2-20 - CornealDegen+Dystrophy+Trauma Flashcards

1
Q

Arcus senilis

A
  • White perilimbal band w/ clear zone
  • Deposition of phospholipid/cholesterol at stroma.
  • Age-related (but if young patient, may indicate high cholesterol)
  • Asymptomatic, no treatment needed
  • Common
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2
Q

Arcus juveniles

A
  • Rare
  • Can involve only sector of peripheral cornea
  • Can be associated w/ genetic high blood cholesterol.
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3
Q

Vogt’s limbal girdle

A
  • Subepithelial degeneration w/ or w/o calcium deposits
  • Common
  • Age-related
  • Asymptomatic, no treatment needed.
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4
Q

Dellen

A
  • Localised thinning of peripheral cornea parallel to limbus
  • Dehydrate + compacted stroma
  • Due to tear film local instability (common in RGP CLs)
  • Fluorescein pools w/o epithelial damage
  • If longstanding, scarring and vascularisation possible.
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5
Q

Band keratopathy

A
  • Calcium deposition in subepithelial space, bowman’s layer, and anterior stroma.
    Due to either:
  • Age (idiopathic)
  • Chronic ocular inflammation
  • Metabolic disturbance
  • Hereditary
    Symptoms (if any):
  • Vision affected if central
  • Ocular irritation
    Signs:
  • Plaque of calcium deposits (generally nasal/temporal but can extend centrally)
  • Small holes or clefts at plaque possible.
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6
Q

Terrien’s marginal degeneration

A
  • Non-inflammatory progressive thinning of peripheral stroma
  • Idiopathic
  • Epithelium fine
  • Asymptomatic early on + slow progression
  • Vascularisation associated possible
  • Irregular astigmatism can decrease vision.
  • Bilateral, rare but more common in young men
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7
Q

Mooren’s ulcer

A
  • Rare type of ulcerative keratitis
  • Uni or bilateral
  • Autoimmune to stroma?
    2 forms:
  • Aggressive in young african descent
  • Less severe in older white men
    Symptoms:
  • Redness
  • Pain
  • Photophobia
  • Vision decrease
    Signs:
  • Progresses circumferentially + centrally
  • Epithelial defect
  • Healing associated w/ corneal thinning, vascularisaton, and scarring.
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8
Q

Roscaea keratitis

A

Rosacea:
- Skin disease w/ bufferfly rash pattern
- Itching, flushing of skin
- Common, idiopathic
- Worse w/ sun exposure
- Common to have dry eye + blepharitis
- Mild to severe
Sometimes associated w/
- Marginal keratitis
- Neovasc

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9
Q

Recurrent corneal erosion syndrome

A

RCES
- Epithelium to BM attachment instable
- Uni/bilateral
- Idiopathic
Either:
- Dystrophic RCE associatd w/ corneal dystrophy
- Post-traumatic RCE – following superficial corneal trauma.
Symptoms:
- Recurrent sharp ocular pain when waking (epithelium rips off BM)
- Variable duration
- Blurred vision
- Lacrimation
- Photophobia
Signs:
- Localised epithelial irregularities (may see detached epithelial pathc)
- Microcysts after healing (maybe raised)

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10
Q

Epithelial basement membrane dystrophy

A

EBMD
a.k.a. “Map-dot Fingerprint” dystrophy, Cogan’s microcystic dystrophy, or anterior basement membrane dystrophy.
- Due to poor epithelial attachment to abnormal BM
Either:
- Maps - Multilaminar BM extends to epithelium
- Dots – Deep epithelial cells, which normally migrate to surface, are trapped under BM
- Fingerprints – Folds of reduplicated BM within epithelium

  • Most common epithelial dystrophy
  • Autosomal dominant, but often unaware of family history.
  • Asymptomatic, but can affect vision if centre.
  • Can be associated w/ (or cause) RCES
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11
Q

Meesmann’s dystrophy

A

a.k.a. juvenile hereditary epithelial dystrophy.
- Many tiny cysts within epithelium
- Early in life, slow progression
- Autosomal dominant inheritance
- Vision minimal affected
- May develop recurrent erosions.
Symptoms:
- Irritation
- Photophobia

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12
Q

Reis-Bücklers dystrophy

A
  • Damage + scar to bowman’s layer + ant. Stroma
  • Irregular bands of collagen progressively replace bowman’s layer in honeycomb pattern
  • Sub-epithelial opacities centrally, most dense in mid-periphery
  • Rare, bilateral
  • Severe, present young
  • Hemi-desmosome loss = Recurrent erosion.
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13
Q

Granular dystrophy

A
  • Rare, autosomal dominant
  • Small granular deposits of hyaline in central ant. stroma, w/ clear zones between. Peripheral spared, deposits can merge.
  • Present within 1st decade
  • Decreased vision when opacities merge
  • May have recurrent corneal erosions.
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14
Q

Lattice dystrophy

A

Deposition of amyloid protein in stroma
- Branching refractile lines
- Diffuse ant. stromal haze
- Significant scarring later
Poor epithelial adhesion = painful recurrent erosions

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15
Q

Macular dystrophy

A
  • Central, grey, poorly defined opacities w/ cloudy stroma
  • Mucopolysaccharide deposits in stromal keratocytes
  • Corneal thinning
  • Rare autosomal recessive
  • Progessive, vision loss in 1st or 2nd decade w/ needing corneal transplant.
  • Does NOT lead to RCES
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16
Q

Fuch’s endothelial dystrophy

A
  • Common, progressive.
  • More in women
  • Generally autosomal dominant, but recessive possible
  • Start at endothelial dystrophy, then becomes Fuch’s dystrophy in 5th/6th decade.

Stage 1 – Corneal Guttata
Stage 2 – Progessivel endothelial loss (due to barrier + active transport breakdown) -> stromal + epithelial oedema.
- Symptoms = Glare, photophobia, blurred vision when waking
- If bullous keratopathy, pain
Stage 3 – Degenerative pannus + scarring + permanent vision loss (requires graft)

17
Q

Corneal guttata

A
  • Collagen deposits thickens descemet’s membrane (where otherwise would be endothelial cells so endothelial loss)
  • Visible under slit lamp w/ specular reflection as “beaten metal”
  • Pleomorphism + Polymegathism of endothelium.
18
Q

Posterior polymorphous dystrophy

A
  • Rare, asymptomatic usually, but if symtpoms, early in childhood.
  • Autosomal dominant
  • Abnormal endothelial cells (w/ more epithelial phenotype)
  • Grouped vesicular/bubble-like lesions on endothelium
  • Linear, band-like lesions (snail track appearnace)
  • Can cause endothelial compromise -> stormal + eptiehlial oedema
  • Endothelial cells can grow into angle -> glaucoma
  • Associated w/ iris abonormalities e.g. iridocorneal adehsions.
19
Q

Acid vs Alkali burns

A
  • Alkali lipophilic so penetrates cornea for more damage
  • Alkali kill cell by binding to lipids and disrupting cell membrane
    Acute:
  • Corneal epithelium sloughing, stromal + endothelial necrosis –> stromal oedema.
    Long term:
  • Serious opacification
  • Limbal blancing (white) = limbal stem cell loss.
  • Poor prognosis