anatomy and diseases of the uvea

7/31/2019 Anatomy and Diseases of the Uvea

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Anatomy and diseases of theuvea

Anatomy:Uvea is the vascular coat of eye ball and

lies between the sclera and retina. Uvea is

composed of three parts i.e. iris, ciliary

body and choroid. These three portions

are intimately connected and a disease of

one part also affects the other portionsthough not necessarily to the same

degree.


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Uvea


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IRIS


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Anterior surface has two zones:

1) Papillary zone: is flat and has a dark

border at the papillary margin , known aspapillary ruff. Junction of papillary and

ciliary zone is marked by a smooth ridge

known as collaret.

2) Ciliary zone: towards the ciliary

border has ciliary crypts. Histologically

iris has got 5 layers (from before

backward).1- Endothelium: flat nucleated cells

absent over the crypts probably to allow

free movement of the aqueous in and out

of the iris.


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2- Vessel layer: consist of blood

vessels lying in collagen fibers,

chromotophores etc.,3- Muscular layer: two muscles:

a) Sphincter pupillae- plain muscle

developed from neuroectoderm- suppliedby parasympathetic fibers coming through

the 3rd nerve (relayed in ciliary ganglion).

b) Dilator pupillae- also arise from

neuroectoderm and supplied by cervicalsympathetic fibers reaching the eye through

long ciliary nerves (not relayed in ciliary

ganglion).


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4- Pigmented epithelium- two layers.

The two layers are loosely attached to

each other and there is a potential space

between the 2 layers. In iridocyclitis

there is adhesion of the iris to the lens.

When a mydriatic is applied the posteriorlayer of pigment epithelium gets partly

detached. This produces pigment

deposition and pigmented patches on the

anterior lens capsule (broken posteriorsynechiae).


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5- Internal limiting membrane- fine and

homogenous structure, not consistently

present.

Function of the iris:

1- Regulates the entry of light into the eye

by changing the size of papillary aperture.

2- Cuts away the peripheral aberrations.

3-Absorption of aqueous also takes place

from its surface.


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Ciliary body


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The inner surface is directed towards

the cavity of the eye ball and is divided

into two portions anterior (pars plicata )

and posterior (pars plana).

Ciliary muscle consists of:

1. Meridional fibers.

2. Circular fibers.

3. Radiating fibers.


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Meridional fibers on contraction pull the

suprachoroidea forwards and release the

suspensory ligament allowing the lens tobecome more convex as in

accommodation. The pars plicata has

about 70 ciliary processes. They secrete

aqueous.

Functions of ciliary body:

1. Brings about accommodation.

2. Formation of aqueous.3. Helps in drainage of aqueous at the

angle of anterior chamber.


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3) Choroid:Choroid is the analogue of pia-arachnoid

of the brain and serves the same purposeof supplying nutrition to the neural

portion of eye i.e. retina. Choroid is

composed of five portions.

1. The outer most is

SUPRACHOROIDEA a potential space

between the choroid and sclera. This is

lined by endothelium and traversed byfibrous trabeculae.


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This space is utilized for the treatment of

aphakic glaucoma in the operation of

cyclodialysis.

Deeper to it are three vascular layers.

2. Layer of LARGE BLOOD VESSELS is

outer most.

3. Next comes MEDIUM SIZED BLOOD

VESSELES.

4. and SMALL BLOOD VESSELES or

CHOROIDO-CAPILLARIES.


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Layer of choriocapillaries is the most

important. It serves to provide nutrition to the

outer layers of retina. The choriocapillaries

are much wider than the capillaries

elsewhere. Their diameter varies from 10 to

30 microns.

5. The innermost layer is avascular known as

MEMBRANE of BRUCHS. This is

composed of elastic and cuticular lamina and

pigment epithelium of retina is intimatelyattached to it.


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Classification:A) Depending upon the site of

inflammation:

1) Anterior uveities

- iritis.

- cyclitis.- iridocyclitis.

As iris and ciliary body are continuous,

iritis seldom occurs without some

inflammation of the ciliary body and viceversa.


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Iritis


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cyclitis


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choroiditis


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choroiditis


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NonGranulomatousGranulomatous

Acute onset of severe

inflammation (red eye).

Short.

Small KPs.

Intense aqueous flare.

Absent.

(11) Onset: insidious,

eye relatively white.

2) Course: chronic.

3) KPs: medium and large

and often mutton fat.

4) Slight aqueous flare.

