Ophthalmology Script ; Jan 2025

*anatomy and structures are better explained in the book “anatomy of dental medicine”
https://archive.org/details/schuenke-michael-anatomy-for-dental-medicine/page/228/mode/2up page 228
and on*

Simplified Eye Anatomy: Layers and Key Components

The human eye is a complex organ designed to focus light, enabling vision. It is structured in layers and
contains key components that work together to process visual information. Here’s an easy-to-understand
breakdown:

Outer Layer: Protection and Focus

1)Cornea:Transparent, dome-shaped front layer of the eye, acts like a window to bend (refract) light into
the eye. No blood vessels but rich in nerves, making it highly sensitive.

2)Sclera:The white, tough outer layer that provides shape and protection, connected to muscles that
move the eye.

Middle Layer: Nourishment and Focus Adjustment

1)Iris: The colored part of the eye, controls the amount of light entering the eye by adjusting the size of
the pupil (the central black opening).

2)Lens:A transparent, flexible structure located behind the iris. changes shape to focus light on the retina
(a process called accommodation).

3)Ciliary Body:Produces aqueous humor (a fluid that nourishes the eye), contains muscles that adjust the
lens shape for focusing.

4)Choroid:A layer between the sclera and retina, rich in blood vessels. Provides oxygen and nutrients to
the retina and other parts of the eye.

Inner Layer: Light Detection and Vision Processing

1)Retina:The innermost layer, made up of light-sensitive cells (photoreceptors).

Rods: Detect dim light and black-and-white vision.
Cones: Detect bright light and color vision.
Converts light into electrical signals sent to the brain via the optic nerve.

2)Macula and Fovea:The macula is the central part of the retina responsible for sharp, detailed vision.
The fovea, at the center of the macula, provides the clearest vision.

Additional Structures

1)Aqueous Humor:Clear fluid in the front of the eye

(anterior chamber). Maintains pressure and
nourishes the cornea and lens.

2)Vitreous Humor:A gel-like substance in the back

of the eye (vitreous chamber). Helps maintain the
eye's shape and allows light to pass to the retina.
3)Optic Nerve: Transmits signals from the retina to the brain, where they are processed into images.

Neurophthalmology:
Features of color vision-
a function of cones, our eyes perceive color with wavelength of light between 400-700nm
below 400nm is ultraviolet and above 720nm is infrared.

Trichromatic theory -
3 types of cones with 3 different photopigments.
each cone is maximally sensitive to one particular color.

Color vision disorders -

1)Congenital: inherited conditions present from birth, typically caused by genetic mutations affecting the
photoreceptor cells in the retina, such as in red-green color blindness.

2)Acquired: develop later in life due to factors like diseases, medications, aging, or damage to the eye or
optic nerve, often resulting in changes to or loss of color perception.

3)Dichromats: individuals with a type of color vision deficiency where one of the three types of cone cells
in the retina is absent or nonfunctional, resulting in the inability to perceive certain colors. There are three
types: protanopia (red cone are absent, difficulty distinguishing red and green), deuteranopia (green cone
are absent, affecting red-green), tritanopia (blue cone are absent, difficulty distinguishing blue and yellow)

4)Monochromates: people that have only one cone system, they can see black, white and grey shades.

Color vision tests -

1)Anameloscops: a specialized device used to diagnose and quantify color vision deficiencies, particularly
red-green color blindness, by measuring the ability to match colors using mixtures of red, green, and
yellow lights. Was first introduced in 1907.

2)Pseudochromatic plates: like the Ishihara test, use patterns of colored dots to assess color vision
deficiencies. Individuals with normal vision can discern numbers or shapes within the dots, while those
with color blindness may struggle to identify them.

3)Eldridge Green Lantern: this machine consists of different colured windows with light source in the
middle, the patient should identidy the colour on the window.
the affect of mist can also be checked during the test, usually sone on railway workrs or pilots.

• Daltonism refers to red-green color blindness, a common type of color vision deficiency where
individuals have difficulty distinguishing between red and green hues. It is named after John Dalton, who
first studied his own color blindness in the late 18th century.
Retina:

Definition: retina is the innermost tunic of the eyeball it’s a thin, delicate and transparent membrane.
The only part of the CNS that can be shown non-invasively in a living organism.
It is responsible for: central visual acuity, color vision and peripheral vision.
its function is to absorb the electromagnetic radiation of the visible spectrum (400-700 nm) and conduct
the signals to the visual cortex.

