ECC2- SA Toxins Drugs

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  1. What is the MOA of NSAID toxicity? (3)
    • inhibit COX-2 and/or 1 (non-selective COX inhibitors cause more adverse effects because COX-1 has protective properties)
    • prostaglandins produced by COX-1 important for maintenance of gastric mucosal barrier, renal perfusion, and platelet function
    • prostaglandins produced by COX-2 responsible for inflammatory response, tissue injury, and nociception
  2. What are clinical signs of NSAIDs toxicity? (by 5 body systems)
    • [dose dependent starting with GI and so on]
    • GI: vomiting, diarrhea, melena, loss of appetite, abdominal pain, hematemesis, peritonitis (if very severe ulceration and perforation)
    • Renal: isosthenuria, azotemia, urine casts, PU/PD, oliguria/ anuria, dehydration, lethargy, GI signs, glucosuria
    • Neurologic: seizures, ataxia, altered mentation
    • Hepatic: [idiosyncratic] lethargy, anorexia, vomiting, icterus, elevated liver enzymes and bili
    • Coagulation: hyper- or hypo-coaguable
  3. What is the cause of the GI signs associated with NSAID toxicity?
    loss of prostaglandin--> decreased protective gastric mucus and bicarb, loss of maintenance of mucosal blood flow, increased gastric acid secretion
  4. What is the cause of the renal signs associated with NSAID toxicity?
    • loss of basal vasodilation that is mediated by prostaglandins--> ischemic injury of the kidney
    • especially profound when dehydrated patients ingest NSAIDs
  5. Why is there hepatic damage associated with NSAID toxicity?
    NSAIDs are primarily metabolized by liver
  6. Why might high dose NSAID toxicity cause coagulation disorders?
    • block COX--> reduce the production of thromboxane (platelet activator)--> hypocoaguable--> bleeding disorders
    • OR lack of prostacyclin (platelet inhibitor) production (another end product of arachadonic acid pathway)-->¬†hypercoaguable--> thromboembolic dz
  7. What is the treatment for NSAID toxicity?
    • Decontamination: emesis, activated charcoal
    • IVF therapy
    • GI protectants: PPI or H2 blocker, anti-emetics, sucralfate
    • +/- misoprostol: if in acute phase, can give synthetic PG analogue; many bad side effects
  8. How do you monitor animals who are being treated for NSAID toxicity? (3)
    • baseline renal panel and liver enzymes
    • monitor urine sediment for casts (isosthenuria is not sensitive because you are diuresing the animal with fluids)
  9. What is the MOA of acetominophen toxicity?
    • metabolites are the toxic component (not acetominophen itself)- N-acetyl-para-benzoquinoneimine (NAPQI)
    • NAPQI generated from cytochrome P-450 pathway--> causes disruption of protein function and cell membrane damage--> generation of reactive oxygen species--> subsequent hepatocellular damage
    • PAP is another metabolite--> causes methemoglobinemia, heinz bodies, and hemolytic anemia
  10. Describe onset of clinical signs of acetominophen toxicity in cats versus dogs.
    • feline hemoglobin has more reactive sulfa-hydroxyl groups--> methemoglobinemia manifests first and liver damage only develops those who survive the acute insult\
    • dogs show hepatic damage first
  11. What are clinical signs of acetominophen toxicity? (8)
    • brown MMs
    • edema of face an paws
    • hypothermia
    • anorexia
    • depression
    • weakness
    • coma
    • elevated liver enzymes, icterus
  12. What is the treatment for acetominophen toxicity? (4)
    • emesis, activated charcoal
    • N-acetylcysteine (replenishes glutathione stores and prevents further accumulation of NAPQI)
    • hepatic protectants- SAMe
    • IVF therapy
  13. What is the MOA of ADHD/ amphetamine toxicity?
    sympathomimetic alkaloids--> release of endogenous catecholamines--> impairing catecholamine metabolism and also increase serotonin levels in the CNS
  14. What are clinical signs of ADHD/ amephetamine toxicity? (9)
    • hypertension [alpha stimulation]
