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eyeballophtho2
| Question | Answer |
|---|---|
| What is the abnormal pressure with a Schiotz? | Dog > 26 / Cat > 32 |
| At what pressure can blindness occur and how fast? | Very high (60-70) and w/in 24-48 hrs if may occur |
| Successful Tx Requirements | Early Dx or Prophylactic therapy / Accurate IOP measurement / Aggressive tx early in the course of the dz |
| What are the functions of aqueous humor? | Holds ocular shape / Nourishes avascular tissues (lens, posterior cornea) / Carries away waste products |
| What produces aqueous and how? | Non pigmented ciliary body epithelium / Active production is predominate (2/3) controlled by carbonic anhydrase & Passive production (1/3) blood aqueous barrier prevents passage of large molecules |
| Where does aqueous outflow occur? | Trabecular meshwork (predominate) and uveoscleral routes |
| Where does aqueous flow? | from posterior chamber -> anterior surface of the lens -> thru the pupil -> anterior chamber |
| What is the main route of aqueous outflow? And what forms it? | Iridocorneal angle (drainage angle) - formed by junction of iris-ciliary body and the cornea-sclera |
| What does the angle consist of: | 1. Pectinate ligaments - spans from iris to peripheral cornea at limbus 2. Ciliary cleft - contains trabecular meshwork 3. Collecting channels lead to scleral venous plexus (communicates with episcleral veins and gen circulation) |
| What is the most common problem causing glaucoma? | impaired outflow, production excessive |
| What are teh common mechanisms of outflow impairments | Closure of drainage angle / adhesions, synechia / inflammatory or neoplastic infiltrates / luxation / recession of drainage apparatus from trauma / accumulation of proteoglycans |
| What can cause the closure of the drainage angle | Developmental abnormalities of pectinate ligaments / reverse pupillary blocks / anteriorly positioned lens attached to zonules / increased axial length of lens or vitreous |
| Elevated IOP causes damage to what? ER? | retina and optic nerve. Neuro ER!!! |
| When should you suscept glaucoma? | Red eye in which cause of vascular injection is not obvious OR in eyes with unexplained corneal edema, pupillary abnormalities, chronic anterior uveitis, lens positional abnormalities or visual impairment |
| Most common breeds associated with Primary Open Angle? | Mixed, Cocker, Basset, Boston, Schnauzer, Beagle |
| Most common breead with Closed angle? | cocker, mixed, basset, smoyed, beagle, husky, chow, fox terrier, toy poodle, standard poodle |
| Most common breeds with Secondary glaucoma? | Mixed, cocker, wire fox, toy poodle, boston, min poodle, lab, husky, basset, beagle |
| Clinical signs of Acute glaucoma | Pain (blepharospasm, epiphora), Episcleral hyperemia, corneal edema, mydriasis (sphincter is paralyzed over 40), cupping of the optic nerve head |
| Clinical signs of chronic glaucoma | Buphthalmia (globe stretching), Decreased pain, Episcleral injection, Striate keratopathy, subluxated/luxated lens, iris degeneration, cataracts, retinal lesions, phthisis bulbi |
| What are common errors in technique of measuring IOP | compressing globe, occluding jugular veins, measure on the sclera or 3rd eyelid, not resting footplate completely on cornea, prolonged application, corneal scarring, infiltrates, thinning |
| What is primary glaucoma? | Increased IOP without antecedent or concomitant ocular dz or injury Usually breed related or heritable |
| What is primary open angle glaucoma (paog)? | Least common. Insidious onset. Mild to mod elevated IOP in both eyes. Vision loss is slow. Cause lies in the metabolism of the trabecular meshwork. |
| What is the primary angle closure glaucoma (pacg)? | More common. Initially unilateral, episodic, acute elevation in IOP that either sponatenously resolves or persists. Bilateral dz will occur. Involves pupil block and abnormal drainage appartus. Basset, artic breeds, cocker, pectinate dysplasia |
