Summary Ophthalmology

Made by Dr.
AMR KHALED
and Dr. MOHAMED O-WIDE
For Medical Student
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CONTENT
1. Lacrimal System and Dry eye:
Chronic Dacrocystitis
Dry eye
2. Eye Lid:
Mal-positions of the lashes (Distichoiasis Trichasis)
Mal Positions & the lid margin( Entropion Ectropion)
Blepharoptosis
Lagopthalms
Congenital Abnormalities of eye lid
Seborrheic (Scaly) Blepharitis
Staphylococcal (Ulcerative) Blepharitis
Stye External Hordeolum
Meibomian Gland Dysfunction
Chalazion
3. Errors of Refractions:
Myopia
Hyperopia
Astigmatism
Anisometropia
Presbyopia
4. Squint:
Paralytic Squint
Concomitant Squint
Latent Squint
Apparent squint
5. Retina & Optic Nerve:
Inflammation of Optic Nerve
Papilloedema
Optic Atrophy
Retinitis Pigmentosa "Night Blindness"
Color Blindness
Retinal Detachment (1ry and 2ry)
Vascular Diseases of Retina
Retinopathies:
Atherosclerosis
Hyper tension
Diabetes mellitus
CRA occlusion
CRV occlusion

6. Uveal tract:
Iridocyclitis
Choroiditis (Endophth. And Panophth.)
Sympathetic Ophthalmitis.
7. Cornea:
Infective Corneal Ulcer (Bacterial and Viral)
Non-infective Corneal Ulcer
Keratoconus
8. Cataract:
Congenital Cataract
Complicated cataract
Senile Cataract
9. Glaucoma:
Secondary Glaucoma
Primary Closed Angle Glaucoma
Primary Open Angle Glaucoma
Primary Buphthalmos "Congenital Glaucoma"
10. Conjunctiva:
Chlamydial Conjunctivitis (Trachoma)
Phlyctenular Keratoconjunctivitis
Vernal Keratoconjunctivitis "Spring Catarrh"
Ophthalmia Neonatorum
Conjunctival Degenerations (Pinguecula and
Pterygium)
11. Collections:(Self-teaching)
Sclera (Staphyloma)
Inflammation of the orbit (orbital cellulites and
cavernous sinus thrombosis)
Proptosis (exophthaloms) and endophthalmos
Eye injuries

Anatomy of the eye
Anatomy of the eye

Anatomy of the eye

Anatomy of the eye

Anatomy of the eye

Lacrimal Apparatus
Chronic Dacrocystitis
Definition:
- Chronic Inflammation of lachrymal sac.
Risk Factors:
I- Predisposing factors (causing Obstruction in passages):
A- Lumen:
Eye lash
B- Wall:
Congestion as nasal catarrhal
Stricture as trauma or inflammation
Trauma
C- Out side from maxillary antrum
Trauma as facture
Tumor as malignant
D- Out let in nasal e.g.:
Nasal polyp.
Rhinoscleroma.
II- precipitating factors:
a- Organism e.g. pneumcocci
b- Rout of infection:
Ascending from nasal cavity
Descending from conjunctival sac (commonest)
Blood borne

Lacrimal Apparatus
Pathology: (3 stages):
1- Obstruction:
Epiphora.
No regurgitation (with pressure on lacrimal sac).
No swelling.
2- Infection:
Epiphora.
Swelling.
Regurgitation (mucous / muco-purullant/ pus)
3- Swelling without regurgitation
Epiphora.
No regurgitation.
Swelling (mucocele- pyocele- heamatocele).
Clinical picture:
Symptoms:
1. Lacrimation
2. Photopia
3. Discharge
4. Disfigurement due to swelling
Signs:
1. Epiphora
2. Regurgitation
3. Swelling
4. No tenderness
Complication:
1- Recurrent conjunctivitis
2- Pneumococcal corneal ulcer
3- Post operative Endophthalmitis.
4- Acute dacryocystitis leading to cavernous thrombus or
lacrimal fistula.
5- Septic focus bacteremia.

Lacrimal Apparatus
Management:
A. Investigation of cause Epiphora
B. Surgery for chronic. Dacryocystitis
C. Treatment for complication.
A- Epiphora:
1- Exclude:
Lacrimation
Ectropion
Orbicularis oculi paresis.
2- Lacrimal passages to detect obstruction ( cause level)
Fluorescent test
Syringing with saline.
Syringing with saline & adrenaline
Probing the passages.
3- Radiology:
Plain X-Ray to detect bone abnormalities.
X-Ray with opaque material to detect stricture show rat
tail appearance or tumor show filling defect.
Lacrimal scintilography by gamma camera
4- E.N.T examination:
Nasal mucosa (Healthy Atrophic).
B- Surgery:
1- Dacryocystectomy: Removal of lacrimal sac. (No
septic focus / with epiphora).
2- Dacryocystorhinostomy (D.C.R.) connection bet.
Lacrimal sac & middle of nasal cavity.
C- Treatment of complication:
1- Lacrimal fistula:
ttt: D.C.R. with Lacrimal cannaliculi openings.
2- Mucocele or pyocele :
ttt: D.C.R with Lacrimal cannaliculi opening.
3- Acute Dacryocystitis:
ttt:
Hospitalization
Antibiotic
Hat water
Pus incision to drain pus
Chronic. Dacryocystitis with fistula DCR with
fistulectomy
N.B:
D. C. R contraindication (indication of Dacryocystectomy):
1- Atrophic Nasal mucosa
2- Diseased Nasal bone.
3- Tumor of lacrimal sac
4- Specific inflammation e.g. T. B

Lacrimal Apparatus
Dry eye
Definition:
Disease where ocular
surface (conjunctive &
cornea) is dissected caused
by (evaporation /
formation of tears)
Types of Dry eye:
According to tear layer:
a. Aqueous deficiency
b. Mucous deficiency
c. Oil lipid deficiency
Causes (Etiology):
I- Evaporation of tears:
1- In lid as:
Short lid
Symblephron
Blinking
Meibomian gland Dysfunction
2- In orbit as:
Proptosis due to tumor or thyroid proptosis
II- formation of tears:
1. Local:
a- Conjunctive:
Trachoma
Beta-blocker drug.
b- Cornea:
Sensation : keratitis surface
Irregular: keratoconus
2. General:
a- pharmacological:
Vit. A
Antihistaminic.
b- Auto-immune:
keratoconjunctivitis sicca
Sarcoidosis.

Lacrimal Apparatus
Clinical picture:
Symptoms:-
1- Local (Ocular):
a- Mild cases: Burning, itching, foreign body sensation.
b- Sever cases: vision, dryness, ptosis, sensation of film
coating the eye.
2- General:
Night blindness
disease of other organs ( saliva dryness oral & vaginal).
Signs:
a- Mild cases:
1. Conjunctival Redness
2. Conjunctival elasticity
3. Conjunctival wrinkling
4. Corneal luster
5. White discharge
6. Tears margin.
b- Sever cases:
1- Bitot spot
2- Yellow discharge
3- Filamentary keratitis
4- Difficult to open upper lid (ptosis).
Investigation: (for each layer of tear film)

Traditional:
1- Schirmer 1 test: No stimulation basic tear film
Accessory lacrimal gland.
2- Schirmer 2 test: stimulation Reflex tear film main
lacrimal gland.
3- Fluroescin breakup time test (BUT): for muscin layer.
4- Rose Bengal dye test: stain Healthy Epithelium.
New tests:
1- Lysozym activity assay
2- Tear function index: compare between (secretion /
evaporation / drainage).

Lacrimal Apparatus
Management:
a- Elimination of predisposing factors:
1- Hypovitaminosis A
ttt vit. A supply
2- Eyelid & orbit anomalies
ttt surgery
b- Substitution therapy:
Medical
1- Tear substitution
Artificial tear
Lubricant methyl cellulose 0.5% drops.
Hypotonic tears osmolarity of tears.
Autologus serum
2- Moist chambers
Surgery
3- Punctual occlusion
4- Lateral tarsoraphy

Eyelid
Eyelid

Eyelid
Mal-positions of the lashes

"Distichiasis"
Abnormal position at lashes behind the gray line
Treatment:
- Cryotherapy After lamellar splitting
"Trichasis "
Abnormal direction of lashes against the globe
Clinical Picture:
Symptoms Signs
- Foreign body sensation - Misdirected Lashes
- Lacrimation - Rubbing against the corner
- Photo phobia and/or conjunctiva
Treatment:
1. Epilation (Temporary).
2. Diathermy (scarring)
3. Cryotherapy (depigmentation)
4. Electrolysis (recurrence)
5. Interpositioning
6. Transpositioning (Z- Plasty)

Eyelid
Mal Positions of the lid margin

"Entropion"
Inward rolling of the lid margin
Classification:
1- Upper lid Entropion: only to scarring mostly following the
trachoma.
2- Lower lid Entropion: According to the cause:
- Cicatricial
- Involution
- Spastic
- Congenital
Surgical Treatment:
1. Upper lid cictricial entropion:
- Normal Trasus:
ttt: Tarsal wedge resection (snellen)
- Thin or short Tarsus:
ttt: Lamellar splitting with post lamellar repositioning
2- Lower lid Inverting entropion:
- Temporary measures:
ttt: Everting Sutures
- Permanent Measures:
ttt: Transverse blepharotomy with marginal rotation
(Wies)
3- Lower lid Cicatricial ectropion:
- Mild cases of fibrosis
ttt: Transverse blepharotomy with marginal rotation
- Moderate advanced cases:
ttt: Tarsal fracturing
- Marked fibrosis:
Treatment: Tarsal grafting
4- Congenital entropion of lower lid
- Treatment:
Everting Sutures
Skin & Mused operation

