DISEASES OF THE CORNEA
Department of Ophthalmology
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IMMUNE MEDIATED KERATITIS
n Phlyctenular keratitis
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n Marginal ulcer( catarrhal ulcer)
n Asso. with acne rosacea
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n Asso with systemic collagen vascular diseasen Chronic serpiginous(Mooren) ulcer
n Interstitial keratitis
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n Disciform keratitis
INTERSTITIAL KERATITIS
n Non ulcerative deep stromal keratitis
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n Infective or allergic in origin
n Causes: Syphilis congenital 90%,
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acquired 10%Tuberculosis
Cogan's syndrome
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Leprosy
Sarcoidosis
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? Local Ag ?Ab reactionn Progressive stage
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n Florid stage
n Stage of regression
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BilateralKeratitis is secondary to uveitis
Treatmemt
n Systemic : penicillin
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n Local: lubricants
steroids
cycloplegics
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MARGINAL(CATARRHAL) ULCERn Form of peripheral ulcerative keratitis
n Immune response to staphylococcal toxins,
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Moraxella, Haemophilus
n Old age
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n Shallow, slightly infiltratedn Typically located at the points of contact of lids
with cornea i.e 4,7,10 and 2 o' clock
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n Clear zone b/w lesion & limbus
n Vascularization + in recurrent cases
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n Treatment Antibiotic+ steroidsROSACEA KERATITIS
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n Ds. of sebaceous glands ofskin
n Women > men
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n Facial eruptions in butterfly
configuration
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n Keratits in 5-10% casesROSACEA KERATITIS
n Infiltrates + small corneal ulcers near limbus
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n Prominent vascularization
n Blepharoconjunctivitis
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n Frequent recurrencesn Local treatment - low dose steroids
n Systemic therapy- Tetracycline 3-6 months
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DoxycyclineKERATITIS IN RHEUMATOID
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ARTHRITISn Sclerosing keratitis
n Perpheral corneal thinning( contact lens
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cornea)
n Acute stromal keratitis
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n Acute corneal meltingSHIELD ULCER IN VKC
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MOOREN'S ULCERn Form of inflammatory peripheral ulcerative
keratitis
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n Two forms Limited form/ Benign
Progressive/Virulent
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? Etiology AutoimmuneIschaemic necrosis
Enzymes produced by conj.
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Degenerative
MOOREN'S ULCER
n Severe pain
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n Signs Superficial infiltration
Shallow ulceration
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Overhanging edgeVascularization at base
Perforation rare
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Sclera uninvolved
NO CLEAR ZONE b/w ulcer & limbus
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DIAGNOSIS OF EXCLUSION--- Content provided by FirstRanker.com ---
TREATMENT OF MOOREN'S ULCER
n Topical antibiotics for infiltration
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n Frequent topical steroidsn Systemic steroids/Cyclosporin
n Conjunctival peritectomy
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n Bandage contact lens
n Lamellar corneal grafts
CORNEAL ECTASIAS
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n Secondary to inflammations
anterior staphyloma
? Non inflammatory
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keratoconuskeratoglobus
pellucid marginal degeneration
KERATOCONUS
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n Non inflammatory, self limiting, ectasia of central
cornea
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n Cornea becomes conicaln Congenital weakness of the cornea
n Manifest after puberty
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? Central/paracentral stromal thinning
? Apical protrusion
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? Irregular astigmatism
Keratoconus
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nn Bilateral in 90% cases, onset asymmetrical
n Etiology
Destruction of stromal tissue by collagenaze
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? Heredity? Asso. with atopic diseases
? Hormonal influences
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? Systemic ds i.e Marfans, Downs, Ehlers Danlos
syndrome
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KERATOCONUSSEVERITY MORPHOLOGY
n Mild K reading
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n Nipple cones
< 48D
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<5mm? Moderate
? Oval cones
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K reading
5-6mm
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48-54 D? Severe
? Globus cones
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K reading
>6mm
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>54 DSYMPTOMS
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n Frequent change of glassesn Decreased tolerance to CL wear
n Monocular diplopia
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n Distortion for distant and near objects
SIGNS
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n Streak retinoscopyn Slit lamp examination
scisssoring reflex
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corneal thinning
stress lines of vogt
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? DDOFleischers ring
oil droplet reflex
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corneal scarring
hydrops
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? KeratometryMunsons sign
malalignment of mires
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Rizzuti's sign
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? Placido discunevenly placed circles
? Corneal topography
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MUNSONS SIGN
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FLEISCHER'S RING
VOGT'S STRIAE
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HYDROPS
TOPOGRAPHY
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n
TREATMENT OF
KERATOCONUS
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n Spectacles early cases
n Contact lenses
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n Epikeratoplastyn Penetrating keratoplasty
n U V cross linking
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DEGENERATIONS
AND
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DESTROPHYDegenerations
Dystrophies
