cortical cataract (soft cataract)- most common type of senile

Etiology: degeneration of lens fibres. Common after 50 years. Both sexes affected, usually bilateral
(one eye develops earlier)
Symptoms: diminished visual acuity, monocular diplopia, glare
Stages:
a) Immature cataract
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1) Stage of lamellar separation: cortical fibres separate by fluid. Pupil appears grey due to
increase in refractive index of the cortex (increased reflection and scattering of light)
2) Incipient cataract: wedge-shaped opacities (Cuneiform opacities) appear in periphery of
lens with clear areas between. Polyopia (irregular refraction), vision impared and
coloured halos are seen
3) Intumescent cataract: deep layers of
cortex cloud and opaque. Swelling of
lens
b) Mature cataract
- Entire cortex is opaque and swelling subsides
- Sclerosis of nucleus
- Iris shadow absent
c) Hypermature (Morganian ) cataract

- Mature cataract progress complete liquefaction of the cortex (milky)
- Nucleus is small, brownish and sinks by gravity in the bag of liquefied cortex. Edge of the
nucleus is seen as a brown semicircular line
- Final stage
-
Cupuliform
cataract: second most
common senile cortical cataract. Aggregation of
opacities usually in the posterior cortex just beneath the
capsule . AKA posterior subcapsular cataract. Leads to early loss of visual acuity. Near field miosis
(near vision worse)
2) Senile nuclear cataract (hard cataract): sclerosis of the central nuclear fibres but cortical
fibres are transparent and clear. There is pressure of the peripheral lens fibres which causes
hardening of the entire lens, especially the nucleus
Etiology:
- Long term effect of UV rays. Photo-oxidation occurs; brown pigment and deposition and
increased calcium concentration. Occurs at 40 (earlier than cortical)
Clinical stages:
1) Black cataract (Cataracta brunscens)- nucleus is cloudy and dark. Can become brown, red or
black due to melanin pigment deposition
2) Clouidness spreads to cortex
3) Mature cataract- sclerosis extens to capsule and entire lens. Progressive myopia
4) No hypermaturity as process is very slow
Symptoms:
- Progressive myopia and central opacity visual impairment
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- ‘second sight’ change in refractive index of nucleus which causes myopia
 Cataract in systemic diseases

Diabetic cataract: senile cataract develops early and progress rapidly. When sugar levels are
elevated, excess glucose is converted to sorbitol which accumulates in the lens fibres causing
osmotic imbalance.
Galasctosemic cataract: bilateral cataract (deep posterior cortical opacity)due to inability to

metabolize galactose to glucose.
 Complicated cataract: occurs as a result of any disease or pathology of the eye.
 Traumatic cataract
- Contusion cataract: contusion of the eyeball and perforating corneal injuries. Rosette-shpaed
cataract is formed usually in posterior (Can be anterior cortex or both)
 Toxic cataract: drug induced e.g. Steroids (topical or systemic corticosteroids) posterior
subcapsular opacity.
Congenital cataract
Can be present at birth or may occur earlier in childhood. Usually stationary and doesn’t progress.
Etiology:
1. Hereditary- genetic mutation, AD
2. Maternal causes- malnutrition (zonular cataract), or infection by virus (rubellia in 1st
trimester)
3. Fetal causes- deficient oxygen due to
placental hemorrhage, galactosemia or GK (-
), down syndrome
Clinical types:
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1) Punctuate/blue-dot cataract  multiple opaque small scattered dots
2) Zonular /lamellar cataract bilateral, opacities in one layer of lens fibers, often ‘riders’ (lens
opacities)
3) Cornoary cataract deep layers of cortex and superficial layers of nucleus. Clup-sphaed
opacities near periphery of the lens

4) Anterior capsular cataract delayed formation of anterior chamber.
5) Posterior capsular cataract
Cataract surgery: most frequently performed procedure in ophthalmology

Incidcations: depends on maturity.
- Bilateral cataracts
- Unilateral cataracts- postponed surgery as long as vision in healthy eye is good
- Mature cataract - undergo surgery ASAP
Preoperative consultations:
- Intraocular lens (IOL)- usually implanted in the place of the natural lens (posterior chamber
lens). Eye with artificial lens= pseudophakia.
Intracapsule cataract extraction= not used with subluxation and dislocation of lens. Entire lens is
frozen and its capsule is removed from the eye through a large corneal incision
Extracapsular cataract extraction: anterior capsule is opened cortex and nucleus of lens removed
whilst posterior capsule and zonule remain intact. Implantation of posterior chamber intraocular
lens
53. Symptamology of vitreous body disorders. Vitreous body diseases

Aging changes:
Synchysis= collagen fibres deteriorates in old age and the fibres condense and flatten
liquefaction small fluid-filled lacunae in the central vitreous body. Vitreous body can collapse and
detach from the retina.
Vitreous detachment:
Definition:
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 Complete or partial detachment of vitreous body from its underlying tissue. Posterior
vitreous detachment (PVD- common), anterior and base of vitreous body detachment is rare
(usually due to blunt trauma- can get hemorrage and dislocation of lens)
PVD: separation of the cortical vitreous from the retina anywhere

posterior to vitreous base
Synchysis- associated with vitreous liquefaction (as above)
Syneresis- collapse of the vitreous due to collection of fluid between the
posterior hyaloid membrane and internal limiting membrane of the
retina
Incidence: above 65 years.
Symptoms:
 Photopsia or flashes of light are seen (in partial vitreous detachment the vitreous body and
retina remain attached, but eye movement in this region will cause traction on the retina
hence the flashes of light. Also, too much traction on the retina can cause the retina to tear)
 Floaters seen- tiny amounts of pigment may come off the retina into the vitreous- look liek
spiders web over the eye
 Vitreous body can detach partially or completely from retina.
Signs: fundus examination to exclude retinal defect. Othalmoscopy

will show collapsed vitreous behind the lens. There’s an optically clear space between the detached
posterior hyaloid phase and the retina. Pathognomic of PVD is annular opacity (Weiss or Fuchs ring)
which shows the vitreous body detached from the attachment at the optic disc.
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Complications: hemorrhage. Retinal breaks
Treatment: once the vitreous is completely detached symptoms resolve. Complications (above) need
treatment e.g. virectomy= removal/excision and replacement of the vitreous.
Vitreous hemorrhage: bleeding into the vitreous chamber or space created by vitreous detachment
Types:
 preretinal or subhyaloid haemorrhage occurs between the retina and the vitreous. Blood
moves with gravity in the macular area forming a fluid meniscus (RBCs sink and form a
horizontal surface)
 intravitreal hemorrhage white fibrous tissue mass
Etiology:
 posterior vitreous
detachment with/wo retinal
tears
 proliferative diabetic
retinopathy
 retinal vein occlusion
 penetrating trauma
Symptoms:
 black spots or cloud seen in front of the eye ‘swarm of black bugs’
 impaired vision and diminished visual acuity if severe
 reduced perception of light
Signs:
1. fundus- faint or no red reflex, grey opacities may be present
2. slit lamp- fresh or clotted blood seen, fluid meniscus
Treatment:
 upright resting position: so bleeding doesn’t spread into the vitreous body, and blood in the
retrohyaloid space will settle more quickly
 treat the underlying cause e.g. retinal tear laser. Vitrectomy will be needed to drain
vitreous hemorrage not absorbed.
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Abnormal opacities of the vitreous body: can cause diminished visual acuity and ‘floaters’
 Asteroid Hyalosis: unilateral opacities of the vitreous body. Linked to DM and
hypercholesterolemia. Deposits are white bodies of calcium soaps resembling snowball. Use
vitrectomy only when visual acuity is diminished
 Synchysis scintillans: freely floating, highly refractive cholesterol crystals in lower vitreous
fluid. Trauma or inflammation.
 Vitreous amyloidosis: AD, bilateral, deposition of amyloid. Diminished visual acuity. Hyaloids
canal unaffected. Vitrectomy.
 Muscae volitantes- harmless black spots in floating in front of the eye.
Viritis and Endophthalmitis:

