Renal: aldosterone and potassium: 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: aldosterone and potassium

Sample item

A 38-year-old woman has blood pressure 170/105 mmHg, serum potassium 2.9 mmol/L and bicarbonate 31 mmol/L, with low plasma renin and raised aldosterone. Which tubular event best explains her hypokalaemia?

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

The answer and the reasoning

A. Increased sodium entry through ENaC in principal cells, creating a lumen-negative potential that drives potassium secretion

This is primary hyperaldosteronism (Conn syndrome). Aldosterone raises ENaC and Na-K-ATPase activity in principal cells, increasing sodium reabsorption and making the lumen negative. This favours potassium secretion; hydrogen secretion from intercalated cells also rises, producing metabolic alkalosis.

Option by option

  • A. Increased sodium entry through ENaC in principal cells, creating a lumen-negative potential that drives potassium secretion (correct)

    Correct. Enhanced principal cell sodium reabsorption drives potassium and hydrogen secretion.

  • B. Blockade of the Na-K-2Cl cotransporter in the thick ascending limb

    Blocking this cotransporter is loop diuretic action and does not cause hypertension.

  • C. Decreased distal tubular flow, which reduces potassium washout

    Reduced flow would limit potassium secretion; aldosterone excess does not do this.

  • D. Reduced Na-K-ATPase activity in principal cells

    Aldosterone increases, not decreases, Na-K-ATPase activity.

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, Increased sodium entry through ENaC in principal cells, creating a lumen-negative potential that drives potassium secretion. This is primary hyperaldosteronism (Conn syndrome).

Why is "Blockade of the Na-K-2Cl cotransporter in the thick ascending limb" not the answer?

Blocking this cotransporter is loop diuretic action and does not cause hypertension.

Why is "Decreased distal tubular flow, which reduces potassium washout" not the answer?

Reduced flow would limit potassium secretion; aldosterone excess does not do this.

Why is "Reduced Na-K-ATPase activity in principal cells" not the answer?

Aldosterone increases, not decreases, Na-K-ATPase activity.

What concept does this question test?

It tests Renal: aldosterone and potassium in Physiology. Aldosterone raises ENaC and Na-K-ATPase activity in principal cells, increasing sodium reabsorption and making the lumen negative. This favours potassium secretion; hydrogen secretion from intercalated cells also rises, producing metabolic alkalosis.

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 Renal: aldosterone and potassium?

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.