Eyelid
"Ectropion"
Out ward rolling of the lid margin
N.B: mainly of lower eye lid except in marked skin scarring
Classification:
1- Cicatricial
2- Involutional
3- Orbicularis paresis
4- Mechanical
Clinical picture:
Symptoms Signs
- Excessive tearing (epiphora) - Mild: punctum can be seen
without eversion
- Cosmetic disfigurement - Sever: palpebral
- Eczema conjunctiva seen without
eversion
Surgical Treatment:
1- Cicatricial ectropion:
- - Localized scar:
Treatment: Z- plasty
- Diffuse scar:
Treatment: skin grafting
2- Involutional ectropion:
- Localized:
Treatment: punctual inversion procedure (the medial
spindle)
- Diffuse:
Treatment: Horizontal lid shortening
3- Paralytic ectropion:
- Temporary measure:
Treatment: lateral tarsorrhaphy
- Permanent measure
Treatment:
1- Supporting lower lid by fascia lata sling Lateral
tarsal sling
2- Lateral tarsal sling

Eyelid
Blepharoptosis
Definition:
- Drooping of the upper eyelid so as to
cover more than 1-2mm of upper cornea
Causes:
1- Congenital as:
Blepharophimosis
2- Acquired as:
Aponeurosis dehiscence
Myogenic as Myasthenia gravis
Neurogenic 3rd nerve paralysis
Mechanical as upper eyelid mass
Types:
1- Levator function better than 5mm
Treatment: levator resection
2- Levator function less than 5mm
Treatment: Frontalis
suspension
3- Levator aponeurosis dehiscence
surgery:
Treatment: Aponeurotic
repairer
Pseudoptosis:
Contra-lateral lid retraction
Shrunken or absent eye

Eyelid
Lagopthalms
Definition:
- Inability to close palpebral fissure
Clinical Picture:
- Inability to close lids Dryness of conjunctiva
Complication:
- Exposure Keratitis corneal ulcer perforation
Endophthalmitis
Causes:
1. Paralysis of lid muscle
2. Saver ectropion
3. Coloboma (cong. or acqied)
4. Protrusion of eye globe
- Big eye globe (psuodoproptosis)
- Thyroid exophthaloms (True proptosis)
5. Symblephron: Adhesion btw palpebral & Bulbar conjunctiva
Treatment:
1. Artificial Tears
2. Treatment the cause.

Eyelid
Congenital Abnormalities of eye lid

1. Ptosis:
- Drop of up. Eye lid
2. Coloboma:
- Facial cleft of lid
3. Epicanthus:
- Fold of skin cover medial canthus angle.
4. Distichiasis:
- Extra rows of lashes grows Behinds the gray line.
5. Ankyloblephoron:
- Narrowing at the palpebral fissure Adhesion between up
& low. Eyelid at out canthus
6. Blepharo-phemosis
Congenital compilation of:
- Narrow of fissure
- Epicanthus
- Ptosis

Eyelid
Seborrheic (Scaly) Blepharitis

Definition:
Inborn disorder of lipid production accompanied with
seborrheic dermatitis without pathogenic organism Infection
Clinical picture:
Symptoms:
1. Burning & Itching
2. Phophapia
3. Lacrimation
Signs:
1. Dry type: Dry flakes
2. Wet type: Oily Secretion & greasy deposits
Complication:
1. Meibomian dysfunction
2. Eczematous dermatitis
3. Ectropion & tearing
4. Deformity of lid margin
5. Loss of lashes
Treatment:
1. Good hygiene & washing by neutral soap.
2. Anti-seborrheic shampoo
3. Anti-seborrheic ointment

Eyelid
Staphylococcal (Ulcerative) Blepharitis

Definition:
Infection hair follicle of lash by staphylococcus aurous
Clinical picture:
Symptoms:
1. Burning itching esp. in morning
2. Difficulty to open eye lid in the morning.
Signs:
1. Lashes matted together
2. Crusting on its base
3. Collarette: fibrinous scale encircles the eye lash
(Prominent feature).
4. Ulceration
Complication:
1. Telangiectasia (red spots) & tylosis (Abnormal lid margin)
2. Modarosis (Abnormal lashes regularly) loss of lashes.
3. Localized piliosis (whitening of lash)
4. External or internal hordeola
5. Chronic conjunctivitis and recurrent keratitis.
Treatment:
1. Good hygiene with neutral soap washing
2. Antibiotic ointment
3. Systemic antibiotic & local
4. Treat the original cause.
5. Steroids may used to fibrosis.

Eyelid
Stye
External Hordeolum
Definition:
Infection of hair follicle & zeis or moll glands by
staphylococcal aurous
Predisposing factors:
1- Staphylococcal Blepharitis
2- Low immune patients as DM
3- Error of refraction
Clinical picture& treatment:

(1) Defuse stage (2) Localized
stage
Clinical Tender swollen lid near the Small localized
picture lid margin abscess pointing
interiorly near the
hair follicles
Treatment Spontaneous resolution Removal of eye
Surgical Incision (If large) lash

Eyelid
Meibomian Gland Dysfunction

Causes:
(1) Initial changes as:
- Keratinization of duct
- Plugging of duct
- Dilatation & cystic formation.
(2) Infection by corynbacterium acnea.
(3) Release of irritant fatty acid from sterol ester.
Clinical picture:
Symptoms:
- Morning irritation & redness. (Improved during day).
Signs:
1. Bilateral foot lid margin information.
2. Thick yellowish oil material excretes.
3. Froth on lid margins.
4. Irritative conjunctivitis
5. Typical pouting orifices occlusion.
Complications:
Internal hordeolum
Chaluzion
Treatment:
1. Periodic expression
2. Oral tetracycline or doxycycline
3. Treatment associated conjunctivitis

Eyelid
Chalazion
Definition:
- Sterile granulomatous inflammation of meibomian gland
Clinical picture:
Symptoms:
- Painless swelling.
Signs:
- Swollen pointing to inner side disappears in forcible closure
of eyelid.
Complication:
1. Mechanical ptosis (if in up lid).
2. Mechanical ectropion (If in low lid).
3. Astigmatism.
4. Internal hordeolum.
5. Mechanical irritation of conjunctives
Treatment:
- Incision of Excision & Curette.

Errors of Refractions
Errors of Refraction
Definitions:
1- Emmeteropia:
Parallel rays coming from infinity to form one focus on the
retina while accommodation at rest.
2- Myopia:
Parallel rays coming from infinity to form one focus in front of
the retina while accommodation at rest.
3- Hyperopia:
Parallel rays coming from infinity to form one focus behind the
retina while accommodation at rest.
4-Astigmatism:
Parallel rays coming from infinity to focus in more than one
point at varying distances from the retina
5- Anisometropia:
Difference in the refractive power of two eyes.
6- Anisokonia:
Difference in the retinal images size between the two eyes.
7- Binocular diplopia:
Anisometropia more than 4D lead to anisokonia which is too
big to fuse images of two eyes in brain.
8- Amblyopia:
Brain suppresses the blurred image leading to ignorantion of
more ammetropic eye.
9- True squint:
Lack of parallism between two visual axes with angle of
deviation.
Types:
Manifested (Heterotropia)
- paralytic
- concomatetant
Latent (Heterophoria)

Grads of Binocular Vision (Detected by Synoptophore):

1. Simultaneous perception (6m)
2. Fusion (9 yr)
3. Stereoscopic vision (above 6 yr)
Accommodation:
1. Eye (lens) power (cont ciliary ms)
2. Myosis (cont. of const. Pupilli )
3. Conversion (cont of M. Rectus).
Clinical Types of Myopia

1- Simple:
start from 14 25 yr.
Error 6D
2- Degenerative:
Dont stop at 25yr
Error up to 25D
3- Congenital:
from childhood
very rare
Clinical Types of Hyperopia

1- Latent: corrected by normal tome of ciliary ms.
2- Facultative: corrected By power of Accommodation.
3- Absolute: No correction by full accommodation.
Etiology of Myopia & Hypermetropia

1- Axial (1mm 3D)
2- Refractive:
Curvature: curve. power
Index:
Index cortex power
Index Nucleus power
Anatomical:
Ant. Displacement at lens Myopia.
Post. Displacement at lens Hyperopia

Myopia Hypermetropia
1- Indistinct for vision 1- No symptoms in
Symptoms 2- eye strain latent type
3- Divergent squint 2- Defect in near vision
4- Masca Volitans in facultative type
5- Degenerative change as central 3- Defect in both near &
vision def for in Absolute type
Only In High error Only In High error
appearance
Big eye Small eye

External
large cornea small cornea

Large puple Small Puple
Deep A.C. shallow A.C.
Simple Myopia: 1- Water silk

- Tigroid Fundus appearance
Signs
Fundus examination
- Temporal crescent 2- Tortuous Retinal

