Pa Mata

PATOLOGI MATA
dr. Hermawan Istiadi, M.Si.Med

Normal Eye
SASARAN BELAJAR
• Histologi normal mata
• Patologi palpebra dan konjungtiva : pinguecula, pterygium,
neoplasma
• Patologi kornea : keratitis, ulkus kornea, keratokonus.
• Patologi Segmen Anterior : Katarak, glaukoma, endoftalmitis,
panoftalmitis
• Patologi uvea, vitreous dan retina : uveitis, retinal
detachment, retinal vascular disease, retinitis, neoplasma,
optic nerve damage, papilledema.
Normal Eye
Normal Eye
Normal Eye
Basic Pathology
Reaksi Radang
Akut
• Infiltrasi sel
PMN
• Ex : Uveitis
anterior -
hipopion
Basic Pathology
Reaksi Radang
Kronik
• Infiltrasi sel
Limfosit, Sel
Plasma
• Ex :
Choroiditis
kronik
Basic Pathology
Reaksi Radang
Kronik
Granulomatosa
• Struktur
Multinucleated Giant cell granuloma –
Multi
nucleated
giant cell
Fragment of hair • Ex : Iritasi
rambut
Basic Pathology
Pyogenic
Granuloma -
Chalazion
• Bendungan
pembuluh
darah –
kapiler dalam
stroma
jaringan ikat
PATOLOGI ORBITA
PATOLOGI ORBITA
• Cavum Orbita – Kompartemen tertutup
pada sisi medial, lateral, dan posterior
• Peningkatan konten didalam cavum
orbita –mendorong bola mata kedepan
(Proptosis)
PATOLOGI ORBITA
Proptosis
Proptosis :
• Axial (Straight forward), Ex : Tumor optic nerve, grave disease
• Positional, Ex : Enlargement lacrimal gland, neoplasm
Eyelids : not cover completely proptotic eye

Tear film : not be distributed evenly across cornea
Chronic corneal exposure to air

(pain, corneal ulceration, infection)
PATOLOGI ORBITA
Proptosis
1. Thyroid Ophthalmopathy (Graves Disease)
Akumulasi Protein matriks ekstraseluler matrix
proteins + fibrosis mm.rectus oculi
Hyperthyroidism
(Increase BMR)
PATOLOGI ORBITA
Proptosis
2. Other Orbital Inflammatory Conditions
Penyebaran infeksi sinusitis (bacteria / fungi) dari
sinus maksilaris (Floor), sinus ethmoidalis (medial
wall) - *immunocompromise state
3. Neoplasm
Capillary hemangioma
Lymphangioma Primary tumor
Adenoma of the lacrimal gland
Secondary tumor (Ex : Metastasis neuroblastoma, wilms tumor)
PATOLOGI KELOPAK MATA
(EYELID)
Normal Eyelids
Normal anatomy
of eyelid
Layers :
1. Skin
2. Striated
muscle
3. Tarsal plate
4. Conjunctival
mucosa
Normal Eyelids
Pathology of Eyelids
Warts
 Sinonim :
Verucca
vulgaris
 HPV
 Hiperkeratosis
- hiperplasia
 Vacuolated cell
Blepharitis
 Inflamasi kronik
pada eyelid margin
 Lipid ekstravasasi –
menymbat
kel.meibom –
reaksi radang
lipogranulomatosa
- lipogranuloma,
or chalazion
Moluskum
Kontagiosum
 Pox virus
 Umbilication
 Hiperplasia
epitel
Neoplasm
 Most common : Basal cell carcinoma (lower, medial
canthus), Sebaceous carcinoma
 Prevent the eyelids from closing completely
 Chronic exposure to air damages the cornea
Basal cell Carcinoma of Eyelid

• Asal : Sel Basal

epidermis
• Risk fact : UV Light
Basal cell Carcinoma of Eyelid
• Asal : Pilosebaceous follicles / sebaceous glands

(Meibomian and Zeiss)
• Klinis : Nodul / mirip nodul karena radang
Sebaceous Gland Carcinoma
• Asal : Pilosebaceous follicles / sebaceous glands

