Toxicology Flashcards
(26 cards)
Toxins that can cause hepatic failure.
Xylitol, amanita mushrooms, acetaminophen
Toxin(s) that can cause Heinz-body anemia.
Onions, garlic, Tylenol
In chocolate toxicity, what ingredients are the main concern and why?
Caffeine and theobromine. These are stimulants, which cause restlessness, agitation, tachycardia, diarrhea, and diuresis.
What is the primary treatment for cardiac medication toxicosis?
Emesis (if warranted), activated charcoal, IVF therapy.
What would be an alternative treatment for severe calcium channel blocker toxicosis?
Insulin therapy or lipids.
Are SSRIs and SNRIs treated the same as far as decontamination?
Yes. They result in similar clinical signs so are treated the same.
Name at least 4 clinical signs of serotonin syndrome related to SSRI and SNRI overdose?
Drooling, vomiting, abdominal pain, diarrhea, CNS stimulation, seizures, mydriasis, tremors.
What are the primary treatments for SSRI and SNRI toxicosis?
Emesis (if warranted), sedation with acepromazine or chlorpromazine, BP and ECG monitoring, muscle relaxants, anticonvulsants, and serotonin antagonists.
Name the primary serotonin antagonist used for SSRI and SNRI toxicosis.
Cyproheptadine
Name at least 3 common SSRIs and SNRIs.
Fluoxetine, Citalopram, paroxetine, sertraline, duloxetine, nefazodone, venafaxine.
What is the mechanism of action of amphetamines?
They act as a sympathomimetic, meaning they stimulate the sympathetic system.
Stimulation of the sympathetic system results in what clinical signs and symptoms?
Similar to those of SSRIs and SNRIs you see serotonin syndrome, vomiting, diarrhea, agitation, mydriasis, tremors, seizures, tachycardia, hypertension, panting.
What is the primary treatment for amphetamine toxicosis?
Similar to SSRI and SNRI. Ace, chlorpromazine, muscle relaxants, anticonvulsants, etc.
What is the mechanism of action of NSAIDS?
Competitive inhibition of prostaglandin synthesis by way of cyclooxygenase.
What animals/breeds are more sensitive to NSAIDS?
Cats and German Shepherds.
What are some clinical signs of NSAID toxicosis?
anorexia, vomiting, hematemesis, melena, lethargy, abdominal pain.
Which organ is most affected by Tylenol toxicity and why?
The liver. Tylenol toxicosis results in oxidative injury to the liver secondary to the buildup of toxic metabolites.
What is the difference between toxicosis and toxicity?
Toxicosis refers to the pathological condition caused by a toxin. Toxicity is the quality of being poisonous.
What pathologies and clinical signs are more likely to occur in cats secondary to Tylenol toxicity?
Methemoglobinemia, swelling of the face or paws, respiratory distress, cyanosis, vomiting, and lethargy.
What pathology and clinical signs are more likely to occur in dogs secondary to Tylenol toxicity?
Hepatic injury, hepatic encephalopathy, vomiting, melena, icterus, and dry eye.
What is the primary treatment for Tylenol toxicosis?
Emesis, activated charcoal, anti-nausea/anti-emetics, antioxidant administration, liver protectants.
What is the antidote to the toxic metabolite NAPQI and its purpose?
N-acetylcysteine. It’s acts as a glutathione substrate and limits the formation of NAPQI by conjugating it with glutathione.
Why are cats more susceptible to Tylenol toxicosis at lower doses than dogs?
They have altered glucuronidation pathway, which results in a decreased ability to metabolize Tylenol.
What specific type of anemia can Tylenol toxicity cause?
Heinz body anemia
