{"id":402,"date":"2019-11-15T19:14:03","date_gmt":"2019-11-15T19:14:03","guid":{"rendered":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/9-5-thyroid-medications\/"},"modified":"2025-01-16T22:29:16","modified_gmt":"2025-01-16T22:29:16","slug":"9-5-thyroid-medications","status":"publish","type":"chapter","link":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/9-5-thyroid-medications\/","title":{"raw":"9.5 Thyroid Medications","rendered":"9.5 Thyroid Medications"},"content":{"raw":"<div class=\"thyroid\">\n\nThis section will review the anatomy and physiology of the thyroid, outline common thyroid disorders, review the anatomy and physiology of the parathyroid gland, outline common parathyroid disorders, apply the nursing process to administering thyroid medications, and then discuss thyroid and osteoporosis medications.\n<h2>Review of Anatomy and Physiology of the Thyroid<\/h2>\nThe thyroid is a butterfly-shaped organ located anterior to the trachea, just inferior to the larynx (see Figure 9.17).<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1811_The_Thyroid_Gland.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1811 The Thyroid Gland.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/3.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 3.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland<\/a>[\/footnote]<\/sup> Each of the thyroid lobes is embedded with parathyroid glands.\n\n[caption id=\"\" align=\"aligncenter\" width=\"737\"]<img title=\"&quot;1811 The Thyroid Gland.jpg&quot; by OpenStax College is licensed under CC BY 3.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland \" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2019\/11\/image11-6.png\" alt=\"Illustration and micrograph showing thyroid and surrounding structures.\" width=\"737\" height=\"1410\"> Figure 9.17 Thyroid Gland[\/caption]\n<h3>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<h3>Regulation of Thyroid Hormone Synthesis<\/h3>\nA negative feedback loop controls the regulation of thyroid hormone levels. As shown in Figure 9.18,<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1813_A_Classic_Negative_Feedback_Loop.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1813 A Classic Negative Feedback Loop.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 4.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" target=\"_blank\" rel=\"noopener noreferrer\">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\"]<img title=\"&quot;1813 A Classic Negative Feedback Loop.jpg&quot; by OpenStax College is licensed under CC BY 4.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image12-6.png\" alt=\"Illustration showing Negative Feedback loop, with labels.\" width=\"941\" height=\"920\"> Figure 9.18 Negative Feedback Loop: Controls Regulation of Thyroid Hormone Levels[\/caption]\n<h3>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 (<em>calor<\/em>- = \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<h3>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 in these ways:\n<ul>\n \t<li>Inhibiting the activity of osteoclasts (bone cells that breakdown bone matrix and release calcium into the circulation)<\/li>\n \t<li>Decreasing calcium absorption in the intestines<\/li>\n \t<li>Increasing calcium loss in the urine<\/li>\n<\/ul>\nPharmaceutical preparations of calcitonin are prescribed to reduce osteoclast activity in people with osteoporosis. Osteoporosis is a disease that can be caused by glucocorticoids.\n\nCalcium is critical for many other biological processes. It is a second messenger in many signaling pathways and is essential for muscle contraction, nerve impulse transmission, and blood clotting. Given these roles, it is not surprising that blood calcium levels are tightly regulated by the endocrine system. The parathyroid glands are primarily involved in calcium regulation.\n<h2>Disorders of the Thyroid Gland<\/h2>\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=\"659\"]<strong>goiter<\/strong>[\/pb_glossary] (see Figure 9.19<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Goitre.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">Goitre.jpg<\/a>\u201d by <a href=\"https:\/\/en.wikipedia.org\/wiki\/User:Almazi\" target=\"_blank\" rel=\"noopener noreferrer\">Almazi<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\" rel=\"noopener noreferrer\">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\"]<img class=\"\" title=\"&quot;Goitre.jpg&quot; by Almazi is licensed under CC0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image13-6.png\" alt=\"Photo showing a female with a goiter.\" width=\"448\" height=\"336\"> Figure 9.19 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 <strong>[pb_glossary id=\"600\"]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, <strong>[pb_glossary id=\"601\"]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. Clients 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.<sup>[footnote]American Thyroid Association. (2019). <em>Radioactive iodine<\/em>. <a href=\"https:\/\/www.thyroid.org\/radioactive-iodine\/\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.thyroid.org\/radioactive-iodine\/<\/a>[\/footnote]<\/sup>\n\n&nbsp;\n<h2>Review of Anatomy and Physiology of the Parathyroid Glands<\/h2>\nThe parathyroid glands are four tiny, round structures usually embedded in the posterior surface of the thyroid gland (see Figure 9.20).<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1814_The_Parathyroid_Glands.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1814 The Parathyroid Glands.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/3.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 3.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands<\/a>[\/footnote]<\/sup>\u00a0The primary function of the parathyroid glands is to regulate blood calcium levels by producing and secreting <strong>[pb_glossary id=\"602\"]parathyroid hormone (PTH)[\/pb_glossary]<\/strong>\u00a0in response to low blood calcium levels.\n\n[caption id=\"\" align=\"aligncenter\" width=\"871\"]<img title=\"&quot;1814 The Parathyroid Glands.jpg&quot; by OpenStax College is licensed under CC BY 3.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image14-1.png\" alt=\"Illustration and micrograph showing paratyroid glands and surrounding structures.\" width=\"871\" height=\"318\"> Figure 9.20 Parathyroid Glands[\/caption]\n\nPTH secretion causes the release of calcium from the bones by stimulating osteoclasts that degrade bone and then release calcium into the bloodstream. PTH also inhibits osteoblasts, the cells involved in bone deposition, thereby keeping calcium in the blood. PTH also causes increased reabsorption of calcium (and magnesium) in the kidney and initiates the production of the steroid hormone calcitriol, which is the active form of vitamin D3. Calcitriol then stimulates increased absorption of dietary calcium by the intestines. A negative feedback loop regulates the levels of PTH, with rising blood calcium levels inhibiting further release of PTH. (See Figure 9.21 for an illustration of the role of parathyroid hormone in maintaining blood calcium homeostasis.)<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1817_The_Role_of_Parathyroid_Hormone_in_Maintaining_Blood_Calcium_Homeostasis.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1817 The Role of Parathyroid Hormone in Maintaining Blood Calcium Homeostasis.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 4.0.<\/a> Access for free at<a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" target=\"_blank\" rel=\"noopener noreferrer\"> https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands<\/a>[\/footnote]<\/sup>\n\n[caption id=\"\" align=\"aligncenter\" width=\"865\"]<img title=\"&quot;1817 The Role of Parathyroid Hormone in Maintaining Blood Calcium Homeostasis.jpg&quot; by OpenStax is licensed under CC BY 4.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image15-1.png\" alt=\"Illustrations showing parathyroid hormone maintaining blood calcium homeostasis\" width=\"865\" height=\"1039\"> Figure 9.21 Parathyroid Hormone in Maintaining Blood Calcium Homeostasis[\/caption]\n<h2>Disorders of the Parathyroid Glands<\/h2>\nAbnormally high activity of the parathyroid gland can cause <strong>[pb_glossary id=\"603\"]hyperparathyroidism[\/pb_glossary]<\/strong>, a disorder caused by an overproduction of PTH that results in excessive degradation of bone and elevated blood levels of calcium, also called hypercalcemia. Hyperparathyroidism can thus significantly decrease bone density, which can lead to spontaneous fractures or deformities. As blood calcium levels rise, cell membrane permeability to sodium is also decreased, and thus the responsiveness of the nervous system is reduced. At the same time, calcium deposits may collect in the body\u2019s tissues and organs, impairing their functioning.