• The retina's anatomy is divided into key regions with specific roles. The eye fundus is the general area
seen at the back of the eye. The macula is the central part of the retina responsible for the clearest vision.
The posterior pole includes the optic nerve and macula, critical for processing
central vision. The middle periphery extends from the central retinal artery and
vein branches to the equator, while the distant periphery lies between the
equator and the ora serrata, marking the outermost edge of the retina. The ora
serrata acts as the boundary, separating the pars optica retinae, which is
involved in vision, from the pars caeca retinae, which is not.

• Histology of retina -

• Photoreceptors
Rods: 110-125 million, responsible for peripheral and night vision, containing rhodopsin.
Cones: 6-7 million, concentrated in the macula, responsible for color and central vision with sensitivity to
blue, green, and red.
• Retinal Blood Supply
The outer retina layers are supplied by choriocapillaris, while the inner retina layers are supplied by the
central retinal artery and the outer plexiform layer is supplied by both choriocapillaris and central retinal
arteries.
Macula is supplied by the superior & inferior temporal branches of the central retinal artery or cilioretinal
artery (20% of the population).

• Retinal Diseases
Symptoms: Central vision loss (macular
diseases), peripheral vision loss
(peripheral retinal diseases).

Types: vascular disorders, degenerative changes, retinal dystrophies, inflammatory diseases, toxic
retinopathies and tumors.

• Vascular Disorders-
Diabetic retinopathy (DR), hypertensive retinopathy, symptoms include; sudden vision changes,
hemorrhages, macular edema.
Diagnostic workup: FA(Visualizes retinal blood flow using dye), OCT(Detailed retinal layer imaging),
systemic tests (Checks diabetes and cholesterol levels).

• Diabetic Retinopathy-
Diabetic retinopathy is a major cause of blindness in developed countries. It has two stages: the non-
proliferative stage, marked by small blood vessel changes like microaneurysms, hemorrhages, and retinal
swelling, and the proliferative stage, where new abnormal blood vessels form, leading to bleeding and
retinal detachment. Treatment includes controlling blood sugar, laser therapy, and anti-VEGF injections to
reduce complications.

• CRVO (Central Retinal Vein Occlusion)- A blockage in the central vein of the retina, causing vision loss
due to swelling and bleeding in the retina.

• CRAO (Central Retinal Artery Occlusion)- A blockage in the central artery of the retina, leading to
sudden, severe vision loss due to lack of blood flow.

• Hypertensive Retinopathy- Damage to the retina's blood vessels caused by high blood pressure, leading
to vision problems like narrowing of vessels, bleeding, and swelling.

• Papillophlebitis - is a rare condition involving inflammation of the optic nerve's veins, often seen in
younger, healthy individuals. It causes mild vision issues, vein swelling, and hemorrhages near the optic
nerve, but usually resolves on its own with a good prognosis.
• AMD (Age-Related Macular Degeneration) Classification divides the condition into two types:

Dry (Non-Exudative): Characterized by drusen (yellow deposits) and thinning of retinal layers, leading to
gradual vision loss.
Wet (Exudative): Involves abnormal blood vessel growth and leakage under the retina, causing faster and
more severe vision loss.

• retinal tumors –

Trauma of the eye, orbit and adnexa :

Pterygium is a pinkish, triangular tissue growth on the cornea of the eye. It typically starts on the cornea
near the nose. It may slowly grow but rarely grows so large that it covers the pupil and impairs vision.
Pterygia are twice as likely to occur in men than women.The cause is unclear. It appears to be partly
related to long term exposure to UV light. Simple Limbal Epithelial Transplantation (SLET) is a surgical
technique first described by Dr. Sangwan in 2012 for the treatment of limbal stem cell deficiency
(LSCD).SLET is a reproducible, single stage technique without the need of a special laboratory setup.
Because it is an autologous transplant, there is no need for systemic immunosuppression.

Orbital tumors :
The eye is protected from mechanical injury by being enclosed in a socket, or orbit, which is made up of
portions of several of the bones of the skull to form a four-sided pyramid, the apex of which points back
into the head. Thus, the floor of the orbit is made up of parts of the maxilla, zygomatic, and palatine
bones, while the roof is made up of the orbital plate of the frontal bone and, behind this, by the lesser
wing of the sphenoid. Orbital tumors can be benign or malignant and arise primarily within the orbit or
secondarily from an adjacent source, such as the eyelid, paranasal sinus, or intracranial compartment.
Orbital tumors can also be metastatic from distant sites types of orbital tumors usually cause proptosis
and displacement of the globe in a direction opposite the tumor. Pain, diplopia, and vision loss may also
be present. The diagnosis of
orbital tumors is suspected
based on the history,
examination, and neuroimaging
(CT, MRI, or both), but
confirmation often ultimately
requires a biopsy. Causes and
treatment vary by age group.

