Final Exam Flashcards
(183 cards)
1
Q
What is the uvea?
A
The vascular tunic of the eye
-composed of the iris, ciliary body and choroid
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
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
4
Q
What makes inflammation of the eye unique?
A
Limited regeneration and unique immune requirements
5
Q
What is inflammation generated by?
A
- The release of chemical mediators by cells
- Presence of certain pathogen-associated molecules (bacteria, fungi)
- Release of pro-inflammatory molecules by immune cells
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)
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
8
Q
What is ciliary flush?
A
360 degree deep vascularization on the cornea
9
Q
T/F: you will often see ciliary flush with corneal surface disease
A
False- will see in cases of intraocular disease
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
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
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
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
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
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
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
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
18
Q
What is hyphema?
A
Blood in the eye
-usually anterior chamber
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
20
Q
What is rubiosis irides?
A
increase in the vasculature of iris
- injection of the iridal blood vessels
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
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
23
Q
How can permanent degeneration result from chronic uveitis?
A
Endothelial degeneration - can be permanent even without active inflammation
24
Q
Why can cataracts result from uveitis?
A
Lens gets its nutrition from AH
25
What is iris bombe?
Posterior synechiae
26
How should you go about your Opthalmic exam?
-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
27
What are some common exam clues that lead you to uveitis as a diagnosis?
-Miosis (spasm of ciliary muscles and pupillary sphincter)
-low IOP (decreased production of aqueous humor)
-aqueous flare, hypopyon, hyphema (due to breakdown of BAB)
28
What are some causes of uveitis?
-Primary ocular disease: cataract, lens rupture, corneal ulcer, intraocular mass
-ocular manifestations of systemic diseases (infectious, metabolic, immune-mediated, neoplastic)
-trauma
29
What percent of cases can you not find a cause of uveitis (idiopathic)?
47% of dogs, 70% of cats
30
What are the most common causes of uveitis in dogs?
-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)
31
What are the most common tumors (primary and secondary) in the eyes of dogs?
Melanoma most common primary, lymphoma most common secondary
32
What are the most common causes of uveitis in cats?
-Infectious: viral (FeLV, FIP, FIV, FHV-1), bacterial (bartonella), fungal (histo, blasto, cocciodioides), protozoal (toxoplasma)
-metabolic: systemic hypertension
-neoplastic: lymphoma most commonly
33
What should you include in your workup in uveitis cases?
-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)
34
What are some of the main treatment goals in uveitis cases?
Control pain, prevent sequele, stabilize and restore BAB
-treat underlying cause when possible
35
What are some topical treatment options for uveitis?
-Topical anti-inflammatories: corticosteroids (prednisolone acetate, dexamethasone), non steroidals (diclofenax, flurbiprofen, ketorolac)
-topical atropine
36
What are some of the benefits of using atropine in uveitis cases?
-Mydriatic to prevent synechia
-Cycloplegic: provides analgesia
-stabilization of BAB
37
T/F: you can use NSAIDs and steroids together in uveitis cases for topical treatment
TRUE
38
When should atropine be avoided?
In glaucoma cases as it could lead to worsening of the IOP
-lens instability
-dry eye (decreases tear production as its a parasympatholytic)
39
What are some contraindications for using steroids in the eye?
-if there is infection present (can potentiate infection)
-if there is an ulcer present (decreases would healing)
-can result in corneal lipid/calcium deposition
40
What are some systemic treatment options for uveitis?
-Corticosteroids (prednisone), NSAIDs
-antimicrobials, antifungals, immunomodulary drugs (cyclosporine, azathioprine)
41
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?
NO- could worsen the infection
42
What is important for the followup in uveitis cases?
Watch for complications such as secondary glaucoma, look for lessening of clinical signs, gradually taper medications to avoid flare ups, educate clients on risks
43
Describe a basic diagnostic approach for a cloudy eye case.
Localize the lesion (what region of eye), qualify the lesion (what is it), determine lesion etiology (whats causing it)
44
What are some important historical questions to ask in a case of cloudy eyes?
