Toxo MT, I

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Toxo MT, I
2013-03-03 20:25:09
Toxo MT

Toxo MT, I
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  1. what species is usually poisoned with strychnine? is it acute or chronic?
    • dogs (LA cases are uncommon)
    • acute (no accumulation)
  2. 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)
  3. what clinical signs are associated with strychnine poisoning?
    • tetanic spasms; convulsions that incr. in frequency
    • saw horse stance; opisthotonus
    • extensor rigidity
  4. 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
  5. 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)
  6. what are clinical signs associated w/rodenticides?
    • hemorrhage disorders (signs vary depending on location of bleed)
    • neuro signs if bleeding in CNS
    • occasional hematuria
  7. 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
  8. Is warfarin highly or low protein bound? how is it metabolised?
    • highly protein bound
    • metab. in liver by mixed function oxidases
  9. what is treatment for warfarin?
    • antidote is vitamin K1 or phytonadione
    • (menadion = vit. K3 and can cause fatal renal failure/anaphylaxis in horses)
  10. what part of the diet enhances absorption of calciferol (vit. D2) from the small intestine?
    enhanced by lipids in the diet
  11. what is problem with calciferol overdose?
    increases absorption of Ca+ and resorption of bone minerals - *hypercalcemia*
  12. 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
  13. what are some findings on necropsy of calciferol poisoning?
    • plaques on larger vessels
    • necrosis of renal tubules
    • minerlization of tissues
  14. 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
  15. what are compounds 1080 and 1081? which species is particularly susceptible?
    • fluoracetate and fluoracetamide
    • dogs
  16. what part of the citrate cycle is blocked by fluoraceate?
    aconitase is blocked so citrate can't become isocitrate
  17. what clinical signs are associated with fluoracetate/fluoracetamide?
    neurotoxic: restlessness, aimless running, frequent urination, tenesmus; tonic-clonic seizures, vocalization
  18. what is treatment for fluoracetates?
    none specific; usually not rewarding
  19. do phosphides require high or low dose to see clinical signs?
    dramatic signs even with low dose
  20. is phosphide more toxic in empty or full stomach?
    empty - stomach acid worsens toxicity
  21. 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
  22. what is treatment for phosphides?
    • no antidotes
    • emetics if asymptomatic
    • gastric lavage ; pain meds
  23. what is the mechanism for bromethalin?
    active metabolite that uncouples oxidative phosphorylation
  24. what are signs associated wtih bromethalin?
    • onset in 10-24 hr
    • tremors, paddling, hyperesthesia, fever, seizures
  25. what is treatment for bromethalin?
    steroids/mannitol to reduce cerebral edema