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SA Optho/Neuro > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is the uvea?

A

The vascular tunic of the eye
-composed of the iris, ciliary body and choroid

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2
Q

What are the functions of the uvea?

A

aqueous humor dynamics, removal of waste, absorption of light (pigment of iris), controlling light (pupil size), and composes a portion of the blood aqueous barrier

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3
Q

Under what conditions can inflammation of the eye occur?

A

It can occur with either ocular or systemic disease
-there is increased blood supply, augmented vessel permeability and white cell migration

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4
Q

What makes inflammation of the eye unique?

A

Limited regeneration and unique immune requirements

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5
Q

What is inflammation generated by?

A
  1. The release of chemical mediators by cells
  2. Presence of certain pathogen-associated molecules (bacteria, fungi)
  3. Release of pro-inflammatory molecules by immune cells
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6
Q

What are the different classifications of uveitis?

A

Anterior (inflammation of iris and ciliary body), posterior (inflammation of choroid), or panuveitis (everything inflamed)

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7
Q

What ocular signs are commonly seen in cases of uveitis?

A

Episceral injection, ciliary flush, corneal flush, miosis, synechiae, aqueous flare, hyphema, hypopyon, keratic precipitates, rubiosis irides

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8
Q

What is ciliary flush?

A

360 degree deep vascularization on the cornea

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9
Q

T/F: you will often see ciliary flush with corneal surface disease

A

False- will see in cases of intraocular disease

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10
Q

Define corneal edema

A

Fluid buildup within the stroma
- occurs with altered function of the corneal endothelium-endothelial cells have sodium potassium pumps that help remove stromal fluid
-results in blue glass appearance of the eye
-fluid buildup within stroma (middle layer of the cornea)
-in the case of uveitis, aqueous not healthy enough to nourish endothelial cells=decrease in sodium potassium pumps

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11
Q

Define miosis

A

A painful spasm of the ciliary body muscle resulting in pupillary constriction.
-due to the action of prostaglandins on sphincter muscle

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12
Q

What is synechiae?

A

An adhesion between the iris to the cornea (anterior) or iris to the lens (posterior) lead by inflammatory cells, fibrin and fibroblasts

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13
Q

What type of synechiae is most common in uveitis cases?

A

Posterior
- one of the main complications- both cosmetically and may predispose to glaucoma

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14
Q

What is pupillary block?

A

A mechanism of glaucoma in which the iris stuck to the lens capsule disrupts the normal flow of aqueous humor to the anterior chamber to be drained out of drainage angle

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15
Q

What is aqueous flare?

A

Occurs when there is protein in the aqueous humor and disruption of the blood aqueous barrier
-appears as a hazy anterior chamber
-looks like “dust in the air” in the front chamber

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16
Q

What is lipid aqueous?

A

A type of aqueous flare in which hyperlipidemia leads to migration of lipid into the eye
- appears milky

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17
Q

What is hypopeon?

A

WBCs in the aqueous humor, particularly neutrophils
- migrates into the eye due to disruption of BAB
-usually seats on ventral aspect of anterior chamber

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18
Q

What is hyphema?

A

Blood in the eye
-usually anterior chamber

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19
Q

Define keratic precipitates

A

Inflammatory cells, fibrin, and iris pigment adhered to endothelium (innermost layer of the cornea)
-can be present in either acute or chronic uveitis

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20
Q

What is rubiosis irides?

A

increase in the vasculature of iris
- injection of the iridal blood vessels

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21
Q

Why is hypotony (low intraocular pressure) a result of uveitis?

A

The ciliary body gets nutrition from aqueous
-nourishment not great to the ciliary body in an eye that is inflamed- will decrease its activity resulting in decreased aqueous humor production
-also a result of the blood aqueous barrier breakdown- fluid is being lost from the eye quicker

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22
Q

What are some common complications from uveitis?

A

Synechiae, iris bombe, corneal edema and degeneration, cataracts, lens instability, vitreous degeneration, retinal detachment, secondary glaucoma, phthisis bulbi

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23
Q

How can permanent degeneration result from chronic uveitis?

