Toxo, Q1, I

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HLW
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200766
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Toxo, Q1, I
Updated:
2013-02-15 12:44:19
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Toxo Q1
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Toxo, Q1, I
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  1. how are free radicals formed?
    • ionizing radiation results in hydroxyl free radicals and hydrogen free radicals;
    • some chemicals are metabolized to free radicals
    • reduced iron can also cause oxidative damage
  2. what do free radicals cause?
    • lipid peroxidation (damages membranes)
    • protein damage
    • DNA damage
  3. how are free radicals dealt with?
    • they are unstable and will decay
    • antioxidants scavenge the radicals
    • enzymes (glutathione peroxidase) scavenge radicals
  4. what are the three forms of oxidative stress and which is most reactive?
    • superoxide free radical (O2)
    • hydrogen peroxide (H2O2)
    • hydroxyl free radical (OH-) = most reactive
  5. what are plant pigments act as anti-oxidants?
    flavonoids (quercetin is an example found in onion, apple, berries, broccoli)
  6. which vitamins act as free radical scavengers?
    vit. C and E
  7. what are 3 sites of action of poisons and phosphorylation?
    • inhibitors of electron transport chain
    • block phosphorylation/ATP
    • uncoupling of oxidative phosphorylation
  8. what are the 3 metabolic pathways for acetaminophen? which is problematic for the cat, and for pigs?
    • sulfation (problem for pigs)
    • glucoronidation (problem for cats)
    • p450
  9. depletion of what pathway results in oxidative damage from acetaminophen?
    depletion of glutathione --> oxidative damage due to accumulation of benzoquinoneimine --> cell toxicity/cell death
  10. What are signs of toxicity from acetominophen in dog? cat?
    • dog: hepatotoxic signs, colic/icterus, methemoglobin at high dose
    • cat: cyanosis, facial/paw edema, dyspnea (hepatoxic signs less common), methemoglobin
    • *apparent recovery*
  11. how do you treat acetaminophen toxicity?
    • decontamination therapy if ingested within 4hr (emetic, charcoal)
    • antidote = N-acetyl cysteine (Mucomyst; incr. glutathione synthesis)
  12. In addition to acetaminophen, what is another toxin that has an apparent recovery and overwhelms glutathione system?
    paraquat
  13. besides acetaminophen, what other toxins lead to methemoglobinemia?
    copper, nitrate/nitrite, chlorates
  14. what is the most common source of lead toxicity?
    car batteries
  15. how much lead is absorbed from the GI following ingestion? how much is excreted in feces?
    • 2-10% absorbed
    • 90-98% of ingested dose is excreted
  16. where is most lead kept in the body?
    carried in RBCs and deposited in the spongy bone (replaces Ca)
  17. With lead, what enzyme is blocked, resulting in build up of substrate?
    • ALA dehydrase (used in screening test)
    • and heme synthetase (-SH group)
  18. How are blood cells affected by accumulation of lead?
    • anemia and basophilic stippling
    • decr. blood supply to CNS
  19. what are the main systems affected by lead toxicity? is toxicity acute or cumulative?
    • *cumulative*
    • CNS (brain edema)
    • PNS (demyelination)
    • Blood (anemia, nucleated RBCs)
    • GIT
  20. what are some common features of lead toxicity in cattle? horse?
    • cow:blindness, head pressing, muscle fasciculations, ataxia, colic/teeth grinding
    • horse: roaring, dysphagia, muscle fasciculations, colic
    • (dog most likely to be wasting w/toxicosis)
  21. what is treatment for lead toxicity?
    • EDTA = antidote
    • or DMSA (Succimer)
  22. is arsenic more toxic to large or small animals?
    large animals (cattle 77% of cases)
  23. is inorganic aresenic acute or cumulative toxicity?
    more rapidly absorbed to acute/subacute
  24. what does inorganic arsenic react with that blocks cell metabolism/respiration?
    sulfhydryl groups

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