Endocrine pathology: Addison disease: practice question

A Pathology 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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Pathology · Endocrine pathology: Addison disease

Sample item

A 34-year-old woman has fatigue, weight loss, postural hypotension, sodium 126 mEq/L, potassium 5.8 mEq/L and darkening of the palmar creases. What explains the pigmentation?

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

The answer and the reasoning

B. Raised ACTH from loss of cortisol feedback, with POMC-derived peptides stimulating melanocytes

In primary adrenal failure, usually from autoimmune adrenalitis, low cortisol removes negative feedback on the pituitary and ACTH rises. ACTH is cleaved from pro-opiomelanocortin along with melanocyte-stimulating peptides that act on melanocortin-1 receptors in skin. Secondary adrenal failure lacks ACTH and gives pale skin.

Option by option

  • A. Direct melanocyte stimulation by excess circulating cortisol

    Cortisol is deficient in this disease, not in excess.

  • B. Raised ACTH from loss of cortisol feedback, with POMC-derived peptides stimulating melanocytes (correct)

    Correct. Raised ACTH and POMC peptides stimulate melanin synthesis.

  • C. Increased thyroid hormone driving melanin synthesis

    Thyroid hormone excess is not the cause of pigmentation in adrenal insufficiency.

  • D. Haemosiderin deposition in the dermis from iron overload

    Haemosiderin causes bronze skin in haemochromatosis, which is not suggested by hyponatraemia and hyperkalaemia.

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 Pathology question

What is the answer to this Pathology question?

The best answer is B, Raised ACTH from loss of cortisol feedback, with POMC-derived peptides stimulating melanocytes. In primary adrenal failure, usually from autoimmune adrenalitis, low cortisol removes negative feedback on the pituitary and ACTH rises.

Why is "Direct melanocyte stimulation by excess circulating cortisol" not the answer?

Cortisol is deficient in this disease, not in excess.

Why is "Increased thyroid hormone driving melanin synthesis" not the answer?

Thyroid hormone excess is not the cause of pigmentation in adrenal insufficiency.

Why is "Haemosiderin deposition in the dermis from iron overload" not the answer?

Haemosiderin causes bronze skin in haemochromatosis, which is not suggested by hyponatraemia and hyperkalaemia.

What concept does this question test?

It tests Endocrine pathology: Addison disease in Pathology. ACTH is cleaved from pro-opiomelanocortin along with melanocyte-stimulating peptides that act on melanocortin-1 receptors in skin. Secondary adrenal failure lacks ACTH and gives pale skin.

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 Endocrine pathology: Addison disease?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.