| What is secondary glaucoma? | Increased IOP as a complication or sequela to other ocular dz or injury. Twice as common as primary glaucoma. MORE common in cats |
| What are the lens associated causes of secondary glaucoma? | Luxated lens in terriers / Intumescent lenses (swollen) / Phacolytic glaucoma (lens protein induced uveitis with fibrosis of drainage angle) |
| What are the traumatic causes of secondary glaucoma? | Hemorrhage / Puncture wounds or FB / Drainage angle recession after trauma |
| What are the inflammatory causes of secondary glaucoma? | Anterior peripheral synechia which closes the angle / Postrior synechia (iris bombe) / Angle obstruction with cels, debris, fibrin |
| What are the intraocular tumors that cause secondary glaucoma? | Primary: melanoma Secondary, any and LSA |
| What else can occlude the pupil and cause secondary glaucoma? | Vitreal prolapse |
| What is the goal of therapy of glaucoma? | save or return vision |
| What four questions should be asked to determine therapy? | Is IOP elevated? Is eye sighted or irreversibly blind? Is glaucoma primary or secondary? Can medical therapy control IOP and and ocular pain or is sx needed? |
| What group of drugs have the most hypotensive ocular effect and how do they work? | Hyperosmotic diuretic agents: dehydrate vitreous, IOP drops in 10 min and lasts for one day / Mannitol: most effective in acute primary glaucoma, Glycerin |
| What is the second most potent hypotensive ocular effects group of drugs? | Prostaglandin derivative: Latanoprost - cleaved by corneal esterases to active drug, increases uveoscleral outflow, induces miosis / Does NOT lower IOP in cats, FIRST choice drug for alleviating pupil blocks in acute PACG |
| What is the third most potent hypotensive ocular drug group? | Carbonic Anhydrase Inhibitor - reduce IOP by 20-30%, reduce aqueous secretion by slowing formation of bicarb with reduct in Na and water transport across ciliary processes. / Corzolamida, brinzolamida, methazolamide, dichlorphenamide |
| How do parasympathomimetic miotics work? | Increase aqueous outflow by contracting longitudinal ciliary muscle NOT effective if IOP is greater than 40-50 due to muscular paralysis Pilocarpine - mimic Ach |
| How do adrenergics work? | Vasoconstricting the ciliary body thereby reducing aqueous production and by improving outflow / Epinephrine bitartrate and dipivalyl epinephrine |
| How do beta blockers work? | Decreasing aqueous production, induce miosis |
| How do anti inflammatories work? | added to reduce uveitis secondary to IOP rise, miotitic drugs or sx |
| Which drugs are animals maintained on for glaucoma? | Pilocarpine or latanprost / Pred / CAI / Epi or beta blocker |
| Which surgeries increase aqueous outflow? | Gonioimplants: anterior chamber to allow draining into subconjuncival space / Filtering proceduring: new outflow routes with holes in iris, sclera or ciliary body |
| Which surgeries decrease aqueous production? | Cyclocryosx: ciliary body frozen / Cyclophotocoagulation: laser ciliary body, less inflammation |
| What is prophylactic tx of fellow eye to prevent glaucoma? | Demarcium bromide, betaxolol, Pred, measure IOP monthly then every 3 mos |
| Short term management of blind eyes due to glaucoma | tramadol, dorzolamide or latanoprost, tear ointments if buphthamlmixc |
| Majority of cases of feline glaucoma | secondary to chronic low grade uveitis, intraocular neoplasia, trauma, or aqueous humor misdirection syndrome |
| Majority of horse glaucoma | secondary to uveitis |
| How does the lens get nutrition? | Aqueous humor, anaerobic glycolysis with glucose (hexokinase) |
| Why is lens sensitive to protein deficiency? | high in protein, mostly soluble in young / with age some crystaline become insoluble -> senile cataractogenesis, more insoluble with cataracts |
