Toxicology: pyrethroid poisoning: practice question

A Forensic Medicine question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Forensic Medicine · Toxicology: pyrethroid poisoning

Sample item

A farmer who sprayed an insecticide without gloves has tingling and burning paraesthesia of the exposed skin and mild cough, with normal pupils and a normal serum cholinesterase. Which mechanism explains this?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Prolonged opening of neuronal sodium channels by pyrethroids

Pyrethroids delay closure of sodium channels, causing repetitive firing; contact causes paraesthesia, and systemic toxicity is low in mammals. Normal pupils and normal cholinesterase make an organophosphate or carbamate unlikely. Treatment is decontamination and symptomatic.

Option by option

  • A. Irreversible inhibition of acetylcholinesterase by an organophosphate

    Organophosphates produce miosis, salivation and low cholinesterase, which are absent.

  • B. Reversible carbamylation of acetylcholinesterase by a carbamate

    Carbamates also lower cholinesterase and cause muscarinic signs, which are absent here.

  • C. Uncoupling of oxidative phosphorylation by a chlorophenol

    Uncouplers cause hyperthermia and sweating, not isolated skin paraesthesia.

  • D. Prolonged opening of neuronal sodium channels by pyrethroids (correct)

    Correct. Skin paraesthesia with normal cholinesterase fits a pyrethroid acting on sodium channels.

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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Questions about this Forensic Medicine question

What is the answer to this Forensic Medicine question?

The best answer is D, Prolonged opening of neuronal sodium channels by pyrethroids. Pyrethroids delay closure of sodium channels, causing repetitive firing; contact causes paraesthesia, and systemic toxicity is low in mammals.

Why is "Irreversible inhibition of acetylcholinesterase by an organophosphate" not the answer?

Organophosphates produce miosis, salivation and low cholinesterase, which are absent.

Why is "Reversible carbamylation of acetylcholinesterase by a carbamate" not the answer?

Carbamates also lower cholinesterase and cause muscarinic signs, which are absent here.

Why is "Uncoupling of oxidative phosphorylation by a chlorophenol" not the answer?

Uncouplers cause hyperthermia and sweating, not isolated skin paraesthesia.

What concept does this question test?

It tests Toxicology: pyrethroid poisoning in Forensic Medicine. Normal pupils and normal cholinesterase make an organophosphate or carbamate unlikely. Treatment is decontamination and symptomatic.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Toxicology: pyrethroid poisoning?

Learn postmortem changes with their timelines, and toxicology as poison, sign, test and antidote. Then use the flashcards and the other Forensic Medicine questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.