A

Endothelial degeneration - can be permanent even without active inflammation

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24
Q

Why can cataracts result from uveitis?

A

Lens gets its nutrition from AH

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25
Q

What is iris bombe?

A

Posterior synechiae

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26
Q

How should you go about your Opthalmic exam?

A

-start in dark room (or create darkness through covering yourself and animal with blanket- be creative)
-Check from outside to inside- look for defects in a systematic manner
- have mental checklist

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27
Q

What are some common exam clues that lead you to uveitis as a diagnosis?

A

-Miosis (spasm of ciliary muscles and pupillary sphincter)
-low IOP (decreased production of aqueous humor)
-aqueous flare, hypopyon, hyphema (due to breakdown of BAB)

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28
Q

What are some causes of uveitis?

A

-Primary ocular disease: cataract, lens rupture, corneal ulcer, intraocular mass
-ocular manifestations of systemic diseases (infectious, metabolic, immune-mediated, neoplastic)
-trauma

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29
Q

What percent of cases can you not find a cause of uveitis (idiopathic)?

A

47% of dogs, 70% of cats

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30
Q

What are the most common causes of uveitis in dogs?

A

-infectious
-lens induced- either phacolytic (soluble lens proteins leaks through an intact lens capsule aka cataracts) or phacoclastic (sudden exposure of intact lens protein due to lens capsule tear/trauma)
-reflex uveitis from corneal or scleral disease
-neoplasia
-breed specific diseases (uveodermatologic syndrome or pigmentary uveitis)
-metabolic disease (hyperlipidemia)

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31
Q

What are the most common tumors (primary and secondary) in the eyes of dogs?

A

Melanoma most common primary, lymphoma most common secondary

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32
Q

What are the most common causes of uveitis in cats?

A

-Infectious: viral (FeLV, FIP, FIV, FHV-1), bacterial (bartonella), fungal (histo, blasto, cocciodioides), protozoal (toxoplasma)
-metabolic: systemic hypertension
-neoplastic: lymphoma most commonly

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33
Q

What should you include in your workup in uveitis cases?

A

-History: vaccination, lifestyle (indoor/outdoor/travel), acute vs chronic, previous medication
-physical exam
-Opthalmic exam
-minimum database (CBC, chem, UA)
-initial serology: fungal, tick titers and toxo in dogs. fungal, FeLV, FIV, FIP toxo in cats
-thoracic radiographs and abdominal ultrasound if fungal/neoplasia is suspected
-ultrasound of eye if you cannot see iris and lens
-additional systemic testing as indicated by species/patient clinical signs or geographic area (urine antigen)

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34
Q

What are some of the main treatment goals in uveitis cases?

A

Control pain, prevent sequele, stabilize and restore BAB
-treat underlying cause when possible

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35
Q

What are some topical treatment options for uveitis?

A

-Topical anti-inflammatories: corticosteroids (prednisolone acetate, dexamethasone), non steroidals (diclofenax, flurbiprofen, ketorolac)
-topical atropine

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36
Q

What are some of the benefits of using atropine in uveitis cases?

A

-Mydriatic to prevent synechia
-Cycloplegic: provides analgesia
-stabilization of BAB

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37
Q

T/F: you can use NSAIDs and steroids together in uveitis cases for topical treatment

A

TRUE

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38
Q

When should atropine be avoided?

A

In glaucoma cases as it could lead to worsening of the IOP
-lens instability
-dry eye (decreases tear production as its a parasympatholytic)

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39
Q

What are some contraindications for using steroids in the eye?

A

-if there is infection present (can potentiate infection)
-if there is an ulcer present (decreases would healing)
-can result in corneal lipid/calcium deposition

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40
Q

What are some systemic treatment options for uveitis?

A

-Corticosteroids (prednisone), NSAIDs
-antimicrobials, antifungals, immunomodulary drugs (cyclosporine, azathioprine)

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41
Q

Is it ok to send a patient home on cyclosporine or another immunomodulary drug and/or steroids if you think there’s any chance of the uveitis being due to infection?

A

NO- could worsen the infection

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42
Q

What is important for the followup in uveitis cases?