(Meibomian and Zeiss)
• Klinis : Nodul / mirip nodul karena radang
Sebaceous Gland Carcinoma
PATOLOGI KONJUNGTIVA
Pathology of Conjunctiva
Normal anatomy
of Conjunctiva
Fornix :
• Pseudostratified
columnar
epithelium rich
in goblet cells
• Accessory
lacrimal tissue
• Ductules of the
main lacrimal
gland superiorly
and laterally
Normal anatomy
of Conjunctiva
Fornix :
• The lymphoid
population most
noticeable
(Enlarge in viral
conjunctivitis)
Papillary Conjunctivitis
Erythematous conjunctiva with numerous small flat-topped
nodules with central vessels. Common causes :
• Bacterial infection
• Chronic blepharitis
• Allergic conjunctivitis
• Contact lens / foreign
body irritation.
Papillary Conjunctivitis
Follicular Conjunctivitis
Small “rice grains” and each is surrounded by blood vessels
Common causes :
• Viral infection
• Chlamydial Infection
• Hypersensitivity
Follicular Conjunctivitis
Conjunctival Scarring
• Infection with Chlamydia trachomatis (trachoma) may produce
significant conjunctival scarring
• Reaction to drugs
• Consequence of surgery (compromise lacrimal gland ductules)
Reduction in the number of goblet cells –

decrease surface mucin
Painful Loss Of Vision

Conjunctival Scarring
Inflammatory Infiltrate
Dense Stromal Fibrosis

Pinguecula and Pterygium
• Submucosal elevations on the conjunctiva, astride the limbus
• Result from Elastotic degeneration
• Pterygium : Submucosal growth of fibrovascular connective
tissue that migrates onto the cornea, does not cross the
pupillary axis, does not pose a threat to vision
• Pinguecula : is a small, yellowish submucosal elevation, does
not invade the cornea
Uneven distribution of tear film over the adjacent cornea - focal

dehydration - saucer-like depression/thinning in corneal tissue (Dellen)
Pterygium Dellen Pinguecula

Neoplasm
Conjunctival nevi
Neoplasm
Squamous Cell Carcinoma
De novo (UV Light risk) / from pre-existing pterygium

Non-pigmented mass , located within interpalpebral fissure - extend
Neoplasm
Squamous Cell Carcinoma
De novo (UV Light risk) / from pre-existing pterygium

Non-pigmented mass , located within interpalpebral fissure - extend
PATOLOGI SKLERA &
KORNEA
Pathology of Sclera
Consists mainly of collagen and contains few blood vessels &
fibroblasts
wounds and surgical incisions tend to heal poorly
1. Necrotizing Scleritis (Immune complex deposits within sclera in
Rheumatoid Arthritis)
2. Sclera appear Blue :
a. Become thin following episodes of scleritis
b. Become thin with high intraocular pressure – staphyloma
c. in osteogenesis imperfecta
d. In congenital melanosis oculi (heavily pigmented congenital
nevus of the underlying uvea)
Pathology of Sclera
Necrotizing Scleritis
Pathology of Cornea
Epithelium
• Major refractive
surface of the eye
Bowman layer
• Corneal stroma
lacks blood vessels
and lymphatics
Stroma
(transparency,
success of corneal
transplantation)
• Descemet
Descement membrane
membrane
increases in
thickness with age.
Endothelium
Pathology of Cornea
• Corneal vascularization may accompany chronic
corneal edema, inflammation, and scarring
• Decrease in endothelial cells or a malfunction of
endothelium results in stromal edema, which may be
complicated by bullous separation of the epithelium
(bullous keratopathy)
Pathology of Cornea
Corneal Oedema Bullous Keratopathy

Pathology of Cornea
Keratitis and Ulcer
• Etiology : bacterial, fungal, viral (especially herpes simplex and
herpes zoster), and protozoal (Acanthamoeba)
• Dissolution of the corneal stroma may be accelerated by
activation of collagenase (Thinned)
• Exudate and cells leaking from iris and ciliary body vessels into
the anterior chamber (hypopyon)
• Chronic herpes simplex keratitis may be associated with a
granulomatous reaction involving
Descemet membrane
Pathology of Cornea
Keratitis and Ulcer
Keratitis Bakterial
Pathology of Cornea
Keratitis and Ulcer
Fibrosis/scar Thinned cornea
Granulomatous reaction in
the Descemet membrane
Chronic herpes simplex keratitis