Degenerative myopia: vessels
1- Post. Staphyloma 3- Pseudo papilloedema
2- Choroidal sclerosis
3- Sub-retinal neouvascularization.
With funchs spot sub-retinal
Hge scarring in foveal region
4- Peripheral chorio-retinal
degeneration (lattice
degeneration).
5- Vitreous Degeneration
Complication
1- PCAG
1- POAG, Cataract & RD
2- Squent: Apparent
2- Squint: Apparent conversion &
diversion &True
True Diversion.
conversion.
1- Glasses:
Under correct to manifested patient
Full correct to comp. Ptn by squent
Treatment
o Concave minus lens o Convex plus lens

o In Myopia. o In Hyperopia.
2- contact lenses Advantages:
Less size diff. In Retinal Image. (Less Anisonia)
wider field of corrected vision
Better cosmetic appearance
* Surgical correction of Myopia:
Error less than 6D PRK
Error less than 12D LASIK
High errors
Yong: Phakic IOL
Old: Clear lens extraction with IOL (Aphokic IOL)

Astigmatism
Classification:
1- Regular :
According to error of refraction:
Simple (Myopia or Hyperopia)
Compound (Myopia or Hyperopia)
Mixed (both Myopia and Hyperopia)
According to the Meridian:
With the Rule
Against the Rule
N.B: Rule = Curvature of vertical meridian more than horizontal.
2- Irregular
Deference between irregular and regular types:

No two main meridian
No right angle
No gradual change in power

Clinical picture of regular Astigmatism:

Symptoms:
1- Eye strain
2- Impair near & far vision
Signs:
1- On examination: Visual acuity show right ring opened in one
direction.
2- Fan test: Not all lines appear sharp
3- Retinoscopy: Difference in refraction of 2 meridian
4- Placidodisc: Rings appear oval rings.
5- Keratometry & Corneal topography: To Identify (Curvature
and Power).
6- Fundus examination: Show oval optic disc and BVs running
in difference planes.
Treatment:
1. Glasses or contact lenses with:
- Cylindrical lens in simple (convex or concave).
- Sphero-cylindrical lens in compound & Mixed type.
2. Hard contact lens Irregular.
Clinical picture of irregular Astigmatism:

See Keratoconus.

Anisometropia
Clinical picture
1- Small degree asymptomatic
2- Eyestrain
3- Binocular diplopia
4- Amblyopia
Treatment:
1- Small degree (difference < 4D) glasses
2- High degree (difference > 4D) contact lenses
Presbyopia
Definition:
Physiological condition in which accommodation. Power is
decreased (Above age of 40 yr.)
Etiology:
1- Physiological:
Power of ciliary ms
Aging:
Elasticity of lens
2- Pathological:
Ischemia at ciliary ms in DM & Glucoma.
Clinical picture
Difficult reading with eye strain.
Treatment:
1- Correct any ammetropia
2- Add suitable plus lens
3- Let reservoir accommodation power
Caused of Eye strain in Error of Refraction:

1- Accommodative:
Due to increase usage of accommodation power
Occure in Hyperopia Astigmatism Presbyopia -
Anisometropia
2- Muscular Asthenopia :
Due to in coordination between Accommodation &
Conversion
Occure in Myopia

Squint
Paralytic Squint
Definition:
Manifested squint in which limitation of eye movement due
paralysis of Extra ocular ms & Angle of deviation not constant.
Causes:
1- Traumatic
2- Metabolic as DM
3- Vascular as embolism
4- Myogenic as Myopathy
5- Neuromascural as Myastheuia gravis
6- Neurogenic.
7- Tumor as Brain Tumor
Clinical picture:
Symptoms:
1- Binocular diplopia:
- Homonymous
- Crossed
2- Vertigo Nausea and vomiting
Signs:
1- Limitation of movement toward action of Affected ms
2- Face turn & Head tilt
3- 2ry Angle at deviation > 1ry Angle of deviation
4- Past- pointing.
Treatment:
I- preoperative:
1- Treatment the cause.
2- Alternate covering (to avoid diplopia and Amblyopia).
3- Relieving prism.
II- Operative (After 6m)
1- Weakening procedure (Recession).
2- Strengthen procedure (As cutting Part of ms).
3- Muscle transplantation In sever ms weak.

Squint
Concomitant Squint
Definition:
Manifest non-paralytic squint in which the eye move without
limitation & same angle of deviation
Causes:
1- Defective vision in one eye (Anisometropia) Anisometropia >
40 diplopia Amblyopia
2- Abnormal relation between Accom. & conv. (Ammetropia) As
in Hypropia & Myopia
3- Central causes absent of binocular vision
Types:
- According To eye : (unilateral - Alternating)
- According To direction: (Vertical - Horizontal)
Management:
1- Treatment at cause.
2- Correct Accommodation / Conversion relation:
Glasses or contact lens
Drugs (Miotic or cycloplagic)
3- Surgery: weaken or strengthen of ms.

Squint
Latent Squint
Definition:
Tendency of the visual axes to deviate when binocular vision
is dissociated
Types:
1- Esophoria (Inward)
2- Exophoria (Out wars)
3- Hyporia (Downward)
4- Hyperhoria (Upward)
5- Cyclophria (Wheel rotation)
Etiology:
Physiological:
1. Prolonged close work
2. General fatigue
3. Age esophoria (young) / exophoria (old)
Error of refraction:
1. Esophoria Hypropia
2. Wxophria Myopia
3. Cyclophoria Astigmatism
Clinical Picture:
Symptoms:
1- usually Asymptomatic due to compensation
2- symptoms of maintain binocular vision:
Diplopia
Difficult to change focus
Photophobia
3- Symptoms of Binocular vision failure (Intermittent):
Diplopia
Blurring of print
Difficult read
Nausea and dizziness
Signs (Diagnosis):
1. Cover test: latent eye show correction
2. Alternate cover test: latent eye show correction
3. Maddox wing: to detect latent squint in near vision
4. Maddox rod: to detect latent squint in far vision

Squint
Management in latent squint:

1- correction of error of refraction
2- Nutrition by Iron & vitamin
3- Orthoptic treatment by using synoptophor
4- Exerting prisms
5- Reliving prisms
6- Surgical treatment
Apparent squint
Definition:
Apparent lack of parallism between two visual axes with
normal parallel visual axes without recovery movement by
cover test and corneal reflex in the center of cornea.
Causes of Apparent squint:
1- Anatomical : - Epicanthus conv.
- Ankyloblephoron Divers
- Blepharophimosis conv.
2- Optical (Abnormal angle
alpha): - Diversion
- Conversion

Retina & Optic nerve
Inflammation of Optic Nerve

Types:
1. Papillitis: Affect only optic head
2. Retro bulbar neuritis: Affect optic nerve portion behind the
eyeball
Etiology:
I- Non Infective as: Demyelinating disease (e.g. M.S), Idiopathic
or Toxic (e.g. Exogenous (Toxic Amblyopia.) or Endogenous.
II- Infective as: viral, extension of infection or granulomatous (e.g
T.B or syphilis)
III- Metabolic disorders as: DM & Avitaminosis
Clinical Picture:
Symptoms:
1- Rapid decrease of vision.
2- Defective color vision
3- No pain except in Retobulbar neuritis periocular pain in
inward & upward movement of eye.
Signs:
1- Visual Acuity: Reduced to 6/60.
2- Color Vision: Impaired
3- Field Examination: Centro-caecal scotoma
4- Pupillary Reaction: Ill to direct light & normal to indirect
5- Fundus Examination:
Appear normal to Retrobulbar Neuritis.
Optic disc affected in papillitis:
- Swollen
- Obliteration of physiological cup. (Filled cup)
- Hyperemia
Treatment:
1- Treat the cause
2- Corticosteroids
3- Vit B12 (Hydroxocobolamin) in Toxic Amblyopia.

Papilloedema
Definition:
Oedema of the optic Nerve Head (due to ICP):
1- Space occupying lesions
2- Benign increased Intracranial tension
3- Subarachnoid hemorrhage
4- Blockage of the ventricular system
D.D of Pailloedema:
Pseudopapilloedema in Hypermetropia
1- General causes & Bilateral swelling O.N.H:
Malignant hypertension
Acute sever anemia
2- Causes of unilateral swelling in O.N.H:
CRV occlusion
Papillitis
Uveitis
Sudden ocular hypotony
On Compression by Tumors
Clinical Picture:
Symptoms :
1- General symptoms of increase ICP e.g. Headache, Vomiting
(without nausea),
2- Visual symptoms:
- Early stage normal relatively
- Late stage (Gradual pain less vision and
Amaurosis Fugax = Transient vision loss).
Signs:
I- Fundus examination:
1- Early stage
2- Established stage
3- Chronic stage
4- Atrophic stage
II- Visual field examination:
1- Early
2- Late

I- Fundus examination:
A- Early papilloedema: Disc (1) & BVs (1)"
1- Blurring of disc Margin
2- Engorgement of R. vein (without normal pulsation)
B- Established Papilldema:
1- Blurring disc margin
2- Elevation of disc surface
3- Obliteration of physiological cup (Filled cup)
4- Obscuration of BVs passing over the disc (Attenuated)
5- Flame shaped hemorrhage
6- Macular star
7- Cotton wool spots
C- Chronic Papilloedema: Disc (3)
1- Resolve of Hge & Exudates.
2- Bulging disc (Champagne cork appearance)
3- Blurring Margin & obliterated cup (filled)
D- Secondary optic atrophy: Disc (3) & BVs (1)
1- White disc
2- Irregular margin (Blurred )
3- Sheathed & Attenuated R.B.Vs
4- Filled cup
II- Visual fild examination
1- Early enlargement of Blind spot
2- Late centro-caecel scotoma Relative central scotoma for
colors.
Treatment:
1- Treat the causes of ICP
2- Medically Dehydrating measures (Manitol, Dextrose,
Diuretic).
3- Surgically orbital decompression.