A

Watch for complications such as secondary glaucoma, look for lessening of clinical signs, gradually taper medications to avoid flare ups, educate clients on risks

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43
Q

Describe a basic diagnostic approach for a cloudy eye case.

A

Localize the lesion (what region of eye), qualify the lesion (what is it), determine lesion etiology (whats causing it)

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44
Q

What are some important historical questions to ask in a case of cloudy eyes?

A

Onset, signalment, symptoms (both ocular and non-ocular)

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45
Q

What are the different locations that cloudiness can be localized to?

A

Cornea, anterior chamber, lens, posterior segment (vitreous or retina)

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46
Q

What can edema of the cornea be a result of?

A

Endothelial dysfunction or ulceration (dehydration of cornea due to epithelial disruption)

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47
Q

What can scarring/fibrosis of the cornea be a result of?

A

Prior ulcer/trauma, chronic exposure, chronic abrasion

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48
Q

What can lipid in the cornea be a result of?

A

Lipid dystrophy, lipid degeneration

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49
Q

What can mineralization of the cornea be a result of?

A

Degeneration or metabolic changes

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50
Q

What is the only way to reliably differentiate between mineral and lipid in the cornea?

A

Histopathology

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51
Q

What are some causes of endothelial dysfunction?

A

Anterior uveitis, glaucoma (physical compression of endothelial cells), endothelial degeneration (breed specific), or localized dysfunction (uncommon)

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52
Q

What is the common presentation of endothelial degeneration cases?

A

Bilateral, non-painful, progressive corneal edema. Fluorescein negative

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53
Q

T/F: Lens instability is usually a unilateral disease

A

False- bilateral

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54
Q

What should you do if you are trying to prevent lens luxation?

A

Constrict the pupil with latanoprost

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55
Q

What can stringiness in the eye be an indication of?

A

Persistent pupillary membrane

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56
Q

What can cause chronic exposure?

A

Lagophthalmos, KCS

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57
Q

What can cause chronic abrasion?

A

Entropion, distichia, ectopic cilia

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58
Q

How can you distinguish corneal edema from corneal scarring?

A

scar usually more focal, more homogenous
-can see blood vessels over scar

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59
Q

What is the common presentation for a dog with chronic exposure?

A

Bilateral horizontal fibrosis
- usually occurs in brachycephalics

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60
Q

What is the difference in etiologies between lipid dystrophy and lipid degeneration?

A

Lipid dystrophy is hereditary

Lipid degeneration due to prior keratitis, infiltrative corneal disease, topical corticosteroids or systemic metabolic disease

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61
Q

T/F: lipid dystrophy often appears homogenous

A

False- usually not homogenous
- looks like glitter/sparkles. made up of numerous coalescing particles

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62
Q

What may you see in terms of a physical difference between lipid dystrophy and degeneration?

A

Degeneration may be accompanied by areas of fibrosis if due to ulcer/trauma
-if due to a metabolic disease, lipid will accumulate at the periphery of the cornea

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63
Q

What are some of the metabolic or degenerative causes leading to corneal mineralization?

A

Degenerative- ocular disease, age related

Metabolic- systemic metabolic disease

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64
Q

What may you see different on ophthalmic exam to differentiate lipid from mineral?

A

Mineral may look more like scratch marks or moth eaten, spiculated appearance
-doesn’t look as shiny

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65
Q

When is a cloudy cornea painful?

A

When it s caused by edema (ulcers, anterior uveitis or glaucoma)
-however edema from endothelial degeneration is not painful

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66
Q

When can mineral lesions causing cloudiness lead to pain?

A

When the mineral flakes off leading to an ulcer
- hard to heal as corneal tissue around it is unhealthy

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67
Q

What can lead to opacity of the anterior chamber?

A

Either aqueous flare caused by uveitis or lipid flare (from hyperlipidemia or uveitis)

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68
Q

Are lipemic aqueous eyes painful?

A

Yes if caused by uveitis
No if a result of a metabolic condition

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69
Q

What can cause cloudiness of the lens?