Pathology of Cornea
Corneal Degenerations and Dystrophies
• Corneal degenerations - unilateral or bilateral and nonfamilial
• Corneal dystrophies - bilateral and hereditary
1. Band Keratopathies
• Corneal degenerations, deposition of calcium in the
Bowman layer, may complicate chronic uveitis
• Actinic band keratopathy, exposed chronically to high
levels of ultraviolet light, a yellow hue to the point
“oil-droplet keratopathy”
Pathology of Cornea
Band Keratopathy
Wing-shaped superficial opacity

Pathology of Cornea
2. Keratoconus
• Progressive thinning and ectasia of the cornea without
evidence of inflammation or vascularization
• Results in cornea has a conical rather than spherical shape
• Generates irregular astigmatism
• Typically bilateral
• Associated with Down syndrome
Marfan syndrome, and
atopic disorders
Pathology of Cornea
• Thinning of the cornea
Keratoconus with breaks in the
Bowman layer are the
histologic hallmarks of
keratoconus
• Descemet membrane
may rupture
precipitously, allowing
aqueous humor in
anterior chamber gain
Hypercellular stroma
access corneal stroma
(Hydrops) followed by
corneal scarring
PATOLOGI SEGMEN
ANTERIOR
Pathology of Anterior Segment
• Lens is a closed epithelial system; the basement membrane of

