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.

Try it

Physiology · Nerve and muscle: organophosphate poisoning

Sample item

A farmer sprays a pesticide without protection and arrives with sweating, miosis and fasciculations, followed by flaccid weakness of the respiratory muscles. What explains the late muscle weakness?

AFailure of calcium entry into the nerve terminalBDepletion of acetylcholine from presynaptic vesiclesCPersistent depolarisation of the end plate from accumulated acetylcholineDBlockade of the nicotinic receptor by the toxin

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

The answer and the reasoning

C. Persistent depolarisation of the end plate from accumulated acetylcholine

Organophosphates inhibit acetylcholinesterase irreversibly, so acetylcholine accumulates. Fasciculations occur first, then the end plate stays depolarised and sodium channels inactivate, causing depolarising block. Atropine and pralidoxime are used.

Option by option

A. Failure of calcium entry into the nerve terminal
Calcium entry failure causes Lambert-Eaton syndrome and magnesium effects, not this picture.
B. Depletion of acetylcholine from presynaptic vesicles
Vesicle depletion is not the mechanism, since acetylcholine is in excess.
C. Persistent depolarisation of the end plate from accumulated acetylcholine (correct)
Correct. Excess acetylcholine keeps the end plate depolarised and produces depolarising block.
D. Blockade of the nicotinic receptor by the toxin
Nicotinic blockade is the mechanism of curare, not of cholinesterase inhibitors.

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.

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is C, Persistent depolarisation of the end plate from accumulated acetylcholine. Organophosphates inhibit acetylcholinesterase irreversibly, so acetylcholine accumulates.

Why is "Failure of calcium entry into the nerve terminal" not the answer?

Calcium entry failure causes Lambert-Eaton syndrome and magnesium effects, not this picture.

Why is "Depletion of acetylcholine from presynaptic vesicles" not the answer?

Vesicle depletion is not the mechanism, since acetylcholine is in excess.

Why is "Blockade of the nicotinic receptor by the toxin" not the answer?

Nicotinic blockade is the mechanism of curare, not of cholinesterase inhibitors.

What concept does this question test?

It tests Nerve and muscle: organophosphate poisoning in Physiology. Fasciculations occur first, then the end plate stays depolarised and sodium channels inactivate, causing depolarising block. Atropine and pralidoxime are used.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. 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.