Optic Atrophy
Definition:
Death of optic nerve fiber (Loss of function visual or Pupillary)
due to lesion at any site from origin (ganglion cell) to termination
(lateral Geniculate body).
Types:
1- Primary Atrophy from start.
2- Secondary Due to disease in optic nerve.
3- Consecuative Due to disease in Eye.
4- Post-glaucoma
Lamina
Surrounding
Types Color Edge Optic Cup cribros Retinal V.
Retina
a
Shallow &
Clearly
saucer
1. 1ry optic seen
White defined shaped attenuated normal
Atrophy with its
(Atrophic
holed
cup)
attenuated 2ry proliferation
Blurred &
2. 2ry optic of R.
White Elevated Filled -
Atrophy Pigmented.epit
Surface
h.
3. Optic attenuated Evidence of
Yellow
consecutive Blurred Filled - causative
(Waxy)
Atrophy disease
4. Post-
glaucomatou Normal with
White Defined deep - Nasal shift
s optic IOP
Atrophy

Retinitis Pigmentosa
(Night Blindness)
Definition:
Bilateral progressive degenerative Heredo-familial diseases
which 1st affect the Rods and starts at the equator (Periphery) later
on affect Macula and Optic nerve.
N.B.:
- May be apart of laurance-Moon -Bidel Syndrome
Clinical Picture:
Symptoms:
1- Night Blindness
2- Gradual progressive field constriction up to tubular vision.
3- Diminution of vision later on
Signs:
1- Fundus Picture (show classic triad):
- bone corpuscles fundus (Black pigments at periphery
- Attenuated BVs
- Waxy yellow optic disc.
2- Field change:
- Ring scotoma
- Progressive concentric contraction till tubular field
Electrophysialgy:
1- Electro - Retingram subnormal A.P
2- Electro - oculogram subnormal R.P
Complication:
1- Complicated Cataract
2- 2ry Glaucoma
3- Consecutive Optic Atrophy.

Color Blindness
Definition:
Bilateral hereditary disease affect male more than females
which patient inability to see one or two of 1ry colors (Red Green
Blue).
Causes:
1. Congenital in origin.
2. Acquired in origin due to:
Retinal disease yellow Blue defects.
Optic nerve disease red green defects.
Clinical Picture:
symptoms:
1. In total world appear Grey.
2. In partial one or two color (common).
Sign:
Ishihara colored palates: Show defect in one or two of 1ry
colors.

Rhegmatogenous RD
Definition:
Full thickness retinal hole or tear with a degree of vitreous
liquefaction.
Etiology:
1- Spontaneous
2- Traumatic
3- Aphakia
Types of Retinal Tears:
1- U- Shaped tears
2- Round holes
3- Retinal dialysis
Clinical Picture:
Symptoms:
- Flash Floater Field defect visual loss
Signs:
1. Red Reflex Grayish
2. IOP Soft
3. Fundus Picture:
- Detached Retina whitish
- Tears Dark
- Vessel Dark & Tortuous
4. Field defect Acc to RD area
5. Degree of vitours Hge & Liquefaction
Complications:
1- Total RD.
2- Atrophic Bulbai.
3- Iridocylitis.
4- Cataract.
Treatment:
1- Break without detachment
- Argon Laser photocoagulation.
2- Retinal Break & Detachment:
- Buckling with drainage sub-Retinal fluid Then,
- Sealing by cryopexy, diathermia or photocoagulation.
3- Neglected RD or Prolifrative Vitro-Retinopathy
- Vitrectomy with oil Injection.

Causes of secondary RD
(Non-Rhegmatogenous)
1- Tractional RD:
2. Prolifrative Diabetic Retinopathy.
3. Organized vitreous Hge.
4. Cyclitic membrane as a complication of Iridocyclitis.
5. Retro-lental fibroplasias in premature Infant who putted in
Incubator under O2 Tension
2- Exudative RD:
Exudative choroiditis
Malignant melanoma.
Rhegmatogenous = Proceeded by tear

Non-Rhegmatogenous = No tear

Vascular Diseases of Retina

1- Retinopathies:
Atherosclerosis
Hyper tension
Diabetes mellitus
2- Central Retinal Vein Occlusion (CRVO)
3- Central Retinal Artery Occlusion (CRAO)
Retinopathies
Definition:
- Bilateral Retinal affection due to General disease.
General Pathology:
- Vascular changes in Retinal BVs leading to:
A- Hemorrhage
1. Superficial (flame shaped) Present in nerve fiber layer.
2. Deep (Dot or Blot) Present in nuclear layer
B- Exudates
1. Hard (yellow white Spot) small Lipoprotein materials
2. Soft (Cotton Wool White) large ( Isch. micro-Infarction).
3. Macular star (Odema in macula) Arranged according to
fibers direction.
Atherosclerotic Retinopathy
1- Vein concealment 2- Vein Deflection.
(obscured).
3- Copper wire appearance 4- Silver wire appearance of
artery with vein distension artery with vein occlusion at
distal to crossing. crossing.
Arterial hypertension:
Grad I : 1- Generalized mild attenuation of arteries
2- No Vein changes
Grad II : 1- Focal attenuation of arteries (+ G. mild
attenuation)
2- Irregular caliber vein (diameter)
Grad III : 1- Angiaspastic retinopathy (Exudates, He &
odema)
2- As above
Grad IV : 1- Paillodema + Macular star + cotton wool spots
+ Flam He.
2- As above

Diabetic Retinopathy
Pathology:
1- Micro vascular occlusion:
- Basement membrane Thickening
- Endothelium Proliferation
- RBCs Defective oxygen transport
- Platelets Aggregation
2- Micro Vascular leakage
- Tight junction loss
- Pericytes loss
Clinical picture:
1- Background DR 2- Pre- Proliferative 3- Proliferative DR
Dilated vein with Irregular cotton-wool (soft) exudates Neovascularization (NVD,
caliber (Micro- Infarction). NVE , NVI)
Micro aneurysm Intra-Retinal Micro-vascular Hge (vitreous & pre. Retinal
Abnormality (IRMA) )
Hard exudates (yellow Dilated veins with beading & Fibrovascular tissue
white spots Looping proliferation tractional
RD & Massive Hge
Retinal Hge (Dot, Blot & Arteriolar narrowing
flam)
Retinal Odema (obscuring Blot Hge.
choroids)
Management:
1- Good control of diabetes mellitus.
2- Local treatment by Laser photo coagulation.
Indication:
Non- Proliferative DR with diabetic maculopthy
Proliferative DR
3- Surgical by vitrectomy
Indication:
Vitrectomy Hge
Tractional RD
4- Cytocrotherapy in neovascular glaucoma
Pre Traetment Investigation:

Funolus examination and colored fundus photograph
Fluoresicien angiography

Central Retinal Vein Occlusion

Etiology:
1- Lumen:
Inc. blood viscosity as polycythemia
2- Wall:
Vasculitis as DM
3- Outside:
Atherosclerosis at lamina cribrosa
Increase IOP.
Clinical picture:
Symptoms:
- Rapid Painless drop of vision
Sings:
A-Early:
1. Artery: Narrowed & Obscured due to odema & Hge
2. Vein: Dilated & Tortuous
3. Retina: Hge, Odema & cotton wool patches (soft exudates)
B- late:
1. Vessels: Attenuated & sheathed
2. Retina: Neovasularization (anastomatic channel due to low
grade Isch.
Complication:
1. Vitreous Hge
2. Nonvascular glaucoma (100 days glaucoma)
3. Tractional RD (If proceeded by tear)
N.B: low greed isch. Leading to noevascular (numerous & weak)
Treatment:
1. Measure to Identify cause as: CBC - BP - IOP - Bl. sugar
level.
2. Measures to avoid Blood cottoning as: Aspirin,
Anticoagulant.
3. Pre-operative: Fluroescin angiography after 3 months to
detect indication of surgery.
4. Operation according to Indication:
Laser photo coagulation:
- In Neovacularization & Macular odema
Cyclocryotherapy:
- In Neovascular glaucoma.
Vitrectomy :
- In vitireous Hge & Tractional RD.
Central Retina Artery Occlusion

Etiology:
1- Lumen:
Emboli as Astheromitus patches
2- Wall:
Arthritis as systemic lupus (SLE)
Arterial spasm as Reynoldss disease
3- Outside:
Tight scleral Buklein in RD surgery
Clinical Picture:
symptoms:
- Sudden Painless loss of vision.
- In spasmic cause transient obscuration of vision may
occur.
Signs:
A- Early:
1. Artery: Thread like
2. Vein: Segmentation
3. Retina:
- Milky white appearance.
- Cherry red spot of fovea (As result of odema).
B- Late:
1. Vessels: Attenuated & sheathed
2. Retina:
- Removal of odema
- Consecutive optic atrophy
Cup: Filled
Edge: Blurred
Color: yellow
Surface: Elevated
BVs & surrounding Retina: CB4

Uveal tract
Uveitis
Definition:
- Inflammation of the uveal tract (Iris- ciliary body choroid)
Classification:
Anatomical classification Clinical classification
1- Anterior uveitis Acute Ant.
(Iridocylitis) Chronic Ant.
2- Posterior uveitis Acute post.
(choroirditis) Chronic Post.
Etiology:-
1-Infective:
- Exogenous
- Endogenous
2- Non- Infective:
- Traumatic
- Allergic (phacoanaphylaxis & sympathetic opthalnatis)
3- Syndrome of unknown etiology as Behset disease and
Vogt-Koyanagi-Harada syndrome.