A

Nuclear sclerosis or cataracts

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70
Q

Define nuclear sclerosis

A

Densification of the nucleus in the lens
- because lens fibers never stop compacting
-occurs in older dogs (8 or older)

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71
Q

Is the path of light blocked to the back of the eye in cases of nuclear sclerosis?

A

NO

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72
Q

How can you differentiate cataracts and nuclear sclerosis?

A

Utilize the oblique and coaxial illumination
- cataracts will prevent light from going to the tapetum

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73
Q

How do you know that you are dealing with a mature cataract?

A

There is a complete obstruction of the tapetal reflex

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74
Q

What unique cataract feature is present in diabetics?

A

Y shaped sclerosis of nucleus

75
Q

What can result in posterior segment cloudiness?

A

Vitreous- haze due to inflammation, asteroid hyalosis, synchesis scintillans

Retina- retinal detachment

76
Q

What is asteroid hyalosis?

A

Part of the natural aging process-incidental finding
-can also be due to trauma or ocular neoplasia
-occurs when vitreous liquifies leading to calcium and phosphorus deposits
-looks like a snowglobe

77
Q

What is synchesis scintillans?

A

Cholesterol deposits in vitreous
- looks the same as asteroid hyalosis

78
Q

Why are red eye cases so frustrating?

A

Because redness is a very unspecific finding
-there are several common etiologies that are painful and potentially blinding
-inappropriate empirical treatment may leave underlying case unaddressed
-can be a presentation of systemic disease

79
Q

What is conjunctival hyperemia?

A

Enlargement of the vessels in the conjunctiva
- can look like diffuse redness or enlargement of a small network of vessels

80
Q

Define episcleral injection

A

Distinct, enlarged straight vessels adherent to the sclera
- run posteriorly towards the equator from the limbus
-usually combined with conjunctival hyperemia

81
Q

What is episcleral injection indicative of?

A

Intraocular disease

82
Q

Describe corneal neovascularization

A

Loss of physiologic corneal transparency
3 types:
- deep/stromal vessels: hedge like, not visible at the limbus
-superficial vessels: tree like branching, cross limbus
-360 degree deep neovascularization

83
Q

What does hemorrhage of the eye look like?

A

Can look like anything- there is no distinct pattern

84
Q

What is a classic presentation of superficial keratitis or keratoconjunctivitis?

A

Long branching vessels
-conjunctival hyperemia

85
Q

Where do ectopic cilia most often occur?

A

On the upper eyelid, dead center

86
Q

What clinical signs are common with intraocular disease?

A

Episcleral injection, maybe conjunctival hyperemia, maybe deep neovasculatization

87
Q

What tests should you perform if suspicious of surface disease? intraocular disease?

A

Surface- schirmer tear test, fluorescein stain, cytology and culture in some cases

Intraocular disease: evaluate pupil size, tonometry

88
Q

What conditions are the most important to rule out before treating anything empircally?

A

Corneal ulcer, dry eye, glaucoma, uveitis
-therefore red eyes should always undergo shirmer, fluorescein stain and tonometry

89
Q

What is the normal for schirmer tear test?

A

> 15

90
Q

Compare and contrast ectopic cilia, dystechia and trichiasis

A

Ectopic cilia is a hair growing out of the conjunctiva

Distichiae- hairs growing out of the meibomian glands on the margin of the eyelid

Trichiasis- normal hairs rubbing on cornea

91
Q

What breeds of dogs are the most predisposed to ectopic cilia?

A

Toy breed dogs
- also usually have a lot of distichia

92
Q

T/F: distichia commonly causes corneal irritation and sometimes ulcers

A

False- this is rare. They are often asymptomatic
-unlike ectopic cilia which commonly cause ulcers, recurrent

93
Q

What are some common clinical signs in a cat with eosinophilic keratoconjunctivitis?

A

Conjunctival hyperemia, corneal neovascularization, plaques

94
Q

What is rhegmatogenous retinal detachment?

A

A tear in the retina that often leads to complete detachment
- can be traumatic, accompanied by hyphema
-usually related to congenital conditions

95
Q

T/F: you should check pressures on every red eye

A

True

96
Q

What are some causes of corneal ulcers?