Definition: acute or chronic intraocular inflammation due to microbes or immunologic causes. Can
also be a result of penetrating trauma to the globe.Inflammation of the vitreous body only possible
when inflammatory gain access to the vitreous chamber from the uveal tract or retinal vessels
Symptoms :
Acute vitreous inflammation/ endophthalmitis: loss of visual acuity, deep dull ocular pain, red
conjunctiva.
Chronic: far less severe, loss of visual acuity is moderate.
Signs:
Acute: hypopyon in the anterior chamber (pus collection). Opthalmoscopy will show yellow-green
discoloration (vitreous body abscess). Roth’s spots (white retinal spots surrounded by hemorrhage).
Treatment: microbial inflammation- ABs, if mycotic- amphotericin B and steroids.
Vitreoretinal Dystrophies:
- Juvenile Retinoschisis- inherited X-linked recessive. Males only. Significant loss of visual acuity.
- Wagner’s disease- AD, involves central liquefaction of the vitreous body, fibrillary
condensation of vitreous stoma.
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Diseases of the uveal tract:
54. Uveitis. Etiology, pathogenesis and treatment
Uveitis= inflammation of the uveal tissue only. However, there’s always associated inflammation of
the adjacent structures e.g. retina, vitreous, sclera, cornea.
Etiology & pathogenesis : mostly not due to a direct infection. Usually due to allergy or
hypersensitivity reaction to infectious agent
1. Exogenous infection- perforating wound or corenal ulcer. Causes iridocyclitis
2. Secondary infection- inflammation spreads from cornea, sclera or retina.
3. Endogenous infection- organisms lodged in some other organ reaches eye via bloodstream-
bacterial septicaemia (Stap, Strep etc.), viral- mumps, measles. TB, syphyllis.
4. Allergic inflammation- sensitized ocular tissue comes in contact again with same organism or
its protein (Ab-Ag rxn) e.g. infection in teeth, tonsils, sinuses
5. Hypersensitivity reaction- autoimmune reaction e.g. SLE, RA, Sarcoidosis
Treatment:
Anterior uveitis & posterior uveitis:
 Atropine (mydriatic)- relax ciliary muscle spasm assoc. with iritis, causing vasodilation to
increase blood supply to anterior uvea (more ABs can reach target tissue)
 Heat application- reduce pain, prevent stasis and increases blood circulation
 Corticosteroids- anti-inflammatory  topical, subconjunctival injection, systemic
 Analgesics, ABs, NSAIDS.
Intermediate uveitis:
 Usually resolves itself
 Can give corticosteroids and immunosupressants
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55. Inflammatory diseases of the anterior uvea
Iritis and iridocyclitis: most frequent form of uveitis. Occurs in combination of cyclitis (iridocyclitis)
i.e. acute inflammation of iris (iritis) and ciliary body (cyclitis)
Etiology: immunologic cause.
Symptoms:
 Redness- congestion
 Severe neuralgic pain refereed to forehead, scalp, cheek, nose and teeth (the iris is richly
supplied by nerves from the ophthalmic division of CN V)
 Epiphora and photophobia (ciliary spasm and papillary constriction due to inflammation)
 Impaired vision
Typical signs:
 Ciliary injection= episcleral and preilimbal vessels may appear blue and red
 Combined injection= conjunctiva is also affected
The iris is hyperaemic- loss of normal pattern and appears muddy due to collections of exudates.
The structure appears diffuse and reactive myosis (water logging and vasodilation. Sluggish
reactions to light due to irritation of CN III endings) is present.
 Cellular infiltration and protein or fibrin accumulation of anterior chamber vision impaired
(Tyndall effect)
 Hyopopyon= exudates accumulation of the floor of anterior chamber
 Hyphemia= bleeding in anterior chamber (viral infection)
 Blocked pupil- exudates along the papillary area raised tension, impaired vision
DDx:
 Acute iritis depth of anterior chamber is normal and reactive myosis is present. Acute
glaucoma anterior chamber is shallow and the pupil is dilated.
Complications:
 Secondary open angle glaucoma
 Anterior synechiae= adhesions between iris and posterior surface of cornea
 Posterior synechiae= adhesion between iris and lens
56. Intermediate and posterior uveitis

Intermediate uveitis: (Chronic posterior cyclitis or pars planitis)
Affects the pars plana of the ciliary body and the peripheral retina and underlying choroid
Both eyes affected (80% of cases). Common in children and young adults. Unknown etiology.
Symptoms:
 Floaters
 Diminished visual acuity due to opacities in anterior aqueous
 Cystoids macular edema (multiple cyst-like areas of fluid in macular causing retinal swelling)-
impaired visual acuity
Signs:
 Grey-white plaques involving the inferior pars plana are seen near ora serrata which
coalesce together giving appearance of snow bank
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Complications:
 Retrolenticular cyclitic membrane – membrane back of the lens
 Macular edema, papilloedema or papillitis
 Vitreous hemorrhage
Posterior uveitis: (choroiditis)
Definition:
 Inflammation in the posterior uveal tract (choroid).
 Focal, multifocal, diffuse
 Outer layers of the retina depend on the choroid for nutrition associated inflammation of
the retina (chorio-retinitis)
Clinical types: according to number and types of lesions
 Diffuse/disseminated choroiditis- lesions scattered all over fundus (syphilis, TB)
 Anterior choroiditis- lesions near equator of fundus (syphilis)
 Central choroiditis- macular area/posterior pole involved (toxoplasmosis, histoplasmosis)
 Juxtapapillary choroiditis- lesion around optic disc.. young persons usually.
Symptoms:
 Floaters- diminished vision
 Photopsia- flashes of light (retina is irritated)
 Metamorphopsia- straight line appears wavy due to edema of retina
 Micropsia- object seems smaller than it actually is (separation of rods and cones)
 Macropsia- objects look larger than it actually is (overcrowding of rods and cones)
 + scotoma seeing black spots in front of eyes (retinal lesions)

 - scotoma black spot in field of vision similar to blind spot
NOTE: choroiditis is painless as the choroid is devoid of sensory nerve fibres
Signs: fundus exam

 Infiltration of choroid and exudates hide the choroidal vessles yellowish areas with ill-
defined edges
 Black spots seen floating in vitreous (vitritis)
 ‘spill over’ uveitis- posterior synechia
 Healing- yellow lesions become white (fibrosis), lesions surrounded by black pigments
Complications: cataract, secondary glaucoma, retinal detachment
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57. Uveitis due to syndrome diseases
1. AIDS (acquired immunodeficiency syndrome)
Cotton wool spots and cytomegalovirus retinitis immune complex deposition
About 50-75% of adult AIDs patients suffer from ocular lesions and complications
1. Eyelids- heres zoster opthalmicus, Kaposi’s sarcoma (raised purple papules on lids)
2. Conjunctival lesions- conjunctivitis (non-specific), dry eye
3. Cornea- herpes simplex keratitis
4. Anterior uveitis- sometimes associated with hypopyon
5. Lens- increased myopia and premature presbyopia
2. Uveoparotitis – seen in sarcoidosis, bilateral involvement of entire uveal tract and parotid
glands, CN III and VII
3. Behcet’s syndrome- recurrent iridocyclitis with hypopyon due to obliterative vasculitis with
immunological basis
4. Reiter’s diseases and uveitis- triad of urethritis, arthritis and conjunctivitis. Associated wit
HLA-B27 antigen
5. Ankylosing spondylitis- recurrent iridocyclitis associated with chronic progressive
involvement of sacroiliac joint
6. Stevens-johnson syndrome (erythema multiforme)- Herpes simplex or reaction to sulpha
group of drugs. acute inflammatory skin disease with rash and bullae of the skin, mm and
conjunctiva. Complication is uveitis.
58. Uveal tumours.

Malignant:
Uveal melanoma (malignant melamona)- most common primary intraocular tumour.
Tumours in the iris are detected earlier than tumours in the ciliary body or choroid.
 Iris melanomas- initially asymptomatic. Isolated nodule that grows rapidly. Can penetrate
through the limbus. Pigmented or unpigmented spidle-shaped or round cells. Metastatic
melanoma cells in the anterior chamber angle can lead to secondary glaucoma. Removed by
segmental iridectomy
 Ciliary body melanomas- changes in accommodation and refraction from displaced lens.
 Choroidal melanomas-
2 main clinical types: pedunculated and flat melanoma
Stages:
i. Quiescent stage- symptomless
ii. Glaucomatous stage- raised tension
iii. Extraocular extension- local spread into orbital tissue
iv. Metastasis- blood bourne to CNS and liver
Diagnosis:
 Defective vision
 Retinal detachment
 Transillumination, US, fluorescein angiography
Treatment:
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 Small (<10mm)- EBRT, laser ablation or brachytherapy
 10-15mm EBRT
 Enucleation excise the eye and cut the optic nerve as far back as possible
 Uveal metastasis- from carcinomas of breast or lung
Retina- diseases
59. Clinical findings in retinal diseases:
- Seeing floaters, specks or cobwebs
- Blurred and distorted vision
- Defects in side vision
- Lost vision
Basically, the following diseases covers it all...
60. Macular degeneration

Age-related Macular degeneration (ARMD)
AKA senile macular degeneration.
 Age related, bilateral, non-hereditary, progressive degeneration of the macula in elderly
patients
 Involves the choriocapillaries, Bruch’s membrane, retinal pigment epithelium and
photoreceptors.
 Most common cause of permanent central vision loss in elderly over 65 in developed
countries.
Etiology:
 Accumulation of metabolic products
 Sclerosis of arteries that nourish the retinadepriving the retina of oxygen and nutrients
Predisposing factors:
 Heredity, age, nutrition, smoking, hypertension, excess sunlight exposure
Types:
 Exudative (wet)- serous fluid or hemorrage
 Dry- atrophic degeneration
Symptoms:
 Diminution of vision- gradual (dry atrophic type) or sudden painless loss of vision (exudative)
 Metamorphopsia- image distortion e.g. straight lines appear wavy, bent or fuzzy
Signs:
 Drusen of Bruch’s membrane (yellow deposits under the retina- they are small, bright,
sharply defined circular points lying below retinal vessels) is one of the early findings seen in
the macular region. The Drusen can join to form a larger round mass
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Treatment: no effective medical therapy. Laser
therapy can be performed in exudative stage.
Hand magnifier or binocular magnifier.
61. Pigment degeneration of the retina.