Uveal tract
Iridocyclitis
Definition:
- Inf1ammation of the iris & ciliary body
Pathology:
1- Vascular phenomenon.
2- Exudative phenomenon.
Clinical Picture:
1- Symptoms:
- Sever pain
- Lacrimation
- Photophobia
- Drop of vision
Causes of Drop of vision:
Turbidity Spasm (Pupillary ms & ciliary ms) Toxic Maculopathy 2ry glaucoma
2- Signs:
- Impaired vision defect
- Cirum corneal ciliary injection (CCCI)
- Chemosis
- Keratic Precipitates (KPs) (small - median - large)
- Aqueous flare
- Loss of Iris pattern (Collorate & crypts)
- Post. & Ant. Synechiae
- Festoon appearance of Iris (Due to Post. Synechiae).
- Vitreous opacities.
- IOP
- Miosis ( Due to spasm insphencter puillims)
Differential diagnosis of acute red eye:

1. Conjunctivitis
2. Cong. Glaucoma
3. Keratitis
4. Iridocyclitis

Uveal tract
Complication of Iridocyclitis:
- Seclusiopupillae &
occlusiopupillae (Post.
Synechiae)
- Peripheral ant. Synechiae
- 2ry glaucoma
- Complicated cataract
- Cyclitic membrane
- Hypotony & phthisis (atrophic)
bulbi
- Traction retinal detachment
(TRD)
- Exudative retinal detachment
(ERD)
- Chorio-retinitis (endophthalmitis)
Management of Iridocyclitis:
1- Investigation to confirm the diagnosis (Help to identify any
syndromes):
- Take Careful history
- General examination
- Lab Investigation
1. Blood test
2. Skin test
3. Tissue Typing
4. ELISA
- Radiological
1. Chest X- ray
2. Sacroiliac X-ray
3. Small joints X-ray
2- Treatment:
- Topical atropine
- Corticosteroids (Topical Systemic)
- NSAIDs
- Treat the cause
- Antibiotic in Infective type

Uveal tract
Choroiditis
Definition:
- Inf1ammation.of the choroids
Types:
1- Supportive:
- Endophthalnitis
- Panophthalnitis
2- Non- Supportive:
- Granulomatous
- Non- granulomatous
Endophthalmitis
Definition:
Supportive Inflammation of the entire uveal tract usually
involves the adjacent tissue away of sclera
Clinical picture:
Symptoms:
Sever pain - Lacrimation - Photophobia - Realness & Marked
drop of vision.
Signs:
In addition to Iridcyclitis
- Injected eye
- Chemosis
- Hypopyon
- Yellow Reflex
Management:
1- Intensive antibiotic (by possible routs up to intravitreal
injection)
2- Vitrectomy (If light perception occur)
3- Enucleation or Evisceration (in Blind painful eye)

Uveal tract
Panopthalinitis
Definition:
- Supportive Inflammation of all three coats of eye.
Clinical Picture:
Symptoms:
- Sever pain & headache Lacrimation and complete loss of
vision
Signs:
In addition to iridocyletis
- Lid odema & proptosis
- Corneal edema
- Loss of light perception
- Self - evisceration
- Chemosis
- Hypopyon
- Yellow reflex
Management:
1- Intensive antibiotic for 48hr only
2- Evisceration is indicated if no response (Enucleation contra-
indicated)

Uveal tract
Sympathetic Ophthalmitis
Definition:
Acute plastic Uveitis affecting healthy eye (Sympathizing eye)
which proceeded by trauma of other eye (Exciting eye) "Uveitis
affecting one eye due to trauma of other eye".
Predisposing causes:
Accidental trauma.
Retained intra ocular foreign body (I.O.F.B.).
Etiology:
Allergic reaction: Due to endogenously circulating uveal
pigment liberated from the injured eye.
Virus infection: Due to precipitated viral infection by the
trauma which leading to liberation of uveal pigment that
circulates in systemic circulation and triggers the uveal
system in the sound eye (Sympathizing eye).
Pathology:
1- Liberation of uveal pigment from the traumatized eye and
circulating in the blood.
2- Uveal pigment acts as an allergen which stimulates Ab
production against uveal tract of other eye.
3- Uveal tract of both eyes shows diffuse mononuclear cellular
infiltration in form of nodules.
4- Each nodule formed of epithelioid cell, small and large
lymphocytes, eosinophils, monocytes, plasma cells and
may be giant cells.
5- Nodules are similar to tuberculous nodules with absent of
caseation.
Clinical picture:
o Exciting eye:
1. History of trauma or I.O.F.B.
2. Evidence of eye trauma.
3. Signs of irritation as ciliary injection.
o Sympathizing eye:
1. Photophobia (earliest sign).
2. Lacrimation and Blepharospasm (occur in remission).
3. Acute symptoms and signs of acute Iridocyclitis.
4. Chronic and recurrent course.

Uveal tract
Prognosis:
In mild case is favorable.
In moderate and sever case is doubtful and usually end by
complete loss of vision.
Investigation:
1. Slit lamp examination shows signs of active Iridocyclitis.
2. Blood examination shows large amount of mononuclears
and eosinophilia.
3. Intra dermal sensitivity test shows +ve to uveal pigment.
Treatment:
Prophylactic treatment:
A. Goggles to avoid industrial injuries.
B. Removal I.O.F.B. as soon as possible.
C. Management of any ocular wound with removal of any ocular
tissue remenants.
D. Excision of the injured eye.
Curative treatment:
A. Exciting eye: immediately excision at any appearance of
earliest sign in the sympathizing eye.
B. Sympathizing eye: treatment of Iridocyclitis mainly by
cortisone.

Cornea
Cornea
Layers:
1- Epithelium
2- Bowmans membrane
3- Stroma
4- Descemats membrane
5- Endothelium
Physiology:
1- Oxygen & nutrition:
Aqueous humor glucose
Tear film Ox
2- Transparency:
Non-keratinized epithelium
uniform arranged collagen fibers
No BVs & No myellnated nerve.
Water in deturgesence against odema
3- Corneal Luster:
Intact epithelium
Intact Tear film
Pathology of corneal ulcer
1- Progressive stage 2- Regressive stage 3- Healing
- Adhering to surface - Infiltration - Necrotic stroma
- Release toxins & enzyme - Multiplications Replaced by
- Disruption of underlining - Destruction of tissue scar scare
tissue. tissue
- Damage of ocular - Slough of necrotic area
structure.
- Diffuse of Toxin - Demarcation of ulcer
- Start of healing
Classification of keratitis
Ulcerative:
1. Infective
2. Non-Infective as Traumatic, Auto-immune Degenerative,
National, Mooren ulcer and keratomalacia
Cornea
Non-ulcerative
Bacterial which Invade Intact cornea
1- Neisseria 2- Diphtheria 3- Lysteria 4-
Hemophilus
Predisposing factors of corneal ulcer:
1- Present of near by septic focus as Decryocystits.
2- Trauma: Mechanical, chemical or physical.
3- Contact lens If infection by pseudomonas.
4- Ocular surface disease.
Corneal exposure as lagophthalmus
Dry eye (xerophthlmus)
Degenerative changes Keratomalacia
corneal sensation Herpetic keratitis
Clinical picture Bacterial corneal ulcer:

Symptoms:
1- Stitching pain
2- Blurring of vision
3- Lacrimation
5- Photophobia
6- Redness
Signs:
1- Loss of luster
2- +ve fluroescin stain
- Staph. & Strept. show oval ulcer dense opaque strom
& clear surround cornea
- Pseudomonas show Irregular ulcer diffuse liquifactive
necrosis of strom & ground glass appearance of
surround cornea
3- Cirum corneal ciliary Injection (CCCI)
4- Miosis due to toxic Iritis
Management: (Threaten condition)
1- Hospitalization
2- Corneal swap to do Culture & sensitivity
3- Medical: (No steroid)
Atropine (To Miosis)
Antibiotic eye drop (Brood spectrum)
- Up to appearance of culture result to determine specific
AB.
Cover the eye (except if associated with conjunctivitis).

Cornea
Management of Resistant corneal ulcer:

1- Re-culture after stoppage of antibiotic for 3days with
exclusion of fungal infection
2- Sub Conjunctival Injection of Antibiotic
3- Therapeutic contact lens
4- Chemical coutery
5- Conjunctival flap
6- Therapeutic corneal graft
Complication of corneal ulcer:

1- Hypopyon (Sterile Pus)
TTT:
- CAI (Diamox)
2-Secondary Closed angle glaucoma
TTT:
- CAI (Diamox)
- Short acting cycloplgic (Tropicamide) Atropine
3- Descematocele:
TTT:
- Pressure Bandage
- Therapeutic contact lens
- Tissue Adhesive (or glue)
4- Perforation (According to size, site & degree)
IOP sublaxation dislocation & Hge
Infection endophthalmitis panophthaluitis
Anatomical damage (According to size & site)
- Small peripheral leucoma & Iris prolapsed
- Small central anterior polar cataract & PAS
- Large partial or total anterior staphyloma

Cornea
Clinical Picture of HSV Keratitis:

Symptoms
(Not reliable due to affect of corneal sensation).
1. Stitching pain or just discomforts.
2. Blurring of visions
3. Lacrimation
4. Photophobia
5. Redness
Signs:
1. Loss of luster
2. +ve fluroescin stain & Rose Bengal stain shows
- Coarse opaque infected cells puncture.
- Satellite pattern of shaded cells.
- Dendritic ulcer or linear ulcer.
- Geographic ulcer (under steroid use).
- Disciform ulcer (in Hypersensitivity).
- Neurotrophic ulcer (with loss of corneal sensation).
3. Circum Corneal Ciliary Injection
Management:
1- Hospitalization
2- Corneal swap (Identify Organism)
3- Medical :
Antiviral:
- Acycloguanosine ointment
- Adinine arabinoside ointment
Atropine (If Associated with mioisis)
Steroid only in disciform ulcer.