• anatomy of the orbit :

• vascularization and innervation :
1)Vascularization: the blood supply to the orbit and eye is primarily derived from the ophthalmic artery, a
branch of the internal carotid artery, entering the orbit through the optic canal alongside the optic nerve.
Key branches include:
- Central retinal artery: Pierces the optic nerve and supplies the inner retina.
- Ciliary arteries: Divided into short and long posterior ciliary arteries, supplying the choroid, sclera, and
outer retina.
- Lacrimal artery: Supplies the lacrimal gland, conjunctiva, and eyelids. Venous drainage occurs via the
superior and inferior ophthalmic veins, which drain into the cavernous sinus.

2)Innervation: Sensory Innervation: Provided by branches of the ophthalmic nerve (V1) of the trigeminal
nerve, including the nasociliary, frontal, and lacrimal nerves, supplying the cornea, conjunctiva, and upper
eyelid.
Motor Innervation: Controlled by cranial nerves:
- Oculomotor (III): Innervates most extraocular muscles and the levator palpebrae superioris.
- Trochlear (IV): Supplies the superior oblique muscle.
- Abducens (VI): Controls the lateral rectus muscle.

Autonomic Innervation: Parasympathetic fibers from the oculomotor nerve control the pupil and lens via
the ciliary ganglion. Sympathetic fibers from the superior cervical ganglion control pupil dilation and blood
vessel tone.

• IgG4-Related Disease (IgG4-RD) - is a systemic, chronic inflammatory condition characterized by tissue

infiltration of IgG4-positive plasma cells, leading to fibrosis and organ enlargement. Commonly affected
organs include the pancreas, salivary glands, lymph nodes, and kidneys. Pathological features include
dense lymphoplasmacytic infiltration, storiform fibrosis, and elevated IgG4 levels. Diagnosis is based on
clinical presentation, imaging of affected organs, histological confirmation, and elevated serum IgG4
levels. Treatment primarily involves corticosteroids, with immunosuppressive therapy for resistant cases.

• Dry eye syndrome-

Pathophysiology of Dry Eye:

Imbalance in tear production or evaporation disrupts the tear film, causing inflammation and damage to
the ocular surface.

Local and Systemic Manifestations: Locally presents as redness, irritation, and vision blurring;
systemically linked to conditions like Sjögren’s syndrome or autoimmune diseases.

Symptoms and Clinical Signs: Patients report dryness, burning, and discomfort; clinically observed are
redness, tear film instability, and surface damage.

Diagnostic Testing: Evaluations include tear break-up time (stability), Schirmer test (tear production), and
staining (surface integrity).

Therapeutical Principles: Aim to restore tear balance, reduce inflammation, and address root causes.

Therapeutic Approaches: Use of artificial tears, anti-inflammatory treatments like cyclosporine, and
lifestyle adjustments to improve eye hydration and reduce irritants.

*some information in this part may be repeated , she will ask one of them for sure*

• Diabetic Retinopathy- In developed countries, diabetic retinopathy is a leading cause of blindness in

individuals aged 30–60. After 20 years of diabetes, 90% of patients show some signs of retinopathy, more
commonly in type 1 diabetes (40%) than type 2 (20%). Diabetic retinopathy is a microangiopathy
characterized by thickened vascular basal membranes and loss of pericytes and endothelial cells. Early
disease progression is driven by hyperglycemia. Capillary blockage leads to retinal ischemia and hypoxia,
triggering angiogenic factors like VEGF and IGF1. These promote neovascularization and disrupt the
blood-retinal barrier, resulting in diabetic macular edema, impairing visual acuity.

Classification:
1) Non-proliferative diabetic retinopathy: Fundus reveals microaneurysms, hemorrhages, and exudates.
Divided into mild, moderate, and severe based on lesion extent. Visual acuity is preserved initially but
declines with macular edema.

2) Proliferative diabetic retinopathy: Progresses from non-proliferative stages without timely intervention.
Features neovascularization (optic disc to posterior hyaloid membrane), rubeosis iridis, secondary
glaucoma, and fibrovascular complications causing vitreous bleeding or traction retinal detachment.

Diagnostics: Fluorescein angiography (FAG), optical coherence tomography (OCT), and ultrasound (for
optical opacity).

Prevention: Maintain good glycemic control and schedule annual ophthalmological exams.

Treatment:
1) Laser photocoagulation: Reduces hypoxia by creating atrophic zones and suppressing
neovascularization.

2) Intravitreal therapy: Anti-VEGF (e.g., bevacizumab) and corticosteroids (e.g., dexamethasone) for
macular edema and neovascularization.
• Hypertensive Retinopathy and Arteriosclerotic-
Hypertension disrupts the blood-retinal barrier, causing hemorrhages, exudates, macular edema, and
optic disc edema. Arteriosclerosis results from arteriole wall thickening and often coexists with
hypertension. Changes may reverse with proper blood pressure control.