Retinitis pigmentosa
Definition:
 Slow, degenerative, hereditary disease of the retina
involving the rods and cones. Recessive trait. Leads to
progressive loss of visual acuity, visual field defects and
night blindness.
 Name comes from pigment deposits that characterize the
disorder.
 Bilateral usually, slow and chronic progression
 Begins in childhood and causes blindness in middle age
Types:
1. Retinitis pigmentosa sine pigmento- no visible pigmentation on the retina
2. Retinitis punctata abescens- white small pigments uniformly. Stationary or progressive
3. Central or inverse pigmentary degeneration- posterior pole
4. Uniocular and atypical form- variation in amount and distribution of pigments
Also, there can be:
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- Rod-cone dystrophy (classic RP) i.e. primarily the rods are affected first. Proliferation of
pigment epithelium of retina in the middle of retina and spreads to the centre and peripherally
- Cone-rod dystrophy- early loss of visual acuity with gradual progressive loss of visual field.
Symptoms:
 Glare, night blindness, progressive visual field defects, loss of visual acuity, colour vision
defects.
Signs:
1. Fundus exam:
 Retina studded with jet black spots (pigments) which resemble bone corpuscles with a
spidery outline.
 Retinal blood vessels= extremely attenuated and thread like. Retinal veins only can have a
sheath of pigment
 Optic disc= atrophy i.e. pale, wax-like, yellowish
2. Visual fields= ring scotoma tubular vision ‘gun barrel vision’ , complete blindness at
later stage
DDx: night blindness (nyctalopia)- e.g. vit A (-), cirrhosis of liver. Congenital syphilis (‘salt and pepper
fundus’)
Diagnosis: electroretinography
Treatment: cannot be treated. Edge-filtered eyeglasses (glasses with orange or blue lenses to filter
out certain wavelengths) and magnifying near vision.
62. Peripheral degeneration of the Retina

Defintion: degenerative changes that lie parallel to the ora serrata in the peripheral portions of the
retina. 2 basic types:
a) Harmless retinal changes- pars plana cysts of the posterior ciliary body or peripheral
chorioretinal atrophy (cobblestone degeneration)
b) Precursors of retinal detachment- local thinning of the retina (snail track or lattice
degeneration)
Asymptomatic.
Diagnosis made by ophthalmoscopic examination of the peripheral retina with dilated pupil.
- Cobblestone degenerations- whitish sharply defined local areas of atrophy of retina, pigment
epithelium and choriocapillaries that lie between the ora serrata and the equator
- Snail track degenerations- yellow-white radiant dots (microglia and astrocytes)
- Lattice degeneration- thinned retinal areas with sclerotic vessels.
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63. Acute vascular disorders of the retina
Retinal vein occlusion:
Definition: obstruction of the venous circulation of the retina due to thrombosis or embolus. Central
retinal vein occlusion= thrombus at the level of lamina cribrosa, branch retinal vein occlusion=
arteriovenous crossing
Etiology: second most common vascular disorder after diabetic retinopathy.

1. Elderly with CVD e.g. hypertension, arteriorsclerosis and diabetes
2. Young people- infective periophlebitis (Branch occlusion) and local causes e.g. orbital
cellulitis
3. Chronic open angle glaucoma
Symptoms: loss of visual acuity if the macula or optic disk involved. Sudden onset of impaired vision.
Not so sudden if the central retinal artery is occluded.
Signs: haemorrhages in all the four quadrants of the retina (tomato splash appearance). In branch
retinal vein occlusion- intraretinal haemorrhages in the area of the vascular supply; bleeding may
only be in one quadrant or in 2 quadrants.
 Cotton wool spots and retinal or optic disk edema.
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DDx: diabetic retinopathy
Treatment: should start as early as possible
1. Complete blockage- no effective treatment
2. Anticoagulants and steroids
Complications:
- Secondary neovascular glaucoma in later stage= sclerosis and neovascularisation of the
anterior chamber angle (rubeosis iriditis)
- Retinal detachment
Retinal Arterial occlusion:
Definition: obstruction of arterial circulation in the retina.
- Renal infarction due to occlusion of an artery in the lamina cribrosa (central retinal artery-
entire retina will be affected) or branch retinal artery occlusion (usually superior temporal
branch- distal vessels will become edematous)
Pathogenesis:
i. Infarction of inner 2/3 of retina
ii. Reflex constriction of whole retinal arterial BVs
iii. Stasis in the retinal capillaries
Symptoms:
- Central retinal artery sudden, painless unilateral blindness
- Branches loss of visual acuity or visual field defects
- Amaurosis fugax in the early stage,
the sudden loss of vision is sudden but
transient- get recovery of vision due to
embolus dislodging in the peripheral
arterioles
Signs: diagnose via opthalmoscopy

- Acute stage of central retinal artery
occlusion retina is greyish-white
(pale retina) due to edema of the layer
of optic nerve fibres (no longer
transparent)
o Only fovea centralis (no nerve
fibres here) remains visible as a
‘cherry red spot’ – the choroid
shows through at this site
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- Chronic stage- atrophy of the optic nerve.
- Branch retinal artery occlusion- retinal edema at site affected.
- Pupil= dilated and doesn’t react to light
- DDx: cherry red spots in Tay-Sachs disease, Niemann-Pick or Gaucher’s disease.
Treatment: ocular massage, medications to reduce intraocular pressure or paracentesis used to try
and drain the embolus in a peripheral retinal vessel. Calcium antagonists and hemodilution.
Poor prognosis irreparable damage to inner retinal layers. Blindness not usually prevented.
Coat’s disease: congenital retinal telangiectasia with vascular anomalies nearly always unilateral.
Can lead to exudative retinal detachment.
64. Diabetic retinopathy

Definition: retinal changes that occur in patients with DM. It is an ocular microangiopathy. It is one
of the main causes of acquired blindness. 90% of all diabetic patients have retinopathy after 20
years. Usually affects the posterior pole.
Pathogenesis:
Microangiopathy affecting the retinal precapillary arterioles, capillaries and venules. Characteristic
changes in the capillaries=
- Damage to endothelial cells
- Loss of cells (intramural pericytes) normally present in basement layers
- BM thickened and fragmented
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Classification and stages:
Symptoms: asymptomatic for a long time. Only in late stages with macular involvement or vitreous
hemorrage visual impairment and suddenly go blind
Signs:
Treatment: macular edema that threatens

vision is managed by laser treatment at the
posterior pole. Proliferative diabetic
retinopathy is treated via scatter
photocoagulation.
Complications: Rubeosis iriditis

(neovascularisation of the iris)
Risk of blindness due t diabetic retinopathy can be reduced by optimum control of blood glucose,
regular ophthalmologic examination and timely therapy. However, it cannot be completely
eliminated.
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65. Vascular changes of the retina due to arterial hypertension, renal diseases and
toxemic retinopathy of pregnancy
Arterial hypertension- vascular changes of the retina
AKA hypertensive retinopathy.
Definition:
 Fundus changes occuring in patients with hypertension
 Usually caused by vasospasm
 Arteriosclerosis causes thickening of the wall of the arteriole
Vascular changes due to arterial hypertension are the most common cause of retinal vein occlusion
Pathogenesis:
High BP breakdown of blood-retina barrier or obliteration of capillaries intraretinal bleeding,
cotton wool spots, retinal edema or swelling of the optic disk
Symptoms: headache or eye pain. Impaired vision or loss of visual acuity only in stages III and IV.
Signs: hypertensive and arteriosclerotic changes in the fundus diagnosed by opthalmoscopy with
the pupil dilated.
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DDx: diabetic retinopathy.
Treatment: treat underlying disorder. Lower BP <140/90mm Hg. Fundus changes due to
arteriosclerosis are untreatable.
Complications: retinal artery and vein occlusion. Formation of macroaneurysm leads to vitreous
hemorrhage.
Toxemic retinopathy of pregnancy:

Occurs late in pregnancy i.e. in 9th month usually. It has many characteristics of hypertensive
retinopathy.
Classification: 3 stages
1. Stage of angiospasm: due to toxins
- Narrowing of retinal arteries usually the nasal branch
- Spasmodic contractions of arteries seen
2. Stage of sclerosis of vessels: depends on severity of hypertension
3. Stage of retinopathy:
- Multiple, superficial and deep haemorrhages seen
- Retinal edema and exudation all over fundus
- Retinal detachment can happen due to massive exudation and hemorrhage
Complications: complete loss of vision in stage of retinopathy. Loss of life of mother and fetus is a
very serious complication
Treatment:
- Control hypertension (rest, sedation, salt reducing diet, diuretics, hypertensives)
- Severe retinopathy not responding to treatment- the termination of pregnancy is advised
66. Inflammations of the retina (Central serous retinopathy and periphlebitis)

Central serous retinopathy (CSR)
Definition: typical example of macular edema localized detachment of the sensory retina at the
macula secondary to local defect in retinal pigment epithelium
Etiology: vasomotor instabilityanigospasm and hyperpremability (due to allergic or toxic

nature)exudation from parafoveal or choroidal capillaries
Symptoms:
- Transient sudden impairment of central vision or visual acuity
- Black path seen in front of eyes [+ scotoma]
- Micropsia or metamorphopsia
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Signs:
- Shallow detachment of sensory macular retina causes a circular grey swelling the size of the
optic disc in the macular region
- Can be a ‘halo’ around the swelling
Complications: fibrovascular scar and tears in the pigment epithelium
Treatment: usually resolves itself within 4-12 weeks. Can do photocoagulation to control exudation
process.
Periphlebitis Retinae (Eale’s disease)

Definition: idiopathic, inflammatory peripheral retinal vasculopathy. Recurrent vitreous and retinal
haemorrhages.
Etiology: periphlebitis (inflammation of retinal wall of veins) commonly associated with TB

(tuberculoprotein hypersensitivity). Young adults affected and occurs usually in males, bilateral.
Symptoms: sudden impairment of vision due to vitreous hemorrhage.
Signs:
1. Peripheral retinal veins- thickened and congested
2. Perivacular sheathing of veins
3. Peripheral neovascularisation seen
4. Vitreous hemorrhage
Complications: loss of vision due to recurrent haemorrhages

and vitreous opacities, retinitis proliferans (fibrous tissue proliferation
due to large vitreous hemorrahge), traction retinal detachment, rubeosis
iridis and glaucoma.
Treatment: treat underlying cause of inflammation, systemic

corticosteroids (control inflammation), photocoagulation, vitrectomy in
cases of retinitis proliferans.
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67. Drug, professional and other intoxications of the Retina and optic nerve
Toxic retinopathy: retinal changes due to medications. Rare.
Pathogenesis: asymptomatic for long time. Loss of visual acuity only when macula is affected.
Chloroquine (>250g) causes retinal damage. (it is an antimalarial drug used to treat SLE and arthritis)
- Macular edema punctate pigment epithelial changes bull’s eye maculopathy with
concentric rings of hypopigmentation and hyperpigmentation in the macular region.
- Bilateral and symmetrical
Toxic amblyopias (chronic retrobulbar neuritis)

Amblyopia= lazy eye  eye fails to achieve normal visual acuity
Optic nerve fibres are damaged by exogenous poisons:
1. Mild toxic agents= tobacco, ethyl alchohol, iodoform. Produce a central scotoma
2. Severe amblyopia= quinine products (as above)
68. Retinal detachment- Types, clinical findings and Treatment

Definition: separation of the 2 retinal layers retina proper and the pigmentary epithelium (to
which is loosely attached).
Classification:
1. Primary or simple detachment AKA. Rhegmatogenous- results from a break/tear in the
retina  allows fluid from vitreous to seep through and raise the retina from its bed.
Mechanism of detachment: Any force sufficient to separate the retina and allow passage of fluid
- Retinal degeneration or trauma
- Degenerated vitreous fluid
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2 types of breaks:
a) Round breaks portion of the retina completely torn out due to a posterior vitreous
detachment
b) Horseshoe tears: retina is only slightly torn
2. Secondary (non-rhegmatogenous) detachment: (very rare)

- Tractional retinal detachment i.e. the vitreous exert forces on the retina
- Exudative retinal detachment caused by fluid (blood,lipids, serous fluid)  link Coat’s disease.
We get the breakdown of the inner or outer blood-retina barrier subretinal fluid
accumulates between retina proper and pigment epithelium
- Tumour-related retinal detachment – transudate form the tumour vasculature or the mass of
the tumour separates retina from its underlying tissue.
Symptoms:
 Photopsia and floaters  acute posterior detachment.
 A posterior vitreous detachment that causes a retinal tear can cause avulsion of retinal
vessels blood will enter the vitreous body black rain (numerous slowly falling black
dots)
 dark shadow in the visual field  occurs when the retina detaches
 break in the centre of the retina sudden loss of visual acuity & metamorphopsia (image
distortion) if the macula is involved
signs: fundus examination

 detached retina looks greyish-white and raised above the surface (loss of transparency and
edematous)
 dark retinal vessels with no central light reflex
 detached retina multiple folds which oscillate with eye movements
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DDx: Senile retinoschisis (splitting of the retina at the level of the inner nuclear and outer plexiform
layers). Choroidal detachment.
Treatment: adhere the torn part of the retina to an area of choroid. Can do argon laser coagulation-
the retina surrounding the break is fused to underlying tissue but the break itself is left open.
69. Tumours of the Retina

Retinoblastoma: malignant tumour of early childhood that develops from immature retinal cells.
Inherited AD trait.
Symptoms:
- Leukocoria whitish-yellow pupil (white reflex)
- Strabismus
- Reddened eye
DDx:
- Cataract (with leukocoria)
- Primary strabismus (with strabismus)
- Infection (with red eye)
Treatment:
- RT – brachytherapy
- Large tumours need enucleation of the eye
Clinical course:
- Can metastasize if untreated and go to the brain death.
Astrocytoma:
Benign tumour that develops from the astrocytes of the neuroglial tissue. Rare.
Symptoms:
- Usually no ocular symptoms
- Calcified astrocytic hamartomas in the region of basal ganglia or ventricles epilepsy and
mental deficit
Signs:
- Single or multiple ‘mulberry’ tumours which are white and often calcified.
Hemangiomas: capillary hemangiomas or hemangioblastomas occur in agniomatosis retinae. Benign

congenital changes. Loss of visual acuity results if exudative retinal detachment occurs. Thick
tortuous arteries and veins. DDx with coats disease. Treated by laser or cryocautery therapy.
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70. Retinopathy of prematurity- diagnosis, clinical findings, treatment
Definition: a retinal disorder where there is disruption of normal development of the retinal
vasculature in preterm infants with birth weight less than 2500g.
Etiology: preterm birth and exposure to oxygen disturbs normal development of retinal
vasculature vessel obliteration proliferative neovascularisation vitreous hemmorhage, retinal
detachment. Late scarring stage retrolenticular fibroplasias as vessels and CT fuse with the
detached retina
Clinical findings: initially asymptomatic, vitreous hemmorhage or retinal detachment accompanied

by secondary strabismus. Leukocoria occurs in the retrolenticular fibroplasias stage
Treatment: laser photocoagulation or cryotherapy in the nonvascularized portion of the retina in

stage III. Stage IV and IV- surgery success rate is rare. Stage I and II- spontaneous resolution in 85% of
cases.
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Optic nerve disorders
71. Optic neuritis

Definition: inflammation of the optic nerve that can occur:
a) Within the globe papillitis (acute inflammation of the optic nerve head- papilla or optic
disc)- rapid loss of vision. Often unilateral
b) Behind the eyeball retrobulbar optic neuritis
Etiology:
a) Papillitis
- Inflammatory processes: infectious diseases e.g. lyme,
malaria, syphilis, inflammation of- orbit, sinuses
- Autoimmune disorders: SLE, chron’s, ulcerative colitis
- Toxic damage: methanol, lead
b) Retrobulbar optic neuritis: demyelinating diseases of the