Cornea
Stages of HZV Opthalmicus

1- 1st stage of papillomacular eruption:
- Skin eruption along nerve distribution and never cross
the midline
- Nasociliary nerve involvements by eruption lip to nose
into shows:
1. Ocular manifestation
- Conjunctivitis
- Keratitis
- Sceleritis
- Ant. uveitis
2. Corneal manifestation.
- Punctate epithelium erosion.
- Microdentritc ulcer.
- Nummular keratitis:
Fine granules surrounded by
Hazy stroma
- Disciform ulcer
nd
2- 2 stage:
- Neurotropic ulcers scarring & visualization.
rd
3- 3 stage:
- Recurrence.

Cornea
Types of Non-Infective Corneal Ulcers

(T H E N D)
1-Tromatics:
- Physical: Ultraviolet.
- Chemical: Acid of Alkaline
2- Hypersensitivity: (FRM)
- Marginal ulcer
- Phlyctenular kerato-conjunction Ring ulcer
- Fascicular ulcer
3- Degenerative: (MK)
- Mooren ulcer (Age related)
- Keratomalacia ( vit. A)
4- Neurotrophic ulcer
5- Exposure Keratopathy (As Lagopthalms).

Cornea
Keratoconus
Definition:
Bilateral congenital progressive bulging of cornea outward
showing conical shape.
Clinical Picture:
Symptoms:
1- Painless progressive vision Impairment by Myopia &
Astigmatism
2- Repeated change of glasses.
3- Intolerance of contact lenses
Signs:
1- Early (Signs of Irregular Astigmatism):
Retinoscopy scissor reflex.
Ophthalmoscopy oil drop reflex
Placidodisc irregular rings
Keratometry & corneal topography changes of
curvature & power.
2- Late:
Poor visual acuity
Steep & thin cornea
Munsons sign (by looking downward)
Fleisher ring (Epithelium Cupper deposition in Wilson's
disease)
Complication:
Acute Hydrops:
Destruction of stroma & basal epithelial Cell.
Descemat membrane tear corneal odema
Management:
1- Glasses (in early stage).
2- Hard contact lens (gas permeable).
3- Surgery: PRK or penetrating keratoplasty (in advanced
stage).

Cataract
The Lens
Function of the lens:
o Focus of light rays to become on retina by:
In the near vision: Contraction of the ciliary ms
releasing the tension on the zonule makes the lens
more spherical body.
In the distant vision: Relaxation of the ciliary ms
tautening the zonule makes the lens less spherical
body.
o Absorption of ultraviolet rays.
Histological parts of the lens

Cataract
Congenital or Developmental Cataract

Etiology: (IF CONG)
I. Infection eg. Rubella
F. Familiarly (Hereditary)
C. Ca++ (hypocalcemia)
O. O2 (hypoxia)
N. Nutration (Malnutrition)
G. Glactosemia (Metabolic disorder).
Morphological Types: (NSFCLP)
N. Nuclear cataract:
opacity of the central
zone between the ant.
and post. Sutures.
S. Satural cataract:
opacity of the one of Y-
sutures.
F. Focal blue dot
opacities: more
common and
insignificant.
C.
Coronary(Supranuclear
) cataract: opacity in the
deep cortex forming
crown like shape around
the nucleus.
L. Lameller cataract:
opacity lies between
clear nucleus and clear
cortex
P. Polar(capsular)
cataract:
o Ant. polar: away
from nodal point
therefore not affect
the vision
o Post. Polar:
accompanied by
persistent hyaloid's
remenants and
vision affection.
Cataract
Management:
A- Pre-operation investigation:
1- Ocular examination:
A- Density can detected by direct & indirect opthalmoscope.
No view of fundus by both very dense opacity.
Fundus seen only by indirect less dense opacity
Fundus seen by both non-significant opacity.
B- Morphology gives an idea about possible etiology
C- Location.
D- Associated ocular pathology.
E- Other features indicative of visual impairment (error of
refraction).
F- Special visual activity test as visual evoked potential
2- Systemic Evaluation of the patient.
B- Operative (Surgery):
Lensectomy & Anterior Vitrectomy
Complication:
- Posterior Capsule Opacification
- Glaucoma (2ry ACG & 2ry OAG).
- Retinal detachment.
C- Post-Operative Visual rehabilitation:
1- Spectacles (Glasses) in bilateral cases.
2- Contact lenses in unilateral & bilateral cases.
3- Intraocular lens still controversial.

Cataract
Complicated cataract
Definition:
Secondary cataract develops as a result of ocular or
systemic disease.
I- Ocular causes:
Central perforated corneal ulcer
Chronic anterior uveitis
Glaucoma (Acute congenital Or Absolute)
High Myopia
Hereditary fundus dystrophy
Neglected retinal detachment
II- Systemic disorders:

DM (True diabetic cataract or presenile cataract).
Hypoparathyroidism:
- Congenital fine punctuated cortical opacity.
- Acquired.
Miscellaneous:
- Galactosemia, Mongolism & Cretinism
(Hypothyroidisms).
Toxic cataract:
- Steroids or Ergot. (Drugs)
Causes of Any 2ry ocular disease

- General causes
- Local causes
Management:
- Pre-operative (Investigation) Local Systemic
- Operative (Surgery)
- Post Operative (Rehabilitation)

Cataract
Senile Cataract
Definition:
- Gradual Opacification of the lens in old age group.
Clinical picture:
Symptoms:
- Painless, bilateral, progressive drop of vision.
Signs:
- According to classification:
I- Sub capsular: (Anterior and posterior)
Near vision more affected than far vision.
Sunlight or bright light causes marked drop of vision.
II- Nuclear cataract: (mainly due to sclerosis):
Induced Myopia
Improvement of near vision (Presbiopic correction) (second
sight).
III- Cortical cataract: (Anterior, Posterior, Equatorial).
Slow progressive, stages:
(1)IMMATURE stage: (4)
Oblique illumination reflect iris shadow
Axial illumination show red reflex
NB:
Many improve into:
1- Incipient cataract (opaque vacuoles & clefts)
Phacomorphic Glaucoma
2- Intumescing cataract. (swollen lens & Pushing iris).
(2) MATUR stage (4)

Oblique illumination no iris shadow
Axial illumination no red reflex
Vision Hand movement
Lens white
(3) HYPER MATURE stage (4)
Lens shrinks, wrinkling and deposition G19 & cholesterol
Anterior Chamber Deep
Iris Tremulous
NB:
Improved into Morgagnian cataract:
Total liquefaction of lens
Nucleons sink inferior
Cataract
Complication of hypermature stage: (3)

1- Phacolytic glaucoma
2- Phacoanaphylactic endophtholmitis glaucoma.
3- Sublaxation & dislocation of lens.
4- Phacomorphic glaucoma of Intomescent cataract (Immature
stage)
Management of senile cataract:

(1) Pre-operative Investigation:
Measurement of visual Acuity.
Examination of ocular surface: eyelids -
tear film conj. & Cornea.
Examination ant segment: Ant. Chamber -
Iris Pupil
Measurement of IOP.
Examination of fundus:
1. Ultrasonography:
A- Scan axial diameter & lens power.
B- Scan anatomy of posterior segment.
2. Assessment of retinal & Mocular function:
Light projection
Electro-physiology:
- Electro retinography (ERG).
- Visual Evocated Potential (VEP).
(2) Operative (Surgery)
Indication of surgery
1. Improvement of vision.
2. Medical indications.
a- Phaco naphylactic Endophthopmitis
b- Lens Induced Glucoma:
Phacomorphic
Phacolytic
Sublaxated lense
Ant. or post. Dislocation

Cataract
Surgical procedure:
1- Large Incision cataract extraction
(A) Intra capsular extraction (B) Extra capsular extraction

Lens removed within its Capsule opened - nucleus
capsule only indicated in dislocation removed - cortex aspirated post.
& sublaxation Capsule leaved.
Disadvantages: Advantages:
Not suitable for young (strong Suitable for young (No traction)
zonule).
Incidence of vitreous loss Incidence of vitreous loss
Incidence of macular odema Incidence of macular odema
Only ant. ch. IOL used Post. Ch. IOL can used
2- Small Incision Cataract extraction:

Fragment of nucleus Cortex aspirated All capsule leaved
Advantages: Disadvantages:
Rapid Need training
Early recovery Machine-dependant
(3) Post-Operative Visual rehabilitation:

Spectacles (Glasses) in bilateral cases.
Contact lenses in unilateral & bilateral cases.
Intraocular lens

Glaucoma
Glaucoma
Definition:
1. Intra-optic pressure (IOP)
2. Damage of optic nerve fibers (ONF)
3. Defect of field
Exceptions:
- Ocular Hypertension = IOP with out damage.
- Low tension glaucoma = normal IOP with damage.
Anatomy of Ant. Chamber angle:
1. Schwalbe line
2. Trabicular wish work
3. Scleral spur
4. Ant. Surface of CB
5. Rood of Iris
6. Canal of schlemm
Classification of Glaucoma:
I- acc. to Age: Adult - Congenital
II- acc. to Etiology: 1ry - 2ry
III- acc. to Gonioscopy: open angle Closed angle
3 Goldman Dievices:
1. Goldman applination tonometer Mesure IOP
2. Goldman 3 mirros Gonioscopy.
3. Goldman perimeter Field Examination

