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Small Animal Optho/Neuro > Intraocular Inflammation > Flashcards

Intraocular Inflammation Flashcards

1
Q

what are the 3 components of the vascular tunic of the eye?

A
  1. iris
  2. ciliary body
  3. choroid
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2
Q

what 2 things make up the anterior uvea?

A
  1. iris
  2. ciliary body
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3
Q

what are the 3 components of the iris?

A
  1. posterior pigment epithelium
  2. stroma
  3. muscles – dilator, sphinctor
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4
Q

which of the following statements if FALSE about the function of the uvea?
A. vitreous humor dynamics (CB – produce and filtrate)
B. removes waste
C. absorbs light (pigment of iris)
D. controls light (through pupil)
E. blood aqueous barrier

A

A. vitreous humor dynamics (CB – produce and filtrate)

its actually AQUEOUS humor production by the ciliary processes and then AH drainage by the iridocorneal angle.

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5
Q

__________ is inflammation of any aspect of the uveal tract.

Bonus if you know the 3 types

A

Uveitis

Anterior Uveitis= iris + CB, Posterior Uveitis=choroid, Panuveitis= all 3

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6
Q

What are the clinical signs associated with uveitis?

A
  • blepharospasm
  • episcleral injection (congestion of the vessels)
  • ciliary flush (360 degree corneal vascularization)
  • corneal edema (build up in stromal layer)
  • miosis
  • synechiae (adherence of iris to cornea or lens)
  • aqueous flare (release of protein into aqueous – breakdown of BAB)
  • hyphema
  • hypopyon
  • keratic precipitates
  • rubiosis iridis (congestion of iridial vasculature)
  • hypotony (low IOP, <15)
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7
Q

What are the complications that can arise from uveitis?

A
  • synechiae
  • glaucoma
  • iris bombe
  • cataracts
  • lens instability
  • retinal detachment
  • phthisis bulbi
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8
Q

How can uveitis cause glaucoma? (3 mechanisms)

A
  1. obstruction of the iridocorneal angle by inflammatory debris
  2. pre-irida fibrovascular membrane
  3. iris bombe + peripheral anterior synechiae
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9
Q

T/F: there is limited regeneration of the uveal tissue

A

true

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10
Q

What 3 events generate inflammation?

A
  1. release of chemical mediators by cells
  2. presence of certain pathogen-associated molecules
  3. release of pro-inflammatory molecules by immune cells
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11
Q

___________ is characterized by 360 degree vascularization on the cornea and is present in cases of INTRAocular disease.

A

ciliary flush

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12
Q

_________ is fluid build-up within the stroma (middle layer of the cornea) and occurs due to the altered function of the corneal endothelium.

A

corneal edema

when a pt has uveitis, aqeous flare can occur; when this occurs, the AH is not healthy enough to nourish the corneal endothelium. This leads to fluid build up d/t alterations of the Na-K pumps within the cornea that typically remove the fluid.

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13
Q

____________ is pupillary constriction that is caused by painful spasms of the ciliary body musculature.

A

miosis

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14
Q

___________ is adherence of the iris to the cornea (anterior) or lens (posterior) which is lead by inflammatory cells, fibrin, and fibroblasts.

A

synechiae

this is a problem because if the iris is stuck to the lens, then light cannot be regulated and the pupil will not move as it should. This will lead to pupillary block. Secondary glaucoma can occur.

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15
Q

____________ is protein in the aqueous humor (anterior chamber) due to a disruption of the blood aqueous barrier.

A

aqueous flare

it appears as a hazy anterior chamber.

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16
Q

__________ is characterized by WBCs in the aqueous humor (anterior chamber), particularly PMNs. Usually appears ventrally-dependent.

A

hypopyon

17
Q

________ is characterized by RBCs in the aqueous humor (anterior chamber)

A

hyphema

18
Q

___________ is inflammatory cells, fibrin, and iris pigment adhered to the endothelium (inner most layer of cornea)

A

keratic precipitates

19
Q

_________ is injection of the iridial blood vessels.

A

rubiosis irides

20
Q

what is the medical term for LOW intraocular pressure?

