Seminar: Abnormal Size/Position of the Eye Flashcards

1
Q

What 3 sources of space occupying lesion may -> exopthalmus?

A
  • infection/iniflammation/abscess/cellulitis
  • neoplasia
  • specific t issue inflam (eg. myositis)
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2
Q

3 clinical signs assocciated with space occupying lesions in the orbit?

A
  • globe displacement (usually dorsolaterally) + exopthalmus
  • protrusion of the TE
  • change in facial symmetry
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3
Q

What specific tissue inflammation may -> exopthalmus? What other CSs may be seen concurrently?

A

extraocular muscle polymyositis

  • acute 1* inflam (autoimmune)
  • thickening of muscles presses on optic nerve -> abnormal PLR
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4
Q

Causes of micropthalmus?

A
  • congenital (from birth, usually bilateral, +- other ocular defects eg. cataracts, rarely very sriking)
  • destruction of the ciliary body (cyclodestruction)
    > as a sequalae of inflammation, called psthisis Bulbi (severe uveitis), targetted surgical destruction (excessive laser cytoablation) or chemical ablation (gentamycin -> vitreous cavity, not nice!)
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5
Q

Which segment of the eye determines IOP?

A

Anterior chamber despite being much smaller

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6
Q

What is bupthalmia? Cilnical signs?

A

= hydropthalmia

  • enlarged globe d/t glaucoma (1/2) streatching globe
  • conjunctival and episcleral hyperaemia/congestion
  • corneal oedema (dmaage to endothelium)
  • Haab’s Striae (stretch marks d/t breaks in Descemet’s membrane)
  • Zonular tears (overstretching of fibres - lens displacement) - Visable lens equator through pupil (Aphakic crescent = “no lens” crescent)
  • Corneal ulcer d/t mild/moderate corneal overexposure
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7
Q

How may glaucoma affect the retina?

A
  • damage to neural retina and optic nerve head
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8
Q

What types of glycoma are possible?

A

1*
> inherited
- breeding advice?
- very complex (cf. GPRA simple recessive allele)
> Goniodysgenesis
- abnormal formation of the iridocorneal angle
> 2 forms:Closed angle (rapid onset, most common in dogs), Open angle (insiduous onset, most common people)
2*
> anything blocking ICA
- uveitis/t cataracts/infectious caues eg. FIP, Leishmania etc. (protein - ICA synechia, iris thickened)
- Hyphema
- PIFMs
- Neoplasia
- Trauma
- lens luxation

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9
Q

How does closed angle goniodysgenesis present?

A

1 eye affected initially, within 6 months other one will be too

  • IOP >40
  • tx prophylactically?
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10
Q

What is visualisation of the iridocorneal angl called?

A

gonioscopy

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11
Q

How does glaucoma present?

A
  • episcleral and conjunctival hyperaemia
  • corneal oedema (d/t endothelial/epithelial causes: fluorocin and IOP to differentiate )
  • Anisocoria (d/t likely slightly differnet pressures) and fixed, mid dilated pupil d/t pressure crushing optic nerve etc.
  • ^ IOP -> Haab’s Striae if IOP >60ish
    +- vision problems (menace/vision maze test)
  • corneal ulcer d/t exposure
  • cupping of optic nerve head
  • lens displacement -> overstratching and tearing of zonules, Aphakic cresent formation
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12
Q

What causes glaucoma in cats most commonly?

A

> 2* to uveitis - FFFT
- FIV, FeLV, FIP, Toxoplasma
- idiopathic
1* form exists in Burmese but much less common

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13
Q

How does differentiating 1* v 2* affect prognosis or decision making?

A

> if 2, possible only ne eye will be affected
- might lose affected eye/treat and prevent re-occurence
- no need to worry about breeding (unless caused by lens luxation)
1
glaucoma will affect both eyes over time FO SHO
- long term monitoring and tx of 2nd eye necessary- breeding advice necessary

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14
Q

Treatment of glaucoma? MEMORISE!!