Onset, signalment, symptoms (both ocular and non-ocular)
45
What are the different locations that cloudiness can be localized to?
Cornea, anterior chamber, lens, posterior segment (vitreous or retina)
46
What can edema of the cornea be a result of?
Endothelial dysfunction or ulceration (dehydration of cornea due to epithelial disruption)
47
What can scarring/fibrosis of the cornea be a result of?
Prior ulcer/trauma, chronic exposure, chronic abrasion
48
What can lipid in the cornea be a result of?
Lipid dystrophy, lipid degeneration
49
What can mineralization of the cornea be a result of?
Degeneration or metabolic changes
50
What is the only way to reliably differentiate between mineral and lipid in the cornea?
Histopathology
51
What are some causes of endothelial dysfunction?
Anterior uveitis, glaucoma (physical compression of endothelial cells), endothelial degeneration (breed specific), or localized dysfunction (uncommon)
52
What is the common presentation of endothelial degeneration cases?
Bilateral, non-painful, progressive corneal edema. Fluorescein negative
53
T/F: Lens instability is usually a unilateral disease
False- bilateral
54
What should you do if you are trying to prevent lens luxation?
Constrict the pupil with latanoprost
55
What can stringiness in the eye be an indication of?
Persistent pupillary membrane
56
What can cause chronic exposure?
Lagophthalmos, KCS
57
What can cause chronic abrasion?
Entropion, distichia, ectopic cilia
58
How can you distinguish corneal edema from corneal scarring?
scar usually more focal, more homogenous
-can see blood vessels over scar
59
What is the common presentation for a dog with chronic exposure?
Bilateral horizontal fibrosis
- usually occurs in brachycephalics
60
What is the difference in etiologies between lipid dystrophy and lipid degeneration?
Lipid dystrophy is hereditary
Lipid degeneration due to prior keratitis, infiltrative corneal disease, topical corticosteroids or systemic metabolic disease
61
T/F: lipid dystrophy often appears homogenous
False- usually not homogenous
- looks like glitter/sparkles. made up of numerous coalescing particles
62
What may you see in terms of a physical difference between lipid dystrophy and degeneration?
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
63
What are some of the metabolic or degenerative causes leading to corneal mineralization?
Degenerative- ocular disease, age related
Metabolic- systemic metabolic disease
64
What may you see different on ophthalmic exam to differentiate lipid from mineral?
Mineral may look more like scratch marks or moth eaten, spiculated appearance
-doesn't look as shiny
65
When is a cloudy cornea painful?
When it s caused by edema (ulcers, anterior uveitis or glaucoma)
-however edema from endothelial degeneration is not painful
66
When can mineral lesions causing cloudiness lead to pain?
When the mineral flakes off leading to an ulcer
- hard to heal as corneal tissue around it is unhealthy
67
What can lead to opacity of the anterior chamber?
Either aqueous flare caused by uveitis or lipid flare (from hyperlipidemia or uveitis)
68
Are lipemic aqueous eyes painful?
Yes if caused by uveitis
No if a result of a metabolic condition
69
What can cause cloudiness of the lens?
Nuclear sclerosis or cataracts
70
Define nuclear sclerosis
Densification of the nucleus in the lens
- because lens fibers never stop compacting
-occurs in older dogs (8 or older)
71
Is the path of light blocked to the back of the eye in cases of nuclear sclerosis?
NO
72
How can you differentiate cataracts and nuclear sclerosis?
Utilize the oblique and coaxial illumination
- cataracts will prevent light from going to the tapetum
73
How do you know that you are dealing with a mature cataract?
There is a complete obstruction of the tapetal reflex
74
What unique cataract feature is present in diabetics?
Y shaped sclerosis of nucleus
75
What can result in posterior segment cloudiness?
Vitreous- haze due to inflammation, asteroid hyalosis, synchesis scintillans
Retina- retinal detachment
76
What is asteroid hyalosis?
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
What is synchesis scintillans?
Cholesterol deposits in vitreous
- looks the same as asteroid hyalosis
78
Why are red eye cases so frustrating?
