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Chapter 27: Thyroid and Antithyroid Drugs

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A 34-year-old woman is being prepared for thyroidectomy. As part of the preparation, she is given a solution containing high iodide concentration. She wonders why she is being treated with something that is added to food (salt). The explanation is that

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a. iodide in food is poorly absorbed.

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b. iodide in food is rapidly taken up by skeletal muscle.

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c. low concentrations of iodide are required for thyroxine synthesis, but high concentrations inhibit thyroxine synthesis and release.

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d. iodide in food is not utilized by the thyroid gland.

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e. high concentrations of iodide block the TRH receptor on the pituitary gland.

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Answer is c. Low levels of iodine are required for thyroid synthesis, but high levels of iodine inhibit thyroid synthesis and release.

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A 38-year-old South American woman has a large protrusion on her neck but is otherwise asymptomatic. Her condition is caused by a dietary deficiency of

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a. iron.

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b. magnesium.

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c. potassium.

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d. sodium.

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e. iodine.

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Answer is e. In some areas of the world, simple or nontoxic goiter is prevalent because of insufficient dietary iodine. Normal thyroid function obviously requires an adequate intake of iodine; without it, normal amounts of thyroid hormone cannot be made, TSH is secreted in excess (see Figures 27-1 and 27-2), and the thyroid becomes hyperplastic and hypertrophic. The enlarged and stimulated thyroid becomes remarkably efficient at extracting residual traces of iodine from the blood and usually succeeds in producing sufficient thyroid hormones. In more severe iodine deficiency, adult hypothyroidism and cretinism may occur.

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Figure 27-1. Major pathways of thyroid hormone biosynthesis and release. D1 and D2, deiodinases; DIT, diiodotyrosine; EOI, enzyme-linked species; HOI, hypoiodous acid; MMI, methimazole; MIT, monoiodotyrosine; PTU, propylthiouracil; Tg, thyroglobulin; TPO, thyroid peroxidase.

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Figure 27-2. Regulation of thyroid hormone secretion. Myriad neural inputs influence hypothalamic secretion of thyrotropin-releasing hormone (TRH). TRH stimulates release of thyrotropin (TSH, thyroid-stimulating hormone) from the anterior pituitary; TSH stimulates the synthesis and release of the thyroid hormones T3 and T4. T3 and T4 feed back to inhibit the synthesis and release of TRH and TSH. Somatostatin (SST) can inhibit TRH action, as can dopamine and high concentrations of glucocorticoids. Low levels of I are required for thyroxine synthesis, but high levels inhibit thyroxin synthesis and release.

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