Special sense 1

2023-2024
ophthalmology
Second year
MSBP-CP
 Special Sense module 1
Ophthalmology (Departments)

1. Ophthalmology
2. Anatomy
3. Physiology
4. Histology
5. Microbiology
6. Pharmacology
7. Biochemistry

Revised by
Curriculum committee
Tanta Faculty of Medicine
 Index
Page
Chapter1 (ORBIT & LACRIMAL SYSTEM) 1
Anatomy of bony orbit 1
Anatomy of the lacrimal system 12
Histology of the lacrimal glands 15
Orbital Infections 16
Diseases of the lacrimal System 18
Chapter2 (EYE LID & CONJUNCTIA) 21
Anatomy of the eye lids 21
Anatomy of the conjunctiva 23
Histology of the conjunctiva and the eye lids 24
Diseases of The eyelid 26
Diseases of The Conjunctiva 32
Microbiology of the eye 36
Drugs used in treatment of eye infection 51
Drugs affecting eye 52
Chapter 3 (EYE BALL) 55
Anatomy of eye ball 55
Histology the photoreceptor system 56
Physiology of the eye 73
Biochemistry of the eye 86
Diseases of the eye ball 96
Microbiology of the eye 101
Pharmacology of the eye 103
Chapter 4 (STRABISMUS & ERROR OF REFRACTION ) 107
The extraocular muscles 107
Physiology of Binocular vision 112
Errors of refraction 114
Strabismus & Amblyopia 117
 ORBIT & LACRINAL SYSTEM CHAPTER 1

Orbit
Bony orbit
- The orbit (orbital cavity) is a skeletal cavity composed of
seven bones situated within the skull.
- The bones that make up the orbit contain several foramina and fissures
through which important neurovascular structures pass.

Walls of the bony orbit

Forming bones Maxilla, Frontal bone, Zygomatic bone, Ethmoid

bone, Lacrimal bone, Sphenoid bone, and Palatine
bone

Base and apex Apex: optic foramen

Orbital margin (rim):
- supra-orbital margin: frontal bone
- medial margin: frontal process of the maxilla
- infra-orbital margin: zygomatic process of the

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ORBIT & LACRINAL SYSTEM CHAPTER 1

maxilla and the zygomatic bone

- lateral margin: zygomatic process of the frontal
bone and the zygomatic bone and its frontal process

Walls Roof (superior): orbital part of the frontal bone,

lesser wing of the sphenoid bone
Medial: orbital plate of the ethmoid bone, lacrimal
bone, frontal process of the maxilla, greater wing of
the sphenoid bone
Floor (inferior): orbital surface of the maxilla,
zygomatic bone, palatine bone
Lateral: zygomatic bone, sphenoid bone

Landmarks and Optic foramen (canal), lacrimal fossa, lacrimal

openings groove, anterior and posterior ethmoidal foramina,
trochlea, superior and inferior orbital fissures

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

� NERVES OF THE ORBIT

� SENSORY NERVES
� Optic Nerve
�� It is the sensory nerve of vision.
�� It is about 4cm long,
�� It begins in the retina by piercing the sclera medial to the
posterior pole of the eyeball
�� It is directed backwards and medially through the posterior part
of the orbit and leaves the orbit through the optic canal.
�� It is pierced along its inferomedial aspect by the central artery
and vein of the retina.
�� It is enclosed by a complete meningeal sheath formed by
extensions of the 3 meninges and extends to the eyeball.

� Zygomatic Nerve
�� It is a branch of the maxillary nerve
�� It divides into 2 nerves which run through their corresponding
canals. These nerves are:
- Zygomatico-facial
- Zygomatico-temporal
�� It also carries postganglionic secretory fibers from the
sphenopalatine ganglion to the lacrimal gland.

Ophthalmic Nerve
It is one of the 3 divisions of the trigeminal nerve.
Before it enters the orbit through the superior orbital fissure it divides
into 3 branches:
�� Lacrimal Nerve
�Arises from the ophthalmic nerve in the cavernous sinus
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 ORBIT & LACRINAL SYSTEM CHAPTER 1

�Enters the orbit through the superior orbital fissure outside the
common tendinous ring.
�Runs forwards along the upper border of the lateral rectus
�It receives a communication from the zygomaticotemporal nerve,
which carries secretory fibers to the lacrimal gland.
�It supplies:
- Lacrimal gland and adjacent conjunctiva
- Palpebral branches: Supply the skin and conjunctiva of the lateral part
of the upper eye lid
�� Frontal nerve
�Enters the orbit through the superior orbital fissure outside the
common tendinous ring.
�Runs forwards on the superior surface of the levator palpebrae
superioris
�Terminates by dividing into 2 terminal branches to the skin of the face
and scalp.
- Supratrochlear
- Supraorbital.
�� Nasociliary nerve
�Enters the orbit through the superior orbital fissure
insidethe common tendinous ring.
�It crosses above the optic nerve together with the ophthalmic artery
from the lateral to the medial side
�It runs forwards along the medial wall of the orbit.
Branches:
� Sensoryrootto the ciliary ganglion.
� 2 or 3 long ciliary nerves
Run medial to the optic nerve and pierce the sclera close to optic nerve.

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

Posterior ethmoidal nerve:

- Passes into the posterior ethmoidal foramen and supplies the mucosa of
sphenoidal and posterior ethmoidal sinuses.
� Terminal branches:
* Infratrochlear nerve
* Anterior ethmoidal nerve

MOTOR NERVES
Oculomotor Nerve
�� It enters the orbit through the superior orbital fissure as 2 divisions
superior and inferior which run inside the common tendinous ring.
�It supplies all the extraocular muscles except:
��Superior oblique; supplied by trochlear SO 4
��Lateral rectus; supplied by abducent LR 6
Superior division
�

- It bends upwards across the lateral side of optic nerve

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

- It pierces and supplies the superior rectus and ends by entering and
supplying the levator palpebrae superioris.
�� Inferior division
�It supplies the medial & inferior rectus and inferior oblique
�The nerve to inferior oblique gives parasympathetic root to the ciliary
ganglion.

Ciliary Ganglion
�� It is a parasympathetic ganglion which lies in the orbital fat lateral to
the optic nerve.
�� It is about the size of pin’s head.
Roots:
�� Sensory root:
� Comes from the nasociliary nerve.
� The fibers pass through the ganglion withoutrelay
� They carry sensation from the cornea, iris and choroid through the
short ciliary nerves.
� Sympathetic root:
� Comes from the plexus around the internal carotid artery.
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 ORBIT & LACRINAL SYSTEM CHAPTER 1

� It consists of postganglionic fibers from the superior cervical

sympathetic ganglion.
� They traverse the ganglion without relay and reach the eye through
the short ciliary nerve to supply the dilator pupillae muscle and the
blood vessels of eye.
�� Parasympathetic root:
�� Runs with the nerve to inferior oblique.
� It is formed from preganglionic parasympathetic fibers which
originate from the Edinger-Westphal nucleus and pass through the
oculomotor nerve.
��They relay in the ciliary ganglion
� The postganglionic fibers reach the eyeball through the short ciliary
nerve to supply the sphincter pupillae and ciliary muscle.
Branches:
�These are 8-10 short ciliary nerves
�They pierce the sclera around the optic nerve.
�They carry the following fibers:
��Sensory
to cornea, iris and choroid
��Sympathetic
to dilator pupillae and blood vessels
��Parasympathetic
to the constrictor pupillae and ciliary muscle.

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

Trochlear Nerve
�� Enters the orbit through the superior orbital fissure outside the
common tendinous ring.
�� Supplies only the superior oblique through its upper border.

Abducent Nerve
�� It enters the orbit through the superior orbital fissure inside the
common tendinous ring.
�� It passes between the two heads of the lateral rectus and supplies it
only through its deep surface.

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

ARTERIES OF THE ORBIT

Ophthalmic Artery
�� Origin:
It is a branch of internal carotid artery as it leaves the cavernous sinus.
�� Course and relation:
�It passes forwards through the optic canal below and lateral to the
optic nerve
�In the orbit, the artery crosses above the optic nerve obliquely from its
lateral to medial side accompanied by the nasociliary nerve.
�It run along the medial wall of the orbit
�It terminates at the medial end of the upper eyelid by dividing into the
supratrochlear and dorsal nasal arteries.
�� Branches:
�Central artery of the retina:
- Arises in the optic canal
- It pierces the optic nerve about 1 cm behind the eyeball
- It runs inside the nerve to the retina

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

- It is an end artery with no anastomosis

�Lacrimal artery:
- Runs forwards along the upper border of the lateral rectus accompanied
by the lacrimal nerve, to reach the lacrimal gland.
�Supraorbital artery:
- It runs forwards in company with the supraorbital nerve
- It leaves the orbit through the supra-orbital foramen to reach the
forehead and scalp.
� Ciliary arteries:
They are divided into 3 groups:
� Long posterior ciliary arteries:
- 2branches, which pierce the sclera on either side of the optic nerve.
- They form the circulus arteriosus major, which supplies the iris.
��Short posterior ciliary arteries:
- 7 branches, which pierce the sclera around the optic nerve.
- They supply the choroid and ciliary processes.
� Anterior ciliary arteries:
- Pierce the anterior part of sclera near the limbus
- Terminate in the circulus arteriosus major.
�Ethmoidal arteries:
� Anterior ethmoidal artery:
Enters into the anterior ethmoidal canal to reach the anterior cranial
fossa
�Posterior ethmoidal artery:
It passes through the posterior ethmoidal canal
�Meningeal branch:
- It passes backwards to enter the middle cranial fossa through the
superior orbital fissure.

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

�Muscular branches:
- They accompany the nerves to extraocular muscles.
�Medial palpebral arteries:
- They are superior and inferior branches to the medial parts of both
eyelids.
�Supratrochlear artery:
- One of the terminal branches.
- It leaves the orbit abovethe trochlea to supply the forehead and scalp.
�Dorsal nasal artery:
- Is the other terminal branch.
- It leaves the orbit belowthe trochlea to supply the dorsum of the nose
and anastomoses with the termination of the angular artery.

Ophthalmic Veins
��They are 2; the superior and inferior.
��They pass backwards through the superior orbital fissure and frequently
unite forming one stem which end in the cavernous sinus
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 ORBIT & LACRINAL SYSTEM CHAPTER 1

��Superior Ophthalmic Vein

- Communicates with the anterior facial vein.
�� Inferior Ophthalmic Vein
- Communicates with the pterygoid plexus of veins through the inferior
orbital fissure.

ANATOMY OF THE LACRIMAL SYSTEM

The lacrimal apparatus consists of:
1. Lacrimal gland and its ducts.
2. Lacrimal canaliculi and puncta.
3. Lacrimal sac.
4. Nasolacrimal duct.
� Main lacrimal gland:
��Responsible for the main part of aquous tear secretion.
��It is almond shaped.
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 ORBIT & LACRINAL SYSTEM CHAPTER 1

��It is formed of a large orbital part and a small palpebral part, which
are continuous around the lateral margin of the aponeurosis of the
levator palpebrae superioris
��Formed of two parts:
a. Orbital portion: the main part of the gland, lies in the shallow
bony fossa in the anterolateral part of the orbital roof.
b. Palpebral portion: is lodged in the lateral part of the upper
eyelid.
Lacrimal ductules:10 - 12 duct that carry the tears arise from the
orbital portion of the gland to pass through the palpebral part and
opens finally in the superior fornix laterally.
� Accessorylacrimal glands:
They are small glands distributed in the conjunctiva, and have fine
ductules, secretes mucin and contribute to some aquous tear
components:
� Excretory (drainage system)
The lacrimal drainage system consists of the 2 puncti, 2 canaliculi,
lacrimal sac and nasolacrimal duct opening in the inferior meatus of
the nose.
- The canaliculi & puncti:
They are two slender ducts 10 mm in length
• They run in the medial parts of the margins of both eyelids
• Each duct begins by an opening called the lacrimal punctum on
the summit of an elevation called the lacrimal papilla
• They drain the lacrimal fluid into the lacrimal sacis lodged in the
lateral part of the upper eyelid.carry the tears from puncti to lacrimal
sac

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 ORBIT & LACRINAL SYSTEM CHAPTER 1

- The lacrimal sac:

Has a size of 8 x 12 mm when distended.
It lies in the lacrimal groove in the medial orbital wall. Below the
medial palpebral ligament.it has body, fundus and neck.
- The nasolacrimal duct:
Is 12 – 24 mm long.
It passes downwards, backwards and slightly lateral.
Opens into the inferior meatus of the nose, lateral to and below the
inferior turbinate.
The nasal opening is covered by a mucosal fold (Hasner’s valve).
Nerve supply:
Sensory: lacrimal nerve (Ophthalmic division of trigeminal).
Sympathetic: vasoconstrictor of blood vessels.
Parasympathetic: secretory to lacrimal glands (from facial nerve).

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ORBIT & LACRINAL SYSTEM CHAPTER 1

Blood supply:
Lacrimal artery (branch from ophthalmic).
Lymph drainage:
Secretory system: to preauricular lymph nodes.
Excretory system: submandibular lymph nodes.

Histology of the lacrimal glands

- They are compound tubulo-alveolar glands present at the supero-lateral
part of the orbit.
- The acini of lacrimal gland are serous acini lined with high cuboidal
cells and surrounded partially by myoepithelial cells.
- The secretion (tears) is watery and rich in the bactericidal lysozyme.
- Each gland opens by about 6-12 excretory ducts into the superior
fornix.
- The tears are drained at the medial end of each eye lid through the
lacrimal puncta to the lacrimal canaliculi which are lined by stratified
squamous epithelium. The upper and lower canaliculi meet in a
lacrimal sac which is drained by the nasolacrimal duct down to the
nasal cavity.
- The lacrimal sac and nasolacrimal duct are lined by pseudostratified
columnar ciliated epithelium.
- Accessory tear glands (of Krause) are small numerous glands present
along the fornices, especially the upper one.

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ORBIT & LACRINAL SYSTEM CHAPTER 1

LM of lacrimal gland
The Orbit
Orbital Infections
Are very serious ocular emergency as they are life and sight threatening
disorders. It may be bacterial or fungal`
Bacterial group is further subdivided into 2 subgroups; Preseptal
cellulites and orbital cellulitis
Preseptal Cellulitis
It is an infection of subcutaneous tissues anterior to the orbital septum.
1. Causes
a. Skin trauma such as laceration or insect bitos. The offending
organism is usually Staph, aureus or b-haemolytic streptococci.
b. Spread of local infection such as an acute hordeolum or
dacryocystitis.
c.From remote infection, either of the upper respiratory tract or middle
ear, which is most frequently caused by H. influenzae and Strep.
pyogenes.