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1.Unilateral and asymmetric1.Bilateral and symmetric
2.Not inherited
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2.Inherited (AD)
3.Located eccentrical y
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3.Central y located4.Usual y accompanied by
4.Avascular
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vascularization
5.Middle life or later
5.Early onset
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6.Progressive lesions
6.Slower in progression
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7.ass. With systemic conditions7.Not related to any systemic or
Ageing, infl amation or trauma
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local conditions
CORNEAL DEGENERATIONS
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n Age related Arcus senilisn Pathological Band shaped keratopathy
Climatic droplet keratopathy
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Salzmann's nodular degeneration
Terrien marginal degeneration
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Arcus senilis
n M/c peripheral corneal opacity
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n Lipoid infiltration of corner seen in elderlyn Present almost universally in people above 60 yrs
of age
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n It is a yellowish white deposit that occurs first in
the inferior then in the superior aspect finally
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joining to form an arcn Lucid interval of Vogt is characteristic, being
sharply defined on the periphery, fading in the
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center
?U/L arcus-associated with carotid ds or ocular
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hypotonyHistology ?lipid first deposited in the
ant.1/2of descemet's membrane and then in
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ant. stroma
ARCUS SENILIS
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Band keratopathy
n Hyaline infiltration of superficial parts of cornea
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followed by deposition of calcium salts in the antpart of Bowmans menbrane
n Causes
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- ocular ? Chr. Ant. Uveitis
- Pth. Bulbi
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- Silicone oil in AC- Chr. keratitis
- Age related
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- Metabolic ? increase ca, CRF- Hereditary
n
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Peripheral inter-palpeberal calcification withclear cornea separating sharp peripheral margins
of the band from the limbus
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n
Spread centrally to form band like chalky
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plaquen
Advance lesion ? nodular & elevated with
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discomfort d/t epi. breakdown
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Treated by chelation- mild casesn Sodium EDTA ? applied with cotton bud
n Exc. Laser keratectomy
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BAND SHAPED KERATOPATHY
Salzmann nod. degn
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n Bluish white avasc. nodule- Sup. Layer of stroma& Bowmann memb.
n Seen with previous corneal Ds
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n Slow progression
n Treat- lam. KP
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SALZMANN'S NODULAR
DEGENERATION
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Spheroidal degn( climatic droplet KP)n Common in people exposed to hot & dry weather
n Exposed inter- palp. cornea sparing the limbus
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n Sign- small amber colored granules in sup.
Stroma,
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n Treat- lamellar KP, PRKTerrien marginal degeneration
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n Usually bilateraln Slow progressive thinning of peripheral cornea
sparing the limbus
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n More frequently seen in males
n Eye is quite with no inflammation
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n Vascularised pannus is seen with yellow depositof lipid
n May cause myopic or irregular astigmatism
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n Perforation can occur with mild trauma
CORNEAL DYSTROPHIES
n Anterior Cogans microcystic dystrophy
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Reis ? Buckler
? Stromal Granular
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Macular
Lattice
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? Endothelial Fuchs endothelial dystrophyPosterior polymorphous
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dystrophy
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Epi. BM dysn Also k/a - Map dot fingerprint dys.
n m/c dys.
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n Onset - 2nd decade
n Recurrent corneal erosions ? 10%
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n Signs- dot like opacity , epi. microcysts, sub-epi maplike pattern
n Treat- same as rec. corneal erosions( saline , bandage
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48hrs, ointment)
Reis ? Buckler dys
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n AD
n Onset- early childhood
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n Arise in region of bow. Membn Recurrent erosions
n Cornea- irregular dense grey sub-epi. Opacity
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arranged in fish net pattern
n Treat- PRK, lam KP
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n HIGH RECURRENCE AFTER CORNEALTRANSPALANT
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REIS-BUCKLERDYSTROPHY
Hereditary stromal corneal dys
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n Bilateral
n Around puberty
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n Central area of cornea, chr. By discrete areas ofopacity in sup. Areas of stroma
n Hyaline deposits b/w the cornel lamellae
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n Symptom less without inflammation
n Progress slowly until visual impairment
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n Treat- KP--- Content provided by FirstRanker.com ---
GRANULAR CORNEALDYSTROPHY
MACULAR CORNEAL
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DYSTROPHY
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GRANULAR MACULAR
LATTICE CORNEAL DYSTROPHY
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ENDOTHELIAL CORNEAL DYS
n M/C Fuch's dys-
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n AD, seen in elderly
n m/c in females
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n d/t changes in endothelium with formation ofhyaline excrescences on DM ( corn. Guttata)
n TREAT- Nacl 5% drop or ointment,
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bandage contact lens.
-Pen KP
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FUCH'S ENDOTHELIALDYSTROPHY
n Stage of cornea guttata
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n Stage of endothelial
decompensation
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n Stage of bullouskeratopathy
n Stage of scarring
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