3.7 cornea Flashcards

1
Q

Causes of Dellen?

A

poor fitting GP lens
pterygia
bleb
tumor

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2
Q

cause of exposure keratopathy?

A

CN VII issue or lid issue causing incomplete lid closure

CN 7 - bells palsy, CVA, aneurysm, MS, HSV, HSZ

orbicular issue - surgery leading to ectropion, TED, lagnopthalmos, FES

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3
Q

what are symptoms that patient experiences with exposure keratopathy?

A

symptoms worse in the morning

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4
Q

what are signs of exposure keratopathy?

A

SPK -> ulcer

decreased sensitivity

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5
Q

causes of filamentary keratitis? What is the.most common?

A

chronic irritation -> dry eye
** most common cause KCS
FES, SLK, CLS, PKP, erosions, neurotrophic keratopathy

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6
Q

what are the filaments made from in filamentary keratitis?

A

degenerated epithelial cells and mucous
*** stain with NAFL

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7
Q

What is thygeson’s ? how long does it take to resolve. Who?

A

bilateral intraepithelial central crumb-like lesions that are raised that occur due to an unknown cause in 20-30 yo

exacerbations - can last 1-2 months if not treated

remissions

can take 10-20 years to resolve

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8
Q

what causes neurotrophic keratopathy?

A
  • damage to V1, VII
    surgery - cut V1- lasik, maxillary repair, etc

chronic corneal injury - cls, corneal
dystrophies

systemic disease - HSV,HSZ, DM

meds: timolol, betaxolol, diclofenac sodium

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9
Q

How does V1 affect the cornea?

A

regeneration, healing, nociceptors for pain

decreased sensitivity
reflex blinking

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10
Q

How can damage to CN 7 cause neurotropic keratitis

A

decreased reflex tearing

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11
Q

what things can affect CN 7?

A

bells
tumor
surgery - acoustic neuroma removal
MA
CVA
MS
HSV/HSZ

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12
Q

signs of neurotrophic keratitis

A

decreased sensitivity
SPK -> ulcer - > can lead to perforation b/c non-healing
no inflammation

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13
Q

what is the pathophys of RCE?

A

poor hemidesmosome attachment
to basement membrane

secondary to trauma, corneal dystrophies, thickening of BM with age

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14
Q

causes of UV/ thermal keratopathy?

A

sun exposure
welding
skiing
using a sun-lamp

high UVc - open K+ channels -> loss of intracellular K+ -> cell death

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15
Q

what layers absorb what wavelength of light in the cornea?

A
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16
Q

tear meniscus height normal

A

0.2 mm or greater

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17
Q

aqueous deficient testing

A

schirmer 1 - no anesthetic (basal, reflex, emotional )
- normal > 10 mm in 5 mins , < 5 mm = abnormal

schirmir 2 - only basal
normal > 5 mm in 5 mins

phenol red
> 10 mm in 15 seconds normal

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18
Q

evaporative testing

A

TBUT < 10 seconds abnormal

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19
Q

rose bengal vs lissamine green

A

dead and devitalized conjunctival and corneal cells, as well as cells that have lost their mucous covering

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20
Q

Tear hyperosmolarity

A

abnormal > 308, or difference > 8 most/L

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21
Q

types of aqueous deficient dry eye

A
  1. Sjögren’s Syndrome Dry Eye
    - primary
    - secondary
  2. Non-Sjögren’s Syndrome Dry Eye
    - gland attacked
    - block ducts
    - cut nerves
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22
Q

Sjögren’s Syndrome Dry Eye categories

A

primary - dry eye, dry mouth

secondary - dry eye, dry mouth + CT disorder (RA>SLE, polyartertis, granulomatosis w/ polyangititis

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23
Q

most common rheumatic disorder?

A

RA

second - Sjögren’s

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24
Q

attacked gland dry eye cause

A

sarcoid
lymphoma
aids
graft vs host disease

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25
Q

blocked gland dry eye causes

A

OBSTUCTION Of lacrimal gland ducts
- trachoma
- pemphigoid
- Erythema multiform
- burns

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26
Q

cut nerves dry eye

A

cls
DM
bells
drugs
NK
infection - HSV/HSZ
surgery

27
Q

extrinsic causes of dry eye

A

vitamin a deficiency
topical anesthetics

cls wear

28
Q

intrinsic causes

A

lid pathology or dynamics

low blink rate (parking sons, concentration)

lid position disorders (TED, lagopthalmos)

MGD, bleh

29
Q

why does vitamin A cause dry eye?

A
  • essential for goblet cell and glycocalyx development.
  • result in aqueous tear-deficient dry eye as a result of lacrimal gland acinar damage
  • Bitot’s spots on the conjunctiva
30
Q

What are corneal ecstasies?

A

keratoconus
pellucid
keratoglobus

31
Q

what do all the corneal ecstasies lead to?