| Nuclear sclerosis | lens continues to grow slowly with compression of nucleus making lens less elastic and less able to accommodate for near vision. compressed nucleus becomes cloudy and is diff from cataracts by visible fundus |
| How do you acquire near vision | lens thickening: ciliary m constrict, zonule tension decreases, elastic lens capsule causes axial thickening |
| What is the most common congenital defect of the lens | Persistent pupillary membrane: anterior remnants of tunica vasculosa - Vascular related, most uncommon is the persistent hyperplastic primary vitreous/persistent hyperplastic tunica vasculosa lentis |
| Other uncommon congential anomalie of the lens | Microphakia (small lens) / lens coloboma (notch like defect) / peter's anomaly (fail to separate from cornea = opaque) |
| Which dz of the lens cause loss of accommodation | With aging - Presbyopia: anterior capsule thickens and nucleus hardens / Following cataract sx |
| Pathogenesis of cataracts | Related to alterations in lens metabolism, any irregularity in the 3D spcing of the lens fibers resulting from changes in lens hydration, protein conformation, cell metabolism, electrolyte imbalances or cel membrane stability |
| When do cataracts occur? | Congenital at birth (nuclear), juvenile, adult, senile |
| Where do cataracts occur? | Can occurs in capsule, cortex or nucleus Many inherited occur in posterior cortex area |
| Incipient stage of development | small opacity and vision is maintained |
| Incomplete/immature stage of development | vision is impaired and fundus is seen indistinctly, tapetal reflex is still seen |
| Intumescent stage of development | swollen, opaque lens which may cause secondary glaucoma due to mechanical compression of the drainage angle |
| Complete/mature stage of development | entire lens is opaque with no tapetal reflex or fundus visible |
| Resorbing/hypermature stage of development | cortex may liquefy and permit visualization of the fundus around the opacity, note wrinkles in the anterior lens capsule or sparkles in the lens consist of very fine particles that reflect light as snow reflects sunlight, assoc with lens induced uveitis |
| Morgagnian cataract stage of development | hypermature lens with liquefied cortex and the solid nucleus sinks to bottom |
| lens consistency differences with age | Old: hard, young: soft |
| Inherited cause of cataracts | most common cause of cataracts in dogs, any age |
| Nutritional cause of cataracts | AA deficiency, Protein deficient/starving, Vit deficiency |
| Toxic cause of cataracts | Disophenol(dewormer), Hygromycin B (anthelmintic), Steroids, Epi, PS Miotics, chlorpromazine |
| Inflammatory/infectious cause of cataracts | Uveitis induced cataracts: most common cause of cataracts in cats and horses / BVD in cattle in utero |
| Senile cause of cataracts | Elderly animals secondary to cumulative effects of chronic exposure to UV light and oxidizing stress |
| Radiation and electric shock cause of cataracts | eye in the field of radiation or if got electric shock from chewing on electric cords |
| Metabolic cause of cataracts | Diabetes mellitus: common / hypocalcemia |
| Traumatic causes of cataracts | lens capsule rupture and lens fiber disruption draws aqueous into the lens, resulting in opacifications |
| Medical therapy of cataracts | Dissolution / Prevention (regulate diabetes) / Palliative (atropine to dilate for better vision) / anti inflammatories (steroids, aspirin, carprofen) |
| Veterinary related factors related to successful outcome with cataracts | recognize it early, recommend lens extraction before complete opacification / refer / refer prior to lens resorption |
| Animal related factros to a successful outcome | good health / free from other eye problems / tolerate tx / sx before 6 mos in a foal |
| Client related factors to successful outcome | know pros and cons / bear expense and time committment |
