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what species is usually poisoned with strychnine? is it acute or chronic?
- dogs (LA cases are uncommon)
- acute (no accumulation)
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Does strychnine stimulate or inhibit the spinal cord? it reversibly antagonizes which receptors?
- spinal cord stimulant (prevents inhibition of renshaw cells)
- antagonizes glycine receptors for post-synaptic inhibition (inhibits inhibition - so enhances reflexes)
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what clinical signs are associated with strychnine poisoning?
- tetanic spasms; convulsions that incr. in frequency
- saw horse stance; opisthotonus
- extensor rigidity
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what is treatment for strychnine?
- no specific antidote
- induce emesis; muscle relaxants
- gastric lavage w/tannic acid to precipitate or KMNO4 to oxidize
- promote urine flow; acidify urine
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rodenticides are anticoagulants due to what mechanism? what species is mostly affected?
- inhibit vitamin K epoxide reductase (can't synthesize vit. K)
- dogs (cow less susceptible)
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what are clinical signs associated w/rodenticides?
- hemorrhage disorders (signs vary depending on location of bleed)
- neuro signs if bleeding in CNS
- occasional hematuria
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what is the difference between first and second generation rodenticides? what is an example of a 1st generation?
- warfarin - 1st gen
- 2nd generations is longer acting and requires more prolonged tx
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Is warfarin highly or low protein bound? how is it metabolised?
- highly protein bound
- metab. in liver by mixed function oxidases
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what is treatment for warfarin?
- antidote is vitamin K1 or phytonadione
- (menadion = vit. K3 and can cause fatal renal failure/anaphylaxis in horses)
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what part of the diet enhances absorption of calciferol (vit. D2) from the small intestine?
enhanced by lipids in the diet
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what is problem with calciferol overdose?
increases absorption of Ca+ and resorption of bone minerals - *hypercalcemia*
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Latent period for calciferol toxicity is 12-36 hours, then what clinical signs are seen?
- GIT, nervous, and cardiac signs; later renal failure
- arched spine
- short Q-T segments
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what are some findings on necropsy of calciferol poisoning?
- plaques on larger vessels
- necrosis of renal tubules
- minerlization of tissues
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what is treatment for calciferol?
- antidote = pamidronate ("aredia")
- older antidote = calcitonin to red. serum Ca (don't use both)
- can tx w/steroids to reduce hyperCa by incr. calciuria, red. absorption, and red. osteoclast activation
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what are compounds 1080 and 1081? which species is particularly susceptible?
- fluoracetate and fluoracetamide
- dogs
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what part of the citrate cycle is blocked by fluoraceate?
aconitase is blocked so citrate can't become isocitrate
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what clinical signs are associated with fluoracetate/fluoracetamide?
neurotoxic: restlessness, aimless running, frequent urination, tenesmus; tonic-clonic seizures, vocalization
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what is treatment for fluoracetates?
none specific; usually not rewarding
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do phosphides require high or low dose to see clinical signs?
dramatic signs even with low dose
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is phosphide more toxic in empty or full stomach?
empty - stomach acid worsens toxicity
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what are clinical signs associated with phosphides? what species usually?
- GIT and hemorrhage -> convulsions -> shock/death w/in 6-48hrs
- "mad dog running" - convulsions, muscle rigidity, howling, snapping
- dogs
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what is treatment for phosphides?
- no antidotes
- emetics if asymptomatic
- gastric lavage ; pain meds
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what is the mechanism for bromethalin?
active metabolite that uncouples oxidative phosphorylation
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what are signs associated wtih bromethalin?
- onset in 10-24 hr
- tremors, paddling, hyperesthesia, fever, seizures
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what is treatment for bromethalin?
steroids/mannitol to reduce cerebral edema
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