A

Trauma, corneal abrasion due to adnexal disease, tear film deficiency, exposure keratitis, infection

97
Q

What type of ulcer can progress to a chronic superficial ulcer?

A

An acute superficial ulcer

98
Q

Describe the normal progression of ulcers if not dealt with?

A

Acute superficial–> mid stromal–> deep stromal–> descemetocele (all the way down to descemets membrane)–> corneal perforation

99
Q

How quickly can corneal ulcers heal?

A

On average heal in 7-10 days, but can heal quicker

100
Q

What diagnostics should be run in corneal ulcer cases?

A

Shirmer tear test, corneal culture and cytology in come cases, usually fluorescein stain (but sometimes can see the ulcer without stain)

101
Q

What are some important risk factors to assess in cases of corneal ulcers in order to guide treatment?

A

-tear production
-is animal able to blink normally
-is it a brachycephalic/is there conformational exopthalmos
-is there any adnexal abnormalities?
-does the ulcer appear infected (discharge, melting)

102
Q

What are some specific causes of delayed healing of corneal ulcers?

A

Corneal infection, unresolved source of corneal abrasion (distichia, ectopic cilia, entropion, foreign body), dry eye, exposure keratitis, neurotropic keratitis, SCCEDs

103
Q

T/F: infections of the cornea are usually primary

A

False- usually secondary
- rarely primary ( in cases of herpesvirus in cats, pinkeye in cattle)

104
Q

Describe the pathogenesis of corneal infection

A

Secondary bacterial or fungal invaders impair healing and result in progressive destruction of the corneal stroma, causing increasing size and depth of ulcers

105
Q

How does entropion lead to corneal ulcers?

A

Inward rolling of eyelids causes hairs to abrade the cornea
-can be conformational or spastic

106
Q

Define distichia

A

Single or multiple hairs protruding from meibomian gland openings of eyelids
-may or may not cause clinical problems: symptoms vary greatly

107
Q

Define ectopic cilia

A

Abnormal hairs protruding through the conjunctival surface of the eyelid
-always symptomatic
-most common in young dogs
-toy breeds most commonly affected

108
Q

Describe keratoconjunctivitis sicca

A

-common cause of corneal ulcers and delayed healing in dogs (rare in cats)
-other clinical signs usually apparent (copious mucopurulent discharge)
-readily diagnosed by schirmer tear test

109
Q

Name some causes of exposure keratitis

A

-conformational exopthalmos
-inability to blink due to facial paralysis
-exopthalmos due to orbital disease
-bupthalmos due to glaucoma

110
Q

What is neurotrophic keratitis?

A

-loss of corneal sensation results in spontaneous non-healing ulcers (due to lesion in opthalmic branch of trigeminal nerve)
-rare disorder-leads to loss of corneal reflex

111
Q

What is SCCEDS syndrome?

A

Spontaneous chronic corneal epithelial defect
-characterized by a chronic non-healing superficial corneal ulcer for which no underlying cause can be determined
-middle aged dogs most commonly affected
-synonyms: boxer ulcer, indolent ulcer, refractory ulcer, recurrent erosion
-diagnosis of exclusion

112
Q

Which types of ulcers are surgical?

A

Descemetocele, corneal perforation, chronic superficial (SCCEDs)
-acute superficial, mid stromal, or deep stromal all can heal medically
-if stroma is left, can heal without surgery

113
Q

What are the goals of medical therapy for ulcer treatment?

A

-prevent/control infection
-prevent/control collagenolysis (enzymes causing loss of stroma)
-increase patient comfort
-promote corneal healing

114
Q

What type of ulcer accounts for the majority of ulcers accounted in practice?

A

Superficial corneal ulcers

115
Q

What is important to consider in acute superficial ulcers?

A

Need to rule out underlying conditions

116
Q

What is the preferred treatment protocol for acute superficial ulcers?

A

-topical broad spectrum antibiotic (neopolybac)
-topical atropine (reduces ciliary spasm)
-analgesia (oral NSAID)

Recheck every 2-3 days, fluorescein stain to monitor ulcer size

117
Q

When is a superficial ulcer considered “chronic”?