| Surgeon related factors to successful outcome | familiar with methods, least amount of trauma (Phaco, Extracapsular cataract extraction), post op refractive errors corrected |
| Etiology of lens luxation | Trauma, Spontaneous, Secondary to chronic uveitis/zonule dissolution, to hypermature cataract and lens shrinkage, to glaucoma and globe streatching |
| Signs of lens luxation | anterior chamber shallow or deep depending on luxation, iridonesis (trembling), lens in anterior chamber, aphakic crescent, corneal edema, glaucoma? |
| 2 forms of lens induced uveitis | trauma - lens tear, protein leakage from cataract |
| Signs of lens rupture | hx, other signs of trauma (hyphema, laceration, uveitis) / if chronic - miotic pupil, deep anterior chamber, smoldering anterior uveitis |
| Tx of lens rupture causing uveitis | Aggressive sx therapy if acute - can save eye/vision, refer / Conservative therapy - Abs, steroids, atropine -- usually blind |
| Signs of cataract induced uveitis | Suspect in ANY red eye with a cataract... Acute: episcleral injection, perilimbal flush, corneal edema, anterior chamber cells and flare, iritis, miosis, low IOP Chronic: synechia, iris bombe, sec glaucoma? |
| Tx of cataract uveitis | anti inflammatory agents, tx glaucoma, lens etraction has high failure rate in chronic LIU, enucleate/eviscerate |
| The divisions of the uvea | Anterior uvea: iris and ciliary body Posterior uvea: choroid |
| Pars plicata | composes of ciliary bodies that produce aqueous humor to supply nutrients and remove waste from eye |
| Blood aqueous barrier | important fxn of uvea: prevents passage of protein into anterior chamber (clear vision) composed of endothelial cells and tight junctions |
| Choroid functions and why predisposed to dz | layers of blood vessels to supply nutrients to retina.. very leaky so proteins can get into interstitial space |
| Functions of Uvea | Par plicata: produce aqueous humor Produces blood aqueous barrier Choroid: supplies nutrients to retina Waste elimination Light regulation Accommodation |
| Layers of the choroid | choriocapillaris, tapetum, medium and large vessel layer with pigment, suprachoroidea |
| Heterochromia irides | multiple colors w/in an iris or b/t 2 |
| Endogenous vs exogenous uveitis | Exo: external to eye, trauma, corneal ulcer, perf End: w/in eye or blood (most common) includes infectious, neoplastic, toxic, metabolic, autoimmune, parasitic |
| Non specific signs of uveitis | lacrimation, blepharospasm, photophobia, red eye |
| Specific signs of uveitis | Miosis: due to PGs (pain due to ciliary body spasm along with constriction of iris sphincter) Aqueous flare: turbid aqueous, breakdown of blood aqueous barrier with inflammation (protein) Hypopyon, hyphema, keratic precipitates, iris swelling/hyperemia |
| What IOC pressure would you expect to find with uveitis | Decreased in acute cases due to decreased aqueous humor production and increased uveoscleral outflow |
| Why would the pupil shape change? | Due to synechia |
| What c/s are seen with chronic uveitis? | cataract formation, secondary glaucoma, phthsis bulbi (small eye), iris pigmentation |
| Uveitis ddx | Algal, bacterial (lepto, septicemia, dental dz), fungal (blasto, coccidio, crypto, histo), parasitic (HW), protozoan (toxo), rickettsial, viral (adeno, distemper, herp, rabies), immune mediated, idiopathic, metabolic, neoplastic, trauma |
| When should you do a work up for systemic dz? | systemic steroids needed, inflam mod to severe, glaucoma, vision threatened, systemic illness present, posterior segment dz, owner concernced |
| Goal of tx of uveitis | Dz and Tx primary cause -- not always possible!!!! So most important to control IO inflammation (dont want to go blind) |
| Topical corticosteroids | BEGIN IMMEDIATELY if cornea intact. Do fluorescein stain. 1% prednisolone acetate or .1% dex alcohol (best corneal penetration) Give one more times a day than grade of flare (2+, give TID) |
