Endocrinology: apparent mineralocorticoid excess: 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 · Endocrinology: apparent mineralocorticoid excess

Sample item

A 45-year-old man who eats large amounts of liquorice sweets has hypertension, hypokalaemia and metabolic alkalosis, with low plasma renin and low aldosterone. Which mechanism explains the mineralocorticoid-like state?

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

The answer and the reasoning

D. Inhibition of 11-beta-hydroxysteroid dehydrogenase type 2, so cortisol occupies renal mineralocorticoid receptors

Mineralocorticoid receptors bind cortisol and aldosterone equally, but in the distal nephron 11-beta-HSD2 normally converts cortisol to inactive cortisone. Glycyrrhetinic acid in liquorice inhibits this enzyme, so cortisol acts on the receptor and causes sodium retention and potassium loss with suppressed renin and aldosterone.

Option by option

  • A. Increased renin release from the juxtaglomerular cells

    Raised renin would increase aldosterone, whereas renin is suppressed in this patient.

  • B. Inhibition of angiotensin converting enzyme in the lung

    ACE inhibition would reduce angiotensin II and aldosterone and would not cause hypertension.

  • C. Direct stimulation of aldosterone synthase in the zona glomerulosa

    Stimulating aldosterone synthase would raise aldosterone, but aldosterone is low here.

  • D. Inhibition of 11-beta-hydroxysteroid dehydrogenase type 2, so cortisol occupies renal mineralocorticoid receptors (correct)

    Correct. Without 11-beta-HSD2, cortisol activates the receptor, giving mineralocorticoid excess with low aldosterone.

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 D, Inhibition of 11-beta-hydroxysteroid dehydrogenase type 2, so cortisol occupies renal mineralocorticoid receptors. Mineralocorticoid receptors bind cortisol and aldosterone equally, but in the distal nephron 11-beta-HSD2 normally converts cortisol to inactive cortisone.

Why is "Increased renin release from the juxtaglomerular cells" not the answer?

Raised renin would increase aldosterone, whereas renin is suppressed in this patient.

Why is "Inhibition of angiotensin converting enzyme in the lung" not the answer?

ACE inhibition would reduce angiotensin II and aldosterone and would not cause hypertension.

Why is "Direct stimulation of aldosterone synthase in the zona glomerulosa" not the answer?

Stimulating aldosterone synthase would raise aldosterone, but aldosterone is low here.

What concept does this question test?

It tests Endocrinology: apparent mineralocorticoid excess in Physiology. Glycyrrhetinic acid in liquorice inhibits this enzyme, so cortisol acts on the receptor and causes sodium retention and potassium loss with suppressed renin and aldosterone.

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 Endocrinology: apparent mineralocorticoid excess?

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.