Bone: postmenopausal osteoporosis: 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 · Bone: postmenopausal osteoporosis

Sample item

A 62-year-old woman has lost 5 cm in height and has a wedge fracture of a lumbar vertebra. Serum calcium, phosphate, alkaline phosphatase and parathyroid hormone are normal. Which statement best describes the pathogenesis of her condition?

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

The answer and the reasoning

C. Oestrogen deficiency increases osteoclast activity through RANKL and cytokines, causing trabecular bone loss

Postmenopausal osteoporosis results from oestrogen loss, which raises IL-1, IL-6 and TNF and increases RANKL signalling, so osteoclast activity outpaces bone formation. Trabecular bone, as in vertebrae and the distal radius, is lost earliest, giving vertebral compression and Colles fractures. Bone is normally mineralised, so calcium, phosphate and alkaline phosphatase are normal.

Option by option

  • A. Excess parathyroid hormone causing subperiosteal resorption

    Excess PTH describes hyperparathyroidism, with hypercalcaemia and raised PTH.

  • B. Defective mineralisation of osteoid from vitamin D deficiency

    Defective mineralisation describes osteomalacia, with low calcium or phosphate and a high alkaline phosphatase.

  • C. Oestrogen deficiency increases osteoclast activity through RANKL and cytokines, causing trabecular bone loss (correct)

    Correct. Increased osteoclastic resorption after oestrogen loss explains the pattern and normal biochemistry.

  • D. Failure of osteoclast function from carbonic anhydrase II deficiency

    Carbonic anhydrase II deficiency causes osteopetrosis, with dense brittle bone.

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 C, Oestrogen deficiency increases osteoclast activity through RANKL and cytokines, causing trabecular bone loss. Postmenopausal osteoporosis results from oestrogen loss, which raises IL-1, IL-6 and TNF and increases RANKL signalling, so osteoclast activity outpaces bone formation.

Why is "Excess parathyroid hormone causing subperiosteal resorption" not the answer?

Excess PTH describes hyperparathyroidism, with hypercalcaemia and raised PTH.

Why is "Defective mineralisation of osteoid from vitamin D deficiency" not the answer?

Defective mineralisation describes osteomalacia, with low calcium or phosphate and a high alkaline phosphatase.

Why is "Failure of osteoclast function from carbonic anhydrase II deficiency" not the answer?

Carbonic anhydrase II deficiency causes osteopetrosis, with dense brittle bone.

What concept does this question test?

It tests Bone: postmenopausal osteoporosis in Pathology. Trabecular bone, as in vertebrae and the distal radius, is lost earliest, giving vertebral compression and Colles fractures. Bone is normally mineralised, so calcium, phosphate and alkaline phosphatase are normal.

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 Bone: postmenopausal osteoporosis?

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.