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ORBIT & LACRINAL SYSTEM CHAPTER 1

d. 2. Signs
a. An unwell, febrile patient with
unilateral, tender, red,
periorbital and lid swelling.
b.Proptosis is absent, and visual
acuity and ocular motility are unimpaired.
3. Treatment is with oral or injection antibiotics under meticulous
observation.

Orbital Cellulitis
Bacterial orbital collulitis is an infection of the soft tissues behind the
orbital septum which is frequently polymicrobial infection, including
anaerobes. The most common causative organisms are Strep.
pneumoniae, Staph. aureus and Strep. pyogenes. In children under the age
of 5 years, the offending organism is frequently H. influenzae.
Causes
1.Sinus-related is by far the most common and is most frequently
secondary to ethmoidal sinusitis. It typically affects children and
young adults.
2. From adjacent structures such as dacryocystitis, and mid-facial or
dental infection. The last condition may cause an orbital cellulitis via
an intermediary maxillary sinusitis.
3. Post-traumatic most commonly develops within 48-72 hours of an
injury that penetrates the orbital septum. In some cases, the typical
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ORBIT & LACRINAL SYSTEM CHAPTER 1

clinical features may be masked by associated laceration or

haematoma.
4. Post-surgical may complicate retinal, lacrimal or orbital surgery.
Clinical Features
1.Presentation is with a rapid onset of severe malaise, fever and orbital
signs.
2. Signs
a.The eyelids are very swollen, red, and warm and tender to
palpation
b.Proptosis, if it can be seen because of the lid swelling.
c. Ocular movements are restricted and painful.
d.Chemosis
Visual impairment and signs of optic nerve dysfunction may be present in
advanced cases.
Thyroid orbitopathy (thyroid eye disease)
(See endocrine module)

The lacrimal System

Congenital Nasolacrimal Duct Obstruction
At birth the lower end of the nasolacrimal duct is frequently non
canalized.
Clinical features:
o Epiphora and watering of the eye.
o Pressure over the lacrimal sac causes reflux of mucoid or
mucopurulent discharge from the puncta.

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ORBIT & LACRINAL SYSTEM CHAPTER 1

2. Dacryocystocele (amniontocele):
Definition:
Is a collection of amniotic fluid or mucus in the lacrimal sac caused
by an imperforate Hasner’s value?
Clinical features:
o Bluish cyctic swelling at or below the medial canthal area.
o Epiphora if the baby was seen after two weeks after labour.
o tense lacrimal sac.
Dacryoadenitis
Definition: inflammation of the lacrimal gland
All lacrimal gland swellings make it palpable and produce S-
shapeddeformity of the upper lid margin.
Canaliculitis
Is caused by Actinomyces israellii.
Clinical features:
1. Unilateral epiphora, chronic conjunctivitis and mucoid discharge.
2. Eyelid erthema and pouting of the punctaum.
3. Concretion within the canaliculus (sulpher granules).
Dacryocystitis
Definition: Dacryocystitis is an inflammation of the lacrimal sac that
occurs because of nasolacrimal duct obstruction.
Causes: Nasolacrimal duct obstruction
Dacryocystitis: may be either: Acute or chronic.

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ORBIT & LACRINAL SYSTEM CHAPTER 1

Acute dacryocystitis

Definition:acute suppurative inflammation of the lacrimal sac.

Clinical manifestations:
Symptoms:Fever, Headache, malaise, Pain, Epiphora.
Signs:Painful swollen mass below the medial canthal tendon.
Conjunctival injection, tearing and watering.
The sac may decompress externally to form dacryocutaneous fistula.
Chronic Dacryocystitis
Definition: Achronic lacrimal sac inflammation secondary to obstruction
of the nasolacrimal duct.
Is the commonest lacrimal sac disorder.
Clinical manifestations:
Symptoms:Epiphora may be the only symptom.
Signs:Occasional mucocele or pyocele and swelling of lacrimal sac .
- Regurgitation of mucopurulent material with digital pressure.
Complications:Hypopyon ulcer, Endophthalmitis, Acute dacryocystitis,
Lacrimal fistula

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 EYE LID & CONJUNCTIVA CHAPTER 2

ANATOMY OF THE EYE LIDS

- They form the boundaries of the palpebral fissure.
- The lateral 5/6 of its free margin are flat and carry eyelashes or cilia
and is called ciliary part
- The medial 1/6 is rounded, devoid of hair and is called lacrimal part.
Structure of the eyelid:

It is formed of the following layers from without inward:

� Skin:
�Thin, delicate, devoid of hair and is continuous with the inner
conjunctival lining at the free margin of the eyelid.

�� Superficial fascia:
�� Formed of loose areolar subcutaneous tissue.
�� It contains no fat to avoid heaviness on the eyelid .
�� Muscle layer:
�The palpebral part of orbicularis oculi runs transversely
�Deep to the muscle there is a thin layer of loose areolar tissue
continuous with that of the scalp.

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 EYE LID & CONJUNCTIVA CHAPTER 2

�� Tarsus:
�It is a thin, dense plate of fibrous tissue
�Lateral palpebralligamentjoins the lateral ends of the tarsal plates
to the lateral margin of the orbit.
�Medial palpebral ligament joins the medial ends to the medial
margin of the orbit.
�Tarsal glands(Meibomean glands) which are modified sebaceous
glands are embedded in vertical grooves in the tarsi.
�The ductsof the tarsal glandsopen on the free margins behind the
eyelashes.
�The orbital septum (palpebral fascia) is a thin fibrous sheet connecting
both tarsi to the orbital margins.
�� Palpebral conjunctiva:lines the deep surface of tarsal plates

Sensory nerves of eyelids

� Upper lid:
�From medial to lateral:
- Supratrochlear nerve.
- Supraorbital nerve
- Palpebral branch of the lacrimal nerve

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 EYE LID & CONJUNCTIVA CHAPTER 2

�Lower lid:
�From medial to lateral:
- Infratrochlear nerve.
- Palpebral branch of infraorbital nerve
Arteries of eyelids
�� Lateral palpebral artery from lacrimal artery.
�� Medial palpebral artery from ophthalmic artery

ANATOMY OF THE CONJUNCTIVA

� Definition: thin membrane which cover the posterior surface of
each eye lid and then reflected on the outer surface of the sclera.
� Extention:it extends on the eye ball to the junction between the
sclera and cornea .
� The conjunctivalsac: is formed when the eye lids are closed ,
the upper and lower extensions of this sac are called superior and
inferior conjunctival fornices, these fornices are loose allowing
the movement of the lids and eye ball.

Part of the conjunctiva �

-Palpebral or tarsal conjunctiva: Lines the eyelids

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EYE LID & CONJUNCTIVA CHAPTER 2

- bulbar conjunctiva: Covers the eyeball, over the anterior sclera:

This region of the conjunctiva is tightly bound to the underlying sclera by
Tenon's capsule and moves with the eyeball movements

HISTOLOGY OF CONJUNCTIVA
- Conjunctiva is a thin mucous membrane that covers the anterior part of
the sclera (bulbar conjunctiva) and is reflected at the fornix to line the
inside of the lid (palpebral conjunctiva).
- It consists of:
1- Epithelium it is:
��Stratified squamous non-keratinized at the bulbar part.
��Stratified columnar with goblet cells at the fornix.
��Stratified squamous non-keratinized at the palpebral part.
2- Lamina propria: is formed of loose connective
tissue rich in blood vessels and lymphocytes.
HISTOLOGY OF EYE LIDS
- Eye lids are movable folds of tissue that protect the eye.
- Histologically, the eye lid consists of the following layers from front
backwards:

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EYE LID & CONJUNCTIVA CHAPTER 2

a) Skin: is loose and elastic with few hair follicles

� The hypodermis is free from fat.
� The eye lashes are rows of long and stiff hair projecting from the
lid margin.
� Glands of Zeis are modified sebaceous glands that open in the hair
follicles.
� Glands of Moll are modified sweat glands that open in the follicles
of the eye lashes.
b) Skeletal muscle: bundles of orbicularis oculi.
c) The tarsus: a fibrous plate containing the Meibomian glands which
are modified sebaceous glands that secrete oily secretion delivered by
ducts which open on the lid margin posterior to the eye lashes.
d) Palpebral conjunctiva: covers the internal surface of eye lid.

The eye lid

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EYE LID & CONJUNCTIVA CHAPTER 2

The eyelid

Blepharitis (bleph= eye lid) (itis =inflammation):

Is a Chronic inflammation of the eye lid especially the lid margin? The
condition is a very common condition met with in the ophthalmology
clinic.
The patient complains of itching, soreness, gritty sensation, lacrimation
and photophobia.
1.SquamousBlepharitis: This is recognized by the whitish scales of
dried greasy secretion, like dandruff, that collect around the roots of the
lashes. These scales can be easily removed revealing a reddened lid
margin without any ulceration. It is often associated with seborrhea of the
scalp.

2.UlcerativeBlepharitis:This is a severe form caused by staphylococcal

infection & is characterized by hyperemia of the lid margin with edema
and thickening. Yellow crusts glue the lashes together. Removal of the
crusts causes bleeding and small ulcers which are seen around the lashes.
The eye lashes are attenuated, thin rounded and distorted.

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EYE LID & CONJUNCTIVA CHAPTER 2

3.Angular Blepharitis: usually affects the outer canthus as there is

relative deficiency of tears, caused by Morax-Axenfeld bacillus. It
produces a proteolytic enzyme which macerates the affected tissue. The
condition is often associated with angular conjunctivitis and the disease is
called angular blepharo-conjunctivitis.

1. Chalazion

Is a chronic inflammatory lipo granuloma of the Meibomian glands? The

patient presents with painless disfiguring swelling that may cause
heaviness of the eye lid.

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EYE LID & CONJUNCTIVA CHAPTER 2

The skin is freely mobile over the swelling. It may present as an acutely
inflamed tender nodule as a result of staph infection (internal hordeolum).

2. Stye

A stye is an acute localized suppurative inflammation at the lid margin

affecting a lash follicle and involving particularly its associated gland of
Zeis. It is caused by staphylococcus aureus. Recurrent styes indicate a
general lowering of resistance to staphylococci, e.g. in debility or
diabetes.

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EYE LID & CONJUNCTIVA CHAPTER 2

Rubbing lashes& Trichiasis

When one or more lashes become misdirected and rub against the cornea
or bulbar conjunctiva are called rubbing lashes. If they are larger than
four maldirected lashes; the condition is called trichiasis.

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EYE LID & CONJUNCTIVA CHAPTER 2

2. Entropion

It is Rolling in words of the lid margin. The whole raw of lashes are
rubbing against the cornea, later on the whole lid will be deformed.

3. Ectropion

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EYE LID & CONJUNCTIVA CHAPTER 2

Ectropion is rolling out of the lid margin resulting in the exposure of a

varying amount of the palpebral conjunctiva. The lower lid is more
commonly involved than the upper lid.
The patient will present with lacrimation due to eversion of the lacrimal
punctum, causing eczematous changes in the skin which tend to
aggravate the ectropion.
Madarosis

Madarosis (Gr. Madaros = Bald) means loss of eyelashes or eyebrow. It

may be (temporary or permanent) or (partial or complete).
Blepharoptosis
Ptosis is drooping of the upper eyelid below its normal position while the
patient looking straight. Normally the upper eyelid covers the upper 1-
2mm of the cornea.

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EYE LID & CONJUNCTIVA CHAPTER 2

Congenital
Acquired
o Neurogenic (Third nerve palsy, Horner's syndrome, synkinetic as

Marcus Gunn phenomena and misdirection of third nerve)

o Myogenic (myathenia gravis and ocular myopathy)

o Traumatic

o Aponeurotic (involutional and postoperative)

o Mechanical (excessive weight as lid edema, tumors and

dermatochalasis or conjunctival scarring).
The Conjunctiva
Inflammation of the conjunctiva (conjunctivitis)

Can be classified according to the etiology into: infective or non-

infective.
According to the clinical presentation into: acute, subacute or chronic.

1- Infective Conjunctivitis: Bacterial, Viral, Chlamydial

2- Non-infectiveConjunctivitis:Allergic: vernal, phlyctenular
Clinical Evaluation of Conjunctivitis
Presentation (symptoms):
Discharge, discomfort, foreign body sensation, heaviness of eye lids, red
eye, itching (in allergic type). Photophobia and lacrimation if cornea is
affected.
Signs: presentation of conjunctival disease
1- Discharge:

- Watery; viral and acute allergic.

- Mucoid; chronic allergic (vernal).
- Ropy; spring catarrh.
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EYE LID & CONJUNCTIVA CHAPTER 2

- Purulent; acute bacterial.

- Mucopurulent; mild bacterial and chlamydial.
2- Conjunctival appearance:
�� Conjunctival injection (redness); non-specific.i.e. present in every
type of conjunctivitis

�� Subconjuctival heamorrhage; mainly in viral conjunctivitis.

�� Follicular reaction; viral, chlamydial, drug

toxicity.

�� Papillary reaction; small: less specific, allergic, bacterial, irritative.

Large: spring catarrh.

�� Oedema (chemosis); in allergy and severe inflammations.

�� Scarring, symblepharon; trachoma, ocular chemical burns,

membranous conjunctivitis.

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EYE LID & CONJUNCTIVA CHAPTER 2

3- Membranes:
- pseudomemranes,removed easily leaving intact epithelium. In
severe adenoviral infection, gonococcal infection, chemical burns.

- True membranes(membranous conjunctivitis),

difficult to remove leaving bleeding due to tearing of epithelium. In
diphtherial and beta heamolytic strept. Infections.
NB: any case of membranous conjunctivitis should be treated as
diphtheria unless conjunctival and throat swabsare negative.
4- lymphadenopathy;viral (tender),
chalamydial, and severe gonococcal infections.

Trachoma (Egyptian Ophthalmia)

This is a very common type of conjunctivitis was considered to be
endemic in Egypt, and hence taken its name.
It is a chronic contagious inflammation caused by Chlamydia
trachomatis characterized by:
�The formation of follicles and papillae
�Subepithelial cellular infiltration
�The formation of pannus
�Healing by cicatrization.