A

Has not healed in 7-10 days

118
Q

What are some of the main clinical characteristics of SCCED

A

-epithelial lip (fluorescein stain moves down under the lip)
-variable corneal pain and vascularization
-may change in size but never completely heal with medical therapy alone
-very rarely become infected

119
Q

What is the pathogenesis of SCCED?

A

Not well understood.
-hyalinized acellular anterior corneal stroma prevents corneal epithelial adhesion
-epithelial non-adherence usually extends well beyond the obvious region of the ulcer

120
Q

What are some of the treatment options for SCEDD

A

-epithelial debridement (not super helpful)
Preferred method:
- anterior stromal puncture (grid or burr keratotomy)
-superficial keratotomy
-adjunctive procedures: 3rd eyelid flap or contact lens, topical antibiotics, Ecollar

121
Q

What does epithelial debridement allow you to determine?

A

How large of a defect is present
-not helpful for treatment but can help understand prognosis
-must be aggressive

122
Q

How does puncture of the anterior stroma help SCCED lesions heal?

A

Exposes type 1 collagen fibers which can facilitate epithelial adhesion complex formation

123
Q

Describe grid keratotomy

A

-use a 25 ga needle to lightly scratch across the ulcer bed
-should begin and end in normal epithelium
-place scratches 1 mm apart

124
Q

Describe the burr keratotomy

A

dremel of eye
- leads to more complications than grid

125
Q

What follow-up is recommended in SCCED cases?

A

-recheck once a week
-if not healed by 2-3 weeks surgical trt should be repeated
-do not debride ulcer for at least 2-3 weeks following surgical procedure (can take up to 6 weeks for adhesions to form)–> dont want to go back to square 1

126
Q

What are some unique considerations for non-healing ulcers in cats?

A

-debridement alone may be effective
-grid/burr keratotomy may induce corneal sequestrum formation

127
Q

What is the approach for treatment of mid stromal ulcers?

A

-investigate underlying cause
-corneal culture and sensitivity, cytology

Treat with topical antibiotics (broad spectrum or as directed by C/S, apply q4-6 hours)
-solutions are preferred over ointments
-protease inhibitors (systemic tetracycline) q4-6 h
-topical atropine to maintain pupil dilation
-analgesia PRN
-recheck every 24 h initially, then every 48 h

128
Q

What do you do differently with deep/melting ulcer cases?

A

Same as mid stromal but more frequent treatments (2-4 h)
-consider hospitalization

129
Q

Describe the diagnosis and treatment of descemetoceles

A

-diagnose with corneal cytology or culture (obtained from ulcer edge), STT, clear spot in middle of ulcer on ophthalmic exam
-surgical treatments: conjunctival flap (trim every 4-6 weeks post op), corneoconjunctival transposition
-must be careful with eye as its very prone to rupture
-post op topical antibiotics, proteolytic inhibitors

130
Q

Define glaucoma

A

Multifactorial disease characterized by elevation of intraocular pressure incompatible with ocular health
-causes irreversible vision loss through optic nerve damage and ganglion cell death

131
Q

What is the normal IOP range

A

10-25
-30 can be normally transiently in stressed animals

132
Q

Describe the normal aqueous humor dynamics in the eye

A

Aqueous humor is produced by the ciliary body. It flows into posterior chamber, flows out through the pupil and drains through the drainage angle

133
Q

What is the main mechanism by which glaucoma develops?

A

Decreased outflow of aqueous humor

134
Q

What are some primary and secondary causes of glaucoma in dogs?

A

Primary- heritable or breed related abnormality of the aqueous drainage angle
Secondary- lens luxation, chronic uveitis, hyphema, intraocular neoplasia, melanocytic glaucoma (cairn terriers), pigmentary uveitis (goldens), pseudophakia/aphakia
-trauma is a very uncommon cause

135
Q

What are some primary and secondary causes of feline glaucoma?

A

Primary- rare. can be a congenital abnormality in siamese, persians, burmese
Secondary- similar causes as dogs, chronic uveitis most commonly, aqueous humor misdirection (unique to cats)

136
Q

What are the mechanisms of vision loss as a result of glaucoma?