\n\nIn contrast, abnormally low blood calcium levels may be caused by parathyroid hormone deficiency, called <strong>[pb_glossary id=\"604\"]hypoparathyroidism[\/pb_glossary]<\/strong>, which may develop following injury or surgery involving the thyroid gland. Low blood calcium increases membrane permeability to sodium, thus increasing the responsiveness of the nervous system, resulting in muscle twitching, cramping, spasms, or convulsions. Severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.\n<h2>Applying the Nursing Process to Administering Thyroid Medications<\/h2>\n<h3>Assessment<\/h3>\nWhen administering thyroid replacement medications, the nurse should plan to monitor TSH levels before and during therapy for effectiveness. Drug interactions may occur with several other medications, so review drug labeling information carefully before administering.\n<h3>Implementation<\/h3>\nLevothyroxine should be administered consistently every morning 30-60 minutes before a meal. For clients who are NPO, levothyroxine can also be given intravenously (IV).\n<h3>Evaluation<\/h3>\nElevated levels of thyroid hormone can cause cardiac dysrhythmias; immediately report any symptoms of tachycardia, chest pain, or palpitations to the provider.\n<h2>Thyroid and Osteoporosis Medication Classes<\/h2>\n<h3>Thyroid Replacement Medication<\/h3>\n<strong>Mechanism of Action: <\/strong>Oral levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present.\n\n<strong>Indications: <\/strong>Levothyroxine is a thyroid replacement drug used to treat hypothyroidism. See Figure 9.22<sup>[footnote]\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Levothyroxine_25mcg_Tablets.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">Levothyroxine 25mcg Tablets.jpg<\/a>\u201d by<a href=\"https:\/\/commons.wikimedia.org\/w\/index.php?title=User:Ash&amp;action=edit&amp;redlink=1\" target=\"_blank\" rel=\"noopener noreferrer\">\u00a0User:Ash<\/a>\u00a0is licensed under\u00a0<a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC0<\/a><span style=\"font-size: 12.8px\">[\/footnote]<\/span><\/sup>\u00a0for an image of levothyroxine.\n\n[caption id=\"\" align=\"aligncenter\" width=\"568\"]<img class=\"\" title=\"&quot;Levothyroxine 25mcg Tablets.jpg&quot; by User:Ash is licensed under CC0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image16.png\" alt=\"Photo showing closeup of open Levothyroxine package with blister pack beside it.\" width=\"568\" height=\"395\"> Figure 9.22 Levothyroxine[\/caption]\n\n<strong>Nursing Considerations: <\/strong>Levothyroxine tablets should be taken with a full glass of water as the tablet may rapidly disintegrate. It should be administered as a single daily dose, on an empty stomach, one-half to one hour before breakfast, and at least four hours before or after drugs known to interfere with levothyroxine absorption. For clients who are NPO, levothyroxine can also be given intravenously (IV).\n\nLevothyroxine is contraindicated for clients with hyperthyroidism and adrenal insufficiency until the condition is corrected. Many clients who undergo treatment for hyperthyroidism may develop hypothyroidism. Overtreatment with levothyroxine may cause symptoms of hyperthyroidism with increased heart rate, cardiac wall thickness, and cardiac contractility that may precipitate angina or arrhythmias, particularly in clients with cardiovascular disease and in older adults. Levothyroxine therapy in this population should be initiated at lower doses. If cardiac symptoms develop or worsen, the nurse should withhold the medication, contact the health care provider, and anticipate a lower dose prescribed or the medication to be withheld for one week and then restarted at a lower dose.\n\nAddition of levothyroxine therapy in clients with diabetes mellitus may worsen glycemic control and result in the need for higher dosages of antidiabetic medication. Carefully monitor glycemic control, especially when thyroid therapy is started, changed, or discontinued.\n\nLevothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the levothyroxine dose is increased. Closely monitor INR results and anticipate dosage adjustments.\n\nLevothyroxine can affect, or be affected by, several other medications, so carefully read drug label information when therapy is initiated.\n\n<strong>Side Effects\/Adverse Effects:<\/strong> There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Because TSH levels may increase during pregnancy, TSH should be monitored, and levothyroxine dosage may require adjustment during pregnancy.<sup>[footnote]This work is a derivative of <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/\" target=\"_blank\" rel=\"noopener noreferrer\">DailyMed<\/a> by <a href=\"https:\/\/www.nlm.nih.gov\/\" target=\"_blank\" rel=\"noopener noreferrer\">U.S. National Library of Medicine<\/a> in the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/\" target=\"_blank\" rel=\"noopener noreferrer\">Public Domain<\/a>. [\/footnote]<\/sup>\n\n<strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take thyroid replacement medications at the same time each day. Clients should be aware that thyroid replacement medications do not cure hypothyroidism and therapy is lifelong. Clients should notify their health care provider if they experience signs of headache, diarrhea, sweating, or heat intolerance. Medications should be spaced four hours apart from medications like antacid, iron, or calcium supplements. Clients will be followed closely by their health care provider regarding their response to medication therapy and serum thyroid levels will be taken.<sup>[footnote]uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a>[\/footnote]<\/sup>\n<h3>Antithyroid Medication<\/h3>\n<strong>Mechanism of Action: <\/strong>Propylthiouracil inhibits the synthesis of thyroid hormones.\n\n<strong>Indications: <\/strong>Propylthiouracil (PTU) is an antithyroid medication used to treat hyperthyroidism or to ameliorate symptoms of hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy.\n\n<strong>Nursing Considerations: <\/strong>Propylthiouracil is administered orally. The total daily dosage is usually given in three equal doses at approximately 8-hour intervals. Propylthiouracil can cause hypothyroidism necessitating routine monitoring of TSH and free T4 levels, with adjustments in dosing to maintain a euthyroid state.\n\n<strong>Side Effects\/Adverse Effects:<\/strong> Liver injury resulting in liver failure, liver transplantation, or death has been reported. Clients should be instructed to report any symptoms of hepatic dysfunction (anorexia, pruritus, and right upper quadrant pain), particularly in the first six months of therapy.\n\nAgranulocytosis is a potentially life-threatening side effect of propylthiouracil therapy. Agranulocytosis typically occurs within the first three months of therapy. Clients should be instructed to immediately report any symptoms suggestive of agranulocytosis, such as fever or sore throat.\n\nCases of vasculitis resulting in severe complications and death have been reported in clients receiving propylthiouracil therapy. If vasculitis is suspected, discontinue therapy and initiate appropriate intervention.\n\nPropylthiouracil crosses the placenta and can cause fetal liver failure, a goiter, and cretinism if administered to a pregnant woman.\n\n<strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take the medication as directed at regular dosing intervals. They should monitor their weight 2-3 times per week. Additionally, clients should be advised that medications may cause drowsiness, and they should report any signs of sore throat, fever, headache, jaundice, bleeding, or bruising.\n<h3>Osteoporosis Medication: Calcitonin<\/h3>\n<strong>Mechanism of Action: <\/strong>Calcitonin is a calcitonin receptor agonist. Calcitonin is released by the thyroid gland. It acts primarily on bone and also has effects on the kidneys and the gastrointestinal tract.\n\n<strong>Indications: <\/strong>Calcitonin is used to treat osteoporosis.