Glaucoma
Causes of Secondary Glaucoma

1- Systemic:
Due to pressure in episcleral vein eg. Sup. venacoma
Obst. (SVO).
2- Local:
a) Cornea ulcer perforation - fistula
b) Ant. Ch Abnormal content e.g exudates, blood, Pus.
c) Iris & Ciliary Body Irialocyclitis
d) Lens cataract - sublaxats Ant. dislocate
e) Retina:
1- Central retinal vein Occlusion (100 days glaucoma)
2- Prolifrative diabetic retinopathy.
3- Retinal isch. VFM Neovascularization Hge Hge
glaucoma Rubiosis Iridis Rubiotic glaucoma.
Low grade Isch. Neovascular vessels (Numerous
Rubiosis Iridis and weak Hge)
f) Intraocular tumors (may causes):
1- Direct invasion of angle
2- Space occupying
3- Pushing Iris lens diaphragm.
4- Vein pressure vessels engagement
5- Separation of malignant cells (malig. emboli)
6- Ischemia
7- Release toxins
g) Steroid Induced Glaucoma

Glaucoma
Primary Closed Angle Glaucoma
Predisposing factors:
35 yr old female with Hypermetropic small eye and shallow Ant. Chamber
usually comes Bilateral
1- Axial hypermetropia with dilated pupil & congested CB.
2- Iris movement on lens during myosis & mydriasis
3- Aqueous pass to ant. Chamber push iris on lens.
Phase of Primary CAG:
1- Intermittent (prodromal).
2- Acute.
3- Chronic.
4- Absolute.
[I] Intermittent (Prodromal attacks):
CCC:
- Rapid partial reversible angle closure
- IOP < 45 mmg
- Proceeded by papillary dilatation & C.B. Congestion.
Clinical picture:
Symptoms:
1. Frontal headache and eye ache.
2. Transient vision impairment.
3. Fogy vision & rainbow haloes around lights.
4. Spontaneous resolve within 1-2 hrs.
Signs:
1. During the attack: (No CCCI) IOP- corneal odema - no
congestion.
2. Between attacks: Normal
Diagnosis:
1. Darkroom test
2. Prone test
3. Darkroom prone test
4. Mydriatic test (dangerous).
Prognosis:
- Acute attack or chronic attacks.

Glaucoma
Management of prodromal attack

During attack:
To resolve the aggravating factors (Pupillary dilatation & CB
congestion.
Miotic (2% pilocorpine) to diseased eye.
Weak miotic (1% pilocorpine) Prophylactic to other eye.
After attack:
Bilateral peripheral Iridectomy
Bilateral Laser Iridotomy (by Argon or YAG)
Atropine is contraindicated
[2] Acute phase:
CCC:
Sudden total angle closure
IOP up to 50 mmHg.
Proceeded by prodromal attack.
Clinical picture:
Symptoms:
Sever headache to periocular pain.
Sever visual impairment
Nausea & vomiting.
Signs:
1. Visual acute up to hand movement.
2. Corneal odema
3. Circum corneal ciliary injection (CCCI)
4. Peripheral Iridocorneal touch
5. Temporal paralysis of sphinctor pupille ms (Oval,
semidilated, irreactive to light)
6. Bluish pupil
7. Stony hard sensation on digital exam.
8. IOP up to 50 mmHg.
D.D. 2ry closed angle glaucoma (KPs is diagnosis sign).

Glaucoma
Management:
1- Hospitalization: (Medical to control IOP)
Hyperosmatic drug (20% Mannitol)
CAI (Acetazolamide)
- Blocker (Timolol 0.5%)
Miotics (Pilocarpin 2%)
2- Operative:
Peripheral Iridectomy
Laser iridotomy
Filtering surgery
Prophylactic iridectomy to other eye.
[3] Chronic [phase]:
CCC:
- Different degrease of close of Angle.
- Mild rise IOP (normal IOP = 25 mmMg)
- Preceded by Prodromal or Acute attack
Clinical Picture:
As Primary Open Angle Glaucoma.
Complication:
1. Progressive cupping open angle of optic head
2. Progressive field loss
Management:
1. Filtering surgery.
2. Prophylactic Iridectomy to other eye.
[4] Absolute Phase:

1- End Stage of neglected glaucoma.
2- Total optic atrophy (Post Glaucomatous Optic Atrophy)
3- Complete Irreversible loss of vision
4- C.B atrople Hypotony ( IOP)

Glaucoma
Primary Open Angle Glaucoma

Characters:
Commonest type
Bilateral & Asymptomatic
Common with High myopes
Causes of POAG:
Retintis pigmentosa
Fochs endothelial dystrophy
Diabetics
Steroid responders
Pathogenesis:
Mechanical theory IOP Damage NF layers
Ischemic theory IOP compress BVs of Retinal NF
layers.
Clinical Picture:
Symptoms:
1. Mainly Asymptomatic.
2. Non - specific symptoms.
Headache, Blurring of vision
Delayed dark adaptation & sens. to light.
Signs & Diagnosis:
1- IOP > 21mm Hg or in border line IOP
a. Diurnal variation > 4mm Hg (day & night)
b. Difference between two eyes > 4 mm Hg
c. Water drinking test IOP > 5 mm Hg
2- Optic Disk & fundus
a- Damage of NFL (exam. By red free illumination)
b- C/D ratio (by fundus exam.)
c- Pallor disc & Nasal shift of CRV (by stereoscopy)
3- Open angle of schlemm (by Gonioscopy)

Glaucoma
4-Visual field defect (by Gold man screen or perimeter)

1. Relative field defect
2. Isolated paracentral Nasal Scatoma
3. Siedel Scatoma
4. Archuate Scatoma
5. Double Archuate Scatoma
6. Nasal Step (Roenne) Scatoma
7. Temporal Island
8. Tubular field
9. Blindness
Management of POAG :
A- Medical therapy:
- Blocker (Timolol 0.5%) drug of choice used 2/day.
Miotics (Pilocarpin 2%) most effective drugs used 4/day.
CAI (Acetazolamide) recently used local CAI 2-3/day.
Epinephrine (Dipivalyl 1%) less systemic effect used 2/day.
Beta-blocker side effect:
o Bradycardia and myocardial contractility # Heart failure and Heart block
o Bronchospasm # Bronchial asthma
Miotics side effect:
o Dimness of vision especially in night.
o Headache and myopic shift due to ciliary ms contraction.
o Enhancement of posterior synechia and ant. cortical cataract.
o Miotic Cysts (cysts in papillary border).
Oral CAI side effect:

o Parathesia (tingling numbness)
o GIT upset
o Generalized malaise anorexia and depression
o Renal stones
Indication of shifting to surgery:
1. Failure of maximum medical treatment.
2. Intolerance to medical treatment.
3. Non-compliance of patient.
4. Patient unable to come for regular follow up.
B- Operative:
Laser Trabeculoplasty ( Agues drainages)
Glaucoma surgery:
Fistulizing operation
- (Subscleral trabeculotomy)
Defunctioning Operation (In Blind eye) (functionless CB)
- Cyclocryo thermy
- Cyclophotocoagulation

Glaucoma
Primary Buphthalmos
(Congenital Glaucoma)
Etiology:
Angle anomalies 75% Bilateral
1- Presence of BarKains membrane. (mesodermal)
Obstruction of ciliary ms.
2- Absent canal of schlemm
Clinical Picture:
Symptoms:
Early:
- In unilat.: Difference in size between of two eyes
- In Bilat.: Photophobia & Lacrimation
Later:
- Changes in eye colour (Hazy cornea & Blue Sclera)
- Poor vision
- Large sized eye.
Signs:
1- Large eye glob (Corneal diameter> 9mm)
2- Corneal Odema
3- Blue Sclera
4- Deep A.C
5- Tremolos Iris
6- IOP
7- Cupping of optic Disc (Reversible)
Management: Surgical as soon as possible
1- Goniotomy widening the angle
2- Trabeculotomy connecting canal of schlemm with A.C
3- Khailis Valve in recurrent cases & failure of repeated
trabeculotomy (Shunt tube is used)

Conjunctiva
Conjunctiva
Anatomical parts of conjunctiva:
1- Palpebral conj.
2- Fornix conj.
3- Bulbar conj.
Histological layers:
1- Surface epithelium
2- Substantia propria:
o Adenoid layer
(superficial)
o Fibrous layer (deep)
Physiological function of the conjunctiva:

1- Related to the tear:
Cooling of the surface
Flushing mechanism
Defense mechanism of abundant lymphoid elements
Bactericidal action of lysozyme
2- Related to epithelium:
Exfoliation
Phagocytosis
3- Normal bacteria flora inhibit the action of some pathogenic strains of
bacteria
Classification of conjunctivitis:
o Infective conjunctivitis:
Acute (Bacteria Viral Chlamydial)
Sub acute (only Chlamydial)
Chronic (Chlamydial as Trachoma Bacterial as
Angular conj. Fungal)
o Non-infective (Allergic or Atopic) conjunctivitis:
Chronic follicular conjunctivitis due to contact lens, eye
drops
Vernal keratoconjunctivitis (spring catarrh)
Phlyctenular conjunctivitis
Atopic conjunctivitis due to autoimmune disease