| Systemic corticosteroids | Do diagnostics first, Rule out bacterial and fungal infections Used acutely if vision loss is imminent. Bloodwork, rads, PE must be normal. Pred |
| Subconjunctival steroids | For low compliance cases or high doses are unsafe. Complicatoins: trauma if needle placed incorrectly. Triamcinolone, Dex, Methylprednisolone acetate |
| Topical NSAIDs | can be used if corneal ulcerated. Additive to steroids. Flurbiprogen, Suprofen 1% |
| Systemic NSAIDs | Can use while waiting for diagnostics or if unsafe to use systemic steroids. Aspirin, carprofen. |
| Immunosuppressive drugs | If unresponsive to other drugs and not infectious. Usually with Uveodermatolgic syndrome. Azathioprine. Cyclosporine. |
| Mydriatics | Reduce change of posterior synechia, stabilize blood aqueous barrier and reduce pain of ciliary spasm. Atropine 1% - cats salivate. |
| Topical Abs | only for uvetitis secondary to bacterial keratitis (don't penetrate well) |
| Systemic Abs/antifungals | Erlichia: oxytet, doxy Toxo: clindamycin |
| What to evaluate at recheck | Conj hyperemia and episcleral injection, comfort, pupil size, aqueous flare, IOP, vision. Taper meds |
| Lens induced uveitis | associated with cataracts or with lens capsule rupture. Diabetic dogs often have due to rapid formation of cataracts |
| Uveodermatologic syndrome | Akita, samoyed, husky, sheltie. immune mediated against melanocytes. Bilateral uveitis, uveal depigmentation, retinal detachment. Derm signs are vitiligo of face, feet. Dx: bx nasal planum |
| Iris atrophy | due to age or secondary to uveitis, glaucoma, or trauma. |
| Uveal cysts | congenital or acquired from trauma or inflammation. |
| Uveal tumors in dogs - signs / tx | C/S: uveitis, ciliary body mass, iris displacement (older dog with unilateral hyphema) Tx: observe, enucleate or exenterate. |
| Kinds of uveal tumors in dogs | Melanocytic: most common, older, anterior, low mets Ciliary body adenoma/carc: 2nd common, low mets Mets: LSA common, poor prognosis |
| Feline uveitis | most common IO dz in cats (commonly systemic) |
| C/S of feline uveitis | ciliary flush, flare, hypopyon, hyperemia, decreased IOP, infiltrate, hyphema |
| Sequelae of feline uveitis | lens luxation, secondary glaucoma, cataracts |
| Endogenous causes in cats | Immune mediated, Idiopathic, Neoplasia, viral (FIP, FeLV, FIV), bacterial (sept), parasitic (toxo), fungal (crypto, blasto, coccidio, histo), metabolic (hypertension), trauma |
| Uveal tumors in cats | More aggressive in cats. Most common is diffuse Iris melanoma. mets to liver and lungs late. Second common is Post traumatic sarcoma, mets down optic nerve LSA most common mets |
| Optic nerve hypoplasia | Occurs sporadically, uni or bilateral, impaired vision or blind if bilateral, absent or incomplete PLR, small, dark optic dix |
| Micropapilla | small optic disc, normal PLR and vision |
| Optic nerve coloboma | focal absence of ocular tissue of optic nerve, common in dogs affected by collie eye anomaly (choroidal hypoplasia), inherited in basenji and in charolais cattle, pits to deep in optic disc, vessels "plungs" at lesion, no vision deficits unless large |
| Congenital Disorders of optic disc and optic nerve | Optic nerve hypoplasia, micropapilla, optic nerve coloboma |
| Acquired disorders of the optic nerve | Papilledema, Optic Neuritis, Optic atrophy, Optic nerve neoplasia |
| Papilledema | swollen, fluffy optic disc / elevated Intra cranial pressure / compression of optic nerve |
| Optic neuritis | Uni or bilateral, sudden loss of vision, reduced/absent PLR, swollen disc |
| DDX for blindness of acute onset and widely dilately pupils that have normal fundic appearance | Optic neuritis bilaterally, SARD, CNS disorders |
| Causes of optic neuritis | systemic infectious dz, extension of local dz, GME, idiopathic --full clinical and neuro exam, U/S of orbit, CSF tap, serology |
| Tx of optic neuritis | Address underlying cause, immunosuppressive steroids --guarded for restoration of vision, recurrence common |