Phlyctenular conjunctivitis:
Is a keratoconjunctivitis due to allergy to endogenous toxin and
characterized by phlycten nodule, more common in malnourished
children.
Etiology: Hypersensitivity to an endogenous antigen which may be:
o Tuberculo-protein

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EYE LID & CONJUNCTIVA CHAPTER 2

o Intestinal parasites.
o Septic focus.
o Staphylococcal blepharoconjunctivitis.

Vernal keratoconjunctivitis(Spring Catarrh):

Bilateral seasonal and recurrent allergic keratoconjunctivitis probably due
to sensitivity to ultraviolet rays and airborne allergens.
It affects mainly children and young adults, more common in boys.
It may be associated with keratoconus.
It is common in patients with asthma, hay fever or atopy.
It may present as palpebral, bulbar, or mixed types
a. Palpebral type:
i. Large flat-topped papillae giving a cobblestone appearance on the
tarsus and absent from the fornix affecting mainly the upper tarsus.
b. Bulbar type: more severe
It manifests as gelatinous limbal masses. It usually starts at the upper
limbus, then later all round. White spot concretions of eosinophils and
necrotic epithelium may be seen (Tranta Spots)
c. Mixed type
The mixed type is a mixture of the palpebral and bulbar types other.

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EYE LID & CONJUNCTIVA CHAPTER 2

Microbiology of the eye

-The most common types of bacteria that causes bacterial
conjunctivitis includes Staphylococcus aureus, Haemophilus
influenzae, Streptococcus pneumoniae and Pseudomonasaeruginosa.

Staphylococcus aureus
Morphology:
Staphylococci are gram positive spherical cells, non-motile, non-spore
forming, usually non-capsulated and arranged in irregular grape like
clusters.

Culture characters:
- Staphylococcusaureusgrows readily on most bacteriologic media
- Gas requirements: aerobe facultative anaerobe
- Incubation temperature: 37°C.
- Incubation time: 24-48 hours.
- Culture media & colony morphology:
�� Nutrient agar: Colonies are grey to deep golden yellow
(endopigment).
�� Blood agar: colonies surrounded by a zone of beta hemolysis.

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EYE LID & CONJUNCTIVA CHAPTER 2

�� Mannitol salt agar (selective differential medium for

Staphylococci): containing 10-15% NaCL (halophilic), the
colonies are yellow.
Biochemical reactions: (see practical lessons)
Antigenic structures:
A. ProteinA: Is a cell wall component which is the major protein in

cell wall, binds to the Fc portion of IgG preventing binding of

complement and inhibiting phagocytosis.
B. Teichoic acid: That mediates adherence of organism to mucosal

cells.
Pathogenicity and virulence factors:
Staphylococcusaureus is responsible for 80% of human suppurative
infections allover the world. The chief source of infections is human
carriers. The organism is transmitted by contact .
virulence factors:
A. Structural factors: Protein A and Capsule
B. Non Structural factors:
I. Enzymes:
1) Catalase:breaks H2O2 into water and O2.
2) Coagulase:An enzyme that clots plasma with deposition of
fibrin on the surface of Staph. that hinders ingestion of the
bacteria by phagocytic cells.
3) Spreadingenzymes:Including 1- hyalourinidase,
2-Fibrinolysin (staphylokinase) which dissolve fibrin clots but more
slowly than streptokinase.
4) β-lactamase: That render the organism resistance to
penecillin and ampicillin.
II.Toxins:
1) Haemolysin:That lyse erythrocytes and damage platelets.
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EYE LID & CONJUNCTIVA CHAPTER 2

2) Leucocidins:killleucocytes and cause necrosis of tissues.

3) Enterotoxins: heat stable, resistant to the action of gut
enzymes. They cause carbohydrate rich food poisoning.
4) Toxic shock syndrome (TSST-1): superantigen responsible
for toxic shock syndrome
5) Exfoliative or epidermatolytic toxin:
That has proteolytic activtiy for matrix of epidermis that lead to bullous
formation of scalded skin syndrome in young children.
Streptococcus pneumoniae (Pneumococci)
Morphology:
Gram positive, ovoid or lanceolate, that are non-motile, non sporing and
capsulated. They are arranged in pairs with broader ends opposed. In
tissue stained with Gram, the capsule appears as an unstained halo.
Culture characters:
- S. pneumoniaecannot grow on ordinary media. It needs enriched
media.
- Gas requirements: aerobe facultative anaerobe, growth is enhanced
by 5-10% Co2
- Incubation temperature: 37°C.
- Incubation time: 24-48 hours.
- Culture media & colony morphology:
�� Blood agar: colonies are small, at first dome shaped and later
developed central plateau (due to natural autolysis) with an
elevated rim, giving the character of draught’s man appearance.
They are surrounded by α haemolysis.
Characters of Pneumococcus that differentiate it from Viridans
streptococci will be shown in practical lessons.
Antigenic structure:

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EYE LID & CONJUNCTIVA CHAPTER 2

The capsule of Pneumococci is polysaccharide and has 90

immunologically distinct types. Types 1-8 are responsible for 75% of
pneumonia and pneumococcal bacteramia .It is essential for virulence of
the organism (resist phagocytosis). Immunity against pneumococciistype
specific.
Quelling reaction:
When Pneumococcusof certain antigenic type is mixed with specific
anti-polysaccharide serum of the same type or with polyvalent antiserum
on a microscope slide, the capsule swells markedly.
Virulence factors:
1. The capsule (anti-phagocytic).
2. IgA protease that destroy secretory IgA.
Pseudomonas
The genus Pseudomonascomprises more than 200 species, mostly
saprophytes found widely in soil and water. Pseudomonasaeruginosais
the species usually associated with human disease.
Pseudomonasaeruginosa
Ps. aeruginosais widely distributed in nature and is commonly present
in the moist environments in hospitals. It can colonize the normal human
intestine, upper respiratory tract and the skin. It only causes disease in
humans with abnormal host defense as patients in hospitals (hospital-
acquired infection), hence it is called an opportunistic pathogen.
Morphology:
Gram-negative bacilli, motile, non-sporing and some strains are
capsulated.
Culture characters:
- It can grow on ordinary media where the media turn greenish blue
due to diffusible exopigments.

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EYE LID & CONJUNCTIVA CHAPTER 2

- Gas requirements: strict aerobe.

- Incubation temperature: 37°C.
- Incubation time: 24-48 hours.
- Culture media & colony morphology:
�� MacConkey's agar where they produce pale yellow non-
lactose fermenting colonies.
�� On blood agar, Most strains produce haemolysis
Biochemical reactions: seepractical lessons
Pathogenicity:
It produces: Infection of respiratory tract, urinary tract, wounds, burns,
ear, eye and osteomyelitis following bone trauma.
Laboratory diagnosis:
� Specimen: according to the disease e.g. sputum, pus, urine, etc.
� Smear& Culture: see practical lessons.
Treatment:
� They are resistant to most antibacterial drugs. The most effective
chemotherapeutics are gentamicin, quinolones and polymyxin B.
� In any case, sensitivity tests must be done before treatment.

Haemophilus aegypticus
Haemophilusaegyptius(Koch-Weeks bacillus) is a small gram-negative
rod that is an important cause of mucopurulent conjunctivitis in
children. Certain strains cause Brazilian purpuric fever, a life-threatening
childhood infection characterized by purpura and shock.

Diagnosis:
1- Specimen:conjunctival swab or discharge.
2- Smear.

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EYE LID & CONJUNCTIVA CHAPTER 2

3- Culture: DD from H.influenza by its ability to agglutinate

blood group O RBCS

Gonococcaland chlamydial conjunctivitis

You can get pink eye from infections from sexually transmitted diseases
including gonorrhea and chlamydia. Newborn babies may be exposed
when they pass through the birth canal of an infected mother.

Neisseria Gonorrhoea (Gonococci)

Differentiation between N. gonorrhoeae& N. meningitides
Points of N. meningitides N. gonorrhoeae
differentiation
1. Capsule -Present -Absent
2. Carrier - Present -Absent
3. Chronicity -Absent -Present
4. Maltose ferm. -Yes -No
5. Transmission -Droplets -Sexual

Morphology,stainingand culture: Similar to those of N. meningitidis.

Biochemicalreactions:practical lessons.

Antigenic structures and virulence factors:

1. Outer membrane proteins: They facilitate invasion of epithelial
cells.
2. Lipopolysaccharide.
3. IgA protease.
4. Pili
Pathogenesis:-
� N. gonorrohoeaeis a strict human pathogen.

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EYE LID & CONJUNCTIVA CHAPTER 2

�� Gonococci attack mucous membranes of the genitourinary tract,

eye, rectum and throat, producing acute suppuration; this is
followed by chronic inflammation and fibrosis.
�� Infection occur mainly by sexual intercourse leading to
Gonorrhoeawhich is a pyogenic disease affecting the male and
female genital systems.
� Non venearal Transmission of N.Gonorrhoeae:
1) Gonococcal ophthalmia neonatorum: an infection of eye of
newborn during passage through infected birth canal.
2) Gonococcal vulvovaginitis: from the contaminated clothes or
toilet seats
Diagnosis: 9Diagnosis of eye)
a) Specimen:Discharge from male or female.
b) Smear stain by Gram: G-ve diplococci, kidney shaped
arranged intra and extra cellular to pus cells (Diagnostic).
c) Culture on chocolate agar or Thayer Martin agar & colonies
identified by: gram film, biochemical reactions.
Treatment: Cefotriaxone is the drug of choice.
Prevention:Prompttreatment of symptomatic patients, Use of condoms.
o Neonatal ophthalmia is prevented by use of erythromycin or
tetracycline eye drops or eye ointment immediately after
birth.
Chlamydia
Chlamydiae are obligate intracellular organisms. They are midway
between viruses and bacteria.

Characters Bacteria Chlamydiae Viruses

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EYE LID & CONJUNCTIVA CHAPTER 2

Obligatory No Yes Yes

intracellular
parasites
Nucleic acids RNA and RNA and DNA RNA or DNA
DNA
Reproduction simple binary complex cycle Synthesis and
fission with fission assembly
Antibiotic Yes Yes No
Sensitivity
Ribosomes Yes Yes No
Metabolic Yes Yes No
enzymes
Energy Yes No No
production

Morphology:
Gram- negative small non motile bacteria. They can be stained by Giemsa
where they are seen as intracytoplasmic basophilic (blue) inclusion
bodies.

(Intracytoplasmic inclusion bodies)

Culture characters:They are obligate intracellular parasites, cultured on
yolk sac of embryonated egg or tissue culture cells.

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EYE LID & CONJUNCTIVA CHAPTER 2

Developmental cycle:

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EYE LID & CONJUNCTIVA CHAPTER 2

Classification of Chlamydia:
Species Diseases
Chlamydiatrachomatis Trachoma (a leading cause of blindness in the
world)
1-Inclusion conjunctivitis
2-Respiratory infection.
3-Genital trachoma.
Lymphogranuloma venereum
(sexually transmitted)
Chlamydia pneumonia Atypical pneumonia
Chlamydia psittaci Atypical pneumonia
Diagnosis of chlamydial infections:
A. Direct diagnosis:
1. Specimens are obtained from the site of the lesion, conjunctival
scrapings, urethral discharge, sputum. etc.
2. Smears: Microscopic examination:
�� Inclusion bodies detection.
�� DIF
3. ELISA to detect chlamydial antigens.
4. PCR.
B. Serological diagnosis: By ELISA or indirect micro
immunofluorescence to detect IgM and IgG formed against
chlamydia.
Treatment:
��Chlamydia is sensitive to tetracycline or macrolides.
��Sexually transmitted Chlamydia trachomatis infection is treated by
azithromycin. Both partners and offspring should be treated
simultaneously to prevent reinfection.

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EYE LID & CONJUNCTIVA CHAPTER 2

��Sulphadiazine eye drops are used in case of ocular trachoma.

-Viral causesof eye infection

Conjunctivitis may accompany the common cold and other systemic
viral infections (especially measles, but also chickenpox, rubella,
and mumps). Localized viral conjunctivitis without systemic
manifestations usually results from adenoviruses and sometimes
enteroviruses.

1- Herpes Simplex Virus:

Types:
�� Herpes simplex virus type 1 (HSV1): oro-facial lesions.
�� Herpes simplex virus type 2 (HSV2): genital lesions
Both viruses cause painful vesicles on the skin at the site of inoculation
Mode of infection:
Direct contact with lesions. For example, through saliva (HSV1) or
sexual intercourse (HSV2).
Clinical features:
a) Herpes simplex virus type 1:
◘ Gingivo-stomatitis:where there is painful vesicles develop at the
following sites:
�� Inside the mouth (on the buccal mucosa and gums), that
ulcerate later.
�� On the lips.
�� On the skin around the mouth.
� Reactivation may be provoked by a number of stimuli that decrease
immunity including sunlight, stress, febrile illnesses, menstruation
or immunosuppression.

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EYE LID & CONJUNCTIVA CHAPTER 2

◘ Conjunctivitis and Keratitis:

� Herpetic lesion on the cornea with pain and photophobia.
� Recurrence can lead to scarring and blindness.
b) Herpes simplex type 2 (Genital Herpes):
� Sexually transmitted herpetic lesions.
� Usually due to HSV2 especially from non-circumcised men to
women causing chronic cervicitis, cervical erosion which may
proceed to cancer cervix.
� Neonatal infections may occur at birth, if the mother has genital
herpes by HSV2 at the time of delivery.
� It may be a cause of recurrent abortion.

2- Varicella Zoster Virus (VZV)

Clinical types
1. Varicella or chicken pox.
2. Herpes zoster or shingless.
The two diseases caused by the same virus, primary infection causes
generalized disease (chicken pox) and secondary infection causes
localized lesion (herpes zoster).
Varicella (chickenpox) (Primary infection)
Incubation period: 14-21 days.
Mode of infection: either by respiratory droplets or by direct contact
with skin lesions.
Clinical picture:
� Mild fever & generalized vesicular rash on the trunk and spread to
the head and extremities.
� The lesions progress from macule to papule to vesicle to pustule to
scab so that lesions of different stages are present at the same time.
Itching is a prominent symptom.

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EYE LID & CONJUNCTIVA CHAPTER 2

Zoster (shingless) (Reactivation lesion)

� The virus establishes a latent infection in sensory ganglia.
Reactivation usually occurs many years after primary infection and
is often associated with immunosuppression of the host.
� Unilateral painful vesicles on the skin commonly across the course
of intercostal nerves.

-Adenoviridae
� At least 40 human serotypes are recognized.
� Some types may be isolated from apparently healthy individuals.
Other types are claimed to be carcinogenic in animals, but no tumors in
humans.
� Diseaseproduced:Ocular infections, upper and lower respiratory
tract infections, myocarditis, mesenteric adenitis, gastroenteritis.
Infections are usually self-limiting.

-Many of different types of fungi can cause eye infections. Common

types include:
� Aspergillus– a common fungus that lives in indoor and outdoor
environments
� Candida– a type of yeast that normally lives on human skin and on
the protective lining inside the body called the mucous membrane

Candida
Several species are found in man but Candida albicans is responsible of
about 90% of infections.
Other species include: C. tropicalis, C. krusei, and others.

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EYE LID & CONJUNCTIVA CHAPTER 2

Candida albicans
Habitat: It is part of the normal flora of mucous membranes of the upper
respiratory, gastrointestinal, and female genital tracts.
Morphologyand staining:Gram positive which has two forms:
Y form: oval yeast budding cells.
M form: Pseudo-hyphae constituting mycelia.
Culture: Aerobic, easily cultivated in 37° C for 24-48 hours
�� On Sabaroud Dextrose Agar (SDA) showing hemispherical
white or creamy colonies with yeasty odour and waxy surface.
� On nutrient and blood agar: addition of inhibitory antibiotic
discs (e.g. chloramphenicol) is useful to inhibit any bacterial
growth.

Identification and differentiated from other speciesby:

��Germ tubes: filamentous outgrowth formed by culturing C.albicans
in serum at 37 °C for 3 hours.
��Chlamydospores: round thick walled resting structures found at the
end of pseudohyphae deep in the agar when C.albicansis cultured
on corn meal agar (nutrition poor media) for 24 hours in 22°C.
��Biochemical reactions: Carbohydrate fermentation reactions
differentiate it from other species.

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EYE LID & CONJUNCTIVA CHAPTER 2

Candida albicans germ tube

http://thunderhouse4-yuri.blogspot.com/2009/12/candida-albicans.html

Candida albicans chlamydospore

http://apitherapy.blogspot.com/2007/01/propolis-may-help-treat-oral.html

Pathogenesis& Clinical Findings:

�� Transmission: usually endogenous but cross infection can occur e.g.
from mother to baby or between babies in nurseries.
�� When local or systemic host defenses are impaired, disease may result
in the form of:

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EYE LID & CONJUNCTIVA CHAPTER 2

Superficial infections:
� Thrush: overgrowth of C.albicans in the mouth producing
white patches.
� Vulvo-vaginitis:with itching and discharge favored by high
pH, diabetes, or prolonged use of antibiotics.
� Skin invasion:in warm, moist areas, which become red and
weeping.
� Fingers and nails: Thickening or loss of the nail can occur
when repeatedly immersed in water e.g. dishwashers in
restaurants are commonly affected.

Systemic (deep):
In immunosuppressed individuals, Candid disseminates to many organs
causing chronic muco-cutaneous candidiasis, lower respiratory tract and
urinary tract infections, septicaemia with localization in eye,
endocardium, meninges, kidney and bone infections.

Drugs used in treatment of eye infection

Eye infection can be caused by bacteria, virus or other microbial
agents which can affect any part of the eye.

A) Common antibacterial drugs usedtopically for ophthalmic use

B)
Azithromycin Conjunctivitis
Levofloxacin
Moxifloxacin
Chloramphenicol Conjunctivitis,
Keratitis
Polymyxin B Conjunctivitis,

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EYE LID & CONJUNCTIVA CHAPTER 2

Keratitis, plepharitis
Bacitracin Conjunctivitis,
Ciprofloxacin Keratitis, plepharitis, dacrocystitis
Gentamycin

C) Common antiviral drugs usedtopically for ophthalmic use

Some examples of : Antiviral agents for ophthalmic use:

Ganciclovir -acyclovir -Valacyclovir -Famciclovir.

D) Common antifungal drugs usedtopically for ophthalmic use

Some examples of : Antifungal agents for ophthalmic use:
Polyenes: amphotricin B.
Imidazoles: Fluconazole – Itraconazole – Ketoconazole – Miconazole

Drugs affecting eye

a) Antiallergic,decongestant and anti-inflammatory agents:
Antiallergic agents:
- Corticosteroids
- H1 Blockers as antazoline
- Mast cell stabilizers as nedocromil eye drops 2%(for
prophylaxis).
Decongestant agents;
- Naphazoline & tetrahydrozoline
Anti-inflammatory agents:
NSAIDs as diclofenac & ketorolac
Glucocorticoids
Topical steroids (dexamethasone, prednisolone, fluorometholone)

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EYE LID & CONJUNCTIVA CHAPTER 2

Used in ocular allegy

Inflammation associated with infection
Anterior uveitis
Systemic and sub-Tenon’s capsule injection
Used in posterior uveitis
Intravitreal injection
Used in diabetic retinopathy
Ocular side effects
Cataract
Ocular hypertension and glaucoma
Secondary infections
Retardation of wound healing post-operative
Inhibition of corneal epithelial & stromal healing
b) Conjunctival irritants:
- Ethyl morphine causes hyperemia that speed healing of
corneal ulcers
- Chloro-aceto-phenone (tear gas or lachrymator)
- Ether , irritates conjunctiva as a side effect.
c) Diagnostic agents: fluorescein
- Used for diagnosis of corneal ulcer
- It is instilled on the eye then washed by saline, any spots of
ulcerated cornea will appear green
d) Drugs toxic to the eye
Atropine glucoma
Nitrate Increase I.O.P
Glucocorticoids See before
Chloropromazine Corneal and lens opacities
Thioredazine Retinopathy

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EYE LID & CONJUNCTIVA CHAPTER 2

Amiodarone Corneal deposits

Oxygen Retrolental fibroplasia
Chloroquine Retinopathy
Ethambutol Optic neuritis
Methyl alcohol Toxic to retina and optic nerve
Digitalis Yellow vision
Practolol Oculomucocutenous syndrome
e) Local anesthetics:
Topical anesthesia
- Proparacaine.
- tetracaine drops.
- lidocaine gel.
Infiltration anesthesia& retrobulbar block anesthesia:
- Infiltration of the ciliary ganglion and surrounding tissues (retro-
bulbar anesthesia)
- Fascial nerve block to produce temporary paralysis of the
orbicularis oculi muscle
- Lidocaine and bubivacaine.
- S/E: globe perforation, haemorrhage, vascular and subdural
injection.

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EYE BALL CHAPTER 3

Anatomy of the Eye Ball

The eye ball is a sphere with a diameter of 24 mm (about 1 inch).
The ocular wall is composedof three coats:
1.Outer fibrous coat: formed of
a. Cornea: anterior transparent 1/6.
b. Sclera: posterior opaque 5/6.
2.Middle vascular coat: Or the uveal coat
Formed of Iris, Ciliary body, and Choroid.
3.Inner nervous coat: the retina.
4. NB: Ocular adenxia (Accessory structures of eye): are
accessory organs related to the eye ball: lids, conjunctiva, lacrimal
apparatus, and extraocular muscles.
The cavity of the eye is divided into:
1.The anterior chamber: the space between the cornea & iris.
Bounded by the angle of the AC.
2.The posterior chamber: is the space between the lens & the iris.
Both chambers communicate through the pupil and filled by
aqueous.
3.The vitreous chamber: lies between the lens & retina and is filled
with vitreous.
Contents of the eye ball:
- Anterior chamber between cornea and iris, filled with aqueous.
- Crystalline lens
- Posterior chamber between iris and lens, filled with aqueous.
- The vitreous cavity filled with the vitreous body

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EYE BALL CHAPTER 3

Histology the photoreceptor system

1-External (Fibrous layer)

The sclera:
-It is a dense opaque layer, made up of tough dense connective tissue that
consists of:
a. Flat collagen bundles in various directions.
b. Moderate amount of ground substance.
c. Few fibroblasts.
Externally, it is covered by Tenon's capsule and the
tendons of the extraocular muscles are attached to its outer
surface. Internally, it is separated from the choroid by a thin
layer of loose connective tissue rich in elastic fibers and
melanocytes called suprachoroidal lamina.
The cornea:
- It is the colorless transparent anterior 1/6 of the fibrous layer.
- It consists of 5 layers:

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EYE BALL CHAPTER 3

1- Epithelium: is stratified squamous non- keratinized

��The basal layer is formed of cuboidal cells resting on a straight
basal lamina (no ridges). It has high regenerative capacity
(turnover time is about one week).
��The intermediate layers: 3-4 layers of polygonal cells with
numerous free nerve endings in between.
��The surface cells are squamous showing microvilli which hold
between them a protective thin layer of tears.
2- Bowman's membrane:
��A thick homogenous non-cellular layer.
��It consists of collagen fibers and a condensation of intercellular
substance.
��It acts as a protective barrier against mechanical injuries and
bacterial invasion.
��If destroyed it does not regenerate, but it heals by irregular fibrous
tissue causing corneal opacities.
3- Stroma (substantia propria):
��It is the thickest layer of the cornea (90%).
��It consists of regularly arranged bundles of collagen type I that
cross at right angles to each other. The collagen fibrils in each
bundle are running parallel to each other and taking the full length
of the cornea.
��The fibroblasts are squeezed in rows in between the bundles and called
corneal corpuscles.
��The fibers and cells of the stroma are immersed in an amorphous
ground substance rich in chondroitin sulphate.
��It is normally non-vascular.
4- Descemet's membrane:
��Thick homogenous structure composed of fine collagen fibrils.

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EYE BALL CHAPTER 3

5- Endothelium:
��It is simple squamous epithelium that covers the posterior surface of
the cornea facing the anterior chamber.
��It plays a role, together with the corneal epithelium, in keeping the
cornea relatively dehydrated by active transport of Na+, followed by
Cl- and water, to their apical surface.

The layers of cornea

-The transparency of the cornea is due to:
1- The relative dehydrated state.
2- The regular arrangement of the thin collagen fibrils.
3- The absence of blood vessels.

CORNEO SCLERAL JUNCTION (LIMBUS)

- It is an area of transition from the transparent collagen bundles of the
cornea to the white opaque fibers of the sclera.
- The following changes are seen at the corneoscleral junction:
1. The corneal epithelium passes to the bulbar conjunctival
epithelium unchanged.
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EYE BALL CHAPTER 3

2. The Bowman's membrane stops abruptly and is replaced by the

subconjunctival connective tissue.
3. The substantia propria (stroma) becomes continuous with the
fibrous tissue of the sclera.
4. The Descemet'smembranebreaks up into fine CT tissue trabeculae
(ligamentum pictinatum) which enclose between them trabecular
spaces of Fontana. These are irregular endothelium-lined spaces that
connect the anterior chamber to canal of Schlemm surrounding the
limbus. This canal drains aqueous humor from the anterior chamber
and is connected externally with the venous system.
5. The endotheliumextends to line the trabecular spaces of Fontana.

Corneoscleraljunction, Iris and ciliary body

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EYE BALL CHAPTER 3

2-Middle (vascular) layer

Layers of eye ball Note (Iris, Ciliary body and choroid of the middle
layer)
A)_The iris :

- The iris is the most anterior part of the middle layer. It is an

extension of the choroid that partially covers the lens. The
rounded opening in its center is called the pupil.
-Histologically, the iris consistsof:
1- The anterior surface:
- It is formed by a discontinuous layer of melanocytes and fibroblasts. It
has no covering epithelium.
2- The stroma:
- It consists of loose C.T. and can be differentiated into two layers:
a) The anterior layer is poorly vascularized and has many melanocytes.
b) The posterior layer is rich in blood vessels.
3- The muscles of the iris:
(i) Sphincterpupillae muscle:it is the inner smooth muscle fibers which
are arranged circularly around the pupillary margin.

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EYE BALL CHAPTER 3

(ii) Dilator pupillae muscle:The outer layer of epithelial cells covering the
posterior surface of the iris have radially directed tongue like extensions
of their basal region creating the dilator pupillae muscle.
4- The posterior surface of the iris is smooth and is lined by two layers of
pigmented epithelium continuous posteriorly with the ciliary epithelium.
N.B. The iris gives the color of the eye:
- In the brown eyes, melanocytes are present in all layers.
- In the blue eyes, melanocytes are to the epithelial layer covering the
posterior surface.

Iris structure

(B) The ciliary body:

- Definition: The ciliary body is the anterior expansion of the

choroid.

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EYE BALL CHAPTER 3

- Shape:It appears triangularin shape in longitudinal section of the

eye ball. (Its apexis continuous posteriorly with the choroid and its
basefaces the iris. Ciliary processes project from its medialborder).
- Structure: It consists of:
a- Covering ciliary epithelium
b- Loose CT tissue rich in blood vessels and melanocytes.
c- Ciliary muscle.
The ciliary epithelium (Pars ciliaris retina)

- It is the covering of the ciliary body and its processes.

- It is a double layer of columnar epithelium sandwiched between
two basement membranes:
- The outer layer is adjacent to the ciliary body, consists of simple
columnar epithelial cells rich in melanin and corresponds to the
forward projection of the pigment epithelium of the retina.
- The inner layer is related to vitreous body and posterior chamber,
consists of simple non-pigmented columnar epithelium and is
derived from the sensory layer of the retina.
- The cells of the two layers meet each other apex to apex and
these apical surfaces are joined together by desmosomes.

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EYE BALL CHAPTER 3

Ciliary epithelium
The ciliary muscle:
It consists of two bundles of smooth muscle;
��One bundle stretches the choroid with most of its fibers has
meridional direction while some fibers are radial or oblique.
��The other bundle runs circularly and when contracted, it relaxes the
tension on the Zonule fibers of the lens.

��The ciliary processes

- They are thin projections from the medial side of the ciliary body.
- They give attachment to the Zonule fibers of the lens.
- They have a loose connective tissue core and numerous fenestrated
blood capillaries from which the aqueous humor is elaborated.
- They are covered by the ciliary epithelium.
(C) The choroid:

- The choroid is a layer of loose connective tissue rich in blood vessels,

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EYE BALL CHAPTER 3

and melanocytes which give the choroid its black color.