\n\n<strong>Nursing Considerations: <\/strong>Calcitonin is administered via nasal spray with one spray in one side of the nose daily. See Figure 9.23<sup>[footnote]\u201c<a href=\"https:\/\/www.flickr.com\/photos\/niaid\/46057881342\" target=\"_blank\" rel=\"noopener noreferrer\">Nasal Spray<\/a>\u201d by\u00a0<a href=\"https:\/\/www.flickr.com\/photos\/niaid\/\" target=\"_blank\" rel=\"noopener noreferrer\">NIAID<\/a>\u00a0is licensed under\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 2.0<\/a><span style=\"font-size: 12.8px\">[\/footnote]<\/span><\/sup>\u00a0for an image of calcitonin nasal spray.\u00a0The nasal spray pump should be primed before the first administration. Unopened calcitonin can be stored in the refrigerator until opened but should not be refrigerated between doses. Opened bottles stored at room temperature should be discarded after 30 days of initial dose.\n\n<strong>Side Effects\/Adverse Effects:<\/strong> Adverse effects include serious hypersensitivity reactions (bronchospasm, swelling of the tongue or throat, anaphylaxis and anaphylactic shock), hypocalcemia, nasal mucosa adverse events, and malignancy.\n\nCalcitonin should not be used during pregnancy.\n\n<strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should be advised to take medications as directed. They should report any signs of hypercalcemia or an allergic response. Clients should receive instruction on the process of self-injection. They should also be advised that they may experience flushing and warmth following injection. Post-menopausal women should adhere to a diet high in calcium and vitamin D and should be educated regarding the importance of exercise for reversing bone loss.<sup>[footnote]uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a>[\/footnote]<\/sup>\n\n&nbsp;\n\n[caption id=\"\" align=\"aligncenter\" width=\"498\"]<img class=\"\" title=\"&quot;Nasal Spray&quot; by NIAID is licensed under CC BY 2.0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image17-5.png\" alt=\"Photo showing woman using nasal spray.\" width=\"498\" height=\"387\"> Figure 9.23 Administration of Calcitonin[\/caption]\n<h3>Osteoporosis Medication: Alendronate<\/h3>\n<strong>Mechanism of Action: <\/strong>Alendronate is a bisphosphonate that inhibits osteoclast-mediated bone resorption. By preventing the breakdown of bone and enhancing the formation of new bone, alendronate assists in reversing bone loss and decreases the risk of fractures.\n\n<strong>Indications: <\/strong>Alendronate is used for the prevention and treatment of osteoporosis in postmenopausal women, to increase bone mass in men with osteoporosis, and for glucocorticoid-induced osteoporosis.\n\n<strong>Nursing Considerations: <\/strong>Check dosages carefully because some formulations are administered daily, whereas others are administered weekly. Alendronate should be taken after arising for the day but should be administered at least one-half hour before the first food, beverage, or medication of the day with plain water only. Other beverages (including mineral water), food, and some medications are likely to reduce the absorption of alendronate. Clients should not lie down for at least 30 minutes and until after their first food of the day. Clients may also require calcium and vitamin D supplementation, especially if concurrently taking glucocorticoids.\n\nAlendronate is contraindicated in the following conditions: pregnancy, hypocalcemia, the inability to sit or stand for 30 minutes after swallowing, esophageal abnormalities that delay emptying, and clients at risk for aspiration. Alendronate is not recommended for clients with kidney disease with creatinine clearance less than 35 mL\/min.\n\nDiscontinue alendronate if severe musculoskeletal pain occurs. A bone mineral density measurement should be made at the initiation of therapy and repeated after 6 to 12 months of combined alendronate and glucocorticoid treatment.\n\n<strong>Side Effects\/Adverse Effects: <\/strong>Side effects include upper GI disturbances, severe musculoskeletal pain, and risk of osteonecrosis of the jaw.\n\n<strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take medication as directed at the same time each day, first thing in the morning. Clients should remain upright after they take medication for 30 minutes to minimize stomach and esophageal irritation. Clients should eat a balanced diet and may seek advice from the health care provider regarding supplementation with calcium and vitamin D. Clients should participate in regular exercise to help increase bone strength.<sup>[footnote]uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a>[\/footnote]<\/sup>\n<h3>Osteoporosis: Calcium + Vitamin D<\/h3>\n<strong>Mechanism of Action: <\/strong>Calcium and vitamin D are essential nutrients that play a vital role in bone health. Calcium is necessary for the formation and maintenance of healthy bones, while vitamin D helps the body absorb and use calcium.\n\n<strong>Indications: <\/strong>Calcium and vitamin D supplements are often prescribed to prevent and treat osteoporosis, as they help maintain bone density and strength.\n\n<strong>Nursing Considerations: <\/strong>The therapeutic effects of calcium and vitamin D supplements may vary depending on the individual's health status and the presence of any underlying medical conditions.\n\n<strong>Side Effects\/Adverse Effects: <\/strong>Side effects include hypercalcemia, kidney stones, and gastrointestinal problems such as constipation, bloating, and abdominal discomfort.\n\n<strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take with food to enhance absorption and monitor for signs of hypercalcemia such as kidney stones and gastrointestinal upset.\n\nNow let\u2019s take a closer look at the medication grid comparing thyroid and osteoporosis medications in Table 9.5.<sup>[footnote]This work is a derivative of <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/\" target=\"_blank\" rel=\"noopener noreferrer\">DailyMed<\/a> by <a href=\"https:\/\/www.nlm.nih.gov\/\" target=\"_blank\" rel=\"noopener noreferrer\">U.S. National Library of Medicine<\/a> in the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/\" target=\"_blank\" rel=\"noopener noreferrer\">Public Domain<\/a>.[\/footnote]<\/sup> Medication grids are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication. Basic information related to each class of medication is outlined below. Detailed information on a specific medication can be found for free at <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/index.cfm\" target=\"_blank\" rel=\"noopener\">DailyMed<\/a>. On the home page, enter the drug name in the search bar to read more about the medication. Prototype\/generic medications listed in the grids below are also linked to a DailyMed page.\n\nTable 9.5 Thyroid and Osteoporosis Medications Grid\n<table class=\"grid\">\n<tbody>\n<tr>\n<th class=\"shaded\" scope=\"col\"><strong>Class\/Subclass<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Prototype\/Generic<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Nursing <\/strong><strong>Considerations<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Therapeutic Effects<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Side\/Adverse Effects<\/strong><\/th>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Thyroid Replacement<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=686ba2cf-7651-44de-9b4d-eeaaf2a0e364\" target=\"_blank\" rel=\"noopener noreferrer\">levothyroxine<\/a><\/td>\n<td>Take levothyroxine sodium tablets with a full glass of water as the tablet may rapidly disintegrate\n\nAdminister levothyroxine as a single daily dose, on an empty stomach, one-half to one hour before breakfast\n\nAdminister levothyroxine at least four hours before or after drugs known to interfere with levothyroxine sodium tablets absorption\n\nAnticipate lower dosages in elderly clients with preexisting cardiac disease\n\nMay interact with several medications, so read drug label thoroughly on initial administration for potential effects<\/td>\n<td>Increases T4 levels in hypothyroidism<\/td>\n<td>Hypersensitivity reactions\n\nCardiac dysrhythmias<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Antithyroid<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a57c49ae-d659-49fa-84e3-cf6d1f9e6f97\" target=\"_blank\" rel=\"noopener noreferrer\">propylthiouracil <\/a><a class=\"rId60\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a57c49ae-d659-49fa-84e3-cf6d1f9e6f97\">(PTU)<\/a><\/td>\n<td>Usually administered every eight hours\n\nMay cause hypothyroidism, so TSH and T4 levels should be monitored\n\nIf a client becomes pregnant, immediately notify health care provider because it can cause fetal harm<\/td>\n<td>Inhibit