5) Nodules on iris present

Koeppe's nodules are

seen on the pupillary

margin. Busacca's

nodules are seen near

coflarette.

C) Clinicopathological classification:


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Fine synechiae.

Tends to affect anterior

uvea.

Fine punctate opacities in

the vitreous.

Allergy.

Complications: few.

6) Dense broad based

posterior synechiae.

7) Tends to affect entire

uvea.

8) Heavyvitreous exudate

or veils common.

9) Etiology: direct

organismal infection.

10)Complications: more


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Etiology:

In most cases it remains obscure.

1) Infection:

a. Exogenous- the organisms reach the eye

from outside.

i) Perforating injury.ii) Perforating corneal ulcer.

iii)Intraocular operation.

This usually leads to suppurative iridocyclitis,

endophthalmitis and even panophthalmitis.

b. Secondary- due to spread from one or other

of the ocular tissue- corneal ulcer, scleritis.


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c. Endogenous: Organisms primarily lodged

in some other organ of the body reach the

eye through the blood stream.i) Viral- herpes simplex, herpes zoster,

measles, mumps, rubella.

ii)Bacterial: tuberculosis- syphilis, leprosy,

gonorrhea, brucellosis.

iii) Fungal: histoplamosis, asperigillosis,

candida albicans, actionomycosis.

iv) Protozoa: Toxoplasmosis.v) Nematodes: ankylostomiasis, filariasis.


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2) Allergy:

a. Bacteria:

i) T.B. usually of the lungs, lymph nodes.ii) Streptococci- teeth, tonsils, sinuses,

urogenital tract.

Primarily source of infection exists at these

sites. At one time the infection wasgeneralized by the escape of organisms into

the blood stream when the ocular tissue- uvea

had become sensitized to them. At a later

date further dissemination of the organisms

or their proteins meeting the sensitized uveal

tissue excites an allergic response.


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b. Lens proteins- phako- anaphylactic

reaction. They have also a toxic action on

iris.c. Uveal pigment- sympathetic ophthalmitis.

3) Constitutional disorders:

Diabetes mellitus, gout, rheumatoid arthritis(adult and juvenile), ankylosing spondylitis.

4) Trauma:

a. Blunt.b. Sympathetic ophthalmitis.


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5) Idiopathic:

a. Sarcoidosis.

b. Vogt- Koyanagi- Harada's disease.c. Behcet's disease.

6) Miscellaneous:

Intraocular haemorrhage, intraocular tumour.

Pathology:

Inflammation of the iris and ciliary body has

the same characteristic as other vascularconnective tissue.


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Sarcoidosis


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1. dilatation of the blood vessels.

2. exudation of protein rich fluid into the

tissue space with leucocytes or

lymphocytes.

1) Pupil: small and reacts sluggishly to

light owing to

a. hyperemia of the radially disposed

vessels of the iris.

b. exudate contains toxic substances whichirritate the sphincter pupillae (this muscle in

more powerful than dilator pupillae).


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2) Delicate patterns of iris:crypts-

become blurred and indistinct (muddy iris).

3) Colour of iris:undergoes change-

brown iris becomes grayish.

4) Exudate in AC:a. Aqueous flare.

b. Sometimes hypopyon.

5)Exudate in posterior chamber:induces adhesion between posterior surface

of iris and the lens (posterior synechiae).


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6) Exudate in vitreous: vitreous haze.

Symptoms:1) Pain the eye ball:

It is dull aching, worse at night, it may be

referred to the forehead along the 1st

division (ophthalmic) of the trigeminal. It isdue to:

a. The iris has a rich nerve supply; the nerve

endings are stimulated by a high

concentration of toxic substances.

b. Spasm of ciliary muscle.

c. Secondary glaucoma.


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2) Diminition of vision due to:

a. Spasm of ciliary muscle- pseudo myopia.

b. turbidity of aqueous, vitreous.c. exudate in papillary area.

d. choroidities when associated in

panuveitis.

e. Secondary glaucoma.

f. complicated cataract.

g. cyclitic membrane.

h. retinal detachment.

3) Photophobia, redness, watering.


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Signs:

1) Oedema lids in severe cases with watery

discharge.2) Ciliary and conjunctival congestion.

3) Cornea:

May show oedema, KPs- These are small

accumulations of cells derived from theuveal tract upon the back of the cornea.

They are found in iridocyclitis, and

choroidities. In iridocyclitis the nutrition of

the corneal endothelium becomes affected

so that the cells become sticky and may

desquamate in places.