- The loose C.T. contains fibroblasts, macrophages, lymphocytes, mast
cells and plasma cells, as well as collagen and elastic fibers.
Layers of the choroid:
1- The suprachoroidal lamina:
It is a layer of elastic tissue that attaches the outer layer of the vascular
choroid to the inner surface of the sclera.
2- The vascular choroids:
It contains large blood vessels and is rich in melanocytes.
3- The choriocapillary layer:
It is the inner layer and is rich in small vessels and wide capillaries.
4- Bruch’s membrane:
The choriocapillary layer is separated from the retina by amorphous
hyaline membrane known as Bruch's membrane which consists of:
1. Basal lamina of choriocapillaris.
2. Two layers of collagen fibers with a layer of elastic fibers in
between.
3. Basal lamina of the pigment epithelium of the retina.

Pigment eithelium
Retina

4- Bruch’s membrane

3-The choriocapillary layer

Choroid
2-The vascular choroids

1-The suprachoroidal lamina

Sclera

Structure of choroid

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EYE BALL CHAPTER 3

Structure of Bruch membrane

The lens
- It has 3 components :
a) Capsule: is thick, elastic and homogenous envelope. It consists
mainly of collagen type IV and amorphous glycoproteins.
b) Subcapsularepithelium: a single layer of cuboidal cells present only
on the anterior surface of the lens. The cells at the equator of the lens
give rise to new lens fibers added during life.
c) Lens fibers: they are highly differentiated cells derived from the
subcapsular epithelial cells that lose their nuclei and organelles and
become greatly elongated.
- The lens is held in place by a radially oriented group of fibers, called
the Zonule, attaching it to the ciliary body.

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EYE BALL CHAPTER 3

The lens
Vitreous body:
-It is a transparent refractile gel occupying the vitreous space.
-It consists of water (99%), collagen type II and glycosaminoglycans
(mainly hyaluronic acid).
-The fluid components of the vitreous body called vitreous humor.
-Small cells called hyalocytesare observed at the periphery of the
vitreous body; these are believed to synthesize collagen fibrils and
hyaluronic acid.

3-INNER (NERVOUS) LAYER

(The Retina)

- The retina consists of ten distinct layers. All (except the outer most
pigmented layer) belong to the photosensitive (neural) retina.
- The retina extends to the posterior border of the ciliary body where the
neural retina ends on a wavy line, the ora serrata.
The pigment epithelium:
- It consists of columnar cells with a basal nucleus.
- The basal regions of the cells adhere firmly to Bruch's membranes with

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EYE BALL CHAPTER 3

numerous basal invaginations of the cell membranes.

- The lateral membranes show junctional complexes (zonulae occludens,
adherence, desmosomes and gap junctions). This junctional complex is
the major component of the blood retinal barrier.
- The apical membrane has abundant microvilli and cylindrical extensions
that invest the tips of rods and cones.
The cytoplasm contains:
��Abundant SER (vitamin "A" transport to the photoreceptors).
��More mitochondria near basal invaginations (ion-transporting
activity).
��Numerous melanin granules in the apical cytoplasm and
microvilli (absorption of light after stimulation of
photoreceptors).
��Numerous dense vesicles (lysosomes) are also present in apical
cytoplasm representing various stages in phagocytosis and
digestion of the tips of the outer segments of rods and cones.

Pigment epithelium

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EYE BALL CHAPTER 3

Photoreceptors (rods & cones):

- The rod and cone cells (1st order neuron) can be divided into outer
segment, inner segment, nuclear region and synaptic region.

ROD CELLS:
- Number:The human retina has about 120 million rods
- Structure:They are thin, elongated cells that are composed of:
a- Outer segment:
��It is rod shaped.
��It is a modified cilium that contains stacks of numerous flattened
membranous disks. These disks are not continuous with the
plasma membrane. They contain the visual pigment rhodopsin.
��The outer segments interdigitated with the cytoplasmic extensions
of the pigment epithelium.
b- The inner segment:
��It is separated from the outer segment by a constriction (connecting
stalk) which contains the nine peripheral doublet microtubules of a
cilium closely associated with a basal body.
��The inner segment is rich in glycogen, mitochondria (near the
constriction), rER& a prominent Golgi complex for protein synthesis
��The inner segment synthesizes the proteins of the membranes of the
flattened disks which are added to the outer segment disks at their
basal region. These disks gradually migrate to the cell apex where
they are phagocytosed by the cells of the pigment epithelium
c- The nuclear region:
��It is expanded region containing the nucleus.
d- The synaptic region:
��It is a club shaped expanded presynaptic terminal
that contains synaptic vesicles and mitochondria.

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EYE BALL CHAPTER 3

- Function:Theyare sensitive to dim light (low intensity of light).

CONE CELLS:

- Number: Each human retina has about 6 million cone cells.

- Structure:The structure of the cone cells is similar to that of rods, but they
differ from the rods in the following.
1. The outer segment is conical in shape.
2. The flattened membranous disks are continuous with the plasma
membrane.
3. The newly synthesized proteins are distributed uniformly
throughout the outer segment, and not only to the recent disks in the
basal region.
4. The flattened disks of the cones contain visual pigment iodopsin
which is sensitive to different colors (red, blue & green).
- Function:They are sensitive to higher intensity of light as well as colour
vision and permit better visual acuity.

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EYE BALL CHAPTER 3

Photoreceptors

Histologically the retina consistsof 10 layers (numbered from outside

inwards):
1- Pigment epithelium.
2- Rods and cones (mainly outer segment).
3- External limiting membrane:
- It is not truly a membrane, but junctional complexes between Muller's
cells (the major supportive glial cells of the retina), and the cell bodies
of the rods and cones.
4- Outer nuclear layer:
- Contains nuclear regions of the rods & cones.
- The nuclei of the cones are adjacent to the external limiting
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EYE BALL CHAPTER 3

membrane.
- The nuclei of the rods occupy several layers next to that of cones
except at the fovea centralis which contains only cone cells.

5- Outer plexiform layer (outer synaptic):

-It is a synaptic layer between:
a. The synaptic regions of the rods and cones.
b. The dendrites of the bipolar neurons (2nd order neurons).
c. The processes of horizontal cells (association
neurons).
6- Inner nuclear layer:
- Contains the cell bodies of:
1- Bipolar neurons.
2- Horizontal cells that lie in the outer part of this layer.
3- Amacrine cells (interconnect bipolar neurons & ganglion cells).
4- Muller cells: supportive neuroglial cells that extend from the
external to internal limiting membranes (whole thickness of
retina).

7-The inner plexiform layer (inner synaptic):

- It is a synaptic layer between:
1- The axons of bipolar cells.
2- Dendrites of ganglion cells.
3- Processes of amacrine cells.

8- Ganglion cell layer: It contains

1- Multipolar ganglion cells (3rd order neuron)
2- Branches of central retinal artery.

9- Nerve fiber layer:

- It is composed of unmyelinated axons of ganglion cells which run

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EYE BALL CHAPTER 3

parallel to the inner surface of the retina then pass through the optic
disk and form the optic nerve which is myelinated.

10- Internal limiting membrane:

- It is formed of the terminal expansions of Muller's cells.

Layers of the retina

-The bipolar cells may synapse with only one cone photoreceptor and only
one ganglion cell (monosynaptic bipolar cells) or have synapses with 2 or
more photoreceptors (diffuse bipolar cells).
- Light must traverse eight (8) layers before arriving at the rods and cones
outer segments to initiate a sensory nerve impulse that passes in the reverse
direction to the ganglion cells, to the optic nerve.
Special regions in the retina:
1- The blind spot:
The region at which axons of ganglion cells come together to form the optic
nerve is devoid of photoreceptors and known as the blind spot
( the papilla of optic nerve, or optic nerve disk).

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EYE BALL CHAPTER 3

2- The fovea centralis

It is a shallow depression of retina in posterior pole of the optical
axis. The bipolar and ganglion cells accumulate in the periphery of
this depression and the center consists only of cone cells. The fovea
is the area with the greatest visual acuity.

Physiology of the eye ball

Physiology of the aqueous humour
� It is a clear and transparent fluid which fills both the anterior & the
posterior chambers of the eye.
� It is alkalinein reaction.
� Its osmoticpressureis3-5milliosmols greater than that of plasma.

Circulation and drainage:

� The aqueous humor is formed by the ciliary process.
� Then, the fluid enters the posteriorchamber��and flows between
the fibers of the suspensory ligament.
� Then, enters the anterior chamberthrough the pupil, �the fluid
flows to the iridocorneal angle (filtration angle)�to the spacesof
Fontana (present between a network of trabeculae) �to reach the
canal of Schlemm.
� From the canal of Schlemm�theaqueous is drained in the aqueous
veins��then, finally in the ipiscleral venousplexus.
� The structure of the canal of Schlemmresembles that of a small
vein; its endothelium layer is permeable to the various contents of the
aqueous even to the large protein molecules.
� The intraocularpressureis the driving force of the aqueous into the
canal of Schlemm.

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EYE BALL CHAPTER 3

� Continuous current occurring in the aqueous because temperature of

the iris is 3-5°C higherthan the cornea. The later looses temperature
due to continuous evaporation of tears that cover it.

Functions of the aqueous humour:

a) It givesnutrients to the avascular structures�(lens & cornea)

b) It maintainsthe I.O.P constant��by means of its steady formation
& drainage.
c) It playsa little role as a refractivemedium�because it has the same
refractive index as that of the cornea.
d) It drains metabolites of surrounding tissues.

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EYE BALL CHAPTER 3

The intraocular pressure(I.O.P.):

Normally I.O.P. is 15-20mmHg.
It shows diurnal variationup to 4mmHgbeing:
Highestinthe morning.
Lowestin the evening.

Regulationof I.O.P.:
I.O.P. remains nearly constantthroughout life �� (if the regulating
mechanism remains normal).
I.O.P. is regulated mainly by controlling the outflow of the aqueous
humour from the anterior chamber into the canal of Schlemmin the
following way:
� The trabeculae that guarding the entrance of the fluid into the canal
of Schlemm are laminar platesthat lie one on top of each other.
� Each of the plates is penetrated by numerous small holes.
� When the plates compressed against each other, the successive
plates partially blocked the holes in the next plate.
� An increaseinI.O.P.�leads to distension of the space between the
plates so leads to �opening of the holes thus, causing �rapid flow
into the canal of Schlemm�and decrease of the pressure back to
normal.
� Decreasesin the I.O.P.�� the plates impinge upon each other
�thus, preventing drainage of aqueous humour��till, the pressure
rises again to normal level.
Importance of I.O.P.:
Normal I.O.P. is sufficient to keep:
i) The wall of the globesphericalin shape.
ii) The eyeball and the optical surface in properposition.

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EYE BALL CHAPTER 3

The focusing mechanismsof the eye depend on normal I.O.P. as

following:
a) If I.O.P. decreases:Thesuspensory ligament relaxes ��the lens
increases its power �� so, the image is focused in front of the
retina.
b) If I.O.P. increases:The suspensory ligament is stretched�� the
lens decreases its power �accordingly, the accommodation for
near vision is impaired.

Physiology of the cornea

The cornea is a clear transparent avascularstructure in the anterior
part of the eyeball.
It has a convex anterior surface moist with tears.
It is similar to small watch glass.
Nutrition and metabolism:
Normally cornea is avascular(i.e. devoid of blood vessels)�in order
to maintain its transparency.
It obtains oxygen, glucoseand nutrition from:
1- O2 directly from atmospheredissolvedin the tears.
2- Aqueoushumour(inthe anterior chamber).
3- Lymphdiffusing through substantiapropria.
4- Bloodcapillariessurrounding corneo-scleral junction.
Causesof transparency of cornea:

1) Regular and uniform arrangement of the epithelial cells and lamellae.

2) Absence of myelinated nerve fibers.
3) Absence of blood vessels.
4) Refractiveindexesofvarious layers of the cornea are the same.
5) VitaminA is essential for healthy epithelium.

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EYE BALL CHAPTER 3

Its absence ��leads to dryness of the cornea (xerophthalmia)�

with subsequent corneal keratinization (thickness) &
keratomalacia(weakness).
6) Tears prevent dryness of the cornea because its dryness disturbs its
transparency.
7) Partial dehydration:
Partial dehydration is essential for transparency of the cornea.
Hydration�causes decrease in the corneal transparency �leads to
its cloudiness.
Partial dehydration of the cornea can be achieved by the
following:
a) Evaporationfromthe outer surface of the cornea through corneal
epithelium to air.
b) Endothelialpump of the inner surface of the cornea expels the
fluids from the cornea into the aqueous �exerts dehydration of
the corneal stroma against strong corneal osmotic pressure.
c) The aqueoushumourand tears are hypertonic relative to cornea
�so, they withdraw water from it.
Functions of the cornea:

1. It is the most important refractive mediumin the eye �because; it

acts as a powerful convex lens of about 45 dioptres.
2. It allowsthe entry of light rays into the eye�due to its transparency.
3. Formation of clear sharp retinal images�� due to its regular
curvature.
4. It is permeabletoisotonicfluids�thus, allows t various kinds of eye
dropsto penetrate into the eye.
5. It protectsthe delicate inner structuresof the eye; this is provided
through:
a) Cornea together with lens absorbs a considerable amount of the
ultraviolet rays.

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EYE BALL CHAPTER 3

b) Cornealreflex which protects the eye from the external harmful

substances e.g. dust and other foreign bodies.

Physiology of the lens

The crystalline lens is a biconvexelastic transparent circular lens.
It has two surfaces (anterior and posterior).

Causesof transparency of the lens:

1- It is avascular.
2- It is devoid of nerves.
3- The uniform arrangement of its fibers.
4- The physico-chemical properties of its proteins and the constancy of
its chemical composition.
5- The refractive indices of the various materials in the lens are nearly
equal.
Functions of the lens:
1) It is one of the important refractive media in the eye:
It provides about 1/3 of the total refractive power of the optical
system of the eye during rest (about 20D).
2) It is important in the processof accommodationfor near vision:
Elasticity of the lens allows it to be more spherical in shape �with
subsequent increase in its power �which is essential to see
nearobjects clearly.
3) It protectsthe retina from harmful effects of ultraviolet rays:
It absorbs together a considerable amount of these rays.

