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A. Thyroid hormones - release, effects, degradation

A. Thyroid hormones - release, effects, degradation

Over Production Thyroxine
B. Endemic goiter and its treatment with thyroxine

Hyperthyroidism and Antithyroid Drugs

Thyroid overactivity in Graves' disease (A) results from formation of IgG antibodies that bind to and activate TSH receptors. Consequently, there is overproduction of hormone with cessation of TSH secretion. Graves' disease can abate spontaneously after 1-2 y. Therefore, initial therapy consists of reversible suppression of thyroid activity by means of antithyroid drugs. In other forms of hyperthyroidism, such as hormone-producing (morphologically benign) thyroid adenoma, the preferred therapeutic method is removal of tissue, either by surgery or administration of 131iodine in sufficient dosage. Radioio-dine is taken up into thyroid cells and destroys tissue within a sphere of a few millimeters by emitting p-(electron) particles during its radioactive decay.

Concerning iodine-induced hyper-thyroidism, see p. 244 (B).

Antithyroid drugs inhibit thyroid function. Release of thyroid hormone (C) is preceded by a chain of events. A membrane transporter actively accumulates iodide in thyroid cells; this is followed by oxidation to iodine, iodina-tion of tyrosine residues in thyroglobu-lin, conjugation of two diiodotyrosine groups, and formation of T4 and T3 moieties. These reactions are catalyzed by thyroid peroxidase, which is localized in the apical border of the follicular cell membrane. T4-containing thyro-globulin is stored inside the thyroid follicles in the form of thyrocolloid. Upon endocytotic uptake, colloid undergoes lysosomal enzymatic hydrolysis, enabling thyroid hormone to be released as required. A "thyrostatic" effect can result from inhibition of synthesis or release. When synthesis is arrested, the antithyroid effect develops after a delay, as stored colloid continues to be utilized.

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