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5) pupil:Is small, irregular (due to posterior

synechiae) and reacts sluggishly to light.This irregularity is exaggerated when pupil

is dilated with mydriatic- festooned pupil

(resembles a wreath such as is placed on a

war memorial). Posterior synechiae may be:

a) filiform seen in non granulomatous

uveitis.

b) broad based posterior synechiae seen ingranulomatous uveitis.

c) annular or ring synechiae or seclusion

pupillae.


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In severe cases of plastic iridocyclitis or after

recurrent attacks the whole circle of the

papillary margin may become tied down to theanterior lens capsule.

It is of great danger to the eye since if

unrelieved it inevitably leads to secondary

glaucoma- the aqueous unable to pass forwards

into the anterior chamber, collects behind the

iris which becomes bowed forward like a sail, a

condition which is called iris bombe. Regardedfrom in front, the anterior chamber is seen to be

funnel shaped, deepest in the centre and

shallowest at the periphery.


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OCCLUSIO PUPILLAE (blockedpupil):

In severe cases of irido cyclitis the exudates

may cover or may organize across the entire

papillary area which becomes ultimately

filled by a film of opaque fibrous tissue- thecondition is called occlusio pupillae

occlusion pupillae and seclusion pupillae

often occur together.

Occlusion pupillae may occur with totalposterior synechiae.


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6) IRIS:a- "Muddy iris"delicate pattern or iris

crypts become blurred and indistinct.b- nodules- these may be of 2 types:

i) pseudo nodules: These consists of

accumulations of lymphocytes and epitheloid

cells which are deposited on the iris koeppes

nodules near the papillary border and

Busacca's nodules near the collarette.They

disappear without fibrosis.

ii)True nodules: These arise in the stroma of

the iris and on healing leave behind a scar or

an atrophic patch.


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nodules


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Ophthalmia

nodosa

Sarcoid

nodule

Leprosy

nodule

Syphilitic

nodule

Tuberculous

nodule

Pink

vascularReddish

vascular

capillaries

pass over and

in the nodule

Pale

avascular

Yellowish-red

avascular

Grey or yellow

avascular

capillaries pass

over nodule.

1.Colour

Any partAny partPupillaryregion

Pupillary or

ciliary regionPupillary or

ciliary region2.Location

Grow slowlyGrow slowlyGrowslowly

Grow

relatively

quickly

Grow slowly3.Progress


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Syphilitic nodule


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9) CILIARY TENDERNESS: particularly when cyclitis


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9) CILIARY TENDERNESS: particularly when cyclitisis predominant.

Active iridocyclitisHealed iridocyclitis

1) symptoms:

Pain, redness,

photophobia, diminished

vision

Diminished vision may be

present.

2)signs:

a- ciliary and conjunctival

congestion

b-KPs grayish white,

circular with regular

margin.

c- Aqueous flare present.

d- Ciliary tenderness

present.

Eye is white

Pigmented KPs with

crenated or serrated

margin.

Absent

Absent


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COMPLICATIONS:

1) Secondary glaucoma:hypertensive

iridocyclitis. This may be due to:i) clogging of trabecular meshwork by

inflammatory exudates- plasmoid aqueous.

ii) seclusio pupillae.

iii) seclusio pupillae produces iris bombewhich gives rise to peripheral anterior

synechiae.

iv) occlusion pupillae.

v) increased capillary hydrostatic pressure

leading to increased aqueous formation.


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2) Complicated cataract:Refer lens

chapter.

3) Cornea:a) a corneal opacity may result from

persistent oedema.

b) band shaped keratopathy particularly in

cases of Stills disease.c) Retrocorneal membrane due to

organization to exudates behind the cornea.4) Cyclitic membrane:

It is a membrane formed in the anterior

vitreous behind the lens due to organization

of inflammatory exudates.


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Significance:

1-causes diminision of vision

2- causes traction retinal detachment.3- one of the causes of pseudoglioma in

children.5) Retinal detachment:a) due to contraction of cyclitic membrane.

b) It may be exudative retinal detachment

when iridocyclitis is associated with

choroiditis.


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Retinal detachment


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6) Phthisis bulbi:a) damage to ciliary body occurs due to

organization of exudates on the surface.b) contraction of cyclitic membrane may

detach the ciliary body. These result in

decreased production of aqueous leading

to ocular hypotony and phthisis bulbi.


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Phthisis bulbi


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INVESTIGATIONS:

1.General examination for evidence of leprosy,

tuberculosis, syphilis, rheumatoid arthritis etc.2.Urinealbumin, sugar and microscopic

examination for pus cells.

