Blood: iron homeostasis: 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 · Blood: iron homeostasis

Sample item

A 55-year-old woman with long-standing rheumatoid arthritis has haemoglobin 9.2 g/dL, MCV 78 fL, low serum iron, low total iron-binding capacity and serum ferritin 420 ng/mL. Which mechanism best explains the low serum iron?

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

The answer and the reasoning

B. Hepcidin excess blocks ferroportin, trapping iron in enterocytes and macrophages

Inflammatory cytokines, especially interleukin-6, raise hepatic hepcidin. Hepcidin degrades ferroportin, so iron cannot leave enterocytes and reticuloendothelial macrophages. Serum iron and transferrin saturation fall while ferritin stays normal or high, the opposite of iron deficiency where total iron-binding capacity rises.

Option by option

  • A. Absent intrinsic factor prevents iron absorption in the ileum

    Intrinsic factor is needed for vitamin B12, not iron, absorption.

  • B. Hepcidin excess blocks ferroportin, trapping iron in enterocytes and macrophages (correct)

    Correct. Hepcidin-induced ferroportin loss sequesters iron within cells despite adequate stores.

  • C. Raised transferrin synthesis binds all circulating iron

    Transferrin is low here (low iron-binding capacity), and it is raised in true iron deficiency.

  • D. Defective haem synthesis from a mutated ALAS2 gene releases iron into plasma

    A sideroblastic defect would give high serum iron and ferritin with ring sideroblasts, not low iron.

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 B, Hepcidin excess blocks ferroportin, trapping iron in enterocytes and macrophages. Inflammatory cytokines, especially interleukin-6, raise hepatic hepcidin.

Why is "Absent intrinsic factor prevents iron absorption in the ileum" not the answer?

Intrinsic factor is needed for vitamin B12, not iron, absorption.

Why is "Raised transferrin synthesis binds all circulating iron" not the answer?

Transferrin is low here (low iron-binding capacity), and it is raised in true iron deficiency.

Why is "Defective haem synthesis from a mutated ALAS2 gene releases iron into…" not the answer?

A sideroblastic defect would give high serum iron and ferritin with ring sideroblasts, not low iron.

What concept does this question test?

It tests Blood: iron homeostasis in Physiology. Hepcidin degrades ferroportin, so iron cannot leave enterocytes and reticuloendothelial macrophages. Serum iron and transferrin saturation fall while ferritin stays normal or high, the opposite of iron deficiency where total iron-binding capacity rises.

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 Blood: iron homeostasis?

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.