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EYE BALL CHAPTER 3

Accommodation to near vision

(The near responseor near reflex)

� Definition:
- It is a physiological process by which the optical system of the eye
increases the power of the lens to focus images of near objects
sharply on the retina and these objects become clearly seen.
� The normal resting optical system of the eye can focus parallelrays
coming from an object (more than 6 metersin front of the eye) on the
retina ��therefore, these objects are clearly seen.
� Near objects (objects placed less than 6 meters from the eye) emit
divergentrays which focus behind the retina �so, images of objects
will be blurred and indistinct.
� In order to see near objects clearly�their images should be brought
on the retina�this is produced through the process of accommodation.

� Changes that occur in the eye during accommodation:

These changes occur in both eyes even if one eye is covered:
(1) Bilateral miosis:

� It is due to contraction of the constrictor pupillae muscle of pupil.

� Its significance:
a- It preventsexcesslightentryinto the eyes from near object.
b- It cuts off a considerable amount of the peripheral rays�
allowing only the central rays to enter the eye�Thus, preventing
both spherical and chromatic aberrations which make the image
blurred �so, it increases the visual acuity.
c- It increasesthe depth of focus �� (i.e. the distance of the object
from the eye can be changed and still its image falls on the retina
without change in accommodation).
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EYE BALL CHAPTER 3

� N.B:
� Spherical aberration:
� It is formation of blurred images as a result of inability of the convex
lens to collect all the rays that it receives into a single focus due to
differences in the refractive powers of its peripheral & central parts
(i.e. the peripheral rays are focused near to lens than the central
rays).
� Chromatic aberration:
��It is formation of images that are surrounded by halos of the various
colors of the spectrum. This occurs because:
� The peripheral parts of lens of the eye act as prisms�so,when a
white light passes through this part �it will be dissociated to the
various colors of the spectral components �which are refracted
to different focal lengths according to the wavelength of each
color.
� So each color will form a separate image.
(2) Increase the diopteric power of the lens:

During near vision��image of the object is formed behind the

retina.
To bring such image on the retina�� the focal length must be
decreased, and this occurs by increasing the diopteric power of the
lens.
So, the lens must be released from the tension of suspensory ligament
and this occurs if the ligament becomes relaxed, this relaxation of the
suspensory ligament occurs if ciliary muscles contract.
So, the lens assumes a more spherical shape because of its elasticity
and the convexity of its anterior surface increases.

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EYE BALL CHAPTER 3

The posterior surface does not change much because of vitreous

humour.
Thus, the diopteric power of the lens will be increased about (10-
14D) according to the age (in children more than young adult and
young adult more than old age) due to loss of its elasticity in old age
(3) Convergence of both visual axes of both eyestowards object:

� It is produced by contraction of the medialrecti muscles.

� This movement brings the image of the near objects on the fovea
centralis of the retina of both eyes to see the object clear.

Nervous pathway of accommodation:

� The blurred image on the retina of a near object initiates impulses

from the photoreceptors that carried by �� the optic nerve to �� the
optic chiasma where the nasal (medial fibers) cross to the opposite
side while its temporal fibers passed uncrossed �� to the optic
tractthen, �� to the lateral geniculate body of thalamus�optic
radiation��then, through the internal capsule→ to the visual cortex.
� The fibers relay first in area 17 of the occipital lobe (visuosensory
area) �� then, in area 18 (visuopsychicarea) �� then in area 19
(occipital eye field area).

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EYE BALL CHAPTER 3

� Form area 19, the fibers take two pathways:

a) Fibers descend directly in the anterior limb of the internal
capsule to �� the tectum of midbrain (occipitotectal fibers)
where they relay in �Edinger-Westephal nucleus
(parasympathetic part of 3rd nerve nucleus) from
which�preganglionic fibersarise �relay in the ciliary
ganglion, then �postganglionicfibersreach �the eye through
the short ciliary nerves��where, they cause contraction of the
ciliary muscles&contraction of constrictorpapillae muscles.

b) Fibers from area 19��reach area 8 (frontal eye field area) to �

the somaticpart of the 3rd nerve nucleuslead to �contraction of
bothmedialrecti leading to �convergence of both eyes towards
the object.

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EYE BALL CHAPTER 3

Retinal adaptation to varying light intensities

� Retinal adaptationmeans that the retina can adjust its sensitivity to

different intensities of light, so that it can see well under different
conditions of illumination (ranging from the bright light of the sun to
the dim light of a star).
� The retinal sensitivityis markedly increased in the dark. While, it
decreases on exposure to light.

(1) Dark adaptation

This is the process by which the retina becomes more sensitive in the
dark.
It occurs when an individual shift suddenly from bright light to a dim
lighted or dark place.
The person at first sees nothing but he gradually begins to identify the
outlines of objects but not their fine details or colors.
As time passes, the retinal sensitivity is increased, and the vision is
improved.
The visual threshold, (which is the minimal amount of light that
produces light sensation), is greatly decreased so, the retina becomes
able to respond to very faint light.
This indicates much increase in the retinal sensitivity which becomes
during maximal dark adaptation 10000-100000times its sensitivity
during exposure to light.
The process of dark adaptation startssoonafter entering into dark. It
becomes moderate after 15minutes and increased to considerable
value within 30 minutes but becomes maximal after one hour or
more.

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EYE BALL CHAPTER 3

Changesoccurring during dark adaptation:

1) Pupillodilatation:
� This allows more light rays to enter the eye which stimulate more
number of rods.
� It is accounts for an increase in retinal sensitivity of only about 12
times.
2) Regeneration of rhodopsin:
� Within 30 minutesin the dark, most of the retinal in the rods is
converted to rhodopsin.
� Vitamin A which is withdrawn from the pigmented cells of the retina
and from the blood to the rods forms more rhodopsin.
� This process was found to continue for several hours after exposure
to darkness.
� The cone pigment (iodopsin) is also regenerated in the dark but its
regeneration is completed within only 5-10 minutes.
� NB:
The time needed for maximal dark adaptation depends on the
regeneration of rhodopsin �� the later depends on the intensity of
illumination to which the subject has been exposed before entering
into darkness.
The greater the intensity of illumination�the longer the time needed
for rhodopsin to regenerate �consequently the slower development
of maximal dark adaptation.
3) Increased retinal sensitivity:
� This is due to regeneration of the photochemical pigment particularly
rhodopsin.
� It is demonstrated by marked decrease in the visual threshold.

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EYE BALL CHAPTER 3

� This increased retinal sensitivity can be demonstrated in a person

while present in the dark, after being exposed to bright light and the
results are presented as dark adaptationcurve.
� From the curve it is noticed that the decrease in the visual threshold
is not continuous but divided into 2 parts:
a) During the first 5 minutes: There is rapid but small drop in the
visual threshold, this is due to dark adaptation of cones.
b) Following the rapid small drop, the visual threshold shows slower
but much greater drop which become almost stable after 30
minutes, this is due to dark adaptation of rods.

Light adaptation

� This occurs when the person shifts suddenly from dim lighted or dark
place to bright one.
� At first, the light seems intensely bright accompanied with
uncomfortable sensation and temporarily the person becomes blind

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EYE BALL CHAPTER 3

(Since all objects in the visual field appear white due to much
breakdown of rhodopsin and iodopsin).
� However, within 5 minutes,this sensation disappears (because after
this time the eyes adapt to bright light). So, sharp vision returns, and
the details of objects and their colors will be clearly seen.
Changesoccurring during light adaptation:

The process of light adaptation is much more rapid taking only about 5
minutes.
1) Pupilloconstriction:
This reduces the amount of light that enters the eyes�thus
decreasing the excessive stimulation of the retina �which helps the
rapid return of acute vision.
2) Bleaching of rhodopsin and iodopsin:
So, the amounts of these photochemical pigments are markedly
decreased.
3) Decreasedretinal sensitivity:
Due to reduction of the photochemical pigments in rods and cones.

BIOCHEMISTRY OF THE EYE

Vitamin A
Anti-night blindnessvitamin
I-Structure& Forms:
1-Vitamin A is derived from carotenesi.e. carotenes are provitamin A.
Carotenes are unsaturated hydrocarbon, photosynthetic pigments that are
synthesized by plants and cannot be made by animals.
2- Carotenes are responsible for the orange colour of carrots and many
other fruits & vegetables.

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EYE BALL CHAPTER 3

3- There are many types of carotenes: α, β, γ, δ, and ε all of them contain

2 iononerings(β ionone & another ionone that differ from type to type,
e.g. β carotene has 2 β ionone rings)

Different forms of carotenes

� There are 4 forms of vitamin A:

1- Retinol.2- Retinal.
3- Retinoic acid.
4- Retinyl esters
N.B. All forms of vitamin A are absorbed in the form of retinol.
1-Retinol:
- It is a primary alcohol containing β-ionone ring.
- The side chain has four double bonds.
- Present in animal tissues as retinyl ester with long chain fatty acids.

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EYE BALL CHAPTER 3

2-Retinal:
-This is an aldehyde form obtained by the oxidation of retinol.
-Retinal and retinol are interconvertible.

3- Retinoic acid:
-This is produced by the oxidation of retinal

- Retinoic acid can`t give rise to retinal or retinol.

4-Retinyl ester:
- When a fatty acyl group is esterified to the hydroxyl terminus of
retinol, a storage form of retinol, the retinyl ester,is formed.

- 88 -
EYE BALL CHAPTER 3

- The most abundant retinyl esters present in the body are those of
palmitic acid, oleic acid, stearic acid, and linoleic acid
II-Sources of vitamin A:
vitamin C is present in a variety of plant & animal sources.
1-Plants source:
All pigmentedvegetablesand fruits as potatoes, carrots, tomatoes and
leafy green vegetables.
2-Animals source:
Liver, milk, fish, butter, eggs and Cod liver.
III- Requirements:
*Recommendeddaily allowance (RDA):
- Children: 300-400 ug/d.
- Adult: 600 ug/d
- Pregnancy: 770 ug/d.
IV-Release & mechanismof action:
1- Vitamin A is released from the liver as retinol (Zn is essential for
retinol metabolism).
2- Retinol is transported in the circulation by the retinol bindingprotein
(RBP) as one molecule of RBP binds one molecule of retinol
3- The retinol-RBP complex binds to specific receptors on the cell
membrane of peripheral tissue and enters the cells.
4- Many cells of target tissues contain a cellular retinol-bindingprotein
(CRBP) that carries retinol to the nucleus and binds to the chromatin
(DNA).
5- Retinol exerts its function in a manner to that of a steroidhormone.
6- Retinoic acid is mainly transported in the blood by binding to
albumin.

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EYE BALL CHAPTER 3

NB: Possibleroutes of vitamin A transfer to cornea & conjunctiva:

- Migration of RBP from blood capillaries in limbus region
- Direct uptake of Vitamin A from tear fluid
- Transfer of Vitamin A from aqueous humour.
- In tears: concentration of retinol is 0.1 umol/L
- In aqueous: retinol barely detectable.
1-Vitamin A & vision:
a- Light falling on retina absorbed by photoreceptors.
b- Photochemical changes in outer segments of photoreceptors initiate
electrical changes.
c- The retina of the eye has two types of cells: rodsand cones.
d- The rods are in the periphery and they are responsible for the dim
light vision, while cones are at the center of retina and they are
responsible for the day vision.
e- Rhodopsinis a conjugated protein present in rods, it contains 11-
cis-retinal & the protein opsin.
(The aldehyde group of retinal is linked to ε –amino group of
lysine of opsin).
f- When light falls on retina, 11-cis-retinal,it is soon isomerized into
all-trans-retinal.
g- All trans-retinal is converted to all trans-retinol by alcohol
dehydrogenase enzyme.
h- All-trans retinol undergoes isomerization into 11-cis retinol
which is oxidized to 11-cisretinal again to participate in the visual
cycle.

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EYE BALL CHAPTER 3

The following figure illustrate the visual cycle:

2- Vitamin A is essentialfor healthy epithelial tissue:

- Synthesis of Goblet cells in epithelial tissues that secrete mucous
containing antimicrobial components.
NB: Vitamin A & Age-related macular degeneration(AMD):
- Adequate dietary intake of vitamin A helps protect against certain
eye diseases, such as age-related macular degeneration (AMD).
- Studies show that higher blood levels of beta-carotene & alpha-
carotene may reduce your risk of AMD by up to 25%
- This risk reduction is linked to carotenoid nutrients’ protection of
macular tissue by lowering levels of oxidative stress.

VI-Deficiency:
1-Night blindness(The inability to seein dim light):
a- First night vision is influenced and day vision is less influenced
b- Regeneration of active rhodopsin requires opsinand 11-cis-retinal.

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EYE BALL CHAPTER 3

NB: (The regeneration of 11-cis-retinal occurs via chemical

transformations called "the visual cycle" & without adequate amounts of
retinal, regeneration of rhodopsin is incomplete and night blindness
occurs).
2- Xerophthalmia (Dry eye):
-Pathologic dryness of the conjunctiva and cornea. The conjunctiva
becomes dry, thick and wrinkled.
-If untreated it leads to corneal ulceration and ultimately to blindness as a
result of corneal damage.
N.B.: Bitot`s spotsare buildup of keratin located superficially in the
conjunctiva, which are oval, triangular or irregular in shape.

Bitot`s Spots

3- Keratomalacia:

-If xerophthalmia persists for a long time, it progresses to

keratomalaciai.e. softening of cornea & degeneration of corneal
epithelium which gets vascularized. Later, corneal opacities develop
bacterial infections leading to corneal ulceration, perforation of cornea
&blindness.

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EYE BALL CHAPTER 3

Keratomalecia

4-Effect on epithelial cells:

-The skin becomes rough and dry.
-Keratinization of epithelial cells of GIT, urinary tract and respiratory
tract with increased incidence of secondary bacterial infection.
Vitamin C
(Ascorbic acid)
I-Structure& Forms:
1-Chemically it is known as ascorbic acid (C6H8O6), It is a water-soluble
vitamin which is a hexose derivative that closely resembles
monosaccharides in structure.
2- Vitamin C existsin two forms:
a- L-ascorbic acid (reduced form) 90%.
b- L-dehydro-ascorbic acid (oxidized form) 10%.
3-On dehydration,dehydroascorbic acid is irreversibly converted to 2,3-
diketogulonic acid which is inactive.

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EYE BALL CHAPTER 3

4- Vitamin C is a good reducing agent; it is lost under oxidizing

conditions like aeration and heating. Thus, many cookedand canned
foods contain little ascorbic acid.
6- Vitamin C is found concentrated in certain parts of human body such
as brain and the white blood cells.