CNS e.g. difuse encephalitis
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Symptoms:
- sudden loss of vision
- field of vision typically impaired by a scotoma and a wedge-shaped visual filed defect up to and
including complete blindness
- pain that increases in extreme positions of gaze and when pressure is applied to the globe
- reduced perception of colour
Signs:
Papillitis:
 edema and hyperemia of the head of optic nerve flattens the optic cup and obscures the
margin of the optic disk
 may be bleeding at margin of optic disc
Retrobulbar optic neuritis:

 optic disk will appear normal
In retrobulbar optic neuritis, the patient sees nothing (due to central scotoma), and the physician ses
nothing (the fundus appears normal)
other findings: afferent papillary defect, red-green colour vision defect
treatment: depends on the underlying disorder. High doses of steroids for severe loss of vision in
retrobulbar optic neuritis.
Prognosis:
- depends on the underlying disorder. Severe permanent loss of vision is possible but so are
significant spontaneous improvements.
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72. Ischeamic optic neuropathy
Anterior Ischemic Optic neuropathy (AION):
Classified according to the cause of the disorder:
1) Arteriorsclerotic AION
Definition: acute disruption of the blood supply to the optic disk i.e. optic disk infarction, resulting
from vascular changes in arteriosclerosis.
- It is a common cause of sudden loss of visual acuity
Etiology: acute disruption of blood flow due to arterioscelrosis narrow optic disk/ known as
diabetic papillopathy
Symptoms:
 Sudden unilateral loss of visual acuity
(infarction of the anterior portion of the
optic nerve)
 Afferent pupillary defect always present
Signs:
 History of HT, DM or hyperlipidemia
 Edema of optic disk, margin obscured in a
segmental pattern NB!! (opthalmoscopy)
 Head of optic nerve hyperaemic with
marginal bleeding
Treatment:
 Nearly impossible to treat
 Steroid to control edema.
 Diagnose underlying cause and treat e.g. DM, HT
2) Arteritic AION
Definition: acute disruption of blood supply to the optic disk due to inflammation of medium-sized
and small arterial branches. Usually occurs after 60 years.
Etiology: Giant cell arteritis  bilateral granulomatous vasculitis

- Temporal arteries and ophthalmic artery, posterior ciliary artery, central retinal arteries and
vertebral arteries
NOTE: giant cell arteritis should be considered in every pt. Presenting with AION
Symptoms:
 Sudden unilateral blindness or severe visual impairment
 Headache, painful scalp in region of temporal arteries, tenderness to palpation in region of
temporal arteries, pain while chewing (a characteristic sign)
Signs:
 Same as above
 NOTE: RBC sedimentation should be measured in every pt. With AION... always elevated
 Prominent temporal arteries, painful to palpation and no pulse.
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Treatment: immediate high dose systemic steroid therapy (prednisone).
73. Edema of the optic disk

Papilledema:
Definition:
 Bilateral optic disk edema secondary to increased intracranial pressure
Etiology:
Pathogenesis:
1. Venous stasis compression of central retinal vein as it crosses the subdural and
subarachnoid spaces
2. Vasodilation of the disk due to hypoxia
3. Nerve fibres at optic disc become swollen which degenerate later
Unilateral Vs Bilateral:
Mostly with raised intracranial pressure bilateral. Due to ocular or orbital lesion it is usually
unilateral.
Special forms:
- Foster Kennedy syndrome: isolated atrophy of the optic nerve due to direct tumour pressure
on one side and papilledema due to increased intracranial pressure on the other side. Can be
due to meningioma of the wing of sphenoid or frontal lobe tumour
- Hypotension papilledema: nerve fibre edema due to ocular hypotension e.g. penetrating
trauma or fistula secondary to intraocular surgery
Symptoms:
1. General symptoms- headache which made worse by coughing or sneezing
2. Projectile vomiting (increased IC pressure)
3. Transient attacks of blurred vision
(amaurosis fugax)
4. Central vision affected only in later
stages (due to atrophy of the optic
nerve)
Signs:
Early phase
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Acute phase optic disc is no longer discernible.
Chronic phase significant optic disk edema. Optic cup is obliteralted

Atrophic phase proliferation of astrocytes results in atrophy of optic nerve- disc becomes pale
with blurred margins.
DDx: psuedopapilledeam, optic disk drusen.

Treatment: treat underlying cause to reduce intracranial pressure once normalized papilledema
will resolve within a few weeks. Can do decompression.
74. Atrophy of the optic disk

Definition: optic nerve is degenerated irreversible loss of axons in the region of the third neuron
(from retinal layer of ganglion cells to lateral geniculate body)
Classification:
1. Primary optic atrophy
2. Secondary optic atrophy
3. Glaucomatous optic atrophy
Etiology:
Secondary papilledema, AION, papillitis
Etiology of atrophy of optic nerve should be determined to
exclude life-threatening intracerebral causes e.g. tumour
Symptoms: broad
 Small peripheral visual field defects (partial atrophy) to
severe concentric visual field defects or even blindness
(total atrophy). Pupil is dilated and doesn’t react to light.
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Signs: need detailed history, ophthalmoscopy and
perimetry testing.
Primary optic atrophy:
 Well defined, pale optic disc
 Pallor can be partial or segmental or even
cover the entire optic disc (chalk white
optic disk in total optic atrophy)
Secondary optic atrophy:

 Pale optic disc which is slightly elevated due to proliferation of astrocytes, margin is blurred
Treatment: irreversible damage to nerve fibres no effective treatment
75. Diseases of the chiasm and central part of the visual analyzer. Localization of
visual disorders of visual pathways according to the visual field defects
Disorders of the visual pathways:
Classified according to 3 main locations:
1) Prechiasmal lesions (lesions of the optic nerve) visual field defects on the same side
2) Chiasmal lesions (disorders of the optic chiasm) bilateral temporal hemianopsia, but can
also cause unilateral or bilateral visual field defects
3) Retrochiasmal lesions (from optic tract to visual cortex) cause homonymous visual field
defects i.e. visual filed loss on the same side of both eyes
Chiasmal lesions:
Remember, the optic chiasm and optic nerves lie on the sella turcica. Around it is the pituitary
gland, ICA, hypothalamus and anterior lobe of the cerebellum. Within the chiasm, inferior nasal
fibroses cross it (link pituitary tumours) as well as superior nasal fibres (link craniopharyngiomas)
and macular fibres.
Etiology:
- Pituitary adenomas when they become bigger they compress nasal fibres initial visual
field defect begins as a bilateral superior temporal defect, can progress to bilateral temporal
hemianopsia.
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- Craniopharyngiomas- slow-growing tumours that compress the optic chiasm affect superior
nasal fibres there. Visual field defects begins in the inferior temporal quadrants and spreads
into the superior temporal quadrants (bilateral temporal hemianopsia)
- Meningiomas : visual field defects on the side of the affected optic nerve, the controlateral eye
may also be affected if fibres in arc of willbrand are compressed. Ipsilateral central scotoma,
controlateral visual field defect in superior temporal quadrants.
- Aneurysms : dilation of ICA due to aneurysm lateral compression of optic chiasm. Initially,
unilateral visual field defect can become bilateral if the chiasm is praised against the
controlateral ICA. Hemianopsia extending nasally and can progress to bilateral nasal
hemianopsia.
NOTE!
- Heteronymous bilateral hemianopsia with decreased visual acuity and unilateral or bilateral
optic nerve atrophy chiasm syndrome
- Bilateral temporal visual field defects are due to chiasmal lesions.
Retrochiasmal lesions:
Etiology: neurologic disorders e.g. tumours, basal meningitis, abscess, vasospasms
Diagnose via perimetry. Bilateral simultaneous visual field defects.

Homonymous visual field defects are a aresult of retrochiasmal lesions
- Lesions of optic tract and lateral geniculate body homonymous hemianopsia. Lesions on the
right produce visual field defect on the left and vice versa. Afferent papillary defect on the
side opposite of lesion is present.
- Lesions in optic radiations homonymous heminopsia if injury to both temporal and parietal
lobes.
- Lesions in the visual cortex homonymous and hemianoptic.
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76. Glaucoma- Definition, types, etiology and pathogenesis
Firstly, we’ll look at the maintenance of normal intraocular pressure before reviewing glaucoma.
1. Formation of aqeous humour
- Fluid that fills the anterior and posterior chamber of the eyeball.
- Production in the ciliary epithelium- secretion and ultrafiltration
2. Outflow of AH
i. Angle of the anterior chamber (conventional route): aqeous formed from ciliary
epithelium flows from the ciliary region to the posterior chamber through the pupil
into the anterior chamber and escapes via drainage channels to episcleral veins.
Trabecular meshwork canal of Schlemm aqueous vein venous circulation
ii. Uveoscleral outflow (unconventional outflow)- secondary exit through ciliary body in
suprachoiroid space an choroid episcleral tissue. Important pathway in
buphthalmos.
Ciliary body suprachoroid space venous circulation of ciliary body, choroid and sclera
3. Pressure in the episcleral veins: there’s a pressure difference between the anterior chamber
and episcleral veins so there is continuous flow of aqeous into the venous system
Glaucoma:
Definition:
 Disorder in which increased intraocular pressure damages the optic nerve. It eventually
leads to blindness in the affected eye.
 Primary glaucoma= glaucoma not caused by other ocular disorders
 Secondary glaucoma= as a result of other ocular disorders or undesired side effect of
medication or other therapy
NOTE: average normal intraocular pressure of 15mmHg in adults
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Etiology:
Obstruction of drainage of aqeous humour through the
i. Angle of the anterior chamber
ii. At the pupil
Types:
 Outflow impediment in
trabecular meshwork
 RBCs, pigment,
inflammatory cells occlude
trabecular meshwork
 Iris occludes the trabecular

meshwork
 Displaced TM produces
anterior synechiae, scarring, and
neovascularisation (rubeosis iridis)
 TM (which is not fully