production of T4<\/td>\n<td>Hypothyroidism\n\nLiver failure\n\nAgranulocytosis\n\nVasculitis\n\nFetal harm<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Calcium Regulator<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=c82eb602-12e1-692b-d660-f8d5b5736b54\" target=\"_blank\" rel=\"noopener noreferrer\">calcitonin<\/a><\/td>\n<td>Administer nasal spray with one spray in one side of the nose daily\n\nContraindicated during pregnancy\n\nDiscard unrefrigerated bottle after 30 days of opening\n\nMay store unopened bottles in refrigerator until expiration date<\/td>\n<td>Treats osteoporosis<\/td>\n<td>Serious hypersensitivity reactions (bronchospasm, swelling of the tongue or throat, anaphylaxis, and anaphylactic shock)\n\nHypocalcemia\n\nNasal mucosa adverse effects\n\nMalignancy<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Bisphosphonates<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a24fd39c-34a7-4de2-9439-781e612189ca\" target=\"_blank\" rel=\"noopener noreferrer\">alendronate<\/a><\/td>\n<td>Administered on rising and at least one-half hour before the first food, beverage, or medication of the day with plain water only\n\nThe client should sit or stand for 30 minutes after administration\n\nContraindicated in pregnancy, hypocalcemia, and kidney disease\n\nConcurrent calcium and vitamin D supplements may be required<\/td>\n<td>Enhances bone mineral density in osteoporosis<\/td>\n<td>Upper GI tract adverse events\n\nSevere musculoskeletal pain\n\nRisk of osteonecrosis of the jaw<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Herbal<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=e84dc181-3dd8-48ca-b1fb-03fb13313369\" target=\"_blank\" rel=\"noopener\">calcium - vitamin D<\/a><\/td>\n<td>Supplement should be taken with meal, as it is better absorbed with food<\/td>\n<td>Improve calcium absorption and bone health<\/td>\n<td>Constipation, bloating, and abdominal discomfort. High doses may lead to hypercalcemia\n\nUse with caution in clients with kidney stone, hyperparathyroidism, or those with vitamin D toxicity<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n&nbsp;\n\n<\/div>\n<div class=\"__UNKNOWN__\">\n<div class=\"textbox textbox--examples\"><header class=\"textbox__header\">\n<h2>Critical Thinking Activity 9.5<img class=\"alignright size-thumbnail wp-image-67\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1-150x150.png\" alt=\"Image of a circle containing a speech bubble with a question mark in it.\" width=\"150\" height=\"150\"><\/h2>\n<\/header>\n<div class=\"textbox__content\" style=\"text-align: left\">\n\nA client has been diagnosed with hypothyroidism and receives a prescription for levothyroxine.\n\nWhat health teaching should the nurse provide regarding this medication?\n\nNote: Answers to the Critical Thinking activities can be found in the \"<a href=\"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/chapter-9\/\" target=\"_blank\" rel=\"noopener\">Answer Key<\/a>\" section at the end of the book.\n\n<\/div>\n<\/div>\n<\/div>","rendered":"<div class=\"thyroid\">\n<p>This section will review the anatomy and physiology of the thyroid, outline common thyroid disorders, review the anatomy and physiology of the parathyroid gland, outline common parathyroid disorders, apply the nursing process to administering thyroid medications, and then discuss thyroid and osteoporosis medications.<\/p>\n<h2>Review of Anatomy and Physiology of the Thyroid<\/h2>\n<p>The thyroid is a butterfly-shaped organ located anterior to the trachea, just inferior to the larynx (see Figure 9.17).<sup><a class=\"footnote\" title=\"\u201c1811 The Thyroid Gland.jpg\u201d by OpenStax College is licensed under CC BY 3.0. Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" id=\"return-footnote-402-1\" href=\"#footnote-402-1\" aria-label=\"Footnote 1\"><sup class=\"footnote\">[1]<\/sup><\/a><\/sup> Each of the thyroid lobes is embedded with parathyroid glands.<\/p>\n<figure style=\"width: 737px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" title=\"&quot;1811 The Thyroid Gland.jpg&quot; by OpenStax College is licensed under CC BY 3.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2019\/11\/image11-6.png\" alt=\"Illustration and micrograph showing thyroid and surrounding structures.\" width=\"737\" height=\"1410\" \/><figcaption class=\"wp-caption-text\">Figure 9.17 Thyroid Gland<\/figcaption><\/figure>\n<h3>Synthesis and Release of Thyroid Hormones<\/h3>\n<p>Thyroid hormone production is dependent on the hormone&#8217;s essential component: iodine. T3 and T4 hormones are produced when iodine attaches to a glycoprotein called thyroglobulin. The following steps outline the hormone&#8217;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.<\/p>\n<h3>Regulation of Thyroid Hormone Synthesis<\/h3>\n<p>A negative feedback loop controls the regulation of thyroid hormone levels. As shown in Figure 9.18,<sup><a class=\"footnote\" title=\"\u201c1813 A Classic Negative Feedback Loop.jpg\u201d by OpenStax College is licensed under CC BY 4.0. Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" id=\"return-footnote-402-2\" href=\"#footnote-402-2\" aria-label=\"Footnote 2\"><sup class=\"footnote\">[2]<\/sup><\/a><\/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.<\/p>\n<figure style=\"width: 941px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" title=\"&quot;1813 A Classic Negative Feedback Loop.jpg&quot; by OpenStax College is licensed under CC BY 4.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image12-6.png\" alt=\"Illustration showing Negative Feedback loop, with labels.\" width=\"941\" height=\"920\" \/><figcaption class=\"wp-caption-text\">Figure 9.18 Negative Feedback Loop: Controls Regulation of Thyroid Hormone Levels<\/figcaption><\/figure>\n<h3>Functions of Thyroid Hormones<\/h3>\n<p>The 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 (<em>calor<\/em>&#8211; = \u201cheat\u201d) raises body temperature.<\/p>\n<p>Adequate 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.<\/p>\n<h3>Calcitonin<\/h3>\n<p>The thyroid gland also secretes another hormone called calcitonin. Calcitonin is released in response to elevated blood calcium levels. It decreases blood calcium concentrations in these ways:<\/p>\n<ul>\n<li>Inhibiting the activity of osteoclasts (bone cells that breakdown bone matrix and release calcium into the circulation)<\/li>\n<li>Decreasing calcium absorption in the intestines<\/li>\n<li>Increasing calcium loss in the urine<\/li>\n<\/ul>\n<p>Pharmaceutical preparations of calcitonin are prescribed to reduce osteoclast activity in people with osteoporosis. Osteoporosis is a disease that can be caused by glucocorticoids.<\/p>\n<p>Calcium is critical for many other biological processes. It is a second messenger in many signaling pathways and is essential for muscle contraction, nerve impulse transmission, and blood clotting. Given these roles, it is not surprising that blood calcium levels are tightly regulated by the endocrine system. The parathyroid glands are primarily involved in calcium regulation.<\/p>\n<h2>Disorders of the Thyroid Gland<\/h2>\n<p>As 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.<\/p>\n<p>Dietary 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 <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_659\"><strong>goiter<\/strong><\/a> (see Figure 9.19<sup><a class=\"footnote\" title=\"\u201cGoitre.jpg\u201d by Almazi is licensed under CC0\" id=\"return-footnote-402-3\" href=\"#footnote-402-3\" aria-label=\"Footnote 3\"><sup class=\"footnote\">[3]<\/sup><\/a><\/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.<\/p>\n<figure style=\"width: 448px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"\" title=\"&quot;Goitre.jpg&quot; by Almazi is licensed under CC0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image13-6.png\" alt=\"Photo showing a female with a goiter.\" width=\"448\" height=\"336\" \/><figcaption class=\"wp-caption-text\">Figure 9.19 Goiter<\/figcaption><\/figure>\n<p>In areas of the world with access to iodized salt, dietary deficiency is rare. Instead, inflammation of the thyroid gland is a common cause of <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_600\">hypothyroidism<\/a><\/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, <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_601\">hyperthyroidism<\/a><\/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. Clients 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.