GI physiology: iron absorption: 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 · GI physiology: iron absorption

Sample item

A 45-year-old woman with rheumatoid arthritis has a hypochromic microcytic anaemia, low serum iron and high ferritin. Raised hepcidin is found. How does hepcidin reduce iron absorption?

AIt blocks the DMT1 transporter on the apical surface of enterocytesBIt causes internalisation and degradation of ferroportin, trapping iron in enterocytesCIt increases the synthesis of transferrin by the liverDIt prevents reduction of ferric iron by duodenal cytochrome b

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

The answer and the reasoning

B. It causes internalisation and degradation of ferroportin, trapping iron in enterocytes

Dietary ferric iron is reduced to ferrous iron by duodenal cytochrome b and enters enterocytes through DMT1, and is exported to plasma through basolateral ferroportin. Hepcidin, a liver peptide raised by inflammation and iron overload, binds ferroportin and causes it to be degraded. Iron then remains in the enterocyte and is lost as the cell is shed, and release from macrophages is also blocked, which explains anaemia of chronic disease.

Option by option

A. It blocks the DMT1 transporter on the apical surface of enterocytes
DMT1 is regulated by iron status of the cell, not blocked directly by hepcidin.
B. It causes internalisation and degradation of ferroportin, trapping iron in enterocytes (correct)
Ferroportin degradation traps iron in enterocytes and macrophages.
C. It increases the synthesis of transferrin by the liver
Transferrin synthesis is not increased by hepcidin; in chronic disease transferrin saturation is low.
D. It prevents reduction of ferric iron by duodenal cytochrome b
Cytochrome b reduction is not the target of hepcidin.

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.

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is B, It causes internalisation and degradation of ferroportin, trapping iron in enterocytes. Dietary ferric iron is reduced to ferrous iron by duodenal cytochrome b and enters enterocytes through DMT1, and is exported to plasma through basolateral ferroportin.

Why is "It blocks the DMT1 transporter on the apical surface of enterocytes" not the answer?

DMT1 is regulated by iron status of the cell, not blocked directly by hepcidin.

Why is "It increases the synthesis of transferrin by the liver" not the answer?

Transferrin synthesis is not increased by hepcidin; in chronic disease transferrin saturation is low.

Why is "It prevents reduction of ferric iron by duodenal cytochrome b" not the answer?

Cytochrome b reduction is not the target of hepcidin.

What concept does this question test?

It tests GI physiology: iron absorption in Physiology. Hepcidin, a liver peptide raised by inflammation and iron overload, binds ferroportin and causes it to be degraded. Iron then remains in the enterocyte and is lost as the cell is shed, and release from macrophages is also blocked, which explains anaemia of chronic disease.

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 GI physiology: iron absorption?

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.