differentiated and/or is occluded
by embryonic tissue)
Pathogenesis:
Damage due to glaucoma is due to a number of factors that affect perfusion of the optic nerve head
1. Mechanical changes coats of the eye can withstand raised ocular pressure except at the
lamina cribrosa which is pushed backwards. This squeezes the nerve fibres and disturb flow
2. Vascular factors perfusion of optic nerve head affected due to decreased blood flow in the
capillaries and in annulus of Zinn which supply nutrition to the laminar and postlaminar optic
nerve head
Also, any increase in the resistance to pupillary outflow (pupillary block) leads to an increase in the
pressure in the posterior chamber; the iris inflates anteriorly and presses against the trabecular
meshwork pathogenesis of angle closure glaucoma
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77. Glaucoma- diagnosis methods
1. Oblique illumination of the anterior chamber: question 25
2. Slit-lamp examination- to view central and peripheral depth of anterior chamber on the
basis of the thickness of the cornea.
The beam should strike the eye at a slight angle to the examiner’s line of sight
3. Gonioscopy- evaluate the angle of the

anterior camber- gonioscope placed
directly on the cornea
It is the method of choice to identify the type of
glaucoma
- Open angle= open angle glaucoma
- Occluded angle= angle closure glaucoma
- Angle access is narrowed= risk of acute
closure glaucoma
- angle is occluded= secondary angle closure
glaucoma e.g. due to neovascularisation in
rubeosis iridis
- angle open with inflammatory deposits,
RBCs or pigment in TM= secondary open
angle glaucoma
4. measuring intraocular pressure

 palpation (compare both eyeballs)
- if examiner can indent the eyeball which
fluctuates under palpation- pressure
<20mmHg
- rock hard (60-79mmHg)- acute angle
closure glaucoma
 tonometry
a) Schiotz indentation tonometry-
measures how much the cornea is
indented in the supine patient; the lower
the IO pressure, the deeper the
tonometer pin sinks and the greater distance the needle moves
b) applanation tonometry- method of choice.
IO pressure of 22mmHg is regarded suspicious
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5. Optic disk opthalmoscopy:
The optic nerve is the eye’s ‘glaucoma memory’. Evaluating this structure will tell
the examiner whether damage from glaucoma is present and how far advanced it
is
The optic cup is nearly

always round. In
glaucoma vertical
elongation and pale
discolouration of the optic
disc
6. Visual field testing: relative scotomas absolute scotomas (later progression)
78. Clinical findings in primary open angle glaucoma- etiology, risk factors,
clinical findings, treatment, prophylaxis
Definition: beings in middle-aged and elderly patients. It is chronic and slowly progressive. The angle
of the anterior chamber characteristically remains open. Most common form of glaucoma (90% of
adult glaucomas). + family history, high myopia= greater risk
Etiology: drainage of aqeous humour is impeded. Sclerosis of the trabecular meshwork and maybe
the lining of canal of Schlemm too.
Symptoms: doesn’t show typical symptoms for years, regular examination is crucial for early
diagnosis.
- Painless, progressive loss of vision
- Mild headache and eyeache
- Defect in visual field
- Failure of accommodative reflex due to pressure on ciliary muscle difficult reading
- Light sense defective light minimum raised and dark adaptation slowed
Signs & diagnostic consideration:
Diagnosis depends on a triad of signs:
Raised IO pressure cupping of optic disc visual field defects
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DDx: ocular hypertension, low-tension glaucoma.
Treatment:
- Should be initiated when there are signs of glaucomatous changes in the optic cup
- Any IO pressure >30mmHg should be treated
- Increasing glaucomatous changes in the optic cup or increasing visual field defects
1) Medical therapy (treatment of choice)
- Inhibit aqeous humour production sympatholytics (BB), carbonic anhydrase inhibitors
- Increase trabecular outflow
- Increase uveoscleral outflow
You begin with BBs (timolol) if miosis is undesirable, or else start with miotic agents (pilocarpine)
2) Surgery: (when medical therapy fails)
Argon laser trabeculoplasty- laser burns the trabecular meshwork causing tissue contraction that
widens the intervening spaces and improves outflow through TM.
Filtration surgery- aqeous humour is drained through the anterior chamber through a
subconjunctival sclera opening
Cyclodialysis- aqeous humour drained via opening into the suprachoroidal space
Cycloablation- inducing atrophy to portions of the ciliary body to reduce IO pressure by decreasing
amount of tissue producing the aqeous humour.
Prophylaxis: none- early diagnosis is crucial- regularly check IOP when 40y and above
79. Clinical findings in closed angle glaucoma. Acute glaucoma- Risk factors,
Clinical findings, Treatment and prophylaxis
Primary angle closure glaucoma:
Definition: raised IOP due to narrow or closed angle of anterior chamber. Obstructed outflow of AH.
Etiology: small and hypermetropic eye, anatomical narrow anterior angle chamber, shallow anterior
chamber, iris lens diaphragm is pushed forwards. Pupillary block increases pressure in posterior
chamber pressure displaces the iris
anteriorly to the trabecular meshword and
117 | P a g e
lbokcs outflow of aqeous humour (angle closure)
Symptoms:
1. Acute onset of intense pain: > IOP acts on corneal nerves (ophthalmic nerve or 1st branch of
trigeminal nerve) to cause a dull pain.
2. Nausea and vomiting: irritation of the vagus nerve
3. Diminished visual acuity: obscured vision and coloured halos around lights in the affected
eye.
4. Prodromal symptoms: transitory episodes of blurred vision
NOTE: the full clinical syndrome of acute glaucoma will not always be present. The diminished visual
acuity can go unnoticed if the other eye is normal. Subjective perception of pain varies with people.
Diagnosis: triad of symptoms:
1. Unilateral red eye with conjunctival or ciliary injection
2. Fixed and dilated pupil
3. Hard eyeball on palpation
DDx: iritis and iridocyclitis (eye is also red and iris appears faded but IOP usually decreased)
Treatment:
Medical therapy- decrease IOP (carbonic anhydrase, hyperosmotic solutions), allow cornea to clear
(for surgery) and relieve pain (analgesics, antiemetics, sedatives)
Surgery- once the cornea is clear, it is treated surgically by creating a shunt between the posterior
and anterior chambers.
- Nd:YAG
- Peripheral iridectomy: incisional procedure to
make a shunt.
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prophylaxis: prodromal symptoms
apparent and the angle of anterior
chamber is constricted the safest
prophylaxis to do is Nd-YAG laser
iridotomy or peripheral iridotomy.
- If one eye has already suffered

an attack, the other eye should be
treated with pilocarpine to minimize risk
of glaucoma attack
80. Congenital glaucoma

AKA Buphthalmos, hydrophthalmos
Definition: any abnormal increase in IOP during first years of life will cause dilation of the wall of the
globe, especially the cornea abnormally large eye (buphthalmos). Usually bilateral
Etiology:
Congenital abnormality at the angle of anterior chamber. AR trait.
1. Iris isn’t completely separated from cornea
2. Absence of canal of Schlemm
3. Embryonic mesodermal tissue covers the trabecular meshwork and impedes flow of AH into
Schlemm canal.
Types:
1. Congenital glaucoma
2. Infantile glaucoma (1-3 years)
3. Juvenile glaucoma (puberty)
Symptoms:
- Photophobia (corneal involvement)
- Epiphora (corneal edema and erosion)
- Corneal opacification causes defective vision (hazy and edematous cornea)
- Uni-/bilateral enlargement of cornea.
Children with this disorder are irritable, poor eaters and rub their eyes often.
Diagnostic considerations/signs:
1. Raised IOP
2. Optic disc ophthalmoscopy- glaucomatous optic cup
3. Inspection of cornea whitish and opacified (epithelial edema). Breaks in Descemet’s
membrane can make the edema worse (haab’s striae). Enlarged corneal diameter is
characteristic. (>10.5mm= childhood glaucoma, normal is approx 9.5mm). Enlargement of
entire globe chronically elevated IOP under 3 years
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4. Gonioscopy of angle of anterior chamber shows abnormalities. Embryonic tissue will be
seen to occlue the trabecular meshwork.
DDx:
- Large eyes (megalocornea/keratoglobus) present since birth
- Deep keratitis and keratoconus vertical striae in Descemet’s membrane (Haab’s striae are
horizontal)
The above don’t have any increase in IOP
Treatment: surgically. The earlier the better.

a) Goniotomy slicing the anterior chamber to the trabecular meshwork and then as far as
the canal of Schlemm to drian AH
b) Trabeculotomy- drainage of AH you basically gain acsess to the canal of Schlemm and you
probe the canal with a trabeculome.
81. Secondary glaucoma

Definition: caused by other ocular diseases e.g. inflammation,trauma, bleeding, tumours,
medication, physical or chemical influences
Secondary open angle glaucoma:

Trabecular meshwork is congested and the resistance to drainage is increased.
Most important forms:
1. Pseudoexfoliative glaucoma- depostis of acellular material in anterior chamber congest the
trabecular meshwork
2. Pigmentary glaucoma- young myopic men. Pigment granules from pigmentary epithelium of
the iris congest trabecular meshwork
3. Cortisone glaucoma- topical or systemic steroid therapy raises IOP. Increased deposits of
mucopolysaccharides in trabecular meshwork
4. Inflammatory glaucoma- influx of protein from inflamed iris vessels increases visocisty of
AH TM congested with inflammatory cells and cellular debris
5. Phacolytic glaucoma- aute glaucoma in the eyes with mature cataracts. Denatured lens
proteins pass through the lens capsule into anterior chamber and phagocytised. TM
congested with macrophages and the protein itself
Secondary angle closure glaucoma
1. Rubeosis iridis: neovascularisation draws the angle
of anterior chamber together like a zipper
(neovascular glaucoma)
- Diabetic retinopathy, retinal vein occlusion or

intraocular tumours can lead to rubeosis iridis with
progressive closure of angle.
2. Trauma- injury, surgery or insufficient treatment of primary angle closure blood or
exudates in anterior angle and prolonged contact between iris and TM collapsed anterior
chamber anterior synechiae and angle closure without rubeosis iridis
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82. Concomitant strabismus- types, treatment, prophylaxis
Strabismus- deviation of an eye’s visual axis from its normal position
Definition: the angle of deviation remains the same in every direction of gaze, the deviating eye
follows the normal eye at a constant angle.
Etiology:
- Genetic factors family history
- Uncorrected refractive errors e.g. children with hyperopia tend to have esotropia (form of
strabismus where both eyes turns inwards i.e. cross-eyed)
- Insufficient fusion: in anisometropia (unequal refractive power of the 2 eyes) and aniseikonia
(unequal retinal image size).
- Unilateral visual impairment: cataract, corneal scarring, macular changes retinal disorders can
cause secondary strabismus.
Types:
Esotropia Inward deviation of the eye
Exotropia Outward deviation
Hypertropia and hypotropia: primary oblique Deviation with one eye higher of lower than the
muscle function and dissociated vertical other
deviation
Cyclotropia Rotation of one eye around its visual axis.
Isolated form of strabismus i.e. doesn’t occur
with paralytic strabismus. Very rare.
Esotropia: most common, 3 forms:

1. Congenital/infantile esotropia: birth or within 1st six
months
- Alternating angle of deviation, lack of binocular vision,
latent nystagmus (involuntary oscillation of eyeballs),
inclination of head in direction of leading eye,
hypertropia
- ‘A pattern deviation’= inward angle of deviation that
increases in upgaze and decreases in downgaze
- ‘V pattern deviation’= inward angle of deviation that

decreases in upgaze and increases indowngaze
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2. Acquired strabismus:
a) Occurring at ages 1-3- age of incomplete sensory development. Unilateral strabismus and
amblyopia
b) Between 3-7years acute late strabismus with normal sensory development- sudden double
vision at the onset of strabismus (the child cannot suppress the images of the deviating eye)
3. Microstrabismus: unilateral esotropia with minimal angle of deviation (<5°)
Exotropia: divergent strabismus

a) Intermittent exotropia: angle of deviation only
present when the patient gazes into a distance, there
is no deviation in near fixation.
b) Secondary exotropia: trauma, reduced visual acuity

in one eye
Hypertropia and hypotropia:
a) Primary oblique dysfunction: upward vertical

deviation of adducting eye during horizontal eye
movements
Treatment:
a) Children:
- Long-term
- Determine if it can be treated with eyeglasses e.g. hyperopia
- Occlusion therapy follows if eyeglasses don’t fully correct strabismus.
- Alignment of eye(s) corrected by surgery;
o Esotropia- medial (reduce the pull) & lateral (increase pull) rectus resection
o Exotropia- posterior lateral rectus resection with medial rectus resection
o Primary oblique muscle dysfunction- inferior oblique resection
b) Adults:
- Surgery
Note: to avoid and treat strabismic amblyopia an eye patching or eyeglass occlusion is the most
effective method the leading eye is patches to improve visual acuity in the deviating amblyopic
eye.
83. Paralytic strabismus- DDx with concomitant strabismus

Paralytic strabismus-
 results from paralysis of one or more eye muscles.
 Differs from concomitant strabismus in that the angle of deviation doesn’t remain constant
in every direction of gaze incomitant strabismus.
 It can be isolated limited motility in one eye or asymmetrical limited motility in both eyes.
Opthalmoplegia- paresis (partial-more common), paralysis.
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Etiology:
 Congenital ocular motility disturbance- encephalitis, aplasia of ocular muscles, birth trauma
 Acquired- DM, intracranial tumours, MS
 Neurogenic ocular motility disturbances- lesions in the nerves supplying ocular muscles,
lesions of the ocular motor nuclei
 Myogenic ocular motility disturbances- Graves disesease, MG
Symptoms:
 Strabismus- link abducent (paralysis of lateral rectus- eye cannot be abducted, medial rectus
dominates-responsible for adduction affected eye medially rotated) and trochlear
(paralysis of superior oblique) nerve palsy
 Gaze palsy- symmetrical paralysis of muscles of both eyes limits ocular motility in certain
directions. Link lesion in the gaze centres
 Double vision- loss of binocular coordination between 2 eyes due to opthalmoplegia leads
to double vision. In time, patients learn to suppress one of the 2 images.
 Compensatory head posture- avoiding diplopia by attempting to avoid using the paralyzed
muscle. He/she tilts their head
 Ocular torticollis- compensatory head posture in trochlear nerve palsy
 Incomitant angle of deviation
Trochlear nerve palsy- superior oblique muscle paralysed upward vertical deviation of the
paralysed eye in adduction and vertical strabismus.
Abducent nerve palsy- lateral rectus is paralysed thus the medial rectus dominates. Abduction
impaired/absent and affected eye is medially rotated.
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Oculomotor nerve palsy- partial or complete (loss of accommodation and pupilary light reaction,
mydriasis, ptosis, paralyzed eye deviated, no diplopia due to ptosis covering pupil)
84. Amblyopia. Treatment

Definition: partial or complete loss of vision in one eye caused by conditions that affect normal
development of vision e.g. strabismus (esotropia and exotropia) and anisometropia.
In amblyopia, the brain favours one eye over the other. The other eye is ignored and inadequately
stimulated. Most common cause of monocular blindness; partial or complete blindness in one eye.
Amblyopia secondary to suppression: constant suppression of strabismus in the form of a central

and fixation scotomas lead to severe amblyopia, especially in children under 6. Amblyopia become
irreversible beyond 8 years. It only occurs in unilateral strabismus.
Treatment and avoidance of strabismic amblyopia: strict occlusion therapy by eyepatching or

eyeglass occlusion is the most effective method for treating and avoiding strabismic amblyopia. The
leading eye is patched
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Procedure: duration of occlusion therapy should
be balanced to avoid loss of visual acuity in the
leading eye.
- Mild amblyopia leading eye is occluded
for several hours at a time
- Severe amblyopia days at a time
Amblyopia is treated in early childhood. The
younger the child, the more favourable the
response to treatment. Upper age limit for
occlusion therapy is 9 years.
85. Trauma of the orbit,eyelids and conjunctiva

Eyelid injury mechanical injury
Etiology: any type of facial injury
- Eyelid lacerations
- Avulstions of the eyelid in the medial canthus with avulsion of the lacrimal canaliculus
Clinical pictures: the highly vascularised and loosely textured tissue of the eyelids causes them to
bleed profusely when injured. Hematoma and severe swelling.
- Abrasions superficial layers of skin is involved
- Punctures, cuts, eyelid evulsions due to blunt trauma (fist) all layers involved
- Bite wounds injury to lacrimal system
Treatment: surgical repair (especially lacerations with involved eyelid margins).
Orbit:
Penetrating injury single full-thickness break or wound of the eyeball caused by sharp objects
(knife, needle, small stone, glass etc.)
Perforating injury double-full thickness break or wound (entrance and exit wounds) in the eyeball
due to sharp objects- emergency due to severe damage to eye
Laceration outside-in injury of eyeball
Rupture inside-out injury of eyeball
Signs of perforation of eyeball:

- Decreased visual acuity
- Low IOP
- Shallow anterior chamber or hyphaema
- Altered pupil size, shape and location
- Chemosis
- Subconjunctival hemorrhage
Treatment:
- Suturing
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- ABs to control and prevent infection
- Follow up topical ABs, atropine and CS
Conjunctiva: laceration due to penetrating wounds