| Optic Atrophy causes and appearance | previous inflammation, glaucoma, trauma, compression (Vit A def in steer, SOL w/in orbit), Ischemia (blood loss in horse) Appears gray and dark disc, shrunken, loss of vasculature with disc |
| Optic nerve neoplasia | uncommon, meningioma more common in dogs Loss of vision/PLR Dx: MR/CT, explore Tx: extenterate |
| Components of the ocular fundus | Vitreous, optic disc/papilla, retinal vasculature, neurosensory retina, retinal pigment epithelium, tapetum/choroid, sclera |
| 2 main components of the retina | Retinal pigment epithelium: outermost monolayer of cells that play role in maintenance of photoreceptor cells. contain melanin BUT lack pigment Neurosensory retina: photoreceptor cells (rods and cones) and all cells that constitute inner part of retina |
| 10 layers of retina | Visual cell/photoreceptor layer, outer limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cell layer, nerve fiber layer, inner limiting membrane |
| Photoreceptor layer | contains rod and cone photoreceptors responsible for generation of electrical signal in response to light. Rods better in dim light (night vision). Better acuity with cones. |
| Ganglion cell layer | axons of which gather int he nerve fiber layer. Pass to optic dix then as optic nerve to brain. |
| Holangiotic blood vessels | well vascularized neurosensory retina (spoke like) (dog) |
| Merangiotic blood vessel retina | moderate vascularization, blood vessels extend medial and lateral to optic disc (rabbit) |
| Paurangiotic blood vessels | very sparsely vascularized (horse) |
| Anagiotic blood vessels | no blood vessels present (bird, reptile, amphibians) Birds have a PECTIN to supply nutrition |
| Stars of Winslow | end on vessels connecting main choroidal vessels with the choriocappilaris layer (dogs, cats born with immature eyes, tapetum developed at 3-4 months) |
| Canine fundus | bright shiny triangular tapetum dorsally, dark pigmented ventral area around tapetum and ventral (melanin of RPE), circular white/pink optic disc, 3-5 major veins converge at disc (circle) |
| Tapetal variations in dogs | different colors, small in smaller, large in larger, may be absent in albino, islands of pigment and tapetum |
| Non tapetal variations in dogs | Degrees of pigment dilution in RPE and choroid lead to variations from reddish tan to striped (lack of pigment in RPE shows underlying vessels) |
| Optic disc variations in dogs | shape may not be circular due to myelin extending beyond margins (retrievers and GSDs) = pseduopapilledema. Hypereflective crescent around disc, ring of pigment around disc |
| Feline fundus | very large, bright tapetum (yellow,green), small round optic disc that is darker grey/pink (no myelination before axons exit globe), 3 pairs of arteries/veins |
| Equine fundus | Extensive tapetum, stars of winslow, ellipsoidal, non myelinated disc in the non tapetal fundus ventrally, notching at 6 oclock, paurangiotic fundus |
| ruminant fundus | blue/green or yellow/green fundus with stars of winslow, darkly pigmented non tapetum, optic disc poorly myelinated so dark with prominent lamina cribrosa and ventral and horizontally oval, holangiotic fundus |
| Procine fundus | NO tapetum, dark pigment, ovoid disc with lamina cribrosa, holangiotic |
| Increased reflectivity of tapetum = | atrophy and thinning of the neurosensory retina. Viewed thru a thinner tissue layer than normal and appears metallic |
| Decreased reflectivity of tapetum = | thickening due to infiltration, edema or folding of the neurosensory retina overlaying the tapetum. less light able to pass back thru neurosensory retina from tapetum - appears gray or dull |
| Altered pigmentation | proliferation, migration and aggregation of the melanocyte and RPE cells are non specific response to insults (inflammation, injury, degen process) -- lighter brown - accumulates in spots and patches in animals with Vit E deficiency or central PRA |