Properties:
• Readily oxidized (in presence of copper and iron), it is for this reason
that the foods cooked in copper utensils lose ascorbic acid
quickly.•Rapidly destroyed by alkalies
• Fairly stable in weak acid solutions
• Drying and storage (loss of vit c)
• Oxidizable in nature (powerful reducing agent)
III-Sources:
1-Plant source:
- Fruits: especially citrus fruits (lemon, orange), melon, tomatoes and
strawberry, guava.
- Vegetables: potatoes, raw cabbage and green peppers.

2-Animal source:
Vitamin C is mostly present in the liver and least present in the muscle.
V-Functions
1-Ascorbic acid is a cofactor for several enzymatic hydroxylation
reactions:
a- Participating in the post-translational hydroxylation of collagen.
b- In the biosynthesis of carnitine.
c- In the conversion of the neurotransmitter dopamine to
norepinephrine.
d- In peptide amidation and in tyrosine metabolism.

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EYE BALL CHAPTER 3

2-Vitamin C is an important regulator of iron uptake, it reduces ferric

Fe3+ to ferrous Fe2+ ions, thus promoting dietary non-haem iron
absorption from the gastrointestinal tract, and stabilizes iron-binding
proteins.
3-Vitamin C is a potent reducing agent and scavenger of free radicals in
biological systems.
4-It acts as a scavenger for oxidizing free radicals and harmful oxygen-
derived species (antioxidant), such as the hydroxyl radical, hydrogen
peroxide, and singlet oxygen.
Vitamin C has two primary actions:
a- First, vitamin C reacts with and inactivates free radicals in the
water-soluble compartments of the body, as in the cytosol,
plasma, and extracellular fluid.
b- Second, and vitamin C regenerates oxidized vitamin E.
5-It also inhibits the excess production of melanin which leads to a tan
and hyperpigmentation.

VI-Deficiency of Vitamin C
SCURVY is the deficiency disease of vitamin C.
Prolonged deprivation of vitamin C (Deficient diet for 20-40 days)
generates defects in the post-translational modification of collagen that
cause scurvy. The main defect is poor deposition of intercellular cement
substance (i.e. collagen). The capillaries are fragile and so there is
tendency to hemorrhage. Wound healing is delayed due to deficiency in
the formation of collagen.
Sign & symptoms:
1- Fragile blood vessels, swollen joint, delayed wound healing and
anemia.
2- Fatigue, pinpoint hemorrhages

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EYE BALL CHAPTER 3

3- Sicca” syndrome (the “sicca” syndrome of Sjögren, which is

usually associated with collagen disorders and includes xerostomia,
keratoconjunctivitissicca, and enlargement of the salivary glands)
� Other Ocular manifestations of vitamins c deficiency.
1.Orbital hemorrhage.
2.Conjunctival and palpebral haemorrage.
3.Keratoconjunctivitis.
4.Cataract.
5.Retinal hemorrhage.

DISEASES OF THE EYE BALL

The Cornea & Sclera
Corneal ulcer
Ulceration of the cornea is a common condition that affects the cornea.
It may be infective or non-infective, central or peripheral.
Infective keratitis is caused by bacterial, viral, fungal or parasitic
infection.
T h e p a t i e n t wi l l b e p r e s e n t e d b y pain, phtophobia, lacrimation
&blepharospasm.

SIGNS OF BACTERIAL CORNEAL ULCER:

1. Oedema of the lids.
2. Ciliary injection of conjunctiva.
3. The cornea shows:
oLoss of luster.
oGreyish infiltration &ulceration.
oPositive fluoreceine test.
4. The anterior chamber: show the hypopyon, so the ulcer is called
(hypopion ulcer). (Hypo=down, pyon=pus).

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EYE BALL CHAPTER 3

1. The iris: is inflamed (secondary iritis) and the pupil is constricted.

Posterior synechiae are common.

SIGNS OF VIRAL (DRNDERETIC) CORNEAL ULCER

1- The conjunctiva shows catarrhal conjunctivitis in the first few days
with influenza before corneal signs
2- The vesicles affect the cornea and occur in groups.
3-They may rupture &coalesce→crenated ulcer.
4- Branches originate from the central ulcer. They rebranch and finally
these branches end in knobs. This picture resembles a tree hence the
name dendritic.
5- The following features are diagnostic:
a) The dendritic appearance.
b) The long course with tendency
to recurrence.
c) The ulcer is superficial and
never perforate.
d) Never become vascularized.
e) Hyposthesia of the affected part
of the cornea.
SIGNS OF FUNGAL KEARATITIS

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EYE BALL CHAPTER 3

• Usually follows trauma by organic material as wood, plant leaves,

and candida is common in
immune compromised patients.
• Thick area of stromal infiltration
• Presence of satellite lesion
• Epithelial defect is smaller than
stromal infiltration
• Atypical hypopion (pyramidal
shape)
• Resistant to antibiotic therapy

SIGNS OFACANTHAMOEBA (PARASITIC) KERATITIS

Common among contact lens wearers especially if bad hygiene is
present.
Characterized by:
Severe pain out of proportion to clinical signs, due to irritation of corneal
nerve endings.
Positive history of contact lens wear with bad hygiene.
Negative culture for bacteria or fungi. Not responding to traditional
measures

The Retina
Central retinal artery Occlusion
o Occlusion of the central retinal artery which is an end artery leads to

sudden painless loss of vision.

Etiology
1.Thrombosis:

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EYE BALL CHAPTER 3

a. Common in older age particularly in patients with diabetes

hypertension and arteriosclerosis.
b. Following trauma: blunt trauma or surgical trauma
2.Embolism:
a. Form large arteries as atheromatous lesion of the carotids.
b. From the heart due to vegetations on the heart valves as in subacute
bacterial endocarditis.
3.Spasm:usually transient as in
migraine and Reynaud’s disease.
Clinical picture
The patient is presented by sudden
painless loss of vision (no PL)
Signs
1.Pupil: dilated non-reactive to direct light but react consensually
2.Fundus picture:
a. Attenuated thread like arteries with segmentation of blood column
inside the vessels (cattle truck appearance).
b. Milky white fundus due to coagulative necrosis of the ganglion
cell layer obscuring the underlying choroidal reflex.
c. Cherry red spot at the fovea due to bright red reflex of the choroid
seen through the thin retina at the fovea.
Central Retinal Vein Occlusion
Etiology
1.Diseased (sclerotic) vessels in old age as in diabetes, hypertension and
arteriosclerosis
2.Inflammatory condition of the retinal vessels which is more common
in young age as infective periphlebitis (typhoid fever) and in some
autoimmune diseases as Behcet’s disease (occlusive vacuities).

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EYE BALL CHAPTER 3

3.Intravascular abnormalities: blood stasis with increased

coagulability as in severe dehydration and polycythaemia.
4.Extravascular causes: pressure on the vein by orbital tumour
orinflammation orbital cellulites
Symptoms
o Rapid painless diminution

of vision usually
discovered in the morning
(venous stasis during
sleep)
o Visual acuity varies from

mild to severe visual loss

depending on type of
occlusion (ischemic or non-ischemic) and degree of macular edema
and macular hemorrhage
Signs
o Sluggish pupillary reaction

o Fundus picture

1. Ischemic CRVO: occlusion occurs anterior to lamina

cribrosa (no collateral circulation) leading to marked fundus
changes
a. Dilated and tortuous retinal veins due to severe engorgement
b. Extensive retinal hemorrhages and soft exudates
c. Diffuse macular edema with cystoid pattern in some cases
d. Optic disc edema (papilledema)
2. Non-Ischemic CRVO: occlusion occurs posterior to
lamina cribrosa with collateral circulation reducing the risk of
ischemia with moderate fundus changes

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EYE BALL CHAPTER 3

a. Dilated and tortuous retinal veins

b. Mild to moderate retinal hemorrhages
c. Macular edema and papilledema
1.Laser photocoagulation: argon laser treatment
For macular edema or neovascularization
2.Treatment of secondary glaucoma:
MICROBIOLOGY OF THE EYE
Aspergillus
Disease: Aspergillus species, especially Aspergillusfumigatus, cause
infection of the skin, eyes, ears, lung and cause allergic
bronchopulmonaryaspergillosis(ABPA).
Morphology: Aspergillusexists only in the filamentous form. They have
septatehyphaethat form V-shape branches. The conidia form
radiating chains.
Distribution: A.fumigatusis cosmopolitan and found almost everywhere.
It is an important pathogen of humans and animals.
Transmission:occurs by airborne conidia.
Pathogenesis& Clinical Findings:
� Invasive aspergillosis: in immunocompromised persons, A.
fumigatus can colonize and later invade abraded skin, wound,
burns, cornea, ears and paranasal sinuses. It can invade the lungs
and other organs producing hemoptysis and granulomas.
� Aspergillomaor fungusball: when it grows in lung cavities (due
to tuberculosis) or sinuses.
� Allergic bronchopulmonaryaspergillosis(ABPA):is an infection
of the bronchi by Aspergillus spp. Patients has asthmatic symptoms
and elevated IgEtitre.

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EYE BALL CHAPTER 3

� Aspergillusflavus:growson cereals or nuts and produces aflatoxin

which is carcinogenic and hepatotoxic.
Laboratory diagnosis:
1- Specimens:Biopsy.
2- Direct microscopicexamination:shows septate, branching
hyphae invading tissue.
3- Culture on SDA:
- Surface:yellow to green, brown, or black, depending on
species. Texture is cottony.
- Reverse:White to brown
4- Colonyidentification:staining with lactophenol cotton blue
shows radiating chains of conidia.
5- Serologicaltests:showshigh levels of IgE in patients with ABPA.

Conidial head of Aspergillusbylactophenol cotton blue.

By:http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Hyphomy
cetes_(hyaline)/Aspergillus/flavus.htm

Immunity against eye infections

The innate immune system:
1- 1st line of natural defense:(at portal of entry)
A. Physical barriers:
Intact epithelial surfaces
Tears and blinking reflex.

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EYE BALL CHAPTER 3

B. Chemical barriers:
Microbicidal action of secreted molecules:
� Lysozymes;basic proteins present in the skin, tears, dissolve
bacterial cell wall.
A. Biologicalbarrier: (normal bacterial flora)which are permanent
residents of certain body sites and suppress the growth of many
pathogenic bacteria and fungi
B. 2ndline of natural defense:
If the invading organism overcomes the defenses at the portal of entry
and enters the tissues, it will meet the followings:
A. Circulating effector cells:(see chapter 1)
� Phagocytes: Polymorphonuclear leucocytes
(neutrophils) & Mononuclear phagocytes (monocytes in
the blood and macrophages in the tissues)
� N.B: Macrophages typically respond to microbes
nearly as rapidly as neutrophils do, but
macrophages survive much longer at the site of
inflammation.
� Natural killer (NK) cells: they are large granular
lymphocytes
� Dendritic cells: They play important roles in innate
responses to infections and in linking innate and adaptive
immune responses.

Pharmacology of the eye

Ocular dosageforms and routes of drug administration
Dosageforms of ocular drugs:
- Solution.
- Suspension.

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EYE BALL CHAPTER 3

- Ointment contain mineral oil or petroleum base (antibiotic,

cycloplegic, miotic delivery).
- Gel (pilocarpine 4% gel).
- Solid inserts (gancyclovirintravitreal implant).
- Soft contact lenses.
- Collagen shields.
Routes of drug administration and side effects of their use:
- Topical(convenient, economic and relatively safe).
Bad compliance and systemic adverse effects from
nasolacrimal absorption.
- Subconjunctival, sub-Tenon,andretrobulbar injections
Optic nerve trauma.
Ocular muscle trauma.
Globe perforation.
- Intraocular (intracameral) injections
Intraocular toxicity.
- Intravitreal injection or device
Retinal toxicity.

Drugs affecting the size of pupil

I-Miotics
A)Parasympathomimetics:
Direct
- Choline esters:
Carbacol&bethanechol.
- Cholinomimetic alkaloids:
Pilocarpine 1-2% (frequent application).

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EYE BALL CHAPTER 3

Indirect
- Revisable:
Physostigmine&demicarium.
- Irreversible:
Ecothiophate.
B)Sympathetic depressants:
Guanthidine
- It causes passive miosis& decreases I.O.P.
- Used in glaucoma & thyrotoxicosis.
C)Morphine (central effect):
- Miosis (pinpoint pupil) due to stimulation of
- ocluomotor nerve nucleus.
II-Mydriatics
A) Sympathomimetics:
Direct
Phenylephrine
Indirect
Amphetamine & hydroxyamphetamine
Dual
Ephedrine
B) Parasympatholytics:
Natural belladonna alkaloids:
- Atropine &hyoscine.
Synthetic atropine substitute:
- Homatropine, cyclopentolate&tropicamide (cycloplasia)
- Eucatropine (no cycloplagia)
C) Cocaine:
Surface anesthesia:Loss of corneal &conjunctival reflexes (not used
clinically)
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EYE BALL CHAPTER 3

Indirect sympathomimetic:Inhibitsneuronal reuptake 1 & MAO leading

to increase endogenous catecholamines, active mydriasis and
deconjestion.
D) Ganglion blockers:
They block ciliary gangliondecrease parasympathetic
atropine like (passive mydriasis, cycloplagia& increase I.O.P).
Parasympathomimetics Sympathomimetics Parasympatholytics
Action on the eye: Blocking of M receptors
Stimulation of M receptors Stim.of α1 receptors -Constrictor pupillae
-Constrictor pupillae -Dilatorpupillae Passive mydriasis
Miosis&widening of angle of Active mydriasis no Narrowing of angel
filtration loss of light reflex) -Cycloplagia
-Ciliary muscle Loss of accomodation
Accommodation for near Closure of canal of
vision & opening of canal of schlem.
schlem. -Lacrimal gland
-Lacrimal gland Decrease lacrimation
Increased lacrimation -Blood vessles -Blood vessles
-Blood vessles V.C, decongestion No effect
Conjunctival V.D &decrease I.O.P
Uses
1-glucoma Fundus examination Atropine: iritis&corneal
2-counteract mydriatics specially in elderly ulcer
3-cut recent adhesions between patients liable for Synthetic atropine
iris and lens(in alternation with glaucoma. substitutes (fundus
mydriatics). examination).

