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FOUNDATION OVERVIEW

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The thyroid gland is located in the front of the neck and operates via negative feedback to synthesize thyroid hormones. The hypothalamus produces thyrotropin-releasing hormone (TRH) which stimulates the pituitary to release thyroid-stimulating hormone (TSH). TSH, also known as thyrotropin, stimulates the synthesis and release of thyroid hormones from the thyroid gland. Formation of thyroid hormones requires iodination of tyrosine residues by thyroid peroxidase to produce monoiodinated and diiodinated residues that couple to form triiodothyronine (T3) and levothyroxine (T4). Circulating levels of T3 and T4 regulate TSH secretion via negative feedback. The thyroid gland is responsible for the production of T4 and less than 20% of T3. Peripheral conversion of T4 to T3 forms the majority of T3. Compared to T4, T3 is more potent, less bound to plasma proteins, and has a shorter half-life. Thyroid hormones affect multiple organ systems throughout the body, and alterations in hormone concentrations and TSH lead to hyper- or hypothyroidism (Tables 61-1 and 61-2).

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TABLE 61-1Physiologic Effects of Thyroid Hormones
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TABLE 61-2Overview of Thyroid Disorders
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Thyrotoxicosis occurs when excessive thyroid hormones are present with the majority of cases caused by hyperthyroidism due to Graves disease. Graves disease is an autoimmune condition in which antibodies form against the thyrotropin receptor and stimulate the production of thyroid hormones. The remaining causes of hyperthyroidism are toxic nodular goiter, adenomas or tumors, and drug-induced. Thyrotoxicosis presents with nervousness, anxiety, palpitations and tachycardia, weight loss, sleep disturbances, frequent bowel movements, and heat intolerance. Women experience irregular menses or decreased fertility, and men have decreased libido or gynecomastia. Graves disease may induce ophthalmopathies including exophthalmos. Select patients present with a thyroid storm, a rare and life-threatening form of ...

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