Human Biochemistry, Volume 2 - Murray R. 1993
Biochemistry of Intracellular and Intercellular Communication
Thyroid Hormones
Pathophysiology
Goiter
Goiter refers to any enlargement of The Thyroid Gland. A simple goiter results from the body's attempt to compensate for diminished thyroid hormone production, meaning all cases of simple goiter are accompanied by elevated thyrotropin levels. The underlying causes of such disorders may include iodide deficiency, iodide excess in the presence of an impaired autoregulatory mechanism, and various rare metabolic defects that highlight Structure/19.html">The Importance of specific stages in thyroid hormone Biosynthesis. These defects include 1) impaired transport; 2) impaired iodination; 3) defective coupling reaction; 4) deiodinase deficiency; and 5) The formation of abnormal iodinated Proteins. Partial impairment of these Functions can cause simple goiter in adults. If any of these causes of simple goiter are severe, they lead to hypothyroidism. Simple goiter is treated with exogenous THYROID Hormones, whereas specific forms of goiter call for either increased or restricted iodine intake.
Hypothyroidism
A deficiency of free T3 or T4 causes the clinical state known as hypothyroidism. Hypothyroidism is typically associated with impaired thyroid function, but it can also result from pituitary or hypothalamic disease. In hypothyroidism, the basal metabolic rate and the rates of other thyroid hormone-dependent processes are decreased. Characteristic Features of this pathology include bradycardia, diastolic Hypertension, lethargy, somnolence, constipation, cold intolerance, dry Skin and Hair, and pallor. Other clinical manifestations depend on the age at which hypothyroidism develops. Cretinism was discussed previously. When hypothyroidism arises in older children, it manifests as growth retardation without delayed intellectual development. Various Forms of hypothyroidism are treated with thyroid hormone replacement therapy.
Hyperthyroidism
Hyperthyroidism, or thyrotoxicosis, is caused by the overproduction of thyroid hormones. Although numerous forms of this pathology exist, the majority of cases in the United States are related to Graves' disease, which results from The production of thyroid-stimulating IMMUNOGLOBULINS (IgG) that activate the thyrotropin receptor (see Table 43.2). This leads to diffuse enlargement of the thyroid gland and excessive, uncontrolled production of T3 and T4, as IgG synthesis is not regulated by feedback inhibition. The manifestations of hyperthyroidism involve multi-organ changes, including tachycardia, widened pulse pressure, nervousness, insomnia, weight loss (despite an increased appetite), weakness, sweating, heat intolerance, and warm, moist skin. The Treatment of hyperthyroidism, or Graves' disease, involves suppressing hormone production through The Use of antithyroid drugs, blocking glandular function with radioactive iodine isotopes (such as 131I), or a combination of both approaches. In some cases, surgical removal of the gland is performed.
Class="center">References
Chopra I. J. et al. Pathways of METABOLISM of thyroid hormones, Recent Prog. Horm. Res., 1978, 34, 531.
Jackson l.M.D. Thyrotropin-releasing hormone, N. Engl. J. Med., 1982, 306, 145.
Larsen P.R. Thyroid-pituitary interaction: Feedback regulation of thyrotropin secretion by thyroid hormones, N. Engl. J. Med., 1982, 396, 23.
Lo G. S. et al. Dependence of renal (Na+ and K+)-ATPase activity on thyroid status, J. Biol. Chem., 1976, 251, 7826. Oppenheimer J. H. Thyroid hormone action at the nuclear level, Ann. Intern. Med., 1985, 102, 374.
Robins J. et al. Thyroxine transport proteins of plasma: Molecular properties and biosynthesis. Recent Prog. Horm. Res., 1978, 34, 477.
Last update: 06/08/2026
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