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
Medical management of lens luxation?
> 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
Surgical management of lens luxation? Prognosis?
> 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
What are the cardinal signs of lens luxation?
- phacodynesis - anterior presentation of the vitreous - deep anterior chamber
28
Presenting signs of pain in the eye with glaucoma?
Will not rub! - may rest on cushion or owner - slow down and sleep more fluctuating pressure so signs will not be present always
29
Which tissues are present in the orbit?
- globe - extraocular muscles - BVs, nn - connective tissue - fat - lacrimal gland, gland of TE, zygomatic salivary gland