Hypertensive Retinopathy Classification (Keith-Wagener-Barker):

1) Narrowed, tortuous arterioles.
2) Vessel constriction and Gunn's sign (artery compresses vein at AV junction).
3) Hemorrhages, edema, exudates.
4) Optic nerve papilla edema.

Arteriosclerotic Classification (Scheie's):

1) Dilation of arteriole reflex.
2) AV junction changes.
3) Copper-colored arteriole reflex.
4) Silver reflex.

• Retinal Venous Occlusions-

The second most common retinal vascular disease after diabetic retinopathy. It results from partial or
complete vein occlusion, causing retinal hemorrhagic infarction.

Types:
1) CRVO (Central Retinal Vein Occlusion): Caused by vein thrombus.
2) HRVO (Hemiretinal Vein Occlusion): Affects upper or lower retinal branches
3) BRVO (Branch Retinal Vein Occlusion): Occurs at AV junctions due to arterial sclerosis compressing
veins.

Findings: Dot hemorrhages, exudates, macular edema, and optic disc edema visible in affected quadrants
or retina.

Diagnostics and Therapy:

Diagnostics: FAG, OCT.
Therapy: Treatment of underlying conditions, anti-VEGF, corticosteroids, and laser photocoagulation.

• Arterial Occlusion Diseases-

Central or branch retinal artery occlusion causes ischemic retinal infarction, leading to sudden, painless,
unilateral vision loss.

Types:
1) CRAO (Central Retinal Artery Occlusion):
80% caused by thrombi (trauma, inflammation, hemorrhage).

2) BRAO (Branch Retinal Artery Occlusion):

90% caused by emboli (from carotid artery, heart).
• Cilioretinal Artery Occlusion-

Findings:
Acute: Grayish-white retina with a "cherry red spot."
Chronic: Optic nerve atrophy and degenerative changes.

Treatment: Local interventions (massage, pressure reduction, paracentesis) within 2 hours.

•Ablation of the Posterior Hyaloid Membrane-

The posterior hyaloid membrane connects to key ocular structures (e.g., vitreous base, optic disc).
Detachment occurs in 65% of individuals aged 55–65, often due to aging or myopia.

Symptoms:Floaters resembling flies or webs, flashes with eye movement (indicating risk of retinal
rupture/detachment).

Types of Retinal Detachment:

1) Rhegmatogenous: Retinal tears allowing vitreous entry, requiring urgent treatment if the macula is
unaffected.
2) Traction: Due to vitreoretinal forces, often in proliferative diabetic retinopathy.

3) Serous/Exudative: Fluid accumulation from inflammatory processes like uveitis.

4) Solid: Subretinal tumors (e.g., melanoma).

Management: Regular check-ups, Laser sealing for ruptures and Surgery for detachment.

Treatment Techniques for Retinal Detachment:

1) Pars Plana Vitrectomy: Most common method. Involves creating three small openings for infusion,
light, and vitrectomy instruments. Removes the vitreous, drains subretinal fluid, and closes ruptures using
endolaser or cryoretinopexy. Retina is reattached using silicone oil, expanding gas, or air.

2) Pneumoretinopexy: Suitable for small detachments in the upper quadrants. introduces a gas bubble
into the vitreous space to help reattach the retina.

3) Conventional Surgery (Scleral Buckling): Involves placing a silicone band around the eye (cerclage).
Drains subretinal fluid, freezes tissues (cryoretinopexy), and places a silicone seal over the rupture site.

• Macular Rupture-
In cases of vitreomacular adhesion, traction forces between the vitreous and the macula can cause a
rupture. It starts as a partial rupture (lamellar) and may become complete.

Symptoms: Gradual decline in visual acuity, more common in women.

Treatment: Pars plana vitrectomy with removal of the internal limiting membrane, followed by air or gas
tamponade.

• Occlusion of the Cilioretinal Artery-

Occlusion of the central retinal artery causes severe neural cell edema, resulting in a grayish-white retina.
The unaffected macular area appears as a "cherry red spot."
Chronic Stage: Optic nerve atrophy and degenerative fundus changes occur.

Therapy: No definitive treatment. Interventions such as bulbar massage, lowering intraocular pressure,
and paracentesis are effective only within 2 hours of symptom onset.