<sup><a class=\"footnote\" title=\"American Thyroid Association. (2019). Radioactive iodine. https:\/\/www.thyroid.org\/radioactive-iodine\/\" id=\"return-footnote-402-4\" href=\"#footnote-402-4\" aria-label=\"Footnote 4\"><sup class=\"footnote\">[4]<\/sup><\/a><\/sup><\/p>\n<p>&nbsp;<\/p>\n<h2>Review of Anatomy and Physiology of the Parathyroid Glands<\/h2>\n<p>The parathyroid glands are four tiny, round structures usually embedded in the posterior surface of the thyroid gland (see Figure 9.20).<sup><a class=\"footnote\" title=\"\u201c1814 The Parathyroid Glands.jpg\u201d by OpenStax College is licensed under CC BY 3.0. Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" id=\"return-footnote-402-5\" href=\"#footnote-402-5\" aria-label=\"Footnote 5\"><sup class=\"footnote\">[5]<\/sup><\/a><\/sup>\u00a0The primary function of the parathyroid glands is to regulate blood calcium levels by producing and secreting <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_602\">parathyroid hormone (PTH)<\/a><\/strong>\u00a0in response to low blood calcium levels.<\/p>\n<figure style=\"width: 871px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" title=\"&quot;1814 The Parathyroid Glands.jpg&quot; by OpenStax College is licensed under CC BY 3.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image14-1.png\" alt=\"Illustration and micrograph showing paratyroid glands and surrounding structures.\" width=\"871\" height=\"318\" \/><figcaption class=\"wp-caption-text\">Figure 9.20 Parathyroid Glands<\/figcaption><\/figure>\n<p>PTH secretion causes the release of calcium from the bones by stimulating osteoclasts that degrade bone and then release calcium into the bloodstream. PTH also inhibits osteoblasts, the cells involved in bone deposition, thereby keeping calcium in the blood. PTH also causes increased reabsorption of calcium (and magnesium) in the kidney and initiates the production of the steroid hormone calcitriol, which is the active form of vitamin D3. Calcitriol then stimulates increased absorption of dietary calcium by the intestines. A negative feedback loop regulates the levels of PTH, with rising blood calcium levels inhibiting further release of PTH. (See Figure 9.21 for an illustration of the role of parathyroid hormone in maintaining blood calcium homeostasis.)<sup><a class=\"footnote\" title=\"\u201c1817 The Role of Parathyroid Hormone in Maintaining Blood Calcium Homeostasis.jpg\u201d by OpenStax is licensed under CC BY 4.0. Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" id=\"return-footnote-402-6\" href=\"#footnote-402-6\" aria-label=\"Footnote 6\"><sup class=\"footnote\">[6]<\/sup><\/a><\/sup><\/p>\n<figure style=\"width: 865px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" title=\"&quot;1817 The Role of Parathyroid Hormone in Maintaining Blood Calcium Homeostasis.jpg&quot; by OpenStax is licensed under CC BY 4.0 Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image15-1.png\" alt=\"Illustrations showing parathyroid hormone maintaining blood calcium homeostasis\" width=\"865\" height=\"1039\" \/><figcaption class=\"wp-caption-text\">Figure 9.21 Parathyroid Hormone in Maintaining Blood Calcium Homeostasis<\/figcaption><\/figure>\n<h2>Disorders of the Parathyroid Glands<\/h2>\n<p>Abnormally high activity of the parathyroid gland can cause <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_603\">hyperparathyroidism<\/a><\/strong>, a disorder caused by an overproduction of PTH that results in excessive degradation of bone and elevated blood levels of calcium, also called hypercalcemia. Hyperparathyroidism can thus significantly decrease bone density, which can lead to spontaneous fractures or deformities. As blood calcium levels rise, cell membrane permeability to sodium is also decreased, and thus the responsiveness of the nervous system is reduced. At the same time, calcium deposits may collect in the body\u2019s tissues and organs, impairing their functioning.<\/p>\n<p>In contrast, abnormally low blood calcium levels may be caused by parathyroid hormone deficiency, called <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_402_604\">hypoparathyroidism<\/a><\/strong>, which may develop following injury or surgery involving the thyroid gland. Low blood calcium increases membrane permeability to sodium, thus increasing the responsiveness of the nervous system, resulting in muscle twitching, cramping, spasms, or convulsions. Severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.<\/p>\n<h2>Applying the Nursing Process to Administering Thyroid Medications<\/h2>\n<h3>Assessment<\/h3>\n<p>When administering thyroid replacement medications, the nurse should plan to monitor TSH levels before and during therapy for effectiveness. Drug interactions may occur with several other medications, so review drug labeling information carefully before administering.<\/p>\n<h3>Implementation<\/h3>\n<p>Levothyroxine should be administered consistently every morning 30-60 minutes before a meal. For clients who are NPO, levothyroxine can also be given intravenously (IV).<\/p>\n<h3>Evaluation<\/h3>\n<p>Elevated levels of thyroid hormone can cause cardiac dysrhythmias; immediately report any symptoms of tachycardia, chest pain, or palpitations to the provider.<\/p>\n<h2>Thyroid and Osteoporosis Medication Classes<\/h2>\n<h3>Thyroid Replacement Medication<\/h3>\n<p><strong>Mechanism of Action: <\/strong>Oral levothyroxine sodium is a synthetic T4 hormone that exerts the same physiologic effect as endogenous T4, thereby maintaining normal T4 levels when a deficiency is present.<\/p>\n<p><strong>Indications: <\/strong>Levothyroxine is a thyroid replacement drug used to treat hypothyroidism. See Figure 9.22<sup><a class=\"footnote\" title=\"\u201cLevothyroxine 25mcg Tablets.jpg\u201d by\u00a0User:Ash\u00a0is licensed under\u00a0CC0\" id=\"return-footnote-402-7\" href=\"#footnote-402-7\" aria-label=\"Footnote 7\"><sup class=\"footnote\">[7]<\/sup><\/a><\/span><\/sup>\u00a0for an image of levothyroxine.<\/p>\n<figure style=\"width: 568px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"\" title=\"&quot;Levothyroxine 25mcg Tablets.jpg&quot; by User:Ash is licensed under CC0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image16.png\" alt=\"Photo showing closeup of open Levothyroxine package with blister pack beside it.\" width=\"568\" height=\"395\" \/><figcaption class=\"wp-caption-text\">Figure 9.22 Levothyroxine<\/figcaption><\/figure>\n<p><strong>Nursing Considerations: <\/strong>Levothyroxine tablets should be taken with a full glass of water as the tablet may rapidly disintegrate. It should be administered as a single daily dose, on an empty stomach, one-half to one hour before breakfast, and at least four hours before or after drugs known to interfere with levothyroxine absorption. For clients who are NPO, levothyroxine can also be given intravenously (IV).<\/p>\n<p>Levothyroxine is contraindicated for clients with hyperthyroidism and adrenal insufficiency until the condition is corrected. Many clients who undergo treatment for hyperthyroidism may develop hypothyroidism. Overtreatment with levothyroxine may cause symptoms of hyperthyroidism with increased heart rate, cardiac wall thickness, and cardiac contractility that may precipitate angina or arrhythmias, particularly in clients with cardiovascular disease and in older adults. Levothyroxine therapy in this population should be initiated at lower doses. If cardiac symptoms develop or worsen, the nurse should withhold the medication, contact the health care provider, and anticipate a lower dose prescribed or the medication to be withheld for one week and then restarted at a lower dose.<\/p>\n<p>Addition of levothyroxine therapy in clients with diabetes mellitus may worsen glycemic control and result in the need for higher dosages of antidiabetic medication. Carefully monitor glycemic control, especially when thyroid therapy is started, changed, or discontinued.<\/p>\n<p>Levothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the levothyroxine dose is increased. Closely monitor INR results and anticipate dosage adjustments.<\/p>\n<p>Levothyroxine can affect, or be affected by, several other medications, so carefully read drug label information when therapy is initiated.<\/p>\n<p><strong>Side Effects\/Adverse Effects:<\/strong> There are risks to the mother and fetus associated with untreated hypothyroidism in pregnancy. Because TSH levels may increase during pregnancy, TSH should be monitored, and levothyroxine dosage may require adjustment during pregnancy.<sup><a class=\"footnote\" title=\"This work is a derivative of DailyMed by U.S. National Library of Medicine in the Public Domain.