{"id":427,"date":"2019-11-15T19:14:03","date_gmt":"2019-11-15T19:14:03","guid":{"rendered":"https:\/\/pressbooks.publishdot.com\/nursingpharmacology\/chapter\/9-5-thyroid-medications\/"},"modified":"2021-12-07T11:28:23","modified_gmt":"2021-12-07T11:28:23","slug":"9-5-thyroid-medications","status":"publish","type":"chapter","link":"https:\/\/pressbooks.publishdot.com\/nursingpharmacology\/chapter\/9-5-thyroid-medications\/","title":{"raw":"9.5 Thyroid Medications","rendered":"9.5 Thyroid Medications"},"content":{"raw":"
\n

Thyroid Basics: A&P Review<\/h2>\nThe thyroid is a butterfly-shaped organ located anterior to the trachea, just inferior to the larynx (see Figure 9.18).[footnote]\"1811 The Thyroid Gland.jpg<\/a>\" by OpenStax College<\/a> is licensed under CC BY 3.0.<\/a> Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland<\/a>[\/footnote]<\/sup>\u00a0Each of the thyroid lobes are embedded with parathyroid glands.\n\n[caption id=\"\" align=\"aligncenter\" width=\"737\"]\"Illustration Figure 9.18 The Thyroid Gland[\/caption]\n

Synthesis and Release of Thyroid Hormones<\/h3>\nThyroid hormone production is dependent on the hormone's essential component: iodine. T3 and T4 hormones are produced when iodine attaches to a glycoprotein called thyroglobulin. The following steps outline the hormone's assembly: Binding of TSH to thyroid receptors causes the cells to actively transport iodide ions across their cell membrane from the bloodstream. As a result, the concentration of iodide ions \u201ctrapped\u201d in the thyroid cells is many times higher than the concentration in the bloodstream. The iodide ions undergo oxidation (i.e., their negatively charged electrons are removed) and enzymes link the iodine to tyrosine to produce triiodothyronine (T3), a thyroid hormone with three iodines, or thyroxine (T4), a thyroid hormone with four iodines. These hormones remain in the thyroid follicles until TSH stimulates the release of free T3 and T4 into the bloodstream. In the bloodstream, less than one percent of the circulating T3 and T4 remains unbound. This free T3 and T4 can cross the lipid bilayer of cell membranes and be taken up by cells. The remaining 99 percent of circulating T3 and T4 is bound to specialized transport proteins called thyroxine-binding globulins (TBGs), to albumin, or to other plasma proteins. This \u201cpackaging\u201d prevents their free diffusion into body cells. When blood levels of T3 and T4 begin to decline, bound T3 and T4 are released from these plasma proteins and readily cross the membrane of target cells. T3 is more potent than T4, and many cells convert T4 to T3 through the removal of an iodine atom.\n

Regulation of Thyroid Hormone Synthesis<\/h3>\nA negative feedback loop controls the regulation of thyroid hormone levels. As shown in Figure 9.19,[footnote]\"1813 A Classic Negative Feedback Loop.jpg<\/a>\" by OpenStax College<\/a> is licensed under CC BY 4.0.<\/a> Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland<\/a>[\/footnote]<\/sup>\u00a0low blood levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus, which triggers secretion of TSH from the anterior pituitary. In turn, TSH stimulates the thyroid gland to secrete T3 and T4. The levels of TRH, TSH, T3, and T4 are regulated by a negative feedback system in which increasing levels of T3 and T4 decrease the production and secretion of TSH.\n\n[caption id=\"\" align=\"aligncenter\" width=\"941\"]\"Illustration Figure 9.19 Negative Feedback Loop. A negative feedback loop controls the regulation of thyroid hormone levels[\/caption]\n

Functions of Thyroid Hormones<\/h3>\nThe thyroid hormones T3 and T4 are often referred to as metabolic hormones because their levels influence the body\u2019s basal metabolic rate, which is the amount of energy used by the body at rest. When T3 and T4 bind to intracellular receptors located on the mitochondria, they cause an increase in nutrient breakdown and the use of oxygen to produce ATP. In addition, T3 and T4 initiate the transcription of genes involved in glucose oxidation. Although these mechanisms prompt cells to produce more ATP, the process is inefficient, and an abnormally increased level of heat is released as a byproduct of these reactions. This calorigenic effect (calor- = \u201cheat\u201d) raises body temperature.\n\nAdequate levels of thyroid hormones are also required for protein synthesis and for fetal and childhood tissue development and growth. They are especially critical for normal development of the nervous system both in utero and in early childhood, and they continue to support neurological function in adults. Thyroid hormones also have a complex interrelationship with reproductive hormones, and deficiencies can influence libido, fertility, and other aspects of reproductive function. Finally, thyroid hormones increase the body\u2019s sensitivity to catecholamines (epinephrine and norepinephrine) from the adrenal medulla by upregulation of receptors in the blood vessels. When levels of T3 and T4 hormones are excessive, this effect accelerates the heart rate, strengthens the heartbeat, and increases blood pressure. Because thyroid hormones regulate metabolism, heat production, protein synthesis, and many other body functions, thyroid disorders can have severe and widespread consequences.\n