the lens epithelium (lens capsule) totally envelops the lens
• With aging, the size of the lens increases
Aqueous humor :
• Pars plicata of the
ciliary body
• Posterior chamber
• Through the pupil
• Anterior chamber
• Trabecular meshwork
• Schlemm canal
Cataract
• Lenticular opacities that may be congenital or acquired
• Condition associated with cataract :
• Galactosemia
• Diabetes mellitus
• Wilson disease
• Atopic dermatitis
• Drugs (especially corticosteroids)
• Radiation
• Trauma
• Many intraocular disorders are associated with cataract
• Age-related cataract typically results from opacification of the
lens nucleus (nuclear sclerosis)
Cataract
• The accumulation of urochrome pigment may render the
lens nucleus brown
• The lens cortex may liquefy
• Occasionally, High-molecular-weight proteins from liquefied
lens cortex may leak through the lens capsule (phacolysis) -
may clog the trabecular meshwork - elevation in intraocular
pressure and optic nerve damage - secondary open angle
glaucoma
Glaucoma
• Collection of diseases characterized by distinctive changes in
the visual field and in the optic nerve cup
• Associated with elevated intraocular pressure, although
some individuals with normal intraocular pressure may
develop characteristic optic nerve and visual field changes
(normal or low-tension glaucoma)
• Classification :
1. Open-angle glaucoma
aqueous humor has complete physical access to the
trabecular meshwork – increase resistance to outflow
2. Angle-closure glaucoma
Iris adheres to the trabecular meshwork
Glaucoma
1. Open-angle glaucoma
a. Primary
• The most common form of glaucoma
• Mutations in the myocilin (MYOC) gene, optineurin
(OPTN) gene
b. Secondary
• Phacolytic glaucoma – (from cataract material)
• Ghost cell glaucoma (RBC)
• Pigmentary glaucoma (Iris)
• Melanomalytic glaucoma (necrotic tumor)
• Elevation of episcleral venous pressure
Glaucoma
2. Angle-closure glaucoma
a. Primary
• Eyes with shallow anterior chambers
• Transient apposition of the pupillary margin of the iris to
the anterior surface of the lens - iris bombé - apposing to
trabecular meshwork - corneal edema and bullous
keratopathy
b. Secondary
• Neovascular glaucoma - iris neovascularization
• Tumors in the ciliary body
Glaucoma
Glaucoma
• Elevated intraocular pressure in infants and children :
• Diffuse enlargement of the eye (buphthalmos) or
• Enlargement of the cornea (megalocornea)
• Adult eye, prolonged elevation of intraocular pressure :
• Focal thinning of sclera
• Uveal tissue may line ectatic sclera (staphyloma)
Endophthalmitis and Panophthalmitis
Intraocular inflammation, vessels in the ciliary body and iris become
leaky, allowing cells and exudate to accumulate in the anterior
chamber
• Keratic precipitates - adhere to the corneal endothelium
• Anterior synechiae - adhesions between the iris and the
trabecular meshwork or cornea
• Posterior synechiae - adhesions between the iris and anterior
surface of Lens - deprive lens epithelium of contact with
aqueous humor - anterior subcapsular cataract
• Endophthalmitis is reserved for inflammation within the
vitreous humor
• Suppurative inflammation in the vitreous humor is poorly
tolerated by the retina - irreversible retinal injury
• Exogenous (originating in the environment through a wound) or
endogenous (delivered to the eye hematogenously).
• Panophthalmitis is applied to inflammation within the eye that
involves the retina, choroid, and sclera and extends into the
orbit
Anterior Synechiae
Posterior Synechiae
Pathology of Uvea
Uveitis
Inflammation in one or more of the tissues that
compose the uvea (Iris, choroid, cilliary body)
Etiology :
1. Infectious agents (e.g., Pneumocystis carinii,
toxoplasmosis)
2. Idiopathic (e.g., sarcoidosis)
3. Autoimmune (sympathetic ophthalmia)
bilateral granulomatous inflammation –
panuveitis
Pathology of Uvea
Uveitis
• Uveal inflammation may be manifest principally in
the anterior segment or both the anterior and
posterior segments
• Inflammation in one compartment is typically
associated with inflammation in the other
Pathology of Uvea
Uveitis
Sympathetic ophthalmia
• Injured eye - retinal antigens sequestered from the
immune system - lymphatics in the conjunctiva -
delayed hypersensitivity – Injured eye and
noninjured eye contralaterally affected (2 weeks -
years after injury)
• Diffuse granulomatous inflammation of uvea
• Tx : systemic immunosuppressive agents
Pathology of Uvea
Uveitis
Sympathetic ophthalmia
Pathology of Uvea
Neoplasm
• Most common intraocular malignancy of adults is
metastasis to the uvea, typically to the choroid
• Uveal Nevi and Melanomas
– Uveal melanoma is the most common primary intraocular
malignancy of adults
– Most uveal melanomas are incidental findings or present
with visual symptoms
– the 5-year survival rate : 80%,
– mortality rate is 40% at 10 years
Pathology of Uvea
Neoplasm
Uveal Nevi and Melanomas
Pathology of Uvea
Neoplasm
Uveal Nevi and Melanomas
PATOLOGI
RETINA & VITREOUS
Pathology of Retina & Vitreous
• Derivative of the diencephalon
• Responds to injury by means of gliosis
• there are no lymphatics
• The adult vitreous humor is avascular
• Incomplete regression of fetal vasculature running
through the vitreous humor : Persistent hyperplastic
primary vitreous
• Posterior vitreous detachment (Posterior hyaloid –
neurosensory retina)
Retinal Detachment
• Separation of the neurosensory retina from the RPE
(Retinal Pigment epithelium)
• Type :
1. Non-rhegmatogenous (without retinal break)
2. Rhegmatogenous (with retinal break)
Retinal Detachment (Non-rhegmatogenous)
• Subretinal space is filled
with protein-rich exudate
• The outer segments of
the photoreceptors are
missing
• Ex: choroidal tumors and
malignant hypertension
Retinal Detachment (rhegmatogenous)
• Associated with a full-
thickness retinal defect
• May develop after the
vitreous collapses
structurally, and the
posterior hyaloid exerts
traction on points of
abnormally strong
adhesion to the retinal
internal limiting
membrane
Retinal Detachment (rhegmatogenous)
• Liquefied vitreous
humor then seeps
through the tear and
gains access to the
potential space between
the neurosensory retina
and the RPE
Retinal Vascular Disease
Hypertension
• Normally, the thin walls of retinal arterioles permit a
direct visualization of the circulating blood by
ophthalmoscopy
• In retinal arteriolosclerosis, the thickened arteriolar
wall changes the ophthalmic perception of
circulating blood
Hypertension
• Reduced Arterioles
diameter
• Blood column color
appears to be less
saturated (“copper wire” to
“silver wire” appearance)
• The vein is compressed
where sclerotic arteriole
crosses over it
Hypertension
• Vessels in the retina and choroid may be damaged -
focal choroidal infarcts (Elschnig spots)
• Damage the overlying RPE and permit the exudate
to accumulate in the potential space between the
neurosensory retina and the RPE – retinal
dettachment
• Occlusion of retinal arterioles may produce infarcts
of the nerve fiber layer of the retina -
“cotton-wool spots”
Retinal Vascular Disease - Hypertension
Hypertensin
The wall of retinal arteriole (arrow) is thick
Exudate (e) in the retinal outer plexiform layer