• Uveitis-
Definition: Inflammation of the middle layer of the eye, which may also affect surrounding structures.
Causes: Idiopathic, Infectious, non-infectious, Masquerade Syndrome (diseases mimicking uveitis, such
as lymphomas, leukemias, intraocular tumors, amyloidosis)

Types (Based on affected structures):

1) Anterior Uveitis (Iritis, Iridocyclitis): Affects iris and pars plicata of the ciliary body; inflammatory cells in
aqueous humor.
2) Intermediate Uveitis (Pars Planitis, Vitritis): Affects pars plana and anterior vitreous.
3) Posterior Uveitis (Choroiditis, Chorioretinitis): Affects choroid ± retina ± posterior vitreous.

Panuveitis: Involves all listed structures.

Figure 1: Division of uveitis according to the affected anatomical structures (panuveitis affects all of the
marked structures).

Symptoms:
Anterior Uveitis: Red eye, tearing, photophobia, reduced visual acuity.
Intermediate Uveitis: Floaters, sometimes reduced vision.
Posterior Uveitis: Floaters, visual loss depending on macular involvement.

Signs:
Anterior Uveitis: Ciliary injection, corneal edema, hypopyon (rare), synechiae, raised intraocular pressure.
Intermediate Uveitis: Inflammatory cells in anterior vitreous, peripheral vasculitis.
Posterior Uveitis: Vitreous cells, choroidal infiltrates, vasculitis, macular edema, retinal detachment.

Complications: Keratopathy, glaucoma, cataract, retinal detachment, maculopathy, ocular atrophy.

Treatment:
Local Therapy: Corticosteroid and NSAID eye drops, mydriatics.
Injections: Subconjunctival or intravitreal corticosteroids, anti-VEGF drugs.
Systemic Therapy: Corticosteroids, NSAIDs, antibiotics, immunosuppressants.
Complications Management: Surgery for cataracts, glaucoma, retinal detachment, or corneal transplants.
∆ Anterior Uveitis (Iridocyclitis)

Causes:
1) Idiopathic (50%)
2) Infectious: Viruses (VZV), syphilis, tuberculosis, Lyme disease.
3) Non-infectious: HLA-B27-related diseases (e.g., ankylosing spondylitis, psoriatic arthritis, reactive
arthritis), juvenile idiopathic arthritis, Behçet’s disease, multiple sclerosis, other autoimmune diseases.
3) Masquerade Syndrome: Mimicking conditions like tumors or amyloidosis.

Figure 2:
Top right: Pronounced ciliary injection.
Top left: Ciliary injection, corneal edema, numerous inflammatory precipitates on the corneal endothelium.
Bottom right: Irregular pupil due to synechiae preventing normal mydriasis.
Bottom left: Dense mature cataract, irregular pupil with partially ruptured synechiae.

∆ Intermediate Uveitis / Vitritis

Causes:
1) Idiopathic (50–70%)
2) Infectious: Lyme disease, syphilis, toxocariasis, tuberculosis, cat scratch disease.
3) Non-infectious: Sarcoidosis (~22%), multiple sclerosis (~8%).
4) Masquerade Syndrome: Conditions mimicking uveitis.

Figure 3:
Top right: Numerous cells in the anterior vitreous visible in slit lamp light.
Bottom right: Inflammatory exudates on the peripheral retina resembling a snowbank.
Bottom middle: Vitreous exudates above the peripheral retina resembling snowballs.
Bottom left: Vitreous opacification caused by inflammatory cells, reducing retinal detail visibility.
Top left: Peripheral retinal scars in the chronic phase without active inflammation.

∆ Posterior Uveitis / Chorioretinitis

Causes:
1) Idiopathic: A group of chorioretinopathies with no systemic disease.
2) Infectious: viral (herpes), fungal (Candida causing endophthalmitis with intense vitritis), atypical
bacteria (tuberculosis, syphilis, lyme disease, cat scratch disease), parasitic.
3) Non-infectious: autoimmune diseases
4) Masquerade Syndrome

Figure 4:
Top right: Intravitreal exudates above the macula, perceived as moving floaters; segmental arteriolitis of
the upper temporal branch of the central retinal artery; larger solitary chorioretinal inflammatory infiltrate.
Top left: Clearer view of arteriolitis and chorioretinal focus.
Bottom right: Peripheral intravitreal exudates connected in a crown-like pattern (string of beads).
Bottom left: After three months, an inactive chorioretinitis scar remains at the site of the focus, with minor
retinal pigment epithelial changes in the macula and minimal vitritis or arteriolitis.
∆ Uveitis and Dentistry
Systemic diseases can manifest in both the oral cavity and eyes. Example: Behçet's Syndrome, recurrent
iridocyclitis and retinal vasculitis, aphthous ulcers on buccal, gingival, lingual, or pharyngeal mucosa.