A
  • control IOP
    > B-blockers
    > Carbonic anhydrase inhibitors (active production of aqueous humour in ciliary body epithelium)
    > PG analogues (inflame the eyes to cause v pressure, v. low conc needed to prevent iris spasm, also causes eyelash growth and hyperpigmentation)
  • If 2*, remove cause if poss
    > treat inflam
    > surgically remove lens from anterior chamber
    > remove eye if neoplastic
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15
Q

Why are b-blockers used to control glaucoma? Eg. drug?

A

> eg. timolol

  • reduce production of aquous
  • weak but cardiac and resp effec in smallies
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16
Q

Why are carbonic anhydrase inhibitors used to control glaucoma? egs.? What can they be given in combo with?

A
  • eg. dorzolamide- v productin of aqeous
  • strong and work well in combo with b blockers
  • work well in cats and horses
17
Q

Why are PG analogues given to control glaucoma? eg.? What conc is needed? Which species are not affected?

A

> eg latanoprost

  • ^ outflow of humour
  • strongest, need v low conc (can cause inflammation!)
  • Does not work in cats
  • WOrks in horses
18
Q

What are IOP curves? How regularly should they be tested?

A

Remember IOP changes over time so may be some periods of high and low pressure
- test q3hours

19
Q

What are phacodonesis and iridodonesis?

A
  • phacodonesis = lens luxation
  • iridodonesis = iris movement
    > often occour together d/t zonule breakdown and lens subluxation (1* stage of lens luxation)
    > seen as wobbly iris when eye moves (video of black and tan dog in lect)
20
Q

In which breeds is lens luxation inherited?

A

Terrier + others (lancashire heeler, chinese crested, australan cattle dog, volpino italiano)
- genetic mutation recently identified
- test developed by AHT
> other breeds = spontaneous

21
Q

What is anterior presentation of the vitreous and when does it occour?

A

lens luxation allows vitreous to leak forward
- appears as mucous like strand floating in AC
- can block ICA and ^ OP -> glaucoma
= PUPIL BLOCK GLAUCOMA
- v. quick onset (mins/hours)

22
Q

Which directions may the lens luxate? Which is better prognosis - outcomes? How woul this be seen clinically?

A
  • anterior and posterior
    > posterior better
  • seen as a “deep” AC as lens is no longer holding iris forward
  • can lead to cataract formation, lens induced uveitis, lens adhesions to the retina (as it floats around the vitreous)
    > anterior
  • causes pupil block glaucoma
  • whole lens visable in AC with pupil seen behind, distorted
  • cornea also damaged
23
Q

What may pupil block glaucoma and other acute ^IOP cause?

A
  • retinal ganglion cells (axons form optic nerve)
  • optic nerve head (axoplasmic flow)
  • damage to BVs
24
Q

Tx pupil block glaucoma or any other rapid ^ IOP?

A

> anterior luxation
- immediate removal of the lens
rarely luxates posteriorly on its own
subluxation can be treated medically/surgically
medical tx necessary to control future IOP spikes

25
Q

Medical management of lens luxation?

A

> xatalan (latanoprost, PG analogue)
- marked miosis (constricts pupil to prevent lens luxating anteriorly)
- can cause uveitis
SID in the morning or BID for max miosis

26
Q

Surgical management of lens luxation? Prognosis?

A

> removal of lens before anterior luxation
-poor prog: ant luxation and ^ IOP
-guarded-poor prog: posterior sub/luxation and ^IOP
- mod good prog-guarded: post sub/luxation and normotension
removal of lens if acutely luxated anteriorly
control of IOP with drugs long term
PREVENTATIVE lasering of ciliary body (endolaser cycloophotocoagulation, lens contents removal done first) leave 30% intact to prevent hypotony and pthisis

27
Q

What are the cardinal signs of lens luxation?

A
  • phacodynesis
  • anterior presentation of the vitreous
  • deep anterior chamber
28
Q

Presenting signs of pain in the eye with glaucoma?

A

Will not rub!
- may rest on cushion or owner
- slow down and sleep more
fluctuating pressure so signs will not be present always

29
Q

Which tissues are present in the orbit?

A
  • globe
  • extraocular muscles
  • BVs, nn
  • connective tissue
  • fat
  • lacrimal gland, gland of TE, zygomatic salivary gland