Conjunctiva
Clinical evaluation of conjunctival

inflammation
1. Symptoms:
Non-specific: Lacrimation, irritation, stinging,
photophobia, and burning.
Corneal involvement symptoms: pain and foreign body
sensation.
Allergic symptoms: itching.
Eyelid edema
2. Discharge:
Watery due to serous exudates and reflex secreted
tears, seen in acute viral and acute allergic
inflammation.
Mucoid due to Mucoid gland stimulation, seen in vernal
conjunctivitis and Kerato-conjunctivitis sicca.
Purulent due to pus formation, seen in sever acute
bacterial infection as gonococcal infection.
Mucopurulent seen in Chlamydial infection and mild
bacterial infection.
3. Conjunctiva appearance:
Conjunctival injection
Sub conjunctival hemorrhage
Follicular reaction due to hyperplasia of lymphoid tissue
in stroma with vascularization develops mostly in
fornices, with high diagnostic value mainly in viral,
Chlamydial and hypersensitivity conjunctival disease.
Papillary reaction due to hyperplasia of conjunctival
epithelium develop only in palpebral conjunctiva and
bulbar at limbus, with less diagnostic value.
Edema of conjunctiva (Chemosis)
Scarring
4. Membranes:
Pseudo membranes in sever adenoviral infection,
gonococcal conjunctivitis and StevenJohnson
syndrome.
True membranes Diphtheria and beta-hemolytic
streptococci infection.
5. Lymphadenopathy:
Affects preauricular and submandibular lymph nodes
Conjunctiva
Ophthalmia Neonatorum
Definition:
Preventable conjunctival infection in newborn infant within
first 2w after birth.
Causes:
1. Chlamydia Oculogenitalis
2. Strept. viridans
3. Staph. aureus
4. Hemophilus influenza
5. Group D Strept.
6. Esch.coli and other gram ve bacteria
7. Nisseria gonorrhea
Tear Glands in conjunctiva

Conjunctiva
Trachoma
Pathology:
Bilateral disease affects all parts of conjunctives and upper
parts cornea.
Chalmydia trachomatis is epitheliotropic and invading the
epith. Cell informs:-
1. Elementary bodies.
2. Initial bodies
3. Inclusion bodies
4. Destruction of cells releasing elementary bodies
5. Leading to toxin diffusion to substantial propria of
conjunctive cornea.
(A) Conjunctival pathology:
Epithelium Substantial propria
1. Papillary formation 1. Follicles formation by
lymphocytes, plasma cells and
giant cells.
2. Shed epithelial cells & 2. Ulceration of conjunctive over
necrotic material the follicles
precipitate undergo.
Calcification (PTC)
Degeneration (PTD)
3. Goblet cells shed & tears 3. Scaring (Aarlt line).
4. Reaction mild and diffuse in
bulbar
(B) Corneal pathology:
1- Trachomatus pannus:
Diffuse odema
Punctuate epith. Necrosis.
Fragmentation of Bowmans membrane.
New capillaries infiltration
2- Herbets rosettes localized follicular reaction.
3- Trachomatus corneal ulcer of pannus.

Conjunctiva
Clinical Picture:
Symptoms:
1. Foreign body sensation
2. Redness
3. Lacrimation
4. Muco-purulent discharge
Signs:
At least two of the following:-
1. Conjunctival follicles.
2. Limbal follicles (Herberts Rosettes)
3. Conjunctival scaring
4. Vascular pannus.
Complication:
(1) Lids (2) Conjunctiva (3) Lacrimal system (4) Cornea
- Mild ptosis - Xerosis (dryness) - Dacryocystitis - Permanent
- Trichiasis - Symblephron - Dacryoadenitis pacification
- Entropion - Hyaline and Amyloidal (ulcer scarring)
- Blepharitis Degeneration of tarsus - Dryness
- Chronic
meibemionitis
D.D.:
1. Follicular trachoma with Follicular conjunctivitis
2. Trachomatus papillae with spring catarrh.
3. Trachomatus pannus with phlyctenular pannus
Treatment:
1. Good personal hygiene
2. Antibiotic:
Topical tetracycline
Erythromycin
Oral tetracycline daily for 3w
Azythromycin only single dose
3. Management of complication
Tear for Dry eye.
Surgery for Trichiasis, Entropion
Picking of PTDs PTCs

Conjunctiva
Phlyctenular Kerato-conjunctivitis
Definition:
Recurrent nodular affects of bulbar conjunctivitis & limbal
cornea due to delayed hypersensitivity of endotoxine mainly in
child (3-14 yr).
Etiology:
Delayed hypersensitivity responses to:
1. Microbial protien.
2. Staph. patient.
3. Bacteria products.
4. Patient of intestinal parasite.
Pathology:
1. Focal sub-epithelium infiltration.
2. Overlying epithelium necroses & sloughs
3. Healing without scarring or opacity.
D.D.:
- Limbus sprain catarrh & Trachomatus pannus
Clinical picture:
Symptoms :
1. Itching
2. Lacrimation
3. 2ry bacterial infection symptoms as muco-purulent discharge
4. Last 1-2 weeks then recurrent.
Signs:
I- Conjunctival signs:
Small nodules in bulber conjunctiva
Surrounded hyperemic zone.
Headed without scarring.
II- Corneal signs:
Small corneal nodules on limbus.
Destroyed over lying epithelium phlyctenular ulcer.
Superficial vascularization & Infiltration phlyctenular pannus.
Headed without scarring.
Management:
General:
- Removal of septic focus or intestinal parasite.
- Desensitization.
- Good nutrition.
Local:
- Topical steroid
- Broad spectrum antibiotic against 2ry infection.

Conjunctiva
Vernal Kerato-Conjunctivitis
(Spring Catarrh)
Definition:
- Bilateral, recurrent, external ocular allergic disorder.
Clinical picture:
Symptoms:
1. Intense itching
2. Lacrimation
3. Photophobia
4. Mechanical ptosis may occur.
Signs:
(1) Palpebral type (2) Limbal type (3) Keratopathy
Light-skin races Dark-skin races Light-skin races
- Conjunctival - Mucoid nodule -Punctate
hyperemia - Trantas spots: epitheliuopathy
- Diffuse papillary While superficial scattered Microerosion.
hypertrophy sports around the limbus - Macroerosion
-Cobble-stones - Plaque: white muro-
appearance of membrane cavers
papillary macrocresion Resists
- Giant papillae the healing and not
wetted by tears
- Sub-epithelia scarring
- Pseudogenotoxon (As
arcus sinilis but reach
the limubus)
Treatment :
As prophylactic
1. Dark glasses
2. Cold compress
3. Antihistaminic
4. Mast cell stabilizer
5. Topical steroid
As Curative
6. Supratarsal injection steroid

7. Topical cyclosporin A
8. Acetyl cystine 5%
9. Lamellar keratectomy To remove plaque
to Asses healing.

Conjunctiva
Conjunctival Degeneration
"Pinguecula"
Definition:
Degeneration of the collagen fibers of conjunctival stroma with
thinning of overlying epith. In form of yellow white deposit on the bulbar
conjunctiva adjacent to nasal or temporal aspect of the limbus and show
slow enlargement.
"Pterygium"
Definition:
Triangular sheet of fibrovascular tissue which encroaches to the
cornea and usually in nasal side
Etiology:
o Hot climates
o Windy and sandy weather
o Chronic dryness
o Exposure to sun "due to Ultra violet sun rays"
Pathology:
o In the conjunctiva: Hyaline degeneration and elastosis.
o In the cornea: Bowman's membrane fragmented and replaced by
hyaline and elastic tissue.
Clinical picture:
Symptoms:
1. Cosmetic disfigurement.
2. Defective vision (if cover the pupil or distort the cornea causing
astigmatism).
Signs:
1. Small grey corneal opacities near the limbus (early sign).
2. Progressive overgrows of conjunctival opacities onto the cornea in a
triangular fashion.
3. According to the types:
o True Pterygium: adhesion of the underlying structures
throughout (fixation of the triangle all through).
o Pseudopterygium: adhesion of a fold of conjunctiva to a
peripheral cornea ulcer (fixation of its apex to the cornea).
Treatment:
Surgical excision
o Indication:
1. Cosmetic disfigurement
2. Affection of vision
o Contra-indication: Stationary and thin pterygia for the fear of very high
recurrence rate

Conjunctiva
Causes of subconjunctival heamorrhage (ecchymosis):

1. Trauma
2. Infective conjunctivitis especially pneumococci and streptococci
3. Arteriosclerosis and hypertension
4. Straining (whooping cough)
5. Blood disease (Leukemia, Scurvy, Purpura, Malaria)
6. Spontaneously (Idiopathic)


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Anatomy of the eye

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Investigation: (for each layer of tear film)

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Mal-positions of the lashes

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Mal Positions of the lid margin

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Congenital Abnormalities of eye lid

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Seborrheic (Scaly) Blepharitis

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Staphylococcal (Ulcerative) Blepharitis

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Clinical picture& treatment:

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Meibomian Gland Dysfunction

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Grads of Binocular Vision (Detected by Synoptophore):

Clinical Types of Myopia

Clinical Types of Hyperopia

Etiology of Myopia & Hypermetropia

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Big eye Small eye

large cornea small cornea

Simple Myopia: 1- Water silk

- Temporal crescent 2- Tortuous Retinal

o Concave minus lens o Convex plus lens

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Deference between irregular and regular types:

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Clinical picture of regular Astigmatism:

Clinical picture of irregular Astigmatism:

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Caused of Eye strain in Error of Refraction:

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Management in latent squint:

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Inflammation of Optic Nerve

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