\" id=\"return-footnote-402-8\" href=\"#footnote-402-8\" aria-label=\"Footnote 8\"><sup class=\"footnote\">[8]<\/sup><\/a><\/sup><\/p>\n<p><strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take thyroid replacement medications at the same time each day. Clients should be aware that thyroid replacement medications do not cure hypothyroidism and therapy is lifelong. Clients should notify their health care provider if they experience signs of headache, diarrhea, sweating, or heat intolerance. Medications should be spaced four hours apart from medications like antacid, iron, or calcium supplements. Clients will be followed closely by their health care provider regarding their response to medication therapy and serum thyroid levels will be taken.<sup><a class=\"footnote\" title=\"uCentral from Unbound Medicine. https:\/\/www.unboundmedicine.com\/ucentral\" id=\"return-footnote-402-9\" href=\"#footnote-402-9\" aria-label=\"Footnote 9\"><sup class=\"footnote\">[9]<\/sup><\/a><\/sup><\/p>\n<h3>Antithyroid Medication<\/h3>\n<p><strong>Mechanism of Action: <\/strong>Propylthiouracil inhibits the synthesis of thyroid hormones.<\/p>\n<p><strong>Indications: <\/strong>Propylthiouracil (PTU) is an antithyroid medication used to treat hyperthyroidism or to ameliorate symptoms of hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy.<\/p>\n<p><strong>Nursing Considerations: <\/strong>Propylthiouracil is administered orally. The total daily dosage is usually given in three equal doses at approximately 8-hour intervals. Propylthiouracil can cause hypothyroidism necessitating routine monitoring of TSH and free T4 levels, with adjustments in dosing to maintain a euthyroid state.<\/p>\n<p><strong>Side Effects\/Adverse Effects:<\/strong> Liver injury resulting in liver failure, liver transplantation, or death has been reported. Clients should be instructed to report any symptoms of hepatic dysfunction (anorexia, pruritus, and right upper quadrant pain), particularly in the first six months of therapy.<\/p>\n<p>Agranulocytosis is a potentially life-threatening side effect of propylthiouracil therapy. Agranulocytosis typically occurs within the first three months of therapy. Clients should be instructed to immediately report any symptoms suggestive of agranulocytosis, such as fever or sore throat.<\/p>\n<p>Cases of vasculitis resulting in severe complications and death have been reported in clients receiving propylthiouracil therapy. If vasculitis is suspected, discontinue therapy and initiate appropriate intervention.<\/p>\n<p>Propylthiouracil crosses the placenta and can cause fetal liver failure, a goiter, and cretinism if administered to a pregnant woman.<\/p>\n<p><strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take the medication as directed at regular dosing intervals. They should monitor their weight 2-3 times per week. Additionally, clients should be advised that medications may cause drowsiness, and they should report any signs of sore throat, fever, headache, jaundice, bleeding, or bruising.<\/p>\n<h3>Osteoporosis Medication: Calcitonin<\/h3>\n<p><strong>Mechanism of Action: <\/strong>Calcitonin is a calcitonin receptor agonist. Calcitonin is released by the thyroid gland. It acts primarily on bone and also has effects on the kidneys and the gastrointestinal tract.<\/p>\n<p><strong>Indications: <\/strong>Calcitonin is used to treat osteoporosis.<\/p>\n<p><strong>Nursing Considerations: <\/strong>Calcitonin is administered via nasal spray with one spray in one side of the nose daily. See Figure 9.23<sup><a class=\"footnote\" title=\"\u201cNasal Spray\u201d by\u00a0NIAID\u00a0is licensed under\u00a0CC BY 2.0\" id=\"return-footnote-402-10\" href=\"#footnote-402-10\" aria-label=\"Footnote 10\"><sup class=\"footnote\">[10]<\/sup><\/a><\/span><\/sup>\u00a0for an image of calcitonin nasal spray.\u00a0The nasal spray pump should be primed before the first administration. Unopened calcitonin can be stored in the refrigerator until opened but should not be refrigerated between doses. Opened bottles stored at room temperature should be discarded after 30 days of initial dose.<\/p>\n<p><strong>Side Effects\/Adverse Effects:<\/strong> Adverse effects include serious hypersensitivity reactions (bronchospasm, swelling of the tongue or throat, anaphylaxis and anaphylactic shock), hypocalcemia, nasal mucosa adverse events, and malignancy.<\/p>\n<p>Calcitonin should not be used during pregnancy.<\/p>\n<p><strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should be advised to take medications as directed. They should report any signs of hypercalcemia or an allergic response. Clients should receive instruction on the process of self-injection. They should also be advised that they may experience flushing and warmth following injection. Post-menopausal women should adhere to a diet high in calcium and vitamin D and should be educated regarding the importance of exercise for reversing bone loss.<sup><a class=\"footnote\" title=\"uCentral from Unbound Medicine. https:\/\/www.unboundmedicine.com\/ucentral\" id=\"return-footnote-402-11\" href=\"#footnote-402-11\" aria-label=\"Footnote 11\"><sup class=\"footnote\">[11]<\/sup><\/a><\/sup><\/p>\n<p>&nbsp;<\/p>\n<figure style=\"width: 498px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"\" title=\"&quot;Nasal Spray&quot; by NIAID is licensed under CC BY 2.0\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2025\/01\/image17-5.png\" alt=\"Photo showing woman using nasal spray.\" width=\"498\" height=\"387\" \/><figcaption class=\"wp-caption-text\">Figure 9.23 Administration of Calcitonin<\/figcaption><\/figure>\n<h3>Osteoporosis Medication: Alendronate<\/h3>\n<p><strong>Mechanism of Action: <\/strong>Alendronate is a bisphosphonate that inhibits osteoclast-mediated bone resorption. By preventing the breakdown of bone and enhancing the formation of new bone, alendronate assists in reversing bone loss and decreases the risk of fractures.<\/p>\n<p><strong>Indications: <\/strong>Alendronate is used for the prevention and treatment of osteoporosis in postmenopausal women, to increase bone mass in men with osteoporosis, and for glucocorticoid-induced osteoporosis.<\/p>\n<p><strong>Nursing Considerations: <\/strong>Check dosages carefully because some formulations are administered daily, whereas others are administered weekly. Alendronate should be taken after arising for the day but should be administered at least one-half hour before the first food, beverage, or medication of the day with plain water only. Other beverages (including mineral water), food, and some medications are likely to reduce the absorption of alendronate. Clients should not lie down for at least 30 minutes and until after their first food of the day. Clients may also require calcium and vitamin D supplementation, especially if concurrently taking glucocorticoids.<\/p>\n<p>Alendronate is contraindicated in the following conditions: pregnancy, hypocalcemia, the inability to sit or stand for 30 minutes after swallowing, esophageal abnormalities that delay emptying, and clients at risk for aspiration. Alendronate is not recommended for clients with kidney disease with creatinine clearance less than 35 mL\/min.<\/p>\n<p>Discontinue alendronate if severe musculoskeletal pain occurs. A bone mineral density measurement should be made at the initiation of therapy and repeated after 6 to 12 months of combined alendronate and glucocorticoid treatment.<\/p>\n<p><strong>Side Effects\/Adverse Effects: <\/strong>Side effects include upper GI disturbances, severe musculoskeletal pain, and risk of osteonecrosis of the jaw.<\/p>\n<p><strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take medication as directed at the same time each day, first thing in the morning. Clients should remain upright after they take medication for 30 minutes to minimize stomach and esophageal irritation. Clients should eat a balanced diet and may seek advice from the health care provider regarding supplementation with calcium and vitamin D. Clients should participate in regular exercise to help increase bone strength.<sup><a class=\"footnote\" title=\"uCentral from Unbound Medicine. https:\/\/www.unboundmedicine.com\/ucentral\" id=\"return-footnote-402-12\" href=\"#footnote-402-12\" aria-label=\"Footnote 12\"><sup class=\"footnote\">[12]<\/sup><\/a><\/sup><\/p>\n<h3>Osteoporosis: Calcium + Vitamin D<\/h3>\n<p><strong>Mechanism of Action: <\/strong>Calcium and vitamin D are essential nutrients that play a vital role in bone health. Calcium is necessary for the formation and maintenance of healthy bones, while vitamin D helps the body absorb and use calcium.