| Vascular changes | Narrowing of retinal blood vessels secondary to retinal degen Peri vascular cuffing with inflam cells due to FIP Hemorrhage due to vascular dz |
| Detachment | Attached at optic disc and ora ciliaris retinae (weak between these points), detachment = separation of neurosensory retina from RPE -- apparea as focal grey areas |
| Causes of retinal detachment | IO inflammation, Vascular dz, Congenital malformations, lens luxation, vitreous dz, trauma, retinal degeneration, neoplasia |
| Collie eye anomaly | rough and smooth collie, sheltie, duck toller, border collie, aussie (recessive trait) --congenital, usually progessive and no vision loss, bilateral --choroidal hypoplasia, coloboma complications: retinal detachment, IO hemorrhage |
| Go normals of collie eye | lesions masked by post natal development of tapetum - NOT normals |
| Retinal dysplasia | leads to thickened areas within neurosensory retina. Primary genetic disorder. Can be acquired due to external insults (herps, FeLV, BVD, Panleuko, Vit A def, radiation) |
| 3 forms of retinal dysplasia | Multifocal: cocker, springer, golden, lab Geographic: spring, golden, lab Total: spring, lab |
| Merle ocular dysgenesis | Aussie, homozygous merle, microphthalmos, blue iris, colobomas, retinal dysplasia, deaf |
| Congenital stationary night blindness in appaloosas | May be anxious/distressed in dark and hard to train, may have strabismus, confirm by ERG test |
| Generalized Progressive retinal atrophy | Cause of blindness in purebreeds. Bilateral. Night blindness --> complete blindness. Photoreceptor dysplasia (early onset) vs degen (late). Autosomal recessive. |
| Findings on oph scope for PRA | narrowing/loss of vessels, hyper reflectivity, mottled non tapetum, secondary optic atrophy, PLR reduced, dilated pupils, 2nd cataract formation |
| Canine multifocal retinopathy | Cmr1 affects mastiffs and pyrenees Cmr2 affects Coton de tulear -- gray/tan blister lesions throughout fundus |
| Major breeds with inherited retinal dz in dogs | Min schnauzer (Type A PRA, pd) / Cocker (prcd) / Poodle (prcd) / Lab (prcd) |
| Sudden acquired retinal degeneration | Acute onset of blindness (hrs-days), dilated pupils, PLRs reduced/absent (some retained), fundus normal --older, obesity, PU/PD, Cushings?, minimal ERG, permanent blindness |
| Feline central retinal degeneration/taurine deficiency | Leads to progessive retinopathy --ellipsoid area of altered tapetal granularity and reflectivity w/in area centralis around optic disc, linear hyperreflective band, loss of vasculature --check for DCM |
| Vit A deficiency | Cattle, young growing susceptible (compression, swelling, hemorrhage), any age (degen, night blindness), may respond to supplments if not day blind |
| Central progressive retinal atrophy (CPRA)/ Vit E deficiency | accumulation of brown/tan lipopigment w/in RPE cells --slow loss of vision, neuro signs? --light brown pigment spots in central tapetum, areas of hyperreflectivity, vascular attentuation --supplement with E |
| Adverse drug rxn: enrofloxacin | Cats, may occur at recommended level, LOSS of vision permanent by retinal degen |
| Adverse drug rsn: Ivermectin | Collies: temp loss of vision/mydriasis |
| Causes of chorioretinitis | Infectious, Immune mediated, Neoplasia |
| Findings with acute chorioretinitis | irregular, gray ill defined area (infiltrates), hemorrhage, vitreous haze, retinal detachment, impaired vision, optic neuritis? |
| Findings with chronic chorioretinitis | regions of tapetal hyper reflectivity, areas of depigmentation with no tapetal fundus, small, localized post inflam lesions --widespread retin degen/detach --> permanent blindness |
| How to manage chorioretinitis | Try to investigate, find and treat any underlying systemic disorder --systemic anti inflam (NSAIDs safer but less effective) --topical steroids if anterior uveitis |
Created by:
hut102023