Reproduction: polycystic ovary syndrome: 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.

Try it

Physiology · Reproduction: polycystic ovary syndrome

Sample item

A 24-year-old obese woman has oligomenorrhoea, hirsutism and acanthosis nigricans. LH is raised relative to FSH and testosterone is raised. Which mechanism contributes most directly to the hyperandrogenism?

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

The answer and the reasoning

A. Raised LH and insulin drive theca cell androgen output while SHBG falls

In polycystic ovary syndrome, high LH pulse frequency and hyperinsulinaemia stimulate theca cells to make androgens. Insulin also lowers hepatic sex hormone-binding globulin, raising free testosterone, and the lack of ovulation gives oligomenorrhoea.

Option by option

  • A. Raised LH and insulin drive theca cell androgen output while SHBG falls (correct)

    Correct. LH and insulin stimulate theca androgen production, and low SHBG raises free testosterone.

  • B. Excess FSH causes granulosa aromatase overactivity

    Excess aromatase activity would convert androgens to oestrogens and lower androgens.

  • C. Failure of 21-hydroxylase in the corpus luteum

    There is no corpus luteum in anovulatory cycles, and the 21-hydroxylase deficiency is a different diagnosis.

  • D. Autonomous cortisol secretion by the zona fasciculata

    Autonomous cortisol secretion causes Cushing syndrome, not this ovarian picture.

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.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Raised LH and insulin drive theca cell androgen output while SHBG falls. In polycystic ovary syndrome, high LH pulse frequency and hyperinsulinaemia stimulate theca cells to make androgens.

Why is "Excess FSH causes granulosa aromatase overactivity" not the answer?

Excess aromatase activity would convert androgens to oestrogens and lower androgens.

Why is "Failure of 21-hydroxylase in the corpus luteum" not the answer?

There is no corpus luteum in anovulatory cycles, and the 21-hydroxylase deficiency is a different diagnosis.

Why is "Autonomous cortisol secretion by the zona fasciculata" not the answer?

Autonomous cortisol secretion causes Cushing syndrome, not this ovarian picture.

What concept does this question test?

It tests Reproduction: polycystic ovary syndrome in Physiology. Insulin also lowers hepatic sex hormone-binding globulin, raising free testosterone, and the lack of ovulation gives oligomenorrhoea.

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 Reproduction: polycystic ovary syndrome?

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.