What is the pathophysiology behind low intraocular pressure?

A

hypotony

The CB is responsible for AH production, so if the eye is inflammed (full of protein, WBCs, etc.), then the CB will not get nutrition from the AH –> CB activity will decrease –> AH production will decrease –> decreased IOP.

another theory: uveitis –> increased permeability of BAB –> fluid goes out of eye –> decreased IOP.

21
Q

what are 3 common exam clues that lead to uveitis?

A
  1. miosis – spasm of CB muscles and pupillary sphincter
  2. low IOP (decreased prod of AH by CB)
  3. aqueous flare, hypopyon, and/or hyphema (d/t breakdown of BAB)
22
Q

what are 3 primary ocular disease causes of uveitis?

A
  1. cataracts
  2. lens rupture
  3. corneal ulcer
23
Q

T/F: uveitis in many cases can be idiopathic

A

true

24
Q

What are the 2 types of lens-induced uveitis in dogs and the difference between them?

A
  1. Phacolytic uveitis – soluble lens protein slowly leaks through an intact lens capsule (ex. cataract)
  2. Phacoclastic – sudden exposure of intact lens protein (Ex. trauma causing lens capsule tear)
25
Q

what are the 6 common causes of uveitis in dogs?

A
  1. infectious
  2. lens-induced uveitis
  3. reflex uveitis (corneal and scleral diseases)
  4. neoplastic (melanoma, lymphoma)
  5. breed-specific / immune-mediated (UVDS, pigmentary uveitus/GRU)
  6. metabolic (hyperlipidemia, diabetes)
26
Q

what are the 3 common causes of uveitis in cats?

A
  1. infectious (FeLV, FIP, FHV, FIV; Bartonella; histoplasma, blastomyces, coccidioides, toxoplasma)
  2. metabolic (systemic hypertension)
  3. neoplastic (lymphoma)
27
Q

How do we diagnose uveitis?

A
  1. history - vxn status, lifestyle, acute/chronic nature, previous medications
  2. PE
  3. optho exam
  4. min database – CBC, Chem, UA
  5. thoracic xray + abd u/s
  6. ocular u/s (only if you cannot see past the iris and lens)
28
Q

What are the GENERAL treatment goals for uveitis?

A
  1. control pain
  2. prevent sequelae
  3. stabilize and restore BAB
  4. treat underlying cause if possible
29
Q

what topical antiinflammatory treatments are available for treating uveitis?

A
  1. Corticosteroids - prednisolone acetate, dexamethasone
  2. NSAIDs- diclofenac, flurbiprofen, ketoclorac
30
Q

what topical treatments are available for treating uveitis pain, preventing synechiae, and stabilizing the BAB?

A

Topical atropine – mydriatic and cycloplegic

31
Q

what are adverse effects of corticosteroid use in cases of uveitis?

A
  1. potentiate infection
  2. decreases wound healing
  3. ulcerative keratolysis
  4. corneal lipid/calcium deposition

always recheck patients frequently when they are on topical corticosteroids, and when they are “out of the woods” switch them to a NSAID

32
Q

what are the contraindications for topical atropine use?

A
  1. lens instability
  2. glaucoma
  3. dry eye (bc its a parasympatholytic, it decreases STT)

it has a bitter taste and can cause hypersalivation in cats

33
Q

what systemic treatments are used in cases of uveitis?

A
  1. systemic corticosteroids (prednisone)
  2. systemic NSAIDs
  3. systemic antimicrobials
  4. systemic antifungals
  5. systemic immunomodulatory drugs (cyclosporine, azathioprine)

the steroids and NSAIDs obviously treat the inflammation, and the others are used on case-by-case basis depending on the underlying cause of the uveitis.

34
Q

What does ‘follow-up’ entail for causes of uveitis?

A

watching for complications
look for reduction of clin signs
gradual tapering of medications to avoid flare ups
educating the client

Small Animal Optho/Neuro (12 decks)

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