Hemorrhage
surrounding nerve fiber
layer infarct
Histology of a cotton-wool spot

Focal swelling of nerve fiber
layer is occupied by numerous
red to pink cytoid bodies
nerve fiber layer infarcts may be detected in a variety

of retinal occlusive vasculopathies, Ex : AIDS
Diabetes Mellitus
• Thickening of the basement membrane of the
epithelium of the pars plicata of the ciliary body
• Retinal microangiopathy
• Types :
1. Nonproliferative diabetic retinopathy
2. Proliferative diabetic retinopathy
1. Nonproliferative diabetic retinopathy
• Microaneurysms – retinal microhemorrhage
• Macular edema
• Exudates that accumulate in the outer
plexiform layer
• vascular micro-occlusions
Retinal neovascularization may be
accompanied by the development of
neovascular membrane on the iris surface –
adhesions between iris and trabecular
meshwork - (neovascular glaucoma)
• Appearance of new vessels sprouting on the surface
of optic nerve head (termed “neovascularization of
the disc”) or surface of retina
• The newly formed vessels breach the internal
limiting membrane of retina – neovascular
membrane
• Scarring associated with organization of retinal
neovascular membrane may wrinkle retina
Tangle of abnormal vessels
Retinal hemorrhage
Posterior hyaloid of the vitreous
White neovascular membrane
Internal limiting membrane

Neovascular membrane
Retinal Artery and Vein Occlusions
• The central retinal artery or its branches can be
occluded by disorders that affect the vessels in
general (Ex : by atherosclerosis – thrombosis)
• Segmental/diffuse infarct of the retina
• The retina swells acutely and becomes optically
opaque
Retinal Artery and Vein Occlusions
• Retinal vein occlusion may occur with or without
ischemia
• In ischemic retinal vein occlusion -
neovascularization of the retina
Other Retinal Degenerations
Retinitis Pigmentosa
• Inherited condition resulting from mutations that
affect rods and cones, or RPE
• May be inherited as X-linked recessive, autosomal
recessive, or autosomal dominant
Retinitis Pigmentosa
• Mutatioin on genes that regulate the visual cascade
and visual cycle, structural genes (transpanins),
transcription factors, retinal catabolic pathways,
and mitochondrial metabolism
• Loss of rods (night blindness) and cones (central
visual acuity)
• Accumulation of retinal pigment around blood
vessels
Retinitis
Etiology :
• Candida, Cytomegalovirus
• Immunocompromise state
• Results in multiple retinal abscesses
Retinal Neoplasm
Retinoblastoma
• Most common primary intraocular malignancy of
children
• Arise from neuronal progenitor
• 40% of cases - germline mutation of RB gene
Retinal Neoplasm
Retinoblastoma
Flexner-Wintersteiner rosettes
PATOLOGI
NERVUS OPTIKUS
Pathology of Optic Nerve
Surrounded by meninges, and cerebrospinal fluid
circulates around the nerve
Anterior Ischemic Optic Neuropathy

