Renal and acid–base: volume versus osmotic control of ADH: 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 · Renal and acid–base: volume versus osmotic control of ADH

Sample item

A patient with severe haemorrhage and a low serum osmolality continues to release ADH. Which statement best explains this?

AADH release is controlled only by osmoreceptorsBMarked hypovolaemia overrides osmotic inhibition of ADH releaseCHaemorrhage destroys the osmoreceptorsDLow osmolality is a potent stimulus of ADH release

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

The answer and the reasoning

B. Marked hypovolaemia overrides osmotic inhibition of ADH release

ADH release is chiefly regulated by plasma osmolality through the hypothalamic osmoreceptors, but a large fall in effective circulating volume stimulates release through baroreceptor input, even if osmolality is low. This protects volume at the cost of hyponatraemia.

Option by option

A. ADH release is controlled only by osmoreceptors
Volume signals also control ADH, not only osmolality.
B. Marked hypovolaemia overrides osmotic inhibition of ADH release (correct)
Correct. Baroreceptor input from low volume overrides the osmotic signal.
C. Haemorrhage destroys the osmoreceptors
The osmoreceptors are not destroyed by haemorrhage.
D. Low osmolality is a potent stimulus of ADH release
Low osmolality suppresses ADH, so it cannot be the cause.

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 B, Marked hypovolaemia overrides osmotic inhibition of ADH release. ADH release is chiefly regulated by plasma osmolality through the hypothalamic osmoreceptors, but a large fall in effective circulating volume stimulates release through baroreceptor input, even if osmolality is low.

Why is "ADH release is controlled only by osmoreceptors" not the answer?

Volume signals also control ADH, not only osmolality.

Why is "Haemorrhage destroys the osmoreceptors" not the answer?

The osmoreceptors are not destroyed by haemorrhage.

Why is "Low osmolality is a potent stimulus of ADH release" not the answer?

Low osmolality suppresses ADH, so it cannot be the cause.

What concept does this question test?

It tests Renal and acid–base: volume versus osmotic control of ADH in Physiology. This protects volume at the cost of hyponatraemia.

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 Renal and acid–base: volume versus osmotic control of ADH?

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.