Figure 5: Ocular manifestations of Behçet's syndrome: Right: Anterior uveitis with hypopyon.
Left: Retinal vasculitis.

Figure 6: Oral manifestations of Behçet's syndrome: right – recurrent aphthous gingivostomatitis; left –
aphthous ulcers of the lingual mucosa

The Lens and Refraction: Structure, Function, and Disorders

•The Lens: lens is a transparent, biconvex structure that works with the cornea to focus light onto the
retina. It is located behind the iris, which regulates the amount of light entering the eye, and its back
surface touches the vitreous body. The lens is held in place by the suspensory ligament, which connects it
to the ciliary body. The lens diameter is 9–10 mm, and its axis is approximately 4 mm, though these
dimensions can change due to accommodation and lifelong growth.

•Structure
Lens Capsule: A thin, protective outer covering.
Lens Epithelium: Located beneath the capsule on the anterior surface.
Lens Fibers: Comprise the bulk of the lens's interior.

The lens depends on nutrients for growth and transparency. During fetal development, it is nourished by
the tunica vasculosa lentis, derived from the hyaloid artery. This blood supply disappears at birth, after
which the lens receives nutrients from the aqueous humor through a dynamic fluid exchange system
maintained by Na+/K+ pumps in the lens epithelium.

•Lens Disorders
1) Aphakia: The absence of the lens, typically due to surgery, injury, or congenital defects.
2) Ectopia Lentis: Displacement of the lens from its normal position.
3) Presbyopia: Age-related difficulty focusing on close objects, caused by changes in lens hardness,
shape, and size.
4) Cataracts: Clouding of the lens, either congenital or degenerative.
Cataracts
Risk Factors: Trauma, smoking, alcohol use, x-rays, UV exposure, diabetes, uveitis, corticosteroids,
and congenital conditions.
Symptoms: Night glare, halos, reduced contrast, and progressive, painless vision blurring. Nuclear
cataracts can cause early nearsightedness, while posterior subcapsular cataracts significantly impair
vision.
Diagnosis: Best assessed with dilated pupils. Cataracts appear as yellow-brown opacities, and a
slit-lamp exam determines their type and extent.
Treatment: Surgical removal followed by lens implantation.

•Refraction in the Eye

Refraction is the bending of light as it passes through the eye's media to focus on the retina. Major
refractive components include the cornea (43 Dpt), lens (10–20 Dpt), and other eye fluids.

•Types of Refraction

1)Emmetropia: Normal vision where light focuses directly on the retina.

2) Ametropia: Vision issues where light does not focus correctly on the retina:
3) Myopia (Nearsightedness): Light focuses in front of the retina, leading to clear near vision but blurry
distance vision.
Causes: Long eyeball (axial myopia) or strong refractive power (refractive myopia).
Correction: Divergent lenses.
4) Hyperopia (Farsightedness): Light focuses behind the retina, causing blurry near vision.
Causes: Short eyeball (axial hyperopia) or weak refractive power (refractive hyperopia).
Correction: Convergent lenses.
5)Astigmatism: Uneven focusing due to an irregular eye shape.
Correction: Cylindrical lenses.

•Accommodation
Accommodation allows the lens to adjust focus for near or distant objects. With aging, this ability declines,
leading to presbyopia, which makes near vision difficult. This is corrected with convergent lenses, with
prescriptions adjusted based on age.

•Other Refraction Anomalies

Anisometropia: Unequal refractive power in both eyes, which can cause amblyopia (lazy eye) if untreated.
Therapy: Glasses, contact lenses, laser correction, or intraocular lenses.

•Testing Visual Acuity

Refraction can be measured:

1) Subjectively: Based on patient feedback.
2) Objectively: Using tools like skiaskopy or refractometry.

These methods ensure accurate correction of refractive errors and optimal visual performance.

Glaucoma: Overview, Classification, and Management

•Definition and Overview

Glaucoma is a chronic optic nerve disease characterized by progressive structural damage, visual field
deterioration, and vision loss. It can be primary or secondary and is not synonymous with elevated
intraocular pressure (IOP), although high IOP is a significant risk factor.

•Types of Glaucoma
1) By Mechanism: Open-angle, Closed-angle.
2) By Onset: Pediatric, Adult.
3) By IOP: Low, Normal, or High Pressure.
4) By Stage: Initial, Developed, Advanced, Terminal.
5) By Cause: Primary, Secondary.

•Intraocular Pressure (IOP)

Normal IOP ranges between 10–21 mmHg, regulated by the balance between aqueous humor production
in the ciliary body and its drainage via the trabecular meshwork and uveoscleral pathways. Elevated IOP
occurs when outflow is reduced, caused by developmental anomalies, trauma, infections, inflammation,
neoplasms, ischemia, or endocrine disorders.