• Spectrum of injuries to optic nerve (ischemia –
infarction)
• Result from inflammation, emboli
• Zones of relative ischemia may surround segmental
infarcts of the optic nerve (pale)
• The optic nerve does not regenerate, and visual loss
from infarction is permanent
Papilledema
• Edema of the head of the optic nerve - consequence
of compression of the nerve (Unilateral) or from
elevations of cerebrospinal fluid pressure
surrounding the nerve (Bilateral)
• Increase in pressure encircling the nerve
• Venous stasis
• Nerve head swelling, hyperemia
• Acute papilledema from increased intracranial
pressure is not associated with visual loss
Acute phases of AION Papilledema

Glaucomatous Optic Nerve Damage
• The majority of individuals with glaucoma have
elevated intraocular pressure
• Small group that develops the visual field and optic
nerve changes
• Diffuse loss of ganglion cells and thinning of retinal
nerve fiber layer – the optic nerve is both cupped
and atrophic
The nerve fiber layer (NFL) and
ganglion cell layer (GC) are atrophic
Normal Glaucoma
The End-Stage Eye: Phthisis Bulbi
Trauma, intraocular inflammation, chronic retinal detachment,

and many other conditions can give rise to an eye that is both
small (atrophic) and internally disorganized
Changes in Phthisis Bulbi :

• Exudate or blood between the ciliary body and sclera and the
choroid and sclera (ciliochoroidal effusion); chronic retinal
detachment; optic nerve atrophy; the presence of
intraocular bone (originate from osseous metaplasia of
the RPE); and a thickened sclera
The End-Stage Eye: Phthisis Bulbi
A 63-year-old woman was diagnosed with type 2 diabetes
mellitus at age 18 years. She has had increasing difficulty with
her vision for the past 10 years. Her most recent hemoglobin A1c
level is 9%. Which of the following pathologic findings is
funduscopy most likely to show?
(A) Corneal stromal dystrophy
(B) Retrolental fibroplasia
(C) Granulomatous uveitis
(D) Capillary microaneurysms
(E) Papilledema
A 50-year-old man was not using protective goggles while
ripping plywood on his table saw and sustained a penetrating
injury to the left eye. A wood splinter is removed. On
funduscopic examination, there appears to be a partial uveal
prolapse, but he has vision in the left eye. Three weeks later, he
has loss of accommodation, photophobia, and blurred
vision in the right eye. Choroidal infiltrates are now seen on
funduscopic examination. What is the most likely diagnosis?
(A) Undiagnosed trauma
(B) Aspergillosis
(C) Sarcoidosis
(D) Fuchs dystrophy
(E) Sympathetic ophthalmia
A 62-year-old woman has had decreasing vision for the past year.
She now has increasing headaches. She has worn
glasses since childhood because of myopia. Funduscopic
examination shows deepening of the optic cup with excavation.
The retina appears normal. Screening of which of the following
would have detected the disease that led to these
findings?
(A) Serum glucose
(B) Serum cholesterol
(C) Homocystine in urine
(D) Blood pressure
(E) Intraocular pressure
SELAMAT BELAJAR

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PATOLOGI MATA

dr. Hermawan Istiadi, M.Si.Med

Eyelids : not cover completely proptotic eye

Chronic corneal exposure to air

Basal cell Carcinoma of Eyelid

• Asal : Sel Basal

• Asal : Pilosebaceous follicles / sebaceous glands

• Asal : Pilosebaceous follicles / sebaceous glands

Reduction in the number of goblet cells –

Painful Loss Of Vision

Dense Stromal Fibrosis

Uneven distribution of tear film over the adjacent cornea - focal

Pterygium Dellen Pinguecula

De novo (UV Light risk) / from pre-existing pterygium

De novo (UV Light risk) / from pre-existing pterygium

Corneal Oedema Bullous Keratopathy

Fibrosis/scar Thinned cornea

Chronic herpes simplex keratitis

Wing-shaped superficial opacity

• Lens is a closed epithelial system; the basement membrane of

Exudate (e) in the retinal outer plexiform layer

Histology of a cotton-wool spot

nerve fiber layer infarcts may be detected in a variety

White neovascular membrane

Internal limiting membrane

Anterior Ischemic Optic Neuropathy

Acute phases of AION Papilledema

Trauma, intraocular inflammation, chronic retinal detachment,

Changes in Phthisis Bulbi :

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