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
What is conjunctival hyperemia?
Enlargement of the vessels in the conjunctiva
- can look like diffuse redness or enlargement of a small network of vessels
80
Define episcleral injection
Distinct, enlarged straight vessels adherent to the sclera
- run posteriorly towards the equator from the limbus
-usually combined with conjunctival hyperemia
81
What is episcleral injection indicative of?
Intraocular disease
82
Describe corneal neovascularization
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
What does hemorrhage of the eye look like?
Can look like anything- there is no distinct pattern
84
What is a classic presentation of superficial keratitis or keratoconjunctivitis?
Long branching vessels
-conjunctival hyperemia
85
Where do ectopic cilia most often occur?
On the upper eyelid, dead center
86
What clinical signs are common with intraocular disease?
Episcleral injection, maybe conjunctival hyperemia, maybe deep neovasculatization
87
What tests should you perform if suspicious of surface disease? intraocular disease?
Surface- schirmer tear test, fluorescein stain, cytology and culture in some cases
Intraocular disease: evaluate pupil size, tonometry
88
What conditions are the most important to rule out before treating anything empircally?
Corneal ulcer, dry eye, glaucoma, uveitis
-therefore red eyes should always undergo shirmer, fluorescein stain and tonometry
89
What is the normal for schirmer tear test?
>15
90
Compare and contrast ectopic cilia, dystechia and trichiasis
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
What breeds of dogs are the most predisposed to ectopic cilia?
Toy breed dogs
- also usually have a lot of distichia
92
T/F: distichia commonly causes corneal irritation and sometimes ulcers
False- this is rare. They are often asymptomatic
-unlike ectopic cilia which commonly cause ulcers, recurrent
93
What are some common clinical signs in a cat with eosinophilic keratoconjunctivitis?
Conjunctival hyperemia, corneal neovascularization, plaques
94
What is rhegmatogenous retinal detachment?
A tear in the retina that often leads to complete detachment
- can be traumatic, accompanied by hyphema
-usually related to congenital conditions
95
T/F: you should check pressures on every red eye
True
96
What are some causes of corneal ulcers?
Trauma, corneal abrasion due to adnexal disease, tear film deficiency, exposure keratitis, infection
97
What type of ulcer can progress to a chronic superficial ulcer?
An acute superficial ulcer
98
Describe the normal progression of ulcers if not dealt with?
Acute superficial--> mid stromal--> deep stromal--> descemetocele (all the way down to descemets membrane)--> corneal perforation
99
How quickly can corneal ulcers heal?
On average heal in 7-10 days, but can heal quicker
100
What diagnostics should be run in corneal ulcer cases?
Shirmer tear test, corneal culture and cytology in come cases, usually fluorescein stain (but sometimes can see the ulcer without stain)
101
What are some important risk factors to assess in cases of corneal ulcers in order to guide treatment?
-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
What are some specific causes of delayed healing of corneal ulcers?
Corneal infection, unresolved source of corneal abrasion (distichia, ectopic cilia, entropion, foreign body), dry eye, exposure keratitis, neurotropic keratitis, SCCEDs
103
T/F: infections of the cornea are usually primary
False- usually secondary
- rarely primary ( in cases of herpesvirus in cats, pinkeye in cattle)
104
Describe the pathogenesis of corneal infection
Secondary bacterial or fungal invaders impair healing and result in progressive destruction of the corneal stroma, causing increasing size and depth of ulcers
105
How does entropion lead to corneal ulcers?
Inward rolling of eyelids causes hairs to abrade the cornea
-can be conformational or spastic
106
Define distichia
Single or multiple hairs protruding from meibomian gland openings of eyelids
-may or may not cause clinical problems: symptoms vary greatly
107
Define ectopic cilia
Abnormal hairs protruding through the conjunctival surface of the eyelid
-always symptomatic
-most common in young dogs
-toy breeds most commonly affected
108
Describe keratoconjunctivitis sicca
-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
Name some causes of exposure keratitis
-conformational exopthalmos
-inability to blink due to facial paralysis
-exopthalmos due to orbital disease
-bupthalmos due to glaucoma
110
What is neurotrophic keratitis?