<\/p>\n<p><strong>Indications: <\/strong>Calcium and vitamin D supplements are often prescribed to prevent and treat osteoporosis, as they help maintain bone density and strength.<\/p>\n<p><strong>Nursing Considerations: <\/strong>The therapeutic effects of calcium and vitamin D supplements may vary depending on the individual&#8217;s health status and the presence of any underlying medical conditions.<\/p>\n<p><strong>Side Effects\/Adverse Effects: <\/strong>Side effects include hypercalcemia, kidney stones, and gastrointestinal problems such as constipation, bloating, and abdominal discomfort.<\/p>\n<p><strong>Health Teaching &amp; Health Promotion: <\/strong>Clients should take with food to enhance absorption and monitor for signs of hypercalcemia such as kidney stones and gastrointestinal upset.<\/p>\n<p>Now let\u2019s take a closer look at the medication grid comparing thyroid and osteoporosis medications in Table 9.5.<sup><a class=\"footnote\" title=\"This work is a derivative of DailyMed by U.S. National Library of Medicine in the Public Domain.\" id=\"return-footnote-402-13\" href=\"#footnote-402-13\" aria-label=\"Footnote 13\"><sup class=\"footnote\">[13]<\/sup><\/a><\/sup> Medication grids are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication. Basic information related to each class of medication is outlined below. Detailed information on a specific medication can be found for free at <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/index.cfm\" target=\"_blank\" rel=\"noopener\">DailyMed<\/a>. On the home page, enter the drug name in the search bar to read more about the medication. Prototype\/generic medications listed in the grids below are also linked to a DailyMed page.<\/p>\n<p>Table 9.5 Thyroid and Osteoporosis Medications Grid<\/p>\n<table class=\"grid\">\n<tbody>\n<tr>\n<th class=\"shaded\" scope=\"col\"><strong>Class\/Subclass<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Prototype\/Generic<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Nursing <\/strong><strong>Considerations<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Therapeutic Effects<\/strong><\/th>\n<th class=\"shaded\" scope=\"col\"><strong>Side\/Adverse Effects<\/strong><\/th>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Thyroid Replacement<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=686ba2cf-7651-44de-9b4d-eeaaf2a0e364\" target=\"_blank\" rel=\"noopener noreferrer\">levothyroxine<\/a><\/td>\n<td>Take levothyroxine sodium tablets with a full glass of water as the tablet may rapidly disintegrate<\/p>\n<p>Administer levothyroxine as a single daily dose, on an empty stomach, one-half to one hour before breakfast<\/p>\n<p>Administer levothyroxine at least four hours before or after drugs known to interfere with levothyroxine sodium tablets absorption<\/p>\n<p>Anticipate lower dosages in elderly clients with preexisting cardiac disease<\/p>\n<p>May interact with several medications, so read drug label thoroughly on initial administration for potential effects<\/td>\n<td>Increases T4 levels in hypothyroidism<\/td>\n<td>Hypersensitivity reactions<\/p>\n<p>Cardiac dysrhythmias<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Antithyroid<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a57c49ae-d659-49fa-84e3-cf6d1f9e6f97\" target=\"_blank\" rel=\"noopener noreferrer\">propylthiouracil <\/a><a class=\"rId60\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a57c49ae-d659-49fa-84e3-cf6d1f9e6f97\">(PTU)<\/a><\/td>\n<td>Usually administered every eight hours<\/p>\n<p>May cause hypothyroidism, so TSH and T4 levels should be monitored<\/p>\n<p>If a client becomes pregnant, immediately notify health care provider because it can cause fetal harm<\/td>\n<td>Inhibit production of T4<\/td>\n<td>Hypothyroidism<\/p>\n<p>Liver failure<\/p>\n<p>Agranulocytosis<\/p>\n<p>Vasculitis<\/p>\n<p>Fetal harm<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Calcium Regulator<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=c82eb602-12e1-692b-d660-f8d5b5736b54\" target=\"_blank\" rel=\"noopener noreferrer\">calcitonin<\/a><\/td>\n<td>Administer nasal spray with one spray in one side of the nose daily<\/p>\n<p>Contraindicated during pregnancy<\/p>\n<p>Discard unrefrigerated bottle after 30 days of opening<\/p>\n<p>May store unopened bottles in refrigerator until expiration date<\/td>\n<td>Treats osteoporosis<\/td>\n<td>Serious hypersensitivity reactions (bronchospasm, swelling of the tongue or throat, anaphylaxis, and anaphylactic shock)<\/p>\n<p>Hypocalcemia<\/p>\n<p>Nasal mucosa adverse effects<\/p>\n<p>Malignancy<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Bisphosphonates<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=a24fd39c-34a7-4de2-9439-781e612189ca\" target=\"_blank\" rel=\"noopener noreferrer\">alendronate<\/a><\/td>\n<td>Administered on rising and at least one-half hour before the first food, beverage, or medication of the day with plain water only<\/p>\n<p>The client should sit or stand for 30 minutes after administration<\/p>\n<p>Contraindicated in pregnancy, hypocalcemia, and kidney disease<\/p>\n<p>Concurrent calcium and vitamin D supplements may be required<\/td>\n<td>Enhances bone mineral density in osteoporosis<\/td>\n<td>Upper GI tract adverse events<\/p>\n<p>Severe musculoskeletal pain<\/p>\n<p>Risk of osteonecrosis of the jaw<\/td>\n<\/tr>\n<tr>\n<th scope=\"row\"><strong>Herbal<\/strong><\/th>\n<td><a class=\"arrow\" href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/drugInfo.cfm?setid=e84dc181-3dd8-48ca-b1fb-03fb13313369\" target=\"_blank\" rel=\"noopener\">calcium &#8211; vitamin D<\/a><\/td>\n<td>Supplement should be taken with meal, as it is better absorbed with food<\/td>\n<td>Improve calcium absorption and bone health<\/td>\n<td>Constipation, bloating, and abdominal discomfort. High doses may lead to hypercalcemia<\/p>\n<p>Use with caution in clients with kidney stone, hyperparathyroidism, or those with vitamin D toxicity<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>&nbsp;<\/p>\n<\/div>\n<div class=\"__UNKNOWN__\">\n<div class=\"textbox textbox--examples\">\n<header class=\"textbox__header\">\n<h2>Critical Thinking Activity 9.5<img loading=\"lazy\" decoding=\"async\" class=\"alignright size-thumbnail wp-image-67\" src=\"https:\/\/pressbooks.ccconline.org\/accdigitalmarketing\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1-150x150.png\" alt=\"Image of a circle containing a speech bubble with a question mark in it.\" width=\"150\" height=\"150\" srcset=\"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1-150x150.png 150w, https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1-65x65.png 65w, https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1-225x225.png 225w, https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-content\/uploads\/sites\/219\/2019\/10\/ORN-Icons_internet-copy_internet-copy-300x300-1.png 300w\" sizes=\"auto, (max-width: 150px) 100vw, 150px\" \/><\/h2>\n<\/header>\n<div class=\"textbox__content\" style=\"text-align: left\">\n<p>A client has been diagnosed with hypothyroidism and receives a prescription for levothyroxine.<\/p>\n<p>What health teaching should the nurse provide regarding this medication?<\/p>\n<p>Note: Answers to the Critical Thinking activities can be found in the &#8220;<a href=\"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/chapter-9\/\" target=\"_blank\" rel=\"noopener\">Answer Key<\/a>&#8221; section at the end of the book.<\/p>\n<\/div>\n<\/div>\n<\/div>\n<hr class=\"before-footnotes clear\" \/><div class=\"footnotes\"><ol><li id=\"footnote-402-1\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1811_The_Thyroid_Gland.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1811 The Thyroid Gland.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/3.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 3.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland<\/a> <a href=\"#return-footnote-402-1\" class=\"return-footnote\" aria-label=\"Return to footnote 1\">&crarr;<\/a><\/li><li id=\"footnote-402-2\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1813_A_Classic_Negative_Feedback_Loop.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1813 A Classic Negative Feedback Loop.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 4.