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Ophthalmology > The Opaque eye > Flashcards

The Opaque eye Flashcards

1
Q

main 2 areas affected causing ocular opacities

A

cornea then lens

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2
Q

Wound healing - The epithelium - Basal cells

A

Transient amplifying cells, capable of mitosis
At the limbus, stem cells are there
Limbal stem cells provide for other basal cells

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3
Q

Wound healing - The epithelium - wing cells

A

non-mitotic

2-4 layers

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4
Q

Wound healing - The epithelium - squamous non-keratinized epithelium

A

slough off with blinking

replaced with cells below

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5
Q

Wound healing - The epithelium - basal lamina

A

needed for permanent adhesions to form

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6
Q

Wound healing - The epithelium - sliding movement

A

abrasion - doesn’t reach basal lamina if stroma not exposed

happens quickly

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7
Q

Wound healing - The epithelium - vertical movement

A

from down, up
1st epithelial then basal cells
1 week cycle

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8
Q

Wound healing - The epithelium - centripetal movement

A

from limbus to centre
affects all layers
in spiral shape

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9
Q

centripetal movement - clinical significance

A

pigment from irritation/corneal scar can migrate over the pupil

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10
Q

Wound healing - The epithelium - healing by sliding

A

1-2mm per day

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11
Q

Wound healing - The epithelium - healing by sliding - depends on…

A

corneal health
existence of limbal basal stem cells
existence of a basal lamina onto which epithelium can adhere

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12
Q

Wound healing - The epithelium - superficial pigment deposition

A

irritants activate melanocytes

pigment deposited in new migrating epithelial cells + superficial stroma

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13
Q

Wound healing - The epithelium - vascularization

A

infl is a stimulus
vessels can coalesce + form granulation tissue
atrophy over time once stimulus has gone
can be superficial or deep

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14
Q

Wound healing - The epithelium - vascularization - what purpose does it serve

A

stabilizing serum
nutrients, growth factors + infl cells
structural suppost

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15
Q

Wound healing - The epithelium -  vascularization - indicator of?

A

chronicity

lag time of 2-4 days to bud, then 1mm/2 days

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16
Q

Wound healing - the stroma - composition - collagen lamellae

A

collagen 1 fibrils
travel from limbus to limbus
relative state of dehydration

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17
Q

Wound healing - the stroma - keratocytes

A

low in number

lamellar creation + myofibroblasts

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18
Q

Wound healing - the stroma - chemicals produced on injury

A

IL-1, EDGF, TNFa, EGF, TGF-beta, collagenases, metaloproteases

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19
Q

Wound healing - the stroma - where are the chemicals produced

A 
Lacrimal glands	
Epithelial cells	
Stromal keratocytes	
Corneal nerves	
Leukocytes that are attracted to the wound
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20
Q

Wound healing - the stroma - cellular attraction

A

monocytes + neutrophils to “clean up”

keratocytes - collagen + GAG production

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21
Q

Wound healing - the stroma - re-establishing corneal curvature

A

part of remodelling
takes time
done by epithelial hyperplasia
can for facets (flat parts)

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22
Q

Wound healing - the endothelium - intercellular Na+K+ATPase pumps

A

in between endothelial cells

put fluid back into the AC

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23
Q

Wound healing - the endothelium - Polimegathism + pleo/polimorphism

A

cells are diffent sizes, shapes (not all hexagonal) and overlap so that they’re not all 1 layer

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24
Q

Wound healing - the endothelium

A

v.sensitive cells with poor ability to regenerate

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25
Q

how does the tissue know its ulcerated

A

cell to cell communication

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26
Q

causes of decr corneal sensation

A

desensitization

“brachycephalic factor” - exposed cornea

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27
Q

stromal collagenolysis (“melting”) - causes

A

unstable repair of stroma
excess infl - continued irritation
secondary infection

28
Q

areas that often cause problems during healing

A

tear film (qual/quantitative)
3rd/eyelids
repair process
make sure the cause of the ulcer is correctly identified

29
Q

general treatment guidelines

A 
Protection from self-harm	
Antibiotic cover for prevention	
Atropine for comfort	
Ciclosporin doesn't interfere with stromal/epithelial healing		
Steroids “a big no-no”
healing aided by vascular growth
30
Q

why use atropine

A

dilation of the pupil (mydriasis)
relaxes the CB (cycloplegia)
can dry out the eye though

31
Q

why not to use steroids

A

enhance collagenolysis

slow healing

32
Q

tarsorrhaphy

A

horizontal mattress suture with stents though eyelids

for corneal protection

33
Q

antibiotics used in the eye

A

fusidic acid
chloramphenicol
aminoglycosides
fluoroquinolones

34
Q

melting - treatment

A

serum eyedrops - antiproteases

freq application + monitoring

35
Q

corneal collagenolysis

A

corneal melting

v.rapidly (hours) to days

36
Q

corneal collagenolysis can lead to

A

local destruction
widespread corneal destruction
perforation

37
Q

descemetocele before perforation - appearance

A

partial bending of descemets membrane
no fluorescein uptake but wall of oedematous stroma around it does
clear centre