Glaucoma-Related Atrophy
Damage at the optic nerve papilla and peripapillary retinal nerve fiber layer (RNFL) impairs axoplasmic
transport, leading to retinal ganglion cell apoptosis and progressive nerve tissue loss.

Diagnosis
1) History and Examination: Includes visual acuity testing, slit-lamp examination, and tonometry.
2) Tonometry: Goldmann applanation is the gold standard; other methods include air-puff tonometry,
indentation, and palpation.
3) Gonioscopy: Evaluates the angle between the iris and cornea to classify glaucoma as open-angle or
closed-angle.
4) Optic Disc Evaluation (PNO): Detects increased excavation, deepening of excavation, and optic nerve
pallor.
5) Functional Tests: Visual field testing identifies sensitivity loss, especially in Bjerrum's area, often
sparing central fixation until late stages.

Childhood Glaucoma
∆ Primary: Abnormal anterior chamber angle development (trabeculodysgenesis/goniodysgenesis).
∆ Secondary: Associated with systemic conditions like Axenfeld-Rieger syndrome or Sturge-Weber
syndrome.

Classification by Age
Congenital: At birth.
Infantile: By age 1–2.
Juvenile: After age 3.

Symptoms: Photophobia, tearing, eye rubbing, blepharospasm.

Signs: Enlarged/cloudy cornea, redness, and buphthalmos (bull’s eye).

Management:
1) Medications: Prostaglandin analogues, Beta blockers
2) Combination therapy combines agents for enhanced effect.
Laser Treatments: Laser iridotomy, trabeculoplasty, iridoplasty, cyclodestructive procedures.
Surgical Procedures:Trabeculectomy, non-perforating procedures, drainage implants.

Strabismus (Squint)

•Definition and Overview

Strabismus is a condition where the eyes do not align when focusing on an object. One eye may turn
inward, outward, upward, or downward, and the misalignment may alternate or remain constant. It affects
about 4% of children in the U.S.

•Effects and Symptoms

If untreated, it can lead to amblyopia (lazy eye) or loss of depth perception.
Symptoms include double vision and eye strain. The brain may suppress the input from the misaligned
eye, reducing depth perception.

•Causes of Strabismus
1) Motor Factors: Anatomical issues.
2) Optical Factors: Refractive errors like farsightedness or nearsightedness.
3) Sensory Factors: Issues with fusion or accommodation.
4) Central Causes: Neurological conditions.

•Types of Strabismus

1)By Consistency of Deviation:

Concomitant: Angle of deviation remains constant.
Non-concomitant: Angle changes with gaze direction.

2)By Timing:
Congenital: Present at birth.
Infantile: Appears within the first few years of life.
Acquired: Develops later.

∆ Specific Types:
1) Infantile Esotropia: Inward crossing in infants.
2) Accommodative Esotropia: Inward turn when focusing.
3) Exotropia: Outward turn, often when tired or daydreaming.

Diagnostic Tests:
1)Cover/Uncover Test: Identifies manifest and latent squints.
2)Prism Test: Measures the degree of deviation.
3)Eye Motility Test: Assesses movement in 9 gaze positions.
4)Convergence Test: Evaluates the ability to focus on near targets.

The aim is to establish normal binocular vision.

Treatment:
Conservative:
Vision therapy, retinal correspondence therapy, mydriatics, botulinum toxin.

Surgical Treatment:
Surgery for large deviations, non-accommodative strabismus, or early cases with abnormal retinal
correspondence.

Corneal Conditions: Overview and Management

•Corneal Erosion
Definition: A defect in the corneal epithelium, the most common eye trauma (10% of emergency
ophthalmology cases).

Symptoms: Severe sharp pain, tearing, photophobia, frequent blinking (blepharospasm), blurred vision
(especially with central erosion).

Diagnosis: Biomicroscopic examination of the cornea; fluorescein staining with blue light for better
visibility.

Treatment: Antibiotics and cycloplegics to reduce ciliary muscle spasm and pain.

•Corneal Foreign Body

Definition: The second most common eye trauma involving a foreign object in the cornea.

Symptoms: Redness, tearing, pain, discomfort, photophobia, and frequent blinking.

Diagnosis: Examination with focal lighting or a biomicroscope; small foreign bodies may be missed
without a biomicroscope.

Treatment:Removal using a needle or special lancet under local anesthesia, for deep stromal foreign
bodies, surgical exploration is required. Post-removal care: antibiotics, cycloplegics, and temporary eye
bandages if necessary. Oral analgesics for pain relief.

