Endocrine: Graves disease: 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 · Endocrine: Graves disease

Sample item

A 32-year-old woman has heat intolerance, weight loss, palpitations, a diffuse non-tender goitre, exophthalmos and pretibial myxoedema. Which mechanism explains her hyperthyroidism?

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

The answer and the reasoning

D. IgG autoantibodies that stimulate the TSH receptor

Graves disease is autoimmune hyperthyroidism in which thyroid-stimulating immunoglobulins bind the TSH receptor and drive unregulated hormone production and follicular hyperplasia. Histology shows tall columnar epithelium with papillary infoldings and scalloped colloid. Extrathyroidal features arise from glycosaminoglycan deposition in orbital and pretibial tissue.

Option by option

  • A. Activating TSH receptor mutation in a single nodule

    A single activating mutation causes a toxic adenoma, with a nodule and not a diffuse goitre or eye signs.

  • B. T cell mediated destruction of thyroid follicles

    T cell mediated follicular destruction with Hurthle change describes Hashimoto thyroiditis, which causes hypothyroidism.

  • C. Autoantibodies that block the TSH receptor

    Blocking antibodies reduce thyroid hormone output and can cause atrophic hypothyroidism.

  • D. IgG autoantibodies that stimulate the TSH receptor (correct)

    Correct. Stimulating anti-TSH receptor antibodies cause Graves hyperthyroidism.

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 D, IgG autoantibodies that stimulate the TSH receptor. Graves disease is autoimmune hyperthyroidism in which thyroid-stimulating immunoglobulins bind the TSH receptor and drive unregulated hormone production and follicular hyperplasia.

Why is "Activating TSH receptor mutation in a single nodule" not the answer?

A single activating mutation causes a toxic adenoma, with a nodule and not a diffuse goitre or eye signs.

Why is "T cell mediated destruction of thyroid follicles" not the answer?

T cell mediated follicular destruction with Hurthle change describes Hashimoto thyroiditis, which causes hypothyroidism.

Why is "Autoantibodies that block the TSH receptor" not the answer?

Blocking antibodies reduce thyroid hormone output and can cause atrophic hypothyroidism.

What concept does this question test?

It tests Endocrine: Graves disease in Pathology. Histology shows tall columnar epithelium with papillary infoldings and scalloped colloid. Extrathyroidal features arise from glycosaminoglycan deposition in orbital and pretibial tissue.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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 Endocrine: Graves disease?

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.