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FOUNDATION OVERVIEW

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; alterations in these hormone concentrations, including TSH, can lead to hyper- or hypothyroidism (Tables 62-1 and 62-2).

TABLE 62-1Physiologic Effects of Thyroid Hormones
TABLE 62-2Overview of Thyroid Disorders

Thyrotoxicosis occurs when excessive levels of thyroid hormones are present. Patients typically experience 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. The majority of cases are caused by hyperthyroidism due to Graves disease, an autoimmune condition in which antibodies form against the thyrotropin receptor and stimulate the production of thyroid hormones. Graves disease may induce ophthalmopathies including exophthalmos. The remaining causes of hyperthyroidism are ...

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