A

High intraocular pressure, optic nerve ischemia, neurotoxic events

137
Q

What are some of the acute signs associated with glaucoma?

A

Blepharospasm, corneal edema, episcleral injection, dilated pupils, variable vision

138
Q

What are the chronic signs associated with glaucoma?

A

All acute signs plus bupthalmos (stretching/enlargement of globe), haabs striae (fractures in descemets membrane), lens subluxation, cupped optic nerve

139
Q

T/F: cupping of optic nerve is reversible

A

False-irreversible

140
Q

How do you reach diagnosis of glaucoma?

A

-clinical signs
-history/signalment- basset hounds, cocker spaniels are at high risk
-IOP measurement (tonometry)-consider disparity between the two eyes moreso than absolute numbers
-gonioscopy (specialist thing)

141
Q

Describe tonometry.

A

-a way to measure IOP
-acceptable tonometry methods include rebound, applanation, or indentation

142
Q

What is the role of tonometry?

A

-primary means of glaucoma diagnosis and assessment of the efficacy of glaucoma therapy
-remember that IOP may vary greatly during the day and from day to day- should take serial pressure measurements to get full picture

143
Q

T/F: relying in tonometry for early prediction of canine glaucoma is likely to be successful

A

FALSE
-not great for a diagnostic on yearly exam-waste of time and money

144
Q

What is gonioscopy?

A

-examination of the drainage angle
-requires specialist lens
-helps to determine likelihood of primary glaucoma based upon angle morphology

145
Q

Describe some clinical features of primary glaucoma?

A

-usually becomes clinically apparent in middle aged dogs
-assessment of the good eye can help to determine prognosis of the eye affected
-usually bilateral, but one eye affected before the other

146
Q

What are the goals of therapy in glaucoma cases?

A

-maintenance of vision where possible
-patient comfort in all cases
-prophylaxis in “at risk” eyes

147
Q

What are some factors that will influence your treatment approach in glaucoma cases?

A

-etiology of the glaucoma
-current intraocular pressure
-presence/absence of vision

148
Q

What are the 3 broad categories of treatment in glaucoma cases?

A

-emergency therapy in acute cases
-maintenance therapy in chronic cases
-end stage/salvage in severe cases

149
Q

What are the specific classes of drugs often indicated in glaucoma treatment?

A

-systemic hyperosmotic medications
-carbonic anhydrase inhibitors
-miotics
-prostaglandin analogues
-beta adrenergic agonists

150
Q

When is topical latanoprost indicated? When is it contraindicated?

A

Indicated: emergent disease, very rapid onset of action
Contraindications: lens luxation/instability

151
Q

What other therapies besides latanoprost might you reach for in acute cases of glaucoma?

A

-Systemic hyperosmotic- IV mannitol or oral glycerin
-has quick acting but short lived response
-contraindicated in cases of cardiovascular insufficiency
-inferior to prostaglandins in most cases

152
Q

Why do carbonic anhydrase inhibitors make a good maintenance glaucoma medication?

A

They are effective in all species and all types of glaucoma (no contraindications)
- topical and systemic options are available (although there is a higher cost and more side effects with systemic)
-go right to the source of aqueous fluid production

153
Q

What are some of the topical CAIs in vet med?

A

Dorzolamide, Brinzolamide

154
Q

How can miotics help with maintenance?

A

include prostaglandins and other miotics
- moderately to very effective
-avoid in glaucoma second to uveitis or anterior lens luxation
-good choice for glaucoma prophylaxis
-includes demacarium bromide and pilocarpine

155
Q

What are the different prostaglandin analogues (miotics) that can be reached for in glaucoma patients?

A

Lantanoptost, Travoprost, Bimatoprost
-none of these are effective in cats

156
Q

T/F: Beta blockers can be used as the sole agent in glaucoma cases

A

False
-they only have mild to moderate effects-aimed for reducing fluid production
-useful for glaucoma prophylaxis
-side effects include bradycardia and worsening asthma
-always use with other agents

157
Q

What is the one carbonic anhydrase, beta blocker combo med for glaucoma?

A

Cosopt- dorzolamide and timolol

158
Q

What general principles should you always follow for glaucoma treatment?