-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
What is SCCEDS syndrome?
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
Which types of ulcers are surgical?
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
What are the goals of medical therapy for ulcer treatment?
-prevent/control infection
-prevent/control collagenolysis (enzymes causing loss of stroma)
-increase patient comfort
-promote corneal healing
114
What type of ulcer accounts for the majority of ulcers accounted in practice?
Superficial corneal ulcers
115
What is important to consider in acute superficial ulcers?
Need to rule out underlying conditions
116
What is the preferred treatment protocol for acute superficial ulcers?
-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
When is a superficial ulcer considered "chronic"?
Has not healed in 7-10 days
118
What are some of the main clinical characteristics of SCCED
-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
What is the pathogenesis of SCCED?
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
What are some of the treatment options for SCEDD
-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
What does epithelial debridement allow you to determine?
How large of a defect is present
-not helpful for treatment but can help understand prognosis
-must be aggressive
122
How does puncture of the anterior stroma help SCCED lesions heal?
Exposes type 1 collagen fibers which can facilitate epithelial adhesion complex formation
123
Describe grid keratotomy
-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
Describe the burr keratotomy
dremel of eye
- leads to more complications than grid
125
What follow-up is recommended in SCCED cases?
-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
What are some unique considerations for non-healing ulcers in cats?
-debridement alone may be effective
-grid/burr keratotomy may induce corneal sequestrum formation
127
What is the approach for treatment of mid stromal ulcers?
-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
What do you do differently with deep/melting ulcer cases?
Same as mid stromal but more frequent treatments (2-4 h)
-consider hospitalization
129
Describe the diagnosis and treatment of descemetoceles
-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
Define glaucoma
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
What is the normal IOP range
10-25
-30 can be normally transiently in stressed animals
132
Describe the normal aqueous humor dynamics in the eye
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
What is the main mechanism by which glaucoma develops?
Decreased outflow of aqueous humor
134
What are some primary and secondary causes of glaucoma in dogs?
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
What are some primary and secondary causes of feline glaucoma?
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
What are the mechanisms of vision loss as a result of glaucoma?
High intraocular pressure, optic nerve ischemia, neurotoxic events
137
What are some of the acute signs associated with glaucoma?
Blepharospasm, corneal edema, episcleral injection, dilated pupils, variable vision
138
What are the chronic signs associated with glaucoma?
All acute signs plus bupthalmos (stretching/enlargement of globe), haabs striae (fractures in descemets membrane), lens subluxation, cupped optic nerve
139
T/F: cupping of optic nerve is reversible
False-irreversible
140
How do you reach diagnosis of glaucoma?
-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
Describe tonometry.
-a way to measure IOP
-acceptable tonometry methods include rebound, applanation, or indentation
142
What is the role of tonometry?
-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
T/F: relying in tonometry for early prediction of canine glaucoma is likely to be successful
FALSE
-not great for a diagnostic on yearly exam-waste of time and money
144
What is gonioscopy?
-examination of the drainage angle
-requires specialist lens
-helps to determine likelihood of primary glaucoma based upon angle morphology
145
Describe some clinical features of primary glaucoma?
-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
What are the goals of therapy in glaucoma cases?
-maintenance of vision where possible
-patient comfort in all cases
-prophylaxis in "at risk" eyes
147
What are some factors that will influence your treatment approach in glaucoma cases?
-etiology of the glaucoma
-current intraocular pressure
-presence/absence of vision
148
What are the 3 broad categories of treatment in glaucoma cases?
-emergency therapy in acute cases
-maintenance therapy in chronic cases
-end stage/salvage in severe cases
149
What are the specific classes of drugs often indicated in glaucoma treatment?
-systemic hyperosmotic medications
-carbonic anhydrase inhibitors
-miotics
-prostaglandin analogues
-beta adrenergic agonists
150
When is topical latanoprost indicated? When is it contraindicated?