N.B Cycloplegic effect is used in

�� Treatment of iridocyclitis.

�� Measurement of errors of refraction.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

THE EXTRAOCULAR MUSCLES

Uniocular motility
elevation, depression, abduction (lateral rotation)
, adduction (medial rotation), extortion (external
rotation, intortion (internal rotation)

Each eye has six extraocular muscles, four recti and two oblique muscles.
The four rectus muscles have common origins posteriorly from the
annulus of Zinn and they insert anteriorly into the sclera some millimeters
from the corneoscleral limbus.
The oblique muscles: originate anteriorly and insert posteriorly. So when
they contract they pull the insertion point forwards.
��Trochlea is the functional origin of the superior oblique.
��The anteromedial aspect of the floor of the orbit is the functional and
anatomical origin of the inferior oblique.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

EXTRINSIC MUSCLES

� RECTI MUSCLES
Origin:
��The 4 recti arise from:
��The common tendinous ring, which surrounds the upper, medial
and lower margins of the optic canal.
��Medial part of the superior orbital fissure
Insertion :
��The muscles pass forwards and widen to form a cone around the
eye ball.
��They are inserted into the sclera in front the coronal equator of the
eye ball at about 6 mm from the limbus (corneoscleral junction).
Nerve supply:
��The superior rectus is supplied by the superior division of
oculomotor nerve .
��The inferior & medial recti are supplied by the inferior division of
oculomotor nerve .
��The lateral rectus is supplied by the abducent nerve.
Action:
��Superior rectus directs the pupil upwards and medially. (elevation ,
adduction and intorsion)
��Inferior rectus directs the pupil downwards and medially .
(depression, adduction, extortion)
��Lateral rectus directs the pupil laterally (abduction)
��Medial rectus directs the pupil medially. (Adduction)

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� OBLIQUE MUSCLES
Superior oblique muscle
Origin:
��From the roof of the orbit, just infront of the optic canal, medial to
the levator palpebrae superioris.
Insertion:
��The muscle runs forwards at the junction between the medial wall
and the roof of the orbit
��Its tendon passes through the trochlea which is a fibrous pulley
attached to the frontal bone.
��At that point the muscle changes direction and runs backwards and
laterally
��It is inserted into the sclera behind the coronal equator of the
eyeball beneath the superior rectus.
Nerve supply:
��Trochlear nerve.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

Action:
��Directs the pupil downwards and laterally. (intortion, depression
and abduction)
��Simultaneous contraction with the inferior rectus moves the
eyeball directly downwards
Inferior oblique muscle
Origin:
��From the floor of the orbit (maxilla) close to the nasolacrimal
duct.
Insertion:
� The muscle runs laterally, backwards and upwards and lies
transversely on the floor of the orbit below the inferior rectus.
� It is inserted into the sclera behind the equator of the eyeball close
to the insertion of the superior oblique.
Nerve supply:
��Inferior division of oculomotor nerve.
Action:
� Directs the pupil upwards and laterally. (extortion, elevation and
abduction).
� Simultaneous contraction with the superior rectus moves the eye
ball directly upwards.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

� Levator palpebrae superioris

Origin:
��From the roof of the orbit just above and in front of the optic
canal.
Insertion:
��It widens as it passes forward
��It ends anteriorly by 2lamellae.
��Superiorlamella ; is inserted into :
��Anterior surface of the superior tarsal plate
��Skin of the upper eyelid.
� Inferior lamella ; is inserted into :
��Upper margin of the superior tarsal plate
��Superior fornix of conjunctiva.

Nerve supply:
��Superior division of oculomotor nerve.
��The inferior lamella contains smooth muscle fibers which are
supplied by sympathetic fibres from the superior cervical
sympathetic ganglion.
Action:
��Elevation of the upper eyelid and superior fornix of the
conjunctiva.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

��In stress conditions (sympathetic overstimulation) the upper eyelid

is strongly elevated and the palpebral fissure is widened due to
contraction of the smooth muscle fibers in the levator palpebrae
superioris

The extraocular muscleshave special properties such as

o They have very rich nerve supply e.g. the lateral rectus has special

cranial nerve that supplies the lateral rectus only.

o They have very rich blood supply.

��They have more elastic fibers than the other striated

muscles so that muscle contractions and relaxations
are smooth.
��They do not show signs of fatigue although they are
voluntary striated muscles. That is because only one
tenth of the muscle fibers is in action and the other
nine tenths are at rest.

Physiology of Binocular vision

Definition:

It is the ability of using both eyesin seeing one object; it is the

phenomena of seeing an object with the two eyes in the same time.

Requirement of binocular vision:

1- Considerable overlapping of both visual fields.

Objects placed in the overlapping areas are seen in the retinae of
both eyes.
Such overlap is most apparentin man and monkeybecause their
eyes are placed in front of head.
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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

In rabbits,the overlapping areas are very small because their eyes

are placed laterally in the head.
So, vision in rabbits and similar animals is mostly monocular.
The monocularfield of visionin man composed of crescentic area
at outer half of both temporal fields. Light rays from objects placed
in this region fall upon nasal half of the retina of the reader eye but
not on temporal half of retina of other eye.
2- The refractive power of both eyesmust be nearly equal.
3- The extraocular muscles and their innervations must be normal to
move eyeball so that both images of objects fall on corresponding
pointsof both retinae.
4- Intact visual cortex��since fusion of images occursin area 17:
� For fusion to occur:
a) The two imagesmust fall on the corresponding points.
These corresponding points are located in the nasal half of one
retina and the temporal half of the other.
The fovea centralis on both sides are also corresponding points.
b) The ocular musclesshould be coordinated:
If the coordination of ocular muscles is deficient ��this leads to
diplopia (double vision), because the images in the displaced
eye do not fall on corresponding points.
Advantages of binocular vision:

1- It givescompensationforweakeye��(i.e. if there is optical defect in

one eye, it will be compensated by the healthy one).
2- It provokesmore accurate perception of depth �(i.e. distance of
objects from the eyes) than that provided by single eye.
3- It is important for stereoscopicvision.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

4- Pathological changes in one retina are masked by activity of

other healthy retina.

Errors of refraction
Ammetropic Eye
The normal eye is called emmetropic eye in which; with accommodation
at rest, parallel rays are not focused on the retina.
If the rays don’t focus on the retina, this condition is called ametropia. Or
error of refraction. This includes: Myopia, Hypermetropia, Astigmatism,
Aphakia, anisometropia, and presbyopia
M yopia (Short or Near Sightedness)
It is the condition of refraction in which with accommodation at rest
parallel rays of light come to focus in front of the retina.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

Aetiology:
1.Axial: increase diameter of the eye (large globe) the commonest
type.
2.Curvature: increase corneal curvature and power (refractive).
3.Index: increase refractive index of the lens or AC.
4.Pathological: keratoconus, lenticonus, Diabetes, senile lens sclerosis,
iritis.
Hypermetropia (Long or Far Sightedness)

It is the condition of refraction in which with accommodation at rest

parallel rays of light come to focus behind the retina

Etiology:
1.Axial: decrease diameter of the eye (small globe) is the commonest
cause.
2.Curvature: decrease corneal curvature or lens curvature and decrease
corneal power
3.Index: decrease refractive index of the lens or AC.
4.Pathological: microphthalmos, cornea plana, retinal detachment etc.
Presbyopia (Senile Hyperopia)
o It is physilogical process in which the near point of distinct vision is

recessed beyond the normal reading or working distance with

relaxed accommodation.
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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

Age of Onset: Error of refraction: Emmetropes at 40years earlier in

hyperopes and later in myopes.
Preferred working distance.
Aetiology: Accommodation Failure due to weakness of ciliary muscle
and sclerosis of lens fibers.
Astigmatism(A=not, Stigma=point)
Astigmatism is an uneven or irregular curvature of the cornea or lens, It is
the condition of refraction in which with accomodation at rest parallel
rays of light do not form a point image on the retina (form 2 focal lines
separated by interval).

Etiology
Most commonly, astigmatism occurs because the cornea is oval or egg-
shaped, along with an irregularly shaped lens, this causes, light rays
entering the astigmatic eye to scatter instead of focusing to a single focal
point on the retina -- some rays fall on the retina while others focus in
front of or behind it. Most people have some degree of astigmatism,
which is usually present at birth and is believed to be hereditary. It can
also result from injury or conditions such as keratoconus. Astigmatism
tends to occur with other refractive disorders e.g. about half of those with
myopia (nearsightedness) are also astigmatic.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

Strabismus & Amblyopia

Strabismus is simply an ocular deviation. It can be defined as an
extraocular muscle imbalance, dysfunction or disturbance so that the two
visual axes do not intersect at the object of regard. Normally the two
visual axes are directed to the object of regard and so they should meet at
the site of that object. If they do not meet there, strabismus exists.

Classification of Strabismus
Strabismus may be:
1. True or
2. Apparent. Apparent strabismus is simply a false or pseudo
strabismus. Pseudo strabismus may be due to epicanthus, wide
interpupillary distance or high errors of refraction.
True strabismus may be:
1. Manifest or
2. Latent.
Manifest strabismus may be:
1. Concomitant (where the angle of deviation is equal in all directions
of gaze) or
2. Incomitant (where the angle of deviation is not equal in all
directions of gaze) as in cases of paretic or restrictive strabismus.
Concomitant strabismus may be:
1. Accommodative,
2. Nonaccommodative or
3. Partially accommodative.
Accommodative strabismus may be:
1. Refractive
2. Non refractive

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3. Mixed

Heterophoria (Latent Strabismus)

Definition: Tendency of one or both eyes to deviate but this tendency is
controlled by the fusional reflexes to maintain binocular single vision and
to avoid diplopia. When one eye deviates, the images of the object of
regard are not formed on corresponding retinal points.
At this situation the visual cortex will not be able to fuse or blend the two
images and so the object is seen double. This diplopia stimulates the
fusional reflexes to readjust the extraocular muscle tone to keep the visual
axes directed to the object of regard to maintain binocular single vision
and eliminate diplopia.
If one eye is covered, diplopia will not be perceived if the covered eye
deviates.
Types of heterophoria:
o Esophoria; a latent tendency of visual axis to deviate inwards i.e.

toward the nose.

o Exophoria;a latent tendency of the visual axis to deviate outwards i.e.

away from the midline.

o Hyperphoria; a latent vertical deviation in which the visual axis of

one eye tends to deviate upwards as compared with that of the other
eye.
o Hypophoria;a latent tendency of the visual axis of one eye to deviate

downwards as compared with that of the other eye.

o Cyclophoria;a latent tendency of the vertical meridian of one eye to

wheel-rotate inwards (incyclophoria) or outwards (excyclophoria) from

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the vertical position. Cyclophoria is usually associated with hyper and

hypophoria.
Manifest Strabismus(Heterotropia)
1. Paralytic strabismus
If the ocular deviation is due to paralysis (complete loss of movement) or
paresis (partial loss of movement) of one or more of the extraocular
muscles, it is called paralytic or incomitant strabismus. Incomitance
means that the angle of deviation is not the same in all directions of gaze.
The deviation increases in the direction of action of the affected muscle
and decreases in the direction of action of its antagonist.
Etiology
It is due a lesion anywhere between the nuclei of the third, fourth and
sixth cranial nerves and the muscles themselves.
Symptoms
1.Binocular diplopia.
2.Deviation of one eye and the deviation increases in certain direction.
3.Vertigo, nausea and uncertain gait. So these symptoms are due to
diplopia.
4.Abnormal head posture:This posture is adopted to avoid diplopia.
Abnormal head posture is simply moving the head instead of the
eye. When the right lateral rectus is paralyzed, the right eye cannot
move to the right, so the head is turned to the right. Abnormal head
posture may be horizontal (in the form of face turn to the right or to
the left), vertical (in the form of chin elevation or depression) or
torsional (in the form of head tilt to the right shoulder or to the left
one).
5.Past pointing; the patient does not see objects in their correct
locations and so he cannot point to them correctly e.g. the patient

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complains that he cannot catch a pen on the desk, he might put his
hand in front, behind or beside the pen.
Signs:
All signsof paralytic squint occur in direction of action of paralyzed
muscle except for the ocular deviation
1. Deviation of one eye; misalignment is obvious in one direction
and less obvious in another direction. This is called incomitant
strabismus.

Right esotropia in right 6th nerve (lateral rectus) palsy

2. Limitation of ocular movement; limitation is seen in the

direction of action of the affected muscle i.e. limitation of
abduction in cases of lateral rectus palsy.
3. The secondary angle of deviation is greater than the
primary angle of deviation. The primary angle is the deviation
elicited when the patient fixes with the sound normal eye and
the secondary angle is the deviation elicited when the patient
fixes with the affected eye. Considering Hering’s law explains
this fact.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

4. Compensatoryhead posture; in the form of face turn, chin

elevation or depression or in the form of head tilt to one
shoulder.

Head tilt to the left shoulder in right superior oblique muscle palsy

5. Falseprojection;the paralyzed eye does not see objects in their

correct location. False projection can be demonstrated by asking
the patient to close his sound eye and telling him to point
quickly to an object in front of him. The finger will be directed
to one side of the object depending on the direction of the main
action of the affected muscle.

2. Concomitant strabismus
It is a type of strabismus where the angle of deviation is constant in all
directions of gaze. Concomitant strabismus may be accommodative, non-
accommodative or partially accommodative.
2.a. Accommodative strabismus
It is a type of concomitant strabismus that is
caused by accommodation and corrected by
glasses.

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STRABISMUS & ERROR OF REFRACTION CHAPTER 4

Accommodative esotropia (above) corrected with glasses(below).

2.b. Non accommodative concomitant strabismus

It is a type of concomitant strabismus not related to accommodation and

so not corrected by glasses.

Strabismic Amblyopia
Amblyopia (lazy eye) denotes diminished visual acuity due to
impairment of foveal vision without demonstrable clinical or structural
anomaly of the eye or the visual pathway. Strabismic amblyopia denotes
reduced foveal vision as a result of manifest deviation in one eye.
Amblyopia develops easier in younger children and also can be corrected
easily in the younger ages. As the child is getting older, amblyopia
develops with difficulty and at the same time is corrected with difficulty.
That is why early development of strabismus (in infants) leads to deeper
amblyopia than that which develops as a result of deviations starting in
older children.
Strabismic amblyopia can be corrected by means of what is called
occlusion therapy of the sound “non amblyopic” eye.

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