    • tachycardia [beta stimulation], sometimes reflex bradycardia from hypertension
    • arrhythmias
    • ataxia
    • mydriasis
    • hyperthermia/ heat stroke
    • tremors
    • seizures
    • hypotension with CV collapse
  15. What is the treatment for ADHA/ amphetamine toxicity? (8)
    • emesis, activated charcoal
    • cyproheptadine (treats CNS signs by addressing excess serotonin)
    • IVF therapy
    • acidification of urine (increases excretion) with ascorbic acid
    • phenothiazine drugs for sedation (no benzos...worsen dysphoria)
    • methocarbamol for muscle tremors
    • +/- anti-seizure meds
    • minimize stimulation- dark quiet room
  16. What is the MOA of marijuana toxicity?
    • THC is psychoactive constituent
    • cannaboid receptors (CB1 and CB2)- CB1 are in CNS and CB2 are in periphery--> CB2 are primarily responsible for clinical signs of toxicity
  17. What are clinical signs of marijuana toxicity? (5)
    • dogs are hyperesponsive to sound and fast movement, but dull/ glazed over when not being stimulated
    • mental depression/ coma if severe
    • dribbling urine
    • vomiting
    • bradycardia (usually)
  18. What is the treatment for marijuana toxicity? (4)
    • emesis if ingested (difficult because THC has anti-nausea properties)
    • activated charcoal (extensive enterohepatic- repeated dosing)
    • IVF therapy
    • if very severe, intralipid therapy (THC is lipid soluble)
  19. What is the MOA of chocolate toxicity?
    theobromine and caffeine= methylxanthines--> antagonism of phosphodiesterase--> increase in cAMP--> increase in catecholamines
  20. What are clinical signs of chocolate toxicity? (8)
    • hyperexcitability
    • tremors
    • tachycardia +/- arrhythmias
    • hypertension
    • seizures
    • vomiting
    • rarely hypotension/ brady
    • pancreatitis
  21. What is the treatment for chocolate toxicity? (5)
    • emesis, activated charcoal (enterohepatic- repeat dosing)
    • +/- beta blockade
    • IVF therapy
    • +/- sedation is super excitable
    • frequent walks for urination or catheter- methylxanthines will be reabsorbed through bladder mucosa if not urinated out fast enough
  22. What is the MOA of grape/ raisin toxicity?
    • unknown- end result is renal damage
    • VERY dependent on patient- some are very sensitive, some can eat grapes all the time and not be effected
  23. What are clinical signs of grape/ raisin toxicity? (8)
    • PU/PD
    • oliguria/ anuria
    • azotemia
    • isosthenuris
    • dehydration
    • vomiting
    • diarrhea
    • anorexia, lethargy
  24. What is the treatment for grape/ raisin toxicity? (3)
    • emesis
    • IVF therapy
    • manage AKI
  25. What is the MOA of xylitol toxicity?
    • stimulates profound insulin release but is not actually used as an energy source--> result in profound hypoglycemia
    • hepatic failure ay also occur
  26. What are clinical signs of xylitol toxicity? (4)
    • weakness
    • ataxia
    • seizures
    • if liver damage, icterus, bleeding disorders, vomiting, diarrhea
  27. What is the treatment for xylitol toxicity? (3)
    • emesis
    • dextrose for hypoglycemia
    • liver protectants- denamarin
  28. What is the MOA of onion toxicity?
    • [allium genus]
    • sulfoxide and disulfide compounds cause oxidative damage to red blood cells--> heinz bodies and eccentrocytes, methemoglobinemia, hemolysis
  29. What are clinical signs of onion toxicity? (6)
    • anemia/ palloe
    • weakness
    • tachycardia, tachypnea
    • hemoglobinuria
    • vomiting
    • diarrhea
  30. What is the treatment for onion toxicity? (3)
    • emesis, charcoal
    • IVF therapy (to minimize renal injury from hemoglobinuria)
    • antioxidants- ascorbic acid, vit E, N-acetylcysteine

Card Set Information

Author:
Mawad
ID:
326183
Filename:
ECC2- SA Toxins Drugs
Updated:
2016-11-30 16:26:51
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vetmed ECC2
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vetmed ECC2
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