A

hydros -> break in descemets

32
Q

keratoconus cause

A
  • 13% AD inheritance
  • most sporadic
  • starts in puberty
  • MMPs -> damage Bowmans causing collagen 1 fibril displacement -> loss of adhesion b/w fibrils -> thinning and profusion
33
Q

keratoconus associated conditions

A
  1. ocular allergic: ocularallegic: VKC, AKS, FES

ocular K-dystrophies: Fuch’s, PPMD, granular, lattice “finger grinding leads to protrusion”

ocular hereditary: RP, lebers, ROP, Anaridia, cone dystrophy

systemic: T-DOME (turners, down, osteogenesis imperfect, marfans , Ehler danlos + atopic dermatitis , mitral valve prolapse

34
Q

early and later signs of KCN

A

early: scissoring reflex, irregular keratometry miers Fleischer’s ring, inferior topo steepening

late: Vogt’s striae (stromal vertical lines, go away with pressure), munson’s sign, Rizuti’s sign ( conical refection on nasal cornea when shine light temporally), hydrops

35
Q

Pellucid cause
What does it lead to

A

collagen abnormality

leads to protrusion above area of thinning! and ATR astigmatism

36
Q

severity of KCN based on K values

A

mild < 48D
mod 48-54
severe > 54

37
Q

who gets pellucid

A

20-40s

38
Q

pellucid vs KCN

A
  • ≠ KCN: (-) cone, Fleischer’s ring, Vogt’s striae
39
Q

keratoglobus
who gets it?
Associated conditions?

A
  • birth AR inheritance

or get it from advanced keratopathy (KCN), trauma, exophthalmos

associated with Ehler’s-danlos and Leber;s

40
Q

what is keratoglobus

A

diffuse thinning in the periphery occurs at birth AR inheritance

41
Q

What do all corneal dystrophies have in common?

A

AD
bilateral
(-) neo

if anterior/stromal -> RCE
if stromal/ posterior -> KCN

42
Q

Cogan’s microcytic dystrophy names

A

EBMD
ABMD
Map dot finger print

43
Q

Cogan’s microcytic dystrophy
who. gets it?

A

AD, females > males

** most common anterior corneal dystrophy

44
Q

what causes EBMD?

complications

A

excessive BM production -> mature corneal cells trapped under BM

-RCE (Usually asymptomatic until get this)
- 10% of ABMD - RCE
- 50% RCE = ABMD

45
Q

Meesmans

A

” multiple cysts”
AD condition that affects epithelium in 1st year of life

  • 100s of bilateral intraepithelial cysts across entire cornea

can lead to RCE

46
Q

Reis- Buckler who? What?

A

AD occurs early in life - 4/5tears old

  • Bowmans layer is replaced with Collagen -> PAIN (RCE) -> decrease with time , but opacities worse with age

grey reticular opacities in central cornea look like “ Reeces pieces”

47
Q

stromal corneal dystrophies

A
  1. macular
  2. granular
  3. Avellino
  4. Lattice
  5. Schnyder’s

” Marilyn Monroe got hers in LA”

all lead to RCE

48
Q

macular dystrophy

A

think “Mac daddy”- AR!!!!!
(least common, most severe ie affect vision early by 30 years old)

diffuse strömal haze (3-9 years old) leads to stromal opacification , stromal thinning, and multiple grey/white opacities in all layers of the cornea everywhere

RCE***

49
Q

what are the macular dystrophies opacities?

A

mucopolysaccarhide deposits

50
Q

granular dystrophy

A

start getting by age 10, vision loss at 60

snowflake granules (hyaline deposits in central stroma) spread to epi and deep stroma

  • become confluent and decrease VA
  • rarely get RCE
51
Q

Avellino dystrophy

A

variant of granular dystrophy

has both granular like and lattice - like deposits in the central cornea

52
Q

lattice dystrophy

A

AD stromal dystrophy

amyloid deposits
Anterior stromal haze with
branching, refractile lattice lines. Decreased va by 30s because of stromal haze and scarring

RCE

53
Q

What stromal dystrophies have a mutation in the TGFB1 gene?

A

granular
lattice
avellino

54
Q

Posterior corneal dystrophies

A

Fuchs
Posterior polymorphous dystrophy

55
Q

Fuchs
Who?
Symptoms?
Causes?
Complications?
What can worsen it?

A

30% hereditary
Post menopausal

56
Q

Posterior polymorphous dystrophy
Who
Symptoms
Signs
Complications

A

20-50 or see hazy cornea at birth
Symptoms: decreased vision secondary to edema , most asymptomatic , bilateral
Complications: Bullae, corneal edema

57
Q

Endothelial cell count normal/abnormal

A
58
Q

Congenital anterior segment anomalies

A

Megalocornea
Microcornea
Cornea plana
Anaridia
Haab striae
Axonfield reiger syndrome
Peters Anomaly
Limbal dermoid
Forceps injury

59
Q

Megalocornea
Who

A

X linked - males

Bilateral corneal diameter > or equal to 13 mm

High myopes with steep cornea - have good VA with correction

Can be associated with lens subluxation and angle abnormalities -> glaucoma because of stretching of the tissue

  • associated with CT disorders - think TDOME
60
Q

Microcornea

A
61
Q

Cornea plana

A

Corneal curvature = scleral curvature
- flat corneas < 38 D , hyperopia, shallow AC, increased risk of angle closure glaucoma

Associations : sclerocornea/ Microcornea

62
Q

Sclerocornea

A
63
Q

Haab striae vs forceps injury

A
64
Q

Axenfield reiger syndrome

A

Angle Anomolies = prominent iris processes to level of PE - can obscure SS