- FB sensation
- Conjunctival reddening and subconjunctival hemorrhage in injured area
Treated- if mild no treatment as conjunctiva heals quickly. Large lacerations absorbable sutures
86. Mechanical eye injuries. Non-penetrating injuries of the eye globe- contusion,
lamellar laceration, superficial foreign bodies. Diagnosis management.
Ocular contusion due to blunt trauma (fist, champagne cork, stone, falling on eye)
- Deformation exerts traction on intraocular structures and can cause them to tear. Blood in
anterior chamber
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superficial FBs:corneal and conjunctival FBs- chips from iron or steel, stone, glass, lead pellet, wood
spciules etc.
- FB sensation with each blink
- Epiphora
- Blepharospasm
Treated by removing FB out of its bed with fine needle or canula.
87. Penetrating injuries of the eye globe- intraocular FBs, penetrating and
perforating ocular trauma
Intraocular FB:
Effects:
1. Mechanical effect- FB pierces hte cornea or sclera and falls to bottom of anterior chamber or
situated in the angle of anterior chamber
2. Infection
3. Action of the metals
- Inert metal- glass, plastic, gold, silver
- Lead can become coated with carbonate
- Aluminium and nickel cause local suppuration
4. Degenerative changes- iron and copper undergo dissociation and get deposited throughout
the eye
a) siderosis bulbiiron deposited in lens (becomes opaque), iris (stained green then later
reddish-brown), retina (retinal degeration). Secondary glaucoma can result and
blindness if FB not removed early
b) Chalicosis FB with pure copper content gives rise to violent suppuration reaction with
shrinkage of the globe. Chalciosis= copper gets deposited in cornea (gold brown ring-
kayser-fleischer ring), lens (sunflower cataract), retina (golden plaques deposited)
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88. Chemical and thermal burns of the eye. First aid
Chemical injury and thermal burns:
Burn injury hot water, steam, hot ashes, explosive powder, molten metals. Because of the eye
closing reflex, eyelids often affected too. Epipohra, blepharospasm and pain. Immediate
opacification of the cornea (scarring of epithelium and tissue necrosis). Prognosis less severe than
chemical injury burns like acid injuries cause superficial coagulation. Heal well when treated with
AB ointment.
Chemical injury;
 Alkali liquefactive necrosis (deeper penetration). Cause severe intraocular damage by
alkalizing the AH.
- Lime, caustic soda, liquid ammonia
- Necrosis of surface epithelium diminished vascularity of anterior segment, corneal
opacification and melting, cataract, symblepharon
 Acids coagulation necrosis
- Sulphuric acid, HCl, nitric acid
- Less serious than alkali bruns as they coagulate the surface proteins and do not penetrate the
eye
Symptoms: epiphora, blepharospasm, severe pain. Acid burns cause immediate loss of visual acuity
due to superficial necrosis. Alkali injuries- loss of visual acuity after several days
Alkali burns may appear less severe initially than acid burns but they lead to blindness
Complication:
1. Symbelparon- adhesion of the lid to the globe due to conjunctival ulceration.
2. Corneal ulcer
First aid:
- Restrain blepharospasm by rigorously holding the eyelids open
- Irrigate the eye within seconds (acids neutralized by sodium bicarbonate, alkalis neutralized bu
milk)
- Notify rescure squad
- Transport the paitent to nearest ophthalmologist or eye clinic
89. Eye injuries due to phycial agents/ electric ophthalmopathy

Ultraviolet keratoconjunctivits:
Injury from UV radiation penetrates slightly superficial necrosis of corneal epithelium. Exposed
areas of the cornea and conjunctiva in the palpebral fissure become edematous, disintegrate and are
finally cast off.
UV keratoconjunctivitis is one of the most common ocular injuries
Symptoms;
- Acute blindness accompanied by pain, photophobia, epiphra and intolerable FB sensation.
Blepharospasm.
- Slit lamp shows epithelial edema and superficial puncate keratitis or erosion in the palpebral
fissure.
Treated: AB ointment
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Radiation injuries (ionizing radiation)
- Gamma or X-rays have high energy and cause ionization and formation of radicals in cellular
tissue.
- Usually a result of tumour irradiation of the eye or nasopharynx

Symptoms:
- Loss of eyelashes and eyelid pigmentation accompanied by blephariitis.
- Dry eye damage to conjunctival epithelium
- Loss of visual acuity due to radiation cataract
- Radiation retinoaphty bleeding, cotton-wool spots, vascular occlusion and retinal
neovascularisation
90. Causes and prevention of blindness

Blindness= inability to see anything.
- Partial blindness limited vision e.g. blurry vision or unable to distinguish shapes and objects
- Complete blindness total darkness
- Legal blindness vision that’s highly compromised
Causes:
- Glaucoma
- Macular degeration
- Cataracts
- Lazy eye (amblyopia)
- Optic neuritis
- Retinitis pigmentosa
- Diabetic retinoapathy
- Retinopathy of prematurity
Prevention:
- Regular eye examination
- If diagnosed with a certain eye condition treatment immediately
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91. Sympathetic opthalmia
Definition: specific bilateral inflammation of uveal tract due to chronic irritation of one eye, caysed
by a perforating wound to the eye or intraocular surgery, produced transferred uveitis to the other
eye. Tissues in the injured eye (uveal tract, lens, retina) act as antigens and provoke an autoimmune
disorder in the unaffected eye.
 Bilateral, granulomatous uveitis that occurs after trauma to the eye.

 Limited range of accommodation and photophobia, later there is diminished visual acuity
and apin.
 Blurry vision, red eye, decreased vision. Keratic precipitates, retinal detachment.
 Clinical symptoms include combined injection, cells and protein in the anterior chamber and
vitreous body, papillary and retinal edema and granulomatous inflammation of the choroid
DDx: iridocyclitis and choroiditis
Treatment: injured eye is usually blind enucleation to eliminate the antigen and prevent SO in the
other eye.. Highg dose topical and systemic steroids. Maybe immunosupressives too
Complication: uveitis, secondary glaucoma, secondary cataract, and shrinkage of eyeball. Lead to
blindness if severe
92. Pharmacological agents in ophthalmology
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Visual Anatomy and Ophthalmic Disease Guide

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Contents

1. General data of the visual analyser/phylogenetic and ontogenetic

General data of the visual analyser

2) Middle vascular layer

Interior the eyeball:

Accessory structures of the eye:

4. Extraocular muscles: Six intrinsic muscles; 4 straight and 2 oblique

Phylogenic and ontogenic development:

2. Blood supply and innervations of the visual analyser

CN IV (trochlear) superior oblique

2) Sensory nerve: CN V (trigeminal) ophthalmic branch supplies whole eye

3. Applied anatomy of the orbit

Remember the bones: frontal,

Surgical spaces of the orbit:

Both open the eyelids- only present in upper eyelids

Blood supply lacrimal arteries

Venous drainage ophthalmic vein

1) Lacrimal gland has 2 parts:

Blood supply: lacrimal branch of ophthalmic artery

Nerve supply: lacrimal brach of ophthalmic nerve

2) Conjunctival sac: membrane that lines the eye

3) Lacrimal puncti, canaliculi, lacrimal sac

Functions of the conjunctival sac:

1) Epithelium- stratified squamous,

It is transparent due to:

8. Applied anatomy of the anterior chamber angle and ocular hydrodynamics

 It is approx 3mm in depth and contains 0.35ml of aqeous humour

The anterior chamber

9. Applied anatomy of the lens and vitreous body

Following structures: iris, ciliary body, choroid

 Coloured, central aperture is the pupil (4mm).

 Ciliary zone= series of radial

Ciliary body: attaches to iris.

Function: regulates temperature, supplies nourishment to outer layers of the retina

11. Applied anatomy of the retina

 Ora serrata: anterior termination of the

12. Applied anatomy of the visual pathway and cortical centres

13. Perception of light, adaptation. Disorders of adaptation

14. Perception of colour. Theory of colour vision. Disorders of colour vision

Theory of colour vision:

15. Central and peripheral vision.Visual acuity. Examination methods

Actual distance/ Standard distance= visual acuity

16. Visual field. Examination methods. Pathological changes of visual field.

Boundary- the peripheral limits

Monocular visual filed= amount of outside world visible to each eye

Normal field of vision= 160-170°

Central field loss Peripheral field loss

Hemianopia: loss of half the field of vision of both eyes

17. Refraction. Emmetropia and ametropia

18. Methods of examination of refraction. Objective and subjective methods

1) Subjective refraction testing:

Automated refractometry: measures refraction automatically with the aid of light-sensitive

19. Myopia. Definition, clinical findings, treatment (glasses, contact lenses,

Etiology: increase in axial length affects the posterior

21. Astigmatism- definition, clinical findings, treatment

22. Accomodation. Disorders of accommodation (insufficiency, paralysis, spasm),

a) Accommodation spasm= inadequate contraction of ciliary muscles

b) Accomodation palsy= failure of accommodation due to paralysis of ciliary muscle

23. Binocular vision

- Remember the position of the eyes are controlled

24. Types of correction for ametropia- glasses, contact lenses, surgery

II) Contact lenses