•Epidemic Keratitis
Definition: Part of keratoconjunctivitis, often characterized by a follicular reaction, conjunctival chemosis,
petechial hemorrhages, and pseudomembranes.

Symptoms: Small subepithelial infiltrates appear after 7–14 days in 80% of cases, reducing visual acuity.
Treatment: Antibiotic-corticosteroid drops and ointments.

•Herpetic Keratitis
Definition: Inflammation of the cornea caused by herpes simplex virus (HSV-1, rarely HSV-2).

Symptoms: Mild pain, photophobia, tearing, redness, and reduced vision if the lesion is central.

Diagnosis: Fluorescein staining reveals lesions resembling tree branches (keratitis dendritica).

Complications: Scarring, particularly in the corneal center, can permanently reduce vision.

Treatment: Antiviral drugs (acyclovir) applied locally and orally.

•Keratoconus
Definition: Bilateral, progressive, non-inflammatory thinning and conical protrusion of the cornea.

Onset: Typically begins during puberty and progresses until the 3rd or 4th decade of life.

Symptoms: Reduced visual acuity, progressive myopia, and irregular astigmatism due to corneal ectasia.

Diagnosis: Corneal topography (e.g., PENTACAM).

Signs: Progressive corneal thinning at the apex, Munson's sign (lower eyelid bulge when looking down),
Corneal scarring, ruptures in Bowman's membrane, and corneal hydrops (acute Descemet/endothelium
rupture).

Treatment:
1)Conservative: Glasses, scleral/corneal contact lenses, and hybrid lenses.
2)Surgical: Cross-linking to strengthen collagen fibers; corneal transplantation for advanced cases (10%).

•Fuchs' Endothelial Corneal Dystrophy

Definition: Bilateral dystrophy affecting the corneal endothelium, more common in women. Often
associated with open-angle glaucoma. leads to edema, cysts.

Symptoms: Gradual vision blurring.

Diagnosis: Specular microscopy identifies cornea guttata (tiny dots on the endothelium).

Treatment:
1)Conservative: 5% NaCl drops.
2)Surgical: Partial or full-thickness corneal transplantation (DSAEK, DMEK, PRK).

•Congenital Corneal Anomalies

Types:
1)Microcornea: Abnormally small cornea.
2)Megalocornea: Enlarged cornea.
3)Cornea Plana: Flat cornea.

Associations: Often part of syndromes and accompanied by refractive errors, glaucoma, optic nerve
hypoplasia, or congenital cataracts.

Conjunctival Conditions
•Pterygium
Pterygium is a pink, triangular tissue that grows over the limbus onto the cornea. It typically grows slowly
and most often originates from the nasal (medial) side of the eye. If it extends deeply into the cornea
towards the center, it can cause a reduction in visual acuity.

Cause: The exact cause is unknown, but it is more common in areas with high UV radiation and occurs
more frequently in men.
Therapy: Treatment is exclusively surgical. Recurrence has been observed in up to 15% of cases after
some types of surgery, and an ideal surgical technique has yet to be identified. Simple Limbal Epithelial
Transplantation (SLET): A surgical method with a very low recurrence rate. In this procedure, limbal
corneal cells from the same eye are transplanted into the area affected by the pterygium.

•Melanoma of the Conjunctiva

Conjunctival melanoma is a rare condition, with an incidence of 0.25% to 0.8% of newly diagnosed cases
per year per 1,000,000 people. It most commonly affects individuals aged 53 to 57 years.

Diagnosis:
Identified through clinical examination with a biomicroscope. Appears as a darkly pigmented growth.
Differential diagnosis must exclude conditions such as nevi, congenital melanosis, cutaneous melanoma
metastases (rare), and blood-filled adrenochromocysts or cysts.

Therapy: Complete surgical excision is the primary treatment. Adjuvant therapies, such as cryotherapy or
radiation (e.g., with 90-strontium), are typically recommended following surgery. Enucleation (removal of
the eye) is indicated only if the melanoma penetrates through the sclera.

Prognosis: Conjunctival melanomas located on the caruncle, in the fornix, or on the tarsus carry the worst
prognosis.

Ocular surface disease

The ocular surface system consists of the cornea, conjunctiva, lacrimal glands, meibomian glands,
nasolacrimal duct, and their associated tear and connective tissue matrices, as well as the eyelids and
eyelashes, all integrated by continuous epithelia and interconnected nervous, endocrine, immune, and
vascular systems. Ocular surface disfunction may accompany numerous systemic diseases.

The course aims to educate students about the most relevant systemic conditions that show the ocular
surface signs and symptoms, to recognize the clinical signs and symptoms, review of dignostic tests,
management strategies and their implications for health and quality of life.