38
Q

keratoconjunctivitis sicca (KCS) - causes

A

evaporative
drug related
anaesthetics + sedatives
primary immune mediated

39
Q

primary KCS - speed of progression

A

slowly progressive

40
Q

primary KCS - effects on the eye

A

mucus accumulation + hyperaemia
+/- vascularization + pigmentation
ulcerative keratitis
ulcers

41
Q

primary KCS - trend A

A

either 0-2 or 6-8 y/o

ulcerative keratitis 50/72% - rapidly perforate

42
Q

primary KCS - trend B

A

5 y/o

ulcerative keratitis 4/22% - mostly superficial

43
Q

primary KCS - causes of central or paracentral ulcers

A 
poor balance of destr/construction
irritant still present (dryness)
change in bacterial flora
incr thick mucoid discharge
infl cells in the surface
44
Q

primary KCS - treatment for central ulcers

A 
Corneolimboconjunctival transposition (CLCT)
uses clear peripheral cornea
45
Q

primary KCS - treatment of peripheral ulcers

A

conjunctival pedicle graft
slightly faster
doesn’t clear much over time but is less important peripherally

46
Q

primary KCS - medical treatment

A

topical ciclosporin
preservative free viscous tears
topical antibiotics
serum eyedrops

47
Q

primary KCS - medical treatment - why use ciclosporin

A

doesn’t interfere with corneal healing

48
Q

feline corneal sequestrum

A

spontaneous

uni or bilateral

49
Q

feline corneal sequestrum - appearance + localization

A

tan/black discolouration of superficial stroma

usually in central/paracentral cornea

50
Q

feline corneal sequestrum - progress over variable period of time causes which prolems

A

Darker plaque
Neovascularization
Ulceration around plaque
Mild to very painful

51
Q

Feline Corneal Sequestrum - Etiology - Idiopathic

A

Associated with corneal trauma
Medial lower eyelid entropion
Superficial grid scraping (“grid keratotomy”)

52
Q

Feline Corneal Sequestrum - Treatment - Surgical

A

Superficial keratectomy +/- bandage lens +/- tarsorrhaphy

Superficial keratectomy and Grafting

53
Q

Feline Corneal Sequestrum - Treatment - Postsurgical supportive medical therapy

A

Topical antibiotic until re-eithelialization

Preservative-free viscous tear preparation

54
Q

Spontaneous chronic corneal epithelial defects (SCCEDDs) - appearance of eye

A 
Loose epithelial edges 
Under-running of fluorescein dye – pulsed saline test 
± corneal edema 
± ocular pain 
± vascularization
55
Q

Spontaneous chronic corneal epithelial defects - treatment

A

Debridement (Db)
Grid Keratotomy (not in cats)/Superficial Scrape (GK/SS)
Keratectomy (K)
mechanical debridement

56
Q

SCCEDs - Medical therapy

A

Topical antibiotic: Chloramphenicol 3x day
Consider serum eye drops 3-4 x day
Protective collar on at all times
Re-evaluation every 2 weeks

57
Q

FHV-1

A

Virus lives in trigeminal ganglion and corneal tissue
Usually infected in kittenhood (cat flu)
Associated with symblepharon in kittens
Corneal ulcerative disease can be severe
Recrudescent disease seen during periods of stress

58
Q

FHV-1 - treating with L-Lysine

A

Interferes with viral replication

Reduced viral shedding

59
Q

FHV-1 - treating with IFN

A

decr cytopathic effects

may have no effect

60
Q

FHV-1 - treating with Idoxuridine & TFT (triflurothymidine)

A 
Thymidine-mimicking pyrimidine analogues 
Use 4x-6x day 
Specificity for FHV1 in vitro 
Tolerance? No trials 
TFT - ok? 
Idox – reportedly bad
61
Q

FHV-1 - treating with Cidofovir

A

Cytosine-mimicking pyrimidine analogue
Bid possible
Reduce severity c-signs/shedding

62
Q

FHV-1 - treating with Pen- Gan- and A- ciclovir

A

Adenosine/guanosisne-mimicking purine analogue
Toxic orally – liver, kidney, BM
Topically, none have been trialled

63
Q

FHV-1 - treating with Famcyclovir is safe orally

A 
Penciclovir is its active metabolite
Same family as Pen- Gan- and A- ciclovir 
Do not reach the target 
But work clinically 
May be used long term
64
Q

Feline Acute Bullous Keratopathy

A

Unknown etiology
Actue development of corneal edema
needs rapid referral

65
Q

Facial Nerve Paralysis - etiologies

A 
Viral (flu- Calici and FHV-1) 
Otitis media (tympanic bulla) 
Ear canal avulsion (trauma) 
Severe otitis externa 
Ear canal neoplasia 
TECA with LBO 
Idiopathic (some might be immune-mediated) 
Part of a polyneuropathy
66
Q

Facial Nerve Paralysis - effects

A

Loss of blink - usually temporary

Interpalpebral fissure ulceration

67
Q

Facial Nerve Paralysis - treatment

A

tarsorrhaphy for 1 to 2 months (horizontal mattress suture)
Protective collar
Topical antibiotic (Fucithalmic bid-tid)
Preservative-free, viscous tear (Celluvisc 1%, bid-tid )

Ophthalmology (7 decks)

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