Graves Disease

Graves' disease is the commonest cause in iodine-sufficient countries.

Graves' Disease

Read this in LECTURE 4: Thyroid Hormones

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Study material on Graves Disease

Practice questions on Graves Disease

A 35-year-old woman undergoes a thyroidectomy for Graves disease. Histologic examination of the thyroid gland shows follicular epithelial cells that are tall and columnar instead of the normal cuboidal shape. This finding is best explained by which of the following processes?

Answer: B. In Graves disease, excessive TSH receptor stimulation leads to both increased number (hyperplasia) and increased size (hypertrophy) of follicular cells, causing them to become tall and columnar. This is a physiologic adaptation to hormonal stimulation, not a neoplastic or metaplastic change.

Graves disease is driven primarily by antibodies to the:

Answer: A. Graves' disease is an autoimmune condition caused by stimulating antibodies directed against the TSH receptor.

Which of the following is NOT a typical feature of Graves' disease?

Answer: A. Graves' disease is an autoimmune disorder causing diffuse toxic goitre and hyperthyroidism, typically mediated by TSH receptor antibodies (TRAb). Exophthalmos is a characteristic feature. Toxic nodular goitre (Plummer's disease) is a different cause of hyperthyroidism. ---

Toxic multinodular goiter (Plummer's disease) differs from Graves' disease in that

Answer: D. Toxic MNG = autonomous function of multiple nodules in a pre-existing goiter. Occurs in iodine-deficient areas in older patients. No TSI, no ophthalmopathy. Treated with radioiodine or surgery. Hot nodules on Tc-99m scan. ---

Which antibody directly causes hyperthyroidism in Graves' disease?

Answer: C. TSI binds and continuously activates TSH receptors causing unregulated thyroid hormone production. Unique features: exophthalmos and pretibial myxedema. ---

Toxic multinodular goiter (Plummer's disease) differs from Graves' disease in that

Answer: A. Graves' disease is an autoimmune disorder where antibodies (Thyroid-Stimulating Immunoglobulins, TSI) bind to and stimulate the TSH receptor, leading to diffuse thyroid overactivity, goiter, and often extrathyroidal manifestations like exophthalmos. In toxic multinodular goiter, one or more nodules within the thyroid gland autonomously produce excess thyroid hormone, typically without the autoimmune features or exoph

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