3.Stools- ova and cyst.

4.TuberculosisMantoux test, X-ray chest5.Syphilisblood VDRL

6.Rheumatoid arthritis- Rose- waaler test.

7.Toxoplasmosis: HA test, dye test and ELISA

test.

8.Thorough dental, ENT, and gynaecological

check up to rule out septic foci


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TREATMENT:-I) Local:

i. Cycloplegic mydriatic therapy:a) 1% atropine drops or ointment t.d.s. This isthe most important drug in the treatment of

iridocyclitis. It acts as follows:

1-puts the iris and ciliary body at rest.2-diminishes congestion of iris and ciliary

body.

3-prevents the formation of posterior

synechiae or tends to break those alreadyformed.

4-has mild anaesthetic action.

b) I h il d dil i h


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b) In cases where pupil does not dilate with

atropine, subconjunctival injection of 0.3 cc

mydricaine is given (this contains atropine,

adrenaline and procaine and is a potent

mydriatic).

c) In cases of atropine allergy- 2%

homatropine, 1% cyclopentolate, 0.5%hyoscine may be used.

ii) Cortisone drops or ointment 3-6 times a

day. This is useful because of the allergicnature of the disease. In severe cases

subconjunctival injection of Dexamethasone is

given.


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NB: Indiscriminate and long term use ofcorticosteroid may cause rise in intraocular

pressure.iii) Hot fomentation t.d.s.

iv) dark glasses.

II) General(11)Treatment of causative factor- T.B.,

infected teeth etc., should be treated or

eliminated.

2) Analgesics- paracetamol.3) Systemic corticosteroid in severe cases of

iridocyclitis or when associated with

choroiditis.


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III) Treatment of complications:

1) secondary glaucoma:

a) local use of 1% atropine,corticosteroid, hot fomentation.

b) Tab. Diamox 250 mg t.d.s.

c) surgical- paracentesis. Peripheral

iridectomy can be done to relieve the

papillary block in cases of iris bombe. In

cases with extensive peripheral anterior

synechiae due to iris bombe,trabeculectomy may be required.


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Earlier, Fuchs four dot iridotomy was

done by passing Von Graefes knife across

AC puncturing and counter puncturingboth cornea and iris. This is now of

historical interest only.

2) Complicated cataract: Refer lens

chapter.


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Choroiditis

Etiology:

I-Infection

1) Endogenous

a. virus - Rubella.

b. bacteria - TB, syphilis.

c. fungi - histoplasmosis.

d. protozoa - toxoplasmosis.

e. Nematodes - ankylostomiasis, filariasis.

2) Exogenous : perforating injury; perforated corneal ulcer ect,these lead to suppurative choroiditis , endophthalmitis and

even panophthalmitis.3) Secondary : spread of inflammation from posterior scleritis

II) Idiopathic: sarcoidosis ,Vogtkoyanagi - haradas disease


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Fundus examination shows :

1) vitreous haze and vitreous opacities.

2) patches of choroiditis. These patches areyellowish or yellowish white with ill definedfluffy margin.

3) Later the exudates undergo resolution byfibrosis and the patches become white with

well defined margin.

Complication :

1) complicated cataract result from defective

nourishment of the lens.2) Exudative retinal detachment due to exudation offluid between pigment epithelium and rods andcones .


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3) optic neuritis : result when the inflammatory

patch is close to optic disc .

4) consecutive optic atrophy : from the destructionof retinal ganglion cells .

Varieties of posterior uveitis :

It classified according to the situation and character

of the patches:1.Circumscribed choroidities.

2.Diffuse choroiditis.

3.Disseminated choroiditis.

4.Anterior choroiditis.

5.Central choroiditis.

6.juxta papillary choroiditis of Jensen.


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Symptoms :Visual disturbances are common:

1) visual acuity may become defective more markedlywhen:

a- the lesion is in the central area near the posteriorpole.

b- cloudiness of vitreous is present.

2) metamorphpsiadistortion of object may be seen .

3) micropsia and macropsiaobjects appear smaaleror bigger, due to separation or crowding ofretinal elements respectively.

4) photopsiasubjective flashes of light, due to

irritation or retinal elements by exudates.


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5) positive scotoma: perception of black spot before the eye.

6) negative scotoma: hiatus in the field of vision ( patient is notaware of this ).

specific type of posterior uveitis :

Tuberculosis of the choroid occurs in acute milliary and chronicforms:

1) acute - in milliary tuberculosis there are multiple small spotsscattered all over the fundus varying in size from pin point to2mm diameter.