Indicated: emergent disease, very rapid onset of action
Contraindications: lens luxation/instability
151
What other therapies besides latanoprost might you reach for in acute cases of glaucoma?
-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
Why do carbonic anhydrase inhibitors make a good maintenance glaucoma medication?
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
What are some of the topical CAIs in vet med?
Dorzolamide, Brinzolamide
154
How can miotics help with maintenance?
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
What are the different prostaglandin analogues (miotics) that can be reached for in glaucoma patients?
Lantanoptost, Travoprost, Bimatoprost
-none of these are effective in cats
156
T/F: Beta blockers can be used as the sole agent in glaucoma cases
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
What is the one carbonic anhydrase, beta blocker combo med for glaucoma?
Cosopt- dorzolamide and timolol
158
What general principles should you always follow for glaucoma treatment?
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
T/F: glaucoma is not cureable
True
160
What is the recommended followup in glaucoma cases?
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
What is the target IOP for glaucoma treatment?
<15-20 mmHg
-high normal is not good enough
162
What meds are the most helpful for prophylaxis in glaucoma cases?
Topical miotics, topical CAIs and beta blockers
163
What are the options for surgical management in glaucoma cases?
Decrease aqueous production: cyclodestructive procedures including cylophotocoagulation (laser)or cyclocryotherapy
Increase aqueous outflow: aqueous shunts or gonioimplant
or combo procedure
164
What is the main complications with aqeous shunts?
Fibrous tissue forms over valve - obstructs fluid and leads to worsening glaucoma
165
Where can failure occur with cyclodestructive procedures?
Ciliary epithelium can regenerate themselves
166
What is the long term prognosis for glaucoma?
-prognosis for vision is poor as you cannot cure the disease
-salvage procedures should be considered in irreversibly blind eyes
167
What are the options for salvage procedures in glaucoma cases?
Enucleation, evisceration or intrascleral prosthesis, chemical ciliary body ablation with intravitreal gentamycin (dont do in visual eyes as you will cause blindness)
168
What is the innervation to the sphincter muscles of the iris?
Parasympathetic innervation originating at CN III
169
What is the innervation of the dilator muscles of the eye?
Sympathetic innervation originating at T1-T3
170
If a lesion is in output of CN III, what might occur to the eye?
The eye will become mydriatic
171
A lesion to the sympathetic innervation to the eye will result in what syndrome?
Horners syndrome
172
When evaluating PLRs in dogs, what is the most confounding issue in old small dogs?
Iris atrophy
- if an animal has poor PLRs and a good dazzle, this is probably what is going on
173
If you have an abnormal optho exam +/- a PLR deficit, what are the main conditions you would look towards?
-opacification of ocular media (cataract)
-retinal disease
174
If you have an abnormal optho exam with diminished or absent PLRs, what should you consider?
-retinal detachment
-optic neuritis, optic nerve hypoplasia
175
If you have a normal ophtho exam and a diminished, incomplete or absent PLR, what should you consider?
-SARDS (PLR often present but diminished)
-Retrobulbar optic neuritis, optic nerve neoplasia, optic tract lesion
176
If you have a normal ophtho exam and a normal PLR, but no menace what should you consider?
-think thalamocortical lesions or cortical blindness
177
What does the ERG (electroretinogram) assess?
retinal function
- main diagnostic for SARDs
178
What are the 3 criteria for diagnosing SARDs?
Acute vision loss, normal looking fundus and flat ERG
179
If fundus appears very abnormal, what structure is affected in a blind dog?
The retina!
180
What type of photoreceptors are affected first in cases of Progressive retinal atrophy?
Rods
-present with loss of night vision
181
Describe some characteristics of progressive retinal atrophy
-hereditary disorder
-rate of progression is variable, but progresses faster in younger dogs that older
-secondary cataract formation is common
182
Do you need to perform an ERG in cases of PRA?
NO- already know retina is affected due to fundus changes
-will often see vascular attenuation, tapetal hyperreflectivity, optic nerve atrophy
183
What is commonly observed in cases of optic neuritis?
-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