A
  1. Treat early and aggressively
  2. Resist temptation to taper drugs in well controlled cases
  3. Consider surgical intervention if available early in the course of disease
159
Q

T/F: glaucoma is not cureable

A

True

160
Q

What is the recommended followup in glaucoma cases?

A

Daily/weekly rechecks until IOP control is established
-recheck every 3-4 weeks after control established
-check at risk eyes every 4-6 weeks

161
Q

What is the target IOP for glaucoma treatment?

A

<15-20 mmHg
-high normal is not good enough

162
Q

What meds are the most helpful for prophylaxis in glaucoma cases?

A

Topical miotics, topical CAIs and beta blockers

163
Q

What are the options for surgical management in glaucoma cases?

A

Decrease aqueous production: cyclodestructive procedures including cylophotocoagulation (laser)or cyclocryotherapy

Increase aqueous outflow: aqueous shunts or gonioimplant

or combo procedure

164
Q

What is the main complications with aqeous shunts?

A

Fibrous tissue forms over valve - obstructs fluid and leads to worsening glaucoma

165
Q

Where can failure occur with cyclodestructive procedures?

A

Ciliary epithelium can regenerate themselves

166
Q

What is the long term prognosis for glaucoma?

A

-prognosis for vision is poor as you cannot cure the disease
-salvage procedures should be considered in irreversibly blind eyes

167
Q

What are the options for salvage procedures in glaucoma cases?

A

Enucleation, evisceration or intrascleral prosthesis, chemical ciliary body ablation with intravitreal gentamycin (dont do in visual eyes as you will cause blindness)

168
Q

What is the innervation to the sphincter muscles of the iris?

A

Parasympathetic innervation originating at CN III

169
Q

What is the innervation of the dilator muscles of the eye?

A

Sympathetic innervation originating at T1-T3

170
Q

If a lesion is in output of CN III, what might occur to the eye?

A

The eye will become mydriatic

171
Q

A lesion to the sympathetic innervation to the eye will result in what syndrome?

A

Horners syndrome

172
Q

When evaluating PLRs in dogs, what is the most confounding issue in old small dogs?

A

Iris atrophy
- if an animal has poor PLRs and a good dazzle, this is probably what is going on

173
Q

If you have an abnormal optho exam +/- a PLR deficit, what are the main conditions you would look towards?

A

-opacification of ocular media (cataract)
-retinal disease

174
Q

If you have an abnormal optho exam with diminished or absent PLRs, what should you consider?

A

-retinal detachment
-optic neuritis, optic nerve hypoplasia

175
Q

If you have a normal ophtho exam and a diminished, incomplete or absent PLR, what should you consider?

A

-SARDS (PLR often present but diminished)
-Retrobulbar optic neuritis, optic nerve neoplasia, optic tract lesion

176
Q

If you have a normal ophtho exam and a normal PLR, but no menace what should you consider?

A

-think thalamocortical lesions or cortical blindness

177
Q

What does the ERG (electroretinogram) assess?

A

retinal function
- main diagnostic for SARDs

178
Q

What are the 3 criteria for diagnosing SARDs?

A

Acute vision loss, normal looking fundus and flat ERG

179
Q

If fundus appears very abnormal, what structure is affected in a blind dog?

A

The retina!

180
Q

What type of photoreceptors are affected first in cases of Progressive retinal atrophy?

A

Rods
-present with loss of night vision

181
Q

Describe some characteristics of progressive retinal atrophy

A

-hereditary disorder
-rate of progression is variable, but progresses faster in younger dogs that older
-secondary cataract formation is common

182
Q

Do you need to perform an ERG in cases of PRA?

A

NO- already know retina is affected due to fundus changes
-will often see vascular attenuation, tapetal hyperreflectivity, optic nerve atrophy

183
Q

What is commonly observed in cases of optic neuritis?

A

-rarely a subtotal condition, usually bilateral blindness
-usually involves optic papilla but can be retrobulbar
-can be due to inflammatory/immune mediated disease, infectious or neoplastic abnormalities
-systemic evaluation is warranted

SA Optho/Neuro (8 decks)

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