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Diseases of Anterior Seg. > cornea pt 1: Corneal anomalies, dysgenesis, and degenerations > Flashcards

cornea pt 1: Corneal anomalies, dysgenesis, and degenerations Flashcards

1
Q

Recurrent Corneal Erosion is a problem with which layer of the cornea

A

basement membrane

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2
Q

it is called recurrent because …

A

its recurrent breakdowns of the epithelium due to the defective adhesions in the basement membrane

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3
Q

what causes RCE?

A

trauma like a clean slice to the cornea or its spontaneous

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4
Q

How long does it take a wound that caused RCE to heal?

A

8-12 weks. The epithelial cells undergo mitosis.

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5
Q

RCE symptons occur most often ____ (am or pm)

A

pain, FBS occurs most often in AM

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6
Q

recurrentces of RCE is how often?

A

every monthy or every year

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7
Q

name the preventative txts for RCE

A

plently of fluids, avoid dry environments, wake up with eyes closed, protective glasses

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8
Q

Someone has RCE. Their slit lamp findings were normal. But on second look you say microsysts (that didn’t staing) , surface irregularity, nafl staining. How are you going to txt?

A

genteal every night until tube is gone, Freshkote, Muro 128 5%(solution and/or ung)

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9
Q

you decide to employ a bandage cl on your patient with RCE. What else should you add to this bandage cl? What are you going to be careful of with bandage cl? In terms of withdrawl.

A

Ofloxacin (prophylatic antibiotic ) , not to withdraw too soon. Need about 4 weeks.

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10
Q

What is the rx for doxycycline? And why is it used in RCE management?

A

50-100mg, once or twice a day . Its used to inhibit the MMP9s with rce

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11
Q

an anomaly is

A

Something different, abnormal, peculiar, or not easily classified; a deviation from the common rule, type, arrangement, or form

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12
Q

normal adult cornea diameter:

A

12

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13
Q

Microcornea defined:

A

10; can be bilateral or unilateral

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14
Q

pts with microcornea are more prone to

A

angle closure glaucoma

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15
Q

Megalocornea is more common in F or M

A

M

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16
Q

t/f. Patients with Megalocornea are not prone to glaucoma.

A

true. They have nomal iop

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17
Q

Megalocornea is defined as

A

bilateral anterior segment enlargement

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18
Q

greater than 13 mm after 2 years is

A

megalocornea

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19
Q

Anteriorly displaced, prominent Schwalbe’s line

A

Posterior Embryotoxon

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20
Q

management of posterior embryotoxon

A

no txt necessary

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21
Q

what is schwalbe line

A

is the termination of decemats membrane marks transition between cornea to sclera

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22
Q

Axenfeld- Rieger’s Anomaly

A

posterior embryotoxon,iris stromal hypoplasia,iris strands that attach to posterior embryotoxon

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23
Q

What would make Axenfeld-reiger’s anomaly a syndrome?

A

Glaucoma

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24
Q

what is the least appropiate option for Axenfeld reigers

A

trabeculoplasty

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25
Q

The best option for axenfeld reiger is aqueous suppressants. Beta blockers or CI

A

true

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26
Q

Peters’ Anomaly description

A

central corneal opacity; focal absence of Descemet’s membrane and endothelium, iridocorneal adhesions, shallow AC

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27
Q

Peters’ Syndrome involves

A

Glaucoma and pt starts to develop systemic problems.

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28
Q

patients may also have ______ with peter’s . tip: another ocular diagnosis.

A

cataract especially if lens adhering to cornea

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29
Q

txt for peter’s anomaly

A

treat glaucoma, penetrating keratoplasty

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30
Q

yellow-white hazy ring of stromal deposits, cholesterol, has a lucid interval between ring and limbus

A

Arcus Senilis (aka Gerontoxon)

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31
Q

arcus senilis starts inferior to superior and encircles cornea

A

TRUE

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32
Q

posterior embroytoxin starts inferior to superior and encircles cornea

A

FALSE. It starts in perphiery

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33
Q

arcus senilis is common in which race?

A

African americans.

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34
Q

incidence of arcus senilis ?

A

50-60 y.o; and older than 80 nearly everyone

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35
Q

management of arcus senilis ?

A

lipid panal

36
Q

main worry of unilateral arcus sensilis?

A

the cartoid artery could be blocked. Listening to bruit here

37
Q

small, irregular chalk-like opacities – subepithelial, irregularly shaped but collectively have a crescent

A

White Limbal Girdle of Vogt

38
Q

white limbal girdle of vogt is located at the limbus more in the termporal .

A

false. Nasal more than termporal

39
Q

whats the difference btwn type I and type II White Limbal Girdle of Vogt

A

Type I – separated by limbus by narrow lucid area; no lucid area between limbus and opacities

40
Q

most common corneal degeneration

A

White Limbal Girdle of Vogt

41
Q

txt for white limbal girdle of vogt

A

none. It has no clinical significance. Just a finding.

42
Q

grayish-white polygonal stromal opacities separated by clear spaces

A

Mosaic (Crocodile) Shagreen

43
Q

which layer of cornea is Mosaic (Crocodile) Shagreen located?

A

stroma. Most noticeably centrally , rarely impacts vision. Involutional

44
Q

dust-like gray dots and flecks in the deep corneal stroma

A

Cornea Farinata

45
Q

cornea farinata’s degenerative pigment must be differentiated from

A

guttata. Guttata is in the endothelium. Cornea farinata is in the stroma.

46
Q

refractile, punctate, comma-shaped and filamentous amyloid deposits most common centrally and posteriorly in stroma

A

Polymorphic Amyloid Degeneration

47
Q

DDX: cornea farinata and lattice dystrophy

A

Polymorphic Amyloid Degeneration

48
Q

Polymorphic Amyloid Degeneration is associated with systemic dz

A

false. Its not associated with disease. You thinking of lattice corneal dystrophy type II with FAP.