Disorders of the Thyroid Gland: Iodine Deficiency, Hypothyroidism, and Hyperthyroidism<\/h3>\nAs discussed above, dietary iodine is required for the synthesis of T3 and T4. For much of the world\u2019s population, foods do not provide adequate levels of iodine because the amount varies according to the level in the soil in which the food was grown, as well as the irrigation and fertilizers used. Marine fish and shrimp tend to have high levels because they concentrate iodine from seawater, but many people in landlocked regions lack access to seafood. Thus, the primary source of dietary iodine in many countries is iodized salt. Fortification of salt with iodine began in the United States in 1924, and international efforts to iodize salt in the world\u2019s poorest nations continue today.\n\nDietary iodine deficiency can result in the impaired ability to synthesize T3 and T4, leading to a variety of severe disorders. When T3 and T4 cannot be produced, TSH is secreted in increasing amounts. As a result of this hyperstimulation, thyroglobulin and colloid accumulate in the thyroid gland and increase the overall size of the thyroid gland, a condition called a [pb_glossary id=\"2435\"]goiter<\/strong>[\/pb_glossary] (see Figure 9.20[footnote]\"Goitre.jpg<\/a>\" by Almazi<\/a> is licensed under CC0<\/a>[\/footnote]<\/sup>). A goiter is only a visible indication of the deficiency. Other disorders related to iodine deficiency include impaired growth and development, decreased fertility, and prenatal and infant death. Moreover, iodine deficiency is the primary cause of preventable mental retardation worldwide. Neonatal hypothyroidism (cretinism) is characterized by cognitive deficits, short stature, and sometimes deafness and muteness in children and adults born to mothers who were iodine-deficient during pregnancy.\n\n[caption id=\"\" align=\"aligncenter\" width=\"448\"]\"Photo Figure 9.20 Goiter[\/caption]\n\nIn areas of the world with access to iodized salt, dietary deficiency is rare. Instead, inflammation of the thyroid gland is a common cause of [pb_glossary id=\"1779\"]hypothyroidism[\/pb_glossary]<\/strong>, or low blood levels of thyroid hormones. Hypothyroidism is a disorder characterized by a low metabolic rate, weight gain, cold extremities, constipation, reduced libido, menstrual irregularities, and reduced mental activity, and requires long-term thyroid hormone replacement therapy. In contrast, [pb_glossary id=\"1780\"]hyperthyroidism[\/pb_glossary]<\/strong>\u2014an abnormally elevated blood level of thyroid hormones\u2014is often caused by a pituitary or thyroid tumor. In Graves\u2019 disease, the hyperthyroid state results from an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland. Hyperthyroidism can lead to an increased metabolic rate, excessive body heat and sweating, diarrhea, weight loss, tremors, and increased heart rate. The person\u2019s eyes may bulge (called exophthalmos) as antibodies produce inflammation in the soft tissues of the orbits. The person may also develop a goiter. Hyperthyroidism is often treated by thyroid surgery or with radioactive iodine (RAI) therapy. Patients are asked to follow radiation precautions after RAI treatment to limit radiation exposure to others, especially pregnant women and young children, such as sleeping in a separate bed and flushing the toilet 2-3 times after use. The RAI treatment may take up to several months to have its effect. The end result of thyroid surgery or RAI treatment is often hypothyroidism, which is treated by thyroid hormone replacement therapy.[footnote]American Thyroid Association. (2019). Radioactive iodine<\/em>. https:\/\/www.thyroid.org\/radioactive-iodine\/<\/a>[\/footnote]<\/sup>\n

Calcitonin<\/h3>\nThe thyroid gland also secretes another hormone called calcitonin. Calcitonin is released in response to elevated blood calcium levels. It decreases blood calcium concentrations by:\n