Nerve and muscle: organophosphate poisoning: practice question

A Physiology 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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Physiology · Nerve and muscle: organophosphate poisoning

Sample item

A farmer who sprayed pesticide has salivation, lacrimation, small pupils, bradycardia and muscle fasciculations followed by weakness. Which enzyme is inhibited, and why does paralysis occur?

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

The answer and the reasoning

A. Acetylcholinesterase, causing persistent end-plate depolarisation and block

Organophosphates phosphorylate and irreversibly inhibit acetylcholinesterase. Acetylcholine accumulates, causing muscarinic effects, nicotinic fasciculations and then depolarisation block of the end plate. Treatment is atropine for muscarinic effects and pralidoxime to reactivate the enzyme.

Option by option

  • A. Acetylcholinesterase, causing persistent end-plate depolarisation and block (correct)

    Correct. Acetylcholine persists in the cleft and holds the end plate depolarised.

  • B. Choline acetyltransferase, so acetylcholine can no longer be made

    Choline acetyltransferase inhibition would deplete acetylcholine and not cause hypersecretion and miosis.

  • C. Carbonic anhydrase, so end-plate pH falls

    Carbonic anhydrase is not the target of organophosphates.

  • D. Monoamine oxidase, so noradrenaline accumulates in the terminal

    Monoamine oxidase inhibition affects catecholamine metabolism, not these cholinergic signs.

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 Physiology question

What is the answer to this Physiology question?

The best answer is A, Acetylcholinesterase, causing persistent end-plate depolarisation and block. Organophosphates phosphorylate and irreversibly inhibit acetylcholinesterase.

Why is "Choline acetyltransferase, so acetylcholine can no longer be made" not the answer?

Choline acetyltransferase inhibition would deplete acetylcholine and not cause hypersecretion and miosis.

Why is "Carbonic anhydrase, so end-plate pH falls" not the answer?

Carbonic anhydrase is not the target of organophosphates.

Why is "Monoamine oxidase, so noradrenaline accumulates in the terminal" not the answer?

Monoamine oxidase inhibition affects catecholamine metabolism, not these cholinergic signs.

What concept does this question test?

It tests Nerve and muscle: organophosphate poisoning in Physiology. Acetylcholine accumulates, causing muscarinic effects, nicotinic fasciculations and then depolarisation block of the end plate. Treatment is atropine for muscarinic effects and pralidoxime to reactivate the enzyme.

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 Nerve and muscle: organophosphate poisoning?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.