Vitamins and minerals: zinc therapy in Wilson disease: practice question

A Biochemistry 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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Biochemistry · Vitamins and minerals: zinc therapy in Wilson disease

Sample item

A 19-year-old with Wilson disease has completed initial chelation and is maintained on oral zinc salts. How does zinc limit copper accumulation?

AIt restores ATP7B function so that biliary copper secretion resumes againBIt chelates copper in the plasma and promotes its excretion in the urineCIt raises hepatic ceruloplasmin output so more copper leaves the liverDIt induces enterocyte metallothionein that traps copper, blocking uptake

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

The answer and the reasoning

D. It induces enterocyte metallothionein that traps copper, blocking uptake

Zinc induces metallothionein in intestinal cells. Metallothionein binds copper more avidly than zinc, so the copper is retained in enterocytes and lost when they are shed, reducing absorption. Penicillamine and trientine act differently, by chelating copper and promoting urinary excretion.

Option by option

A. It restores ATP7B function so that biliary copper secretion resumes again
The ATP7B gene is mutated in the disease and zinc cannot restore its function.
B. It chelates copper in the plasma and promotes its excretion in the urine
Urinary excretion after chelation is the action of penicillamine or trientine, not zinc.
C. It raises hepatic ceruloplasmin output so more copper leaves the liver
Ceruloplasmin synthesis is not the mechanism; it is low in the disease because copper loading fails.
D. It induces enterocyte metallothionein that traps copper, blocking uptake (correct)
Correct. Metallothionein induced by zinc sequesters copper in the enterocyte and prevents absorption.

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 Biochemistry question

What is the answer to this Biochemistry question?

The best answer is D, It induces enterocyte metallothionein that traps copper, blocking uptake. Zinc induces metallothionein in intestinal cells.

Why is "It restores ATP7B function so that biliary copper secretion resumes a…" not the answer?

The ATP7B gene is mutated in the disease and zinc cannot restore its function.

Why is "It chelates copper in the plasma and promotes its excretion in the ur…" not the answer?

Urinary excretion after chelation is the action of penicillamine or trientine, not zinc.

Why is "It raises hepatic ceruloplasmin output so more copper leaves the liver" not the answer?

Ceruloplasmin synthesis is not the mechanism; it is low in the disease because copper loading fails.

What concept does this question test?

It tests Vitamins and minerals: zinc therapy in Wilson disease in Biochemistry. Metallothionein binds copper more avidly than zinc, so the copper is retained in enterocytes and lost when they are shed, reducing absorption. Penicillamine and trientine act differently, by chelating copper and promoting urinary excretion.

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 Vitamins and minerals: zinc therapy in Wilson disease?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry 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.