Mineral and Trace Element Metabolism (Iron, Copper, Zinc, Calcium-Phosphate) MCQs

Biochemistry · 18 free questions with answers & explanations.

1. Hepcidin is the master regulator of iron homeostasis. In anaemia of chronic disease (ACD), hepcidin levels are INCREASED. What is the molecular mechanism by which elevated hepcidin causes hypoferraemia?
2. Wilson's disease results from mutations in ATP7B, a copper-transporting P-type ATPase. Which biochemical consequence of ATP7B dysfunction explains both the hepatic copper accumulation and low serum caeruloplasmin?
3. Zinc deficiency classically causes acrodermatitis enteropathica. Zinc is a cofactor for >300 enzymes. Which enzyme's zinc dependence explains impaired wound healing in zinc deficiency?
4. FGF-23 (fibroblast growth factor-23), secreted by osteocytes, is central to phosphate homeostasis. In X-linked hypophosphataemia (XLH), PHEX mutations cause elevated FGF-23. What is the resulting biochemical phenotype?
5. In Wilson's disease, copper accumulates in the liver, brain, and cornea (Kayser-Fleischer rings). What is the PRIMARY biochemical defect responsible for copper accumulation?
6. Hepcidin is the master regulator of systemic iron homeostasis. In anemia of chronic disease (ACD), hepcidin levels are typically:
7. A patient with celiac disease develops hypocalcemia and osteomalacia despite adequate calcium intake. What is the SEQUENTIAL biochemical mechanism of bone disease in this condition?
8. Acrodermatitis enteropathica is caused by zinc deficiency due to a mutation in ZIP4 transporter. What is the ROLE of zinc that explains the dermatitis, alopecia, and immune deficiency seen in this condition?
9. A 30-year-old woman presents with hemochromatosis-like features, low ceruloplasmin, Kayser-Fleischer rings, and liver cirrhosis. Ferrous iron (Fe²⁺) is elevated because ceruloplasmin-mediated ferroxidase activity is impaired. Which copper transport protein is defective in Wilson's disease?
10. Hepcidin is the master regulator of iron homeostasis. In which of the following conditions is hepcidin inappropriately elevated, contributing to the anemia?
11. Zinc is an essential trace element. Which of the following biochemical functions is directly dependent on zinc as a structural or catalytic cofactor?
12. FGF-23 (fibroblast growth factor-23) is a phosphatonin secreted by osteocytes. In X-linked hypophosphatemia (XLH), which mutation leads to FGF-23 excess and what is the biochemical consequence?
13. Hepcidin is the master regulator of iron homeostasis. In anaemia of chronic disease (ACD), hepcidin is elevated. The mechanism by which elevated hepcidin causes iron restriction is:
14. A patient with Wilson's disease has corneal Kayser-Fleischer rings, liver disease, and haemolytic anaemia. The biochemical basis of haemolysis in Wilson's disease is:
15. Zinc is required as a cofactor for many enzymes. Zinc deficiency causes impaired wound healing, acrodermatitis enteropathica, and immune dysfunction. The molecular basis of immune impairment is PRIMARILY due to:
16. In chronic renal failure, secondary hyperparathyroidism develops through which sequence of biochemical events?
17. Selenium is an essential trace element incorporated into selenoproteins. The MOST important selenoprotein protecting cells from oxidative damage is:
18. A 6-year-old child from a rural area presents with anaemia, abdominal pain, peripheral neuropathy, and 'lead lines' on the gums. Blood lead level is 65 mcg/dL. The MECHANISM by which lead causes anaemia is: