Term
| Metabolic causes of diffuse CNS disease: bovine vs. equine |
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Definition
-bovine: hypomagnesemia, polioencphalomalacia, nervous ketosis, hypovitaminosis A
-Equine: hepatoencephalopathy, electrolyte depletion |
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Term
| Hypomagnesemic tetany: epidemiology and clinical findings |
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Definition
-epidemiology: grass tetany-lush grass pasture in spring; milk tetany-veal calves; transport tetany-after extended transport, serum magnesium levels less than 1 mg/dl
-Clinical findings:
-early signs: anxious expression, muscle twitching
-progressive signs: hyperesthesia, frenzied galloping
-convulsions may be episodic
-death within one or two hours of first signs |
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Term
| Hypomagnesemic tetany: differentials, dx |
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Definition
-differentials: rabies, lead poisoning, nervous ketosis
-Dx: serum Mg, clinical response to tx |
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Term
| Polioencephalomalacia: epidemiology |
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Definition
-sporadic or herd
-major management changes precede
-up to 50% case fatality rate
-animals 6-18 months of age |
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Term
| Polioencephalomalacia: pathogenesis |
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Definition
-thiamine deficiency
-high rumen H2S gas
-intracellular edema
-Neuronal degeneration |
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Term
| Polioencephalomalacia: clinical signs |
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Definition
-blindness
-PLR normal
-"Star Gazers"-incoordination, depression interrupted by excitment, dorsomedial strabismus
-later: muscle tremors, incoordination
-terminal: recumbency with opisthotonos, convulsions, coma and death
-clinical course: 24-48 hours in young cattle, sheep, and goats |
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Term
| Polioencephalomalacia: Clin Path and Dx |
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Definition
Clin path-hemogram normal, CSF: normal, necropsy: diffuse cerebral edema, UV fluorescence observed in necrotic areas
-Dx: response to early thiamine therapy, determination of sulfur content of diet, maximal tolerated conc. of sulfur is considered to be 0.4 % dry matter |
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Term
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Definition
-thiamine HCl, IV
-remove grain, forage ration
-response in 6-8 hours
-corticosteroids
-severe cases respond poorly |
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Term
| Nervous ketosis: epidemiology, clinical signs, and dx and tx |
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Definition
-epidemiology: nervous form-hypoglycemia
-clinical signs: belligerence, delirium, awkward stance, head pressing, licking, intermittent nervous signs lasting 1-2 hours
-dx: urine or milk ketones, response to IV glucose therapy, intermittent signs
-tx: IV glucose, oral propylene glycol (tranquilize, correct underlying cause of ketosis) |
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Term
| Hypovitamosis A epidemiology, clinical syndromes, and dx/tx |
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Definition
-epi: drough conditions, poor quality stored feed, young/growing animals
-Clinical syndromes:
-blindness: stenosis of optic foramen, increase in CSF pressure, pupils will be dilated and unresponsive to light
-encephalopathy: increasing CSF pressure, clonic tonic convulsions
-progressive paresis or paralysis: destruction of peripheral nerve
-dx: serum vitamin A concentration, analysis of ration
-tx: vitamin A |
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Term
| Hepatoencephalopathy etiology and risk factors |
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Definition
-etiology: acute hepatitis, chronic liver dz, neonatal foals
-risk factors: equine origin biological (#1 tetanus antitoxin, vax chicken embryo, plasma), portal-systemic shunt |
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Term
| Hepatoencephalopathy pathophysiology, dx, adn tx |
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Definition
-pathophysiology: increased ammonia, ammonia plus glutamine, GI-derived toxin, decreased BCAA:AAA ration, increased GABA activity
-dx: confirmation of liver dz (serum chem profile)
-tx: prognosis is always grave, maintain blood glucose, electrolyte disturbance |
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Term
| Toxic causes of diffuse CNS dz |
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Definition
-Equine: Leukoencephalomalacia, nigropallidal encephalomalacia, RARELY lead
-Bovine: lead toxicity, salt, organophosphates |
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Term
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Definition
-contaminated corn-Fusarium
-signs: may resemble viral enceph; hepatic signs, colic
-white matter liquefactive necrosis
-degeneration: cerebral hemisphere, brainstem, cerebellum, spinal cord
-cavitation |
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Term
| Nigropallidal encephalomalacia |
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Definition
-chronic consumption: yellow star thistle, russian knapweed
-Pathophysiology: Repin, Lactones, Inhibition of dopamine release
-difficulty prehending food and water
-Substantia nigra, globus pallidus |
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Term
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Definition
-chronic toxicity
-peripheral neuropathies
-no acute toxicity |
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Term
| Lead poisoning in cattle: epidemiology, clinical signs |
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Definition
-epidemiology: common, major sources: paint, car batteries, oil
-clinical signs: single, large ingestion of lead: blindness (*most consistent finding), ataxia, head pressing, abdominal pain (bloat or diarrhea) |
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Term
| Lead poisoning in cattle: clinical path and tx |
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Definition
-clin path: lead levels-blood, tissues
-tx: rumenotomy, cathartics, calcium disodium EDTA |
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Term
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Definition
-blindness
-ataxia
-seizures |
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Term
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Definition
-product overdose
-accidental access to insecticides
-organophosphates inactivate cholinesterases resulting in over stimulation of PS nerves
-clinical signs: midriasis, increase GI motility, increase secretions, increase muscle tone, bronchoconstriction |
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Term
| Organophosphates: clinical signs, dx, tx |
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Definition
-clinical signs: dyspnea, diarrhea, apparent blindness from miosis, protruding tongue, drooling, bloat, collapse
-dx: clinical signs, blood cholinesterase activity
-tx: atropine (choinergic blocker), activated charcoal if oral |
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