49
Q

progressive non-inflammatory conical-shaped corneal thinning (ectasia), usually inferior to center of cornea

A

Keratoconus

50
Q

easy way to remember cornea farinata

A

it has a flower like appearance

51
Q

keratoconus is non progressive

A

false. Its progressive. Onset is young adulthood and progresses throughout life

52
Q

which of the following is not a late change of keratoconus? A. visible fleischer’s ring, vogt’s lines (vertical stress lines in desments membrane, increased thing of interior stroma, munsons sign, steep mires on keratometry

A

steep mires on keratometry. That’s an early change not a late change. Other early changes involve refraction too.

53
Q

corneal scarring, prominent nerves, and acuity 20/60 or worse are late changes in

A

Keratoconus

54
Q

a pertinent negative in keratoconus

A

fletchers sign

55
Q

acute corneal hydrops is an additional complication keratoconus. What are acute corneal hydrops?

A

Ruptures in Descemet’s membrane which allows aqueous fluid to invade the cornea. Management with bandage cl, pressure patch, cycloplegic and nacl 5%

56
Q

this condition has been associated with marfan syndrome, down syn, ehlers danols syndr, atic disease. Atopic kertoconjunctivies VKC, RP, and FLOPPY eyelid syndrome

A

Keratoconus

57
Q

management of keratoconus

A

spx, rgp cl, corneal intacs, corneal cross linkin, penetrating keratoplasty

58
Q

limbus to limbus corneal thinning

A

Keratoglobus

59
Q

Keratoglobus may be associated with what systemic syndrome?

A

Ehlers-Danlos syndrome

60
Q

what is true about keratoglobus?

A

treatment options are limited and not very successful

61
Q

t/f kertoglobus pts are more prone to trauma.

A

ture. They have a ectasia (cornela thining)

62
Q

narrow arcuate band of inferior corneal thinning (4-8 o clock); peripheral band of normal cornea, stoma clear

A

Pellucid Marginal Degeneration

63
Q

area of protrusion of normal cornea occurs superior to the thinning band

A

Pellucid Marginal Degeneration

64
Q

DDX for pellucid marginal degeneration

A

Keratoconus. The pellucid doesn’t have a Fletchers ring, and theing of pellucid is 4-8 o clock postion

65
Q

what type of surgery do you want to avoid in pellucid marginal degen pts?

A

refractive

66
Q

noninflammatory and asymptomatic and non progressive corneal degeneration. Is pellucid.

A

false. Marginal furrow degen is noninflamm and asymptomic. ITS also nonprogressive.

67
Q

thinning of cornea in area adjacent to limbus

A

Marginal Furrow Degeneration aka Senile Corneal Furrow degen

68
Q

Terrien’s Marginal Degeneration is more common in

A

males .

69
Q

marginal thinning of cornea with opacification and superficial vasculariation; yellow-white line (lipid deposit) noted central to
thinned edge

A

Terrien’s Marginal Degeneration

70
Q

easy way to remember prllucid degener appearance

A

kissing claws

71
Q

t/f epi is intact in terriens marginal degen.

A

true . Theres no inflammation so its intact.

72
Q

what is the least appropiate option for terriens marginal

A

lamellar or pentrationg kertoplase.

73
Q

there is treatment to slow the progression of terriens marginal

A

fasle . Theres no txt for to slow its progression.

74
Q

terriens marginal degen are often asymptomatic unless astigma occurs

A

true

75
Q

elevated gray-white (or sometimes light blue) corneal nodules; single or multiple separated by clear cornea

A

Salzmann’s Nodular Degeneration

76
Q

Often found in eyes with chronic dryness or inflammation, more common in women than males

A

Salzmann’s Nodular Degeneration

77
Q

most common association of alzmann’s Nodular Degeneration (other than dryness

A

phlyctenular keratitis

78
Q

salzmanns can be asymtomatic or sympatheic. For symptomatic txt :

A

txt is lubricants, rgp cl, nodule removal (PTK, PK, LAMERLLAR, SUPERFICIAL

79
Q

band keratopathy is associated with ____ _____

A

chronic inflammation

80
Q

calcium deposits in the subepithelial space, Bowman’s layer and anterior stroma Swiss cheese appearance

A

Band Keratopathy

81
Q

band keratopathy is associated with hyerpcalceimia, hyperparathyoidism, excissive vitamin d intack, renal failure, sarcoidosis, juvenile idiopatch arthris.

A

true and there are many others.

82
Q

txt for band kertophaty

A

Ocular lubricants, Manage RCE, EDTA, Surgical

83
Q

Deposition of iron, yellowish-brown line in the corneal epithelium, Causes no symptoms. Often in the junction between middle and lower third, No clinical significance

A

Hudson Stähli Line

84
Q

chronic progressive, painful peripheral ulceration of the cornea,

A

Mooren’s Degeneration (Mooren’s Ulcer)

85
Q

Unilateral, older patients, responds well to medical treatment

A

Mooren’s Degeneration (Mooren’s Ulcer) Type 1

86
Q

Bilateral, usually younger individuals, progressive destruction of cornea despite treatment

A

Mooren’s Degeneration (Mooren’s Ulcer) Type 2

87
Q

Mooren’s Degeneration (Mooren’s Ulcer) Type 2 responds well to topical steriods and conjunctival resection.

A

FALSE. Type 1 responds well to topical steroids, type 2 of moorens ulcer has poor prognosis, reduce likilihood of perferation is all we can do.

Diseases of Anterior Seg. (11 decks)

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