2) chronic tuberculosis - may result in:

-diffuse choroiditis.- disseminated choroiditis.

- solitary or conglomerate tubercle.


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Differences between active and healed choroiditis :

Active choroiditis Healed choroiditis

1-Vitreous haze is present.

2-Yellow patch with

feathery margin.

3-Borders are not

pigmented.

4-Produces passive scotoma

due to inflammatory

exudates in front of

light sensitive element.

5-Underlying choroidal

vessels obscured.

6- Often requires treatment.

Vitreous is clear.

White patch with

circumscribed margin.

Borders are pigmented.

Produce negative scotoma

due to destruction of

photoreceptors.

Large choroidal vessels.

No treatment required.


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congenital abnormalities of the uveal tract:

persistent pupillary membrane - in the early foetaleye pupil is covered over by a delicatemembrane known as pupillary membrane.

conginital aniridia : failure of iris to develop.There is usually associated nystagmus andfoveal hypoplasia.

heterochromia iridis : part of the same irisusually a sector may differ in colour from theremainder .

heterochromia iridum : one iris may havedifferent colour from the other.

behcets syndrome: it is an acute iridocyclitis seenin young adult associated with:- hypopyon,ulcerative lesion in mouth.


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Congenital aniridia


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Iris coloboma


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heerfordts disease: it is a bilateral affection characterized byinvolvement of the entire uveal tract, the parotid gland andcranial nerve.

Vogt koyanagi haradas syndromeFuchs heterochromic iridocyclitis

Sympathetic ophthalmitis

Rubeosis iridis: it is characterized by the development of newand enlarged vessels on iris.and is seen in:

i) diabetes mellitusii)After central retinal vein occlusion

iii)After central retinal artery occlusion

In cases of diabetes mellitus with rubeosis and mature cataractiridectomy may have to be omitted or peripheral iridectomydone in an area where rubeosis is not present

Complication:secondary glaucoma due to fibro vascularmembrane blocking trabecular meshwork and due torecurrent hyphaema


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Vogt koyanagi haradas


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og oya ag a adasyndrome


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Nodules on the iris are seen in the following disease

1) Iridocyclitis: due to tuberculosis, syphilis, leprosy

2)Iris melanoma:usually seen in people between 40 and 50years and presents as a solitary pigmented nodule on thelower half of iris feature that should arouse suspicion ofmalignancy include:

- ectropion uveae

- pupillary distortion

- neovascularization

- raised IOP

- increase in nodule size

3) Lisch nodules

4) Juvenile xanthogranuloma


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Iris melanoma


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Lisch nodules


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PANOPhTHALMITISDefinition:

An intense suppurative inflammation of the entire uvealtract which fills the eye ball with pus, extends to all thestructures of the eye and ends in complete destruction ofthis organ.

Etiology:

Infection is by pyogenic organisms:

1) ps. Pyocyanea

2) pneumococcus

3) staph

4)strept5) E. coli

6) gonococcus


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i) Exogenous infection:

1) perforated corneal ulcer

2) penetrating wounds

3) intraocular operation

ii) Endogenous infection

Results from septic embolism of a retinal or a choroid vessels.Such cases occur in the course of infectious diseasepneumonia, meningitis


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5) AC filled with pus


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5) AC filled with pus.

6) increased I.O.P .

7) in severe cases the pus bursts through the wallof the globe.

Treatment:

I- At early stage :1) intensive treatment by antibiotics both localand systemic.

2) analgesics- tap.paracetamol.

3)hot fomentation.

II A it b id t th t th


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II- As soon as it becomes evident that the eye

cannot be saved evisceration is done.

Frill excision: if the entire sclera is left. There is

considerable pain, reaction and delayed healing.

It is not considered advisable to enucleate in cases

of panophthalmitis on account of the danger of

causing meningitis.

Prognosis:is always bad. However the condition does not

cause sympathetic ophthalmitis.

H t h i d h


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Hetrochromia waardenhurgs

l


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Iris prolapse

Iris hemangioma


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Iris hemangioma

Iris cyst


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y

Iris nevus


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Iris nevus


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Iris tumor


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Iris neovascuralization


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Herberts pits


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hypopyon


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Keratouveitis

' d l


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Koeppe's nodule

S h


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Synechiae posterior


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pseudo exfoliation


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anatomy and diseases of the uvea

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