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Forensic Medicine · Toxicology: amatoxin mushroom poisoning
Sample itemA family eats wild mushrooms and 10 hours later develops severe vomiting and watery diarrhoea. They improve at 24 hours but on day 3 develop jaundice and coagulopathy. What is the mechanism of toxicity?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Inhibition of RNA polymerase II by amatoxin, causing hepatocyte necrosis
Amanita phalloides contains amatoxins, which inhibit RNA polymerase II and halt protein synthesis, particularly in the liver. The typical course is delayed gastrointestinal illness after 6 to 24 hours, an apparent recovery, and then hepatic failure on days 2 to 4. Treatment includes supportive care, silibinin or N-acetylcysteine and transplantation in fulminant failure.
Option by option
A. Inhibition of RNA polymerase II by amatoxin, causing hepatocyte necrosis (correct)
Correct. Amatoxins block RNA polymerase II and injure hepatocytes.
B. Inhibition of acetylcholinesterase by muscarine
Muscarine mushrooms cause early cholinergic features within an hour or two.
C. Binding of the toxin to sodium channels causing paralysis
Paralysis from sodium channel toxins does not fit this delayed hepatic course.
D. Blockade of GABA receptors by muscimol
Muscimol mushrooms cause early confusion and delirium, not delayed liver failure.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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