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-4-the-thyroid-gland<\/a> <a href=\"#return-footnote-402-2\" class=\"return-footnote\" aria-label=\"Return to footnote 2\">&crarr;<\/a><\/li><li id=\"footnote-402-3\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Goitre.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">Goitre.jpg<\/a>\u201d by <a href=\"https:\/\/en.wikipedia.org\/wiki\/User:Almazi\" target=\"_blank\" rel=\"noopener noreferrer\">Almazi<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC0<\/a> <a href=\"#return-footnote-402-3\" class=\"return-footnote\" aria-label=\"Return to footnote 3\">&crarr;<\/a><\/li><li id=\"footnote-402-4\">American Thyroid Association. (2019). <em>Radioactive iodine<\/em>. <a href=\"https:\/\/www.thyroid.org\/radioactive-iodine\/\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.thyroid.org\/radioactive-iodine\/<\/a> <a href=\"#return-footnote-402-4\" class=\"return-footnote\" aria-label=\"Return to footnote 4\">&crarr;<\/a><\/li><li id=\"footnote-402-5\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1814_The_Parathyroid_Glands.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1814 The Parathyroid Glands.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax College<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/3.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 3.0.<\/a> Access for free at <a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands<\/a> <a href=\"#return-footnote-402-5\" class=\"return-footnote\" aria-label=\"Return to footnote 5\">&crarr;<\/a><\/li><li id=\"footnote-402-6\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1817_The_Role_of_Parathyroid_Hormone_in_Maintaining_Blood_Calcium_Homeostasis.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">1817 The Role of Parathyroid Hormone in Maintaining Blood Calcium Homeostasis.jpg<\/a>\u201d by <a href=\"https:\/\/openstax.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">OpenStax<\/a> is licensed under <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 4.0.<\/a> Access for free at<a href=\"https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands\" target=\"_blank\" rel=\"noopener noreferrer\"> https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-5-the-parathyroid-glands<\/a> <a href=\"#return-footnote-402-6\" class=\"return-footnote\" aria-label=\"Return to footnote 6\">&crarr;<\/a><\/li><li id=\"footnote-402-7\">\u201c<a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Levothyroxine_25mcg_Tablets.jpg\" target=\"_blank\" rel=\"noopener noreferrer\">Levothyroxine 25mcg Tablets.jpg<\/a>\u201d by<a href=\"https:\/\/commons.wikimedia.org\/w\/index.php?title=User:Ash&amp;action=edit&amp;redlink=1\" target=\"_blank\" rel=\"noopener noreferrer\">\u00a0User:Ash<\/a>\u00a0is licensed under\u00a0<a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC0<\/a><span style=\"font-size: 12.8px\"> <a href=\"#return-footnote-402-7\" class=\"return-footnote\" aria-label=\"Return to footnote 7\">&crarr;<\/a><\/li><li id=\"footnote-402-8\">This work is a derivative of <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/\" target=\"_blank\" rel=\"noopener noreferrer\">DailyMed<\/a> by <a href=\"https:\/\/www.nlm.nih.gov\/\" target=\"_blank\" rel=\"noopener noreferrer\">U.S. National Library of Medicine<\/a> in the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/\" target=\"_blank\" rel=\"noopener noreferrer\">Public Domain<\/a>.  <a href=\"#return-footnote-402-8\" class=\"return-footnote\" aria-label=\"Return to footnote 8\">&crarr;<\/a><\/li><li id=\"footnote-402-9\">uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a> <a href=\"#return-footnote-402-9\" class=\"return-footnote\" aria-label=\"Return to footnote 9\">&crarr;<\/a><\/li><li id=\"footnote-402-10\">\u201c<a href=\"https:\/\/www.flickr.com\/photos\/niaid\/46057881342\" target=\"_blank\" rel=\"noopener noreferrer\">Nasal Spray<\/a>\u201d by\u00a0<a href=\"https:\/\/www.flickr.com\/photos\/niaid\/\" target=\"_blank\" rel=\"noopener noreferrer\">NIAID<\/a>\u00a0is licensed under\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/\" target=\"_blank\" rel=\"noopener noreferrer\">CC BY 2.0<\/a><span style=\"font-size: 12.8px\"> <a href=\"#return-footnote-402-10\" class=\"return-footnote\" aria-label=\"Return to footnote 10\">&crarr;<\/a><\/li><li id=\"footnote-402-11\">uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a> <a href=\"#return-footnote-402-11\" class=\"return-footnote\" aria-label=\"Return to footnote 11\">&crarr;<\/a><\/li><li id=\"footnote-402-12\">uCentral from Unbound Medicine. <a href=\"https:\/\/www.unboundmedicine.com\/ucentral\" target=\"_blank\" rel=\"noopener noreferrer\">https:\/\/www.unboundmedicine.com\/ucentral<\/a> <a href=\"#return-footnote-402-12\" class=\"return-footnote\" aria-label=\"Return to footnote 12\">&crarr;<\/a><\/li><li id=\"footnote-402-13\">This work is a derivative of <a href=\"https:\/\/dailymed.nlm.nih.gov\/dailymed\/\" target=\"_blank\" rel=\"noopener noreferrer\">DailyMed<\/a> by <a href=\"https:\/\/www.nlm.nih.gov\/\" target=\"_blank\" rel=\"noopener noreferrer\">U.S. National Library of Medicine<\/a> in the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/\" target=\"_blank\" rel=\"noopener noreferrer\">Public Domain<\/a>. <a href=\"#return-footnote-402-13\" class=\"return-footnote\" aria-label=\"Return to footnote 13\">&crarr;<\/a><\/li><\/ol><\/div><div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_402_659\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_659\"><div tabindex=\"-1\"><p>A visible enlargement of the thyroid gland when there is hyperstimulation of TSH due to deficient levels of T3 and T4 hormones in the bloodstream or an autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland, causing hyperthyroidism.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_402_600\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_600\"><div tabindex=\"-1\"><p>Abnormally low blood levels of thyroid hormones T3 and T4 in the bloodstream.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_402_601\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_601\"><div tabindex=\"-1\"><p>Abnormally elevated blood level of thyroid hormones T3 and T4, often caused by a pituitary tumor, thyroid tumor, or autoimmune reaction in which antibodies overstimulate the follicle cells of the thyroid gland.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_402_602\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_602\"><div tabindex=\"-1\"><p>The hormone released by parathyroid glands and is involved in the regulation of blood calcium levels.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_402_603\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_603\"><div tabindex=\"-1\"><p>A disorder caused by an overproduction of PTH that results in excessive calcium resorption from bone, causing significantly decreased bone density and spontaneous fractures, decreased responsiveness of the nervous system, and calcium deposits in the body\u2019s tissues and organs, impairing their functioning.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_402_604\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_402_604\"><div tabindex=\"-1\"><p>Abnormally low blood calcium levels caused by parathyroid hormone deficiency, which may develop following thyroid surgery. Low blood calcium can cause muscle twitching, cramping, spasms, or convulsions; severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><\/div>","protected":false},"author":83,"menu_order":5,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[48],"contributor":[],"license":[],"class_list":["post-402","chapter","type-chapter","status-publish","hentry","chapter-type-numberless"],"part":370,"_links":{"self":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapters\/402","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/wp\/v2\/users\/83"}],"version-history":[{"count":2,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapters\/402\/revisions"}],"predecessor-version":[{"id":771,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapters\/402\/revisions\/771"}],"part":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/parts\/370"}],"metadata":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapters\/402\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/wp\/v2\/media?parent=402"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/pressbooks\/v2\/chapter-type?post=402"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/wp\/v2\/contributor?post=402"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/wp-json\/wp\/v2\/license?post=402"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}