Toxo, Q1, III

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HLW
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200764
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Toxo, Q1, III
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2013-02-15 12:44:08
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Toxo Q1 III
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Toxo, Q1, III
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  1. what is the characteristic name for subacute selenium toxicity?
    "blind staggers" due to lost weight, impaired vision and stumbling/blind
  2. What is the characteristic name for chronic selenium toxicity? what are presenting signs of this in horses' hooves? what about in cattle?
    • "alkali disease"
    • horse: sloughs hoof
    • cow: corkscrew claw
  3. how do you treat selenium toxicity?
    • no antidote
    • symptomatic/supportive only
    • increase sulfur containing proteins in the diet
  4. What is most common source for sulfur toxicity? what has sulfide been linked to in feedlots?
    • water source (also onions, molasses)
    • polioencephalomalacia
  5. What is common sign with acute/subacute sulfur toxicity? how is this treated?
    • diarrhea
    • NO antidote
    • sodium sulfate/Glauber's salt as saline purgative
  6. Zinc is found in footbaths and galvanized objects. Once ingested what two things can it antagonize in the hematopoietic process?
    • antagonize copper and iron
    • also affects glutathione reductase
  7. what are main clinical signs seen in dogs with excess Zn?
    • GIT signs, CNS depression
    • chronically anemia/hemolysis/DIC and lameness from affected collagen
  8. what is treatment for Zn?
    • antidote = EDTA
    • tx: diuresis and blood transfusion
  9. Fluorine is an inorganic anion that mainly affects what species? where do 95% of accumulates go?
    • mainly cattle
    • bones and teeth (fracture pedal bones = kneeling cows)
  10. what is treatment for fluorine?
    • no antidote
    • non specific; aim is prevention
  11. what is mechanism for organophosphates (insecticides)? are these compounds stable in the environment?
    • lead to build up of ACh so overstimulation of nicotinic, muscarinic and neuromuscular junctions (not all OP groups cause neurotoxicity)
    • -not stable, rapidly degraded in environment by sun/microbes
  12. Seizures from organophosphates are not responsive to atropine if not given early enough because what two mechanisms come into play?
    glutamate and NMDA
  13. what are commonly described signs associated with OPs at muscarinic v. nicotinic receptors?
    • muscarinic: "SLUD" signs
    • (parasympathetic signs = salivation, lacrimation, urination, defecation)
  14. nicotinic: fasciculations and respiratory failure/bronchoconstriction
  15. what is treatment for OPs?
    antidote = Atropine if started early and 2PAM/Prlaidoxime
  16. What is treatment for carbamates?
    Antidote = atropine ONLY
  17. what are clinical signs associated with carbamates?
    • SLUD signs (reversible inhibitors of cholinesterase)
    • overstim of musc/nicotinic but less severe than OPs
  18. Where do organochlorides distribute to?
    distribute to body fat (and blood cells)
  19. what are some behavioral clinical signs associated with organochlorides?
    licking, chomping jaws
  20. what is treatment for organochlorides?
    • no antidote but good prognosis
    • tx: anticonvulsants, purgatives, etc
  21. what species is most sensitive to pyrethrins?What is added to pyrethrins to potentiate effects/incr. mammalian toxicity?
    • cats (fish and bees also affected)
    • MFO inhibitors (mixed function oxidase)
  22. what is treatment for pyrethrin toxicity?
    • no antidote
    • symptomatic/supportive
  23. what is mechanism of amitraz?
    alpha-2 adrenergic agonist (CNS sedative)
  24. what is treatment for amitraz?
    antidote = atipamezole and yohimbine
  25. what is treatment for DEET?
    no antidote for deet
  26. what are clinical abnormalities and tx for Naphthalene (moth balls)? which species is more susceptible?
    • (cats more susceptible) hemolytic anemai/heinz body and mehtemoglobinemia
    • antidote is slow IV methylene blue;
    • tx blood transfusion

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