Question:hard
Assertion (A): Hyperkalemia is not a feature of ACTH deficiency (secondary adrenal insufficiency).
Reason (R): ACTH increases potassium reabsorption by the distal renal tubule.
Assertion (A): Hyperkalemia is not a feature of ACTH deficiency (secondary adrenal insufficiency).
Reason (R): ACTH increases potassium reabsorption by the distal renal tubule.
Show Hint
Remember that aldosterone, not ACTH, is the hormone that controls potassium at the distal tubule.
Updated On: Jul 7, 2026
- Both A and R are true and R is the correct explanation of A
- Both A and R are true but R is NOT the correct explanation of A
- A is true but R is false
- A is false but R is true
Show Solution
The Correct Option is C
Solution and Explanation
Step 1: Separate cortisol control from potassium control.
ACTH deficiency mainly cuts down cortisol output, since ACTH's chief job is to drive the cortisol producing part of the adrenal gland. The salt and potassium regulating hormone, aldosterone, has its own separate control system built around blood pressure, sodium level, and potassium level, running through the renin angiotensin pathway. Because that system does not depend on ACTH, aldosterone output continues close to normal even when ACTH is low.
Step 2: Trace what that means for potassium.
With aldosterone still working, the kidney keeps pushing potassium out into the urine as usual, so blood potassium stays in the normal range. This is why hyperkalemia is not typically seen in secondary adrenal insufficiency, unlike in primary adrenal failure, where aldosterone is also lost. The Assertion is therefore true.
Step 3: Check the claim about ACTH and the tubule.
The Reason says ACTH raises potassium reabsorption at the distal tubule, but ACTH does not act directly on the kidney tubule at all, and the hormone that does act there, aldosterone, works to remove potassium from the blood rather than hold onto it. So the Reason is incorrect on both counts.
Step 4: Put it together and clear the other codes.
A true Assertion resting on preserved aldosterone cannot be explained by a false claim about ACTH acting on the tubule. This rules out both codes needing R true, and it rules out the code needing A false, since hyperkalemia really is absent here.
Final Answer:
The Assertion is true while the Reason is false, based on standard adrenal physiology since the printed key was unreadable.
ACTH deficiency mainly cuts down cortisol output, since ACTH's chief job is to drive the cortisol producing part of the adrenal gland. The salt and potassium regulating hormone, aldosterone, has its own separate control system built around blood pressure, sodium level, and potassium level, running through the renin angiotensin pathway. Because that system does not depend on ACTH, aldosterone output continues close to normal even when ACTH is low.
Step 2: Trace what that means for potassium.
With aldosterone still working, the kidney keeps pushing potassium out into the urine as usual, so blood potassium stays in the normal range. This is why hyperkalemia is not typically seen in secondary adrenal insufficiency, unlike in primary adrenal failure, where aldosterone is also lost. The Assertion is therefore true.
Step 3: Check the claim about ACTH and the tubule.
The Reason says ACTH raises potassium reabsorption at the distal tubule, but ACTH does not act directly on the kidney tubule at all, and the hormone that does act there, aldosterone, works to remove potassium from the blood rather than hold onto it. So the Reason is incorrect on both counts.
Step 4: Put it together and clear the other codes.
A true Assertion resting on preserved aldosterone cannot be explained by a false claim about ACTH acting on the tubule. This rules out both codes needing R true, and it rules out the code needing A false, since hyperkalemia really is absent here.
Final Answer:
The Assertion is true while the Reason is false, based on standard adrenal physiology since the printed key was unreadable.
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