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Thyroid hormone excess

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. [Pg.608]

Many disorders are associated with thyroid hormone excess or deficiency in the absence of definable thyroid disease. These states of euthyroid hyperthyroxinemia or euthyroid hypothyroxinemia often result from alterations in the concentration of thyroid hormone—binding proteins, the actions... [Pg.2061]

The clinical signs and symptoms of thyroid hormone excess or deficiency are generally vague and nonspecific (see Box 52-4). Therefore when hypothyroidism or hyperthyroidism is suspected, confirmation with laboratory tests is generally required. Guidelines for the selection of appropriate laboratory tests for thyroid function have been published... [Pg.2063]

M16. Moses, C., Sunder, J. H., Vester, J. W., and Donowski, T. S., Hydrocortisone and/or desiccated thyroid in physiological dosage. XI. Effects of thyroid hormone excesses on lipids and other blood and serum solutes. Metab., Clin. Exptl. 13, 717-728 (1964). [Pg.207]

The main role of the human thyroid gland is production of thyroid hormones (iodinated amino acids), essential for adequate growth, development, and energy metaboHsm (1 6). Thyroid underfunction is an occurrence that can be treated successfully with thyroid preparations. In addition, the thyroid secretes calcitonin (also known as thyrocalcitonin), a polypeptide that lowers excessively high calcium blood levels. Thyroid hyperfunction, another important clinical entity, can be corrected by treatment with a variety of substances known as antithyroid dmgs. [Pg.46]

The common causes of thyrotoxicosis are shown in Table 41-6.29,30 Thyrotoxicosis can be related to the presence or absence of excess hormone production (hyperthyroidism). Graves disease is the most common cause of hyperthyroidism. Thyrotoxicosis in the elderly is more likely due to toxic thyroid nodules or multinodular goiter than to Graves disease. Excessive intake of thyroid hormone may be due to overtreatment with prescribed therapy. Surreptitious use of thyroid hormones also may occur, especially in health professionals or as a self-remedy for obesity. Thyroid hormones can be obtained easily without a prescription from health food stores or Internet sources. [Pg.676]

Excess thyroid hormone intake (thyrotoxicosis factitia)... [Pg.676]

Excess production of thyroid hormone can be reduced in four ways iodides, antithyroid drugs, radioactive iodine, and... [Pg.678]

In patients with excess thyroid hormone production, reduce hormone production with an antithyroid drug and/or radioactive iodine. Choose therapy based on patient-specific factors and preference. [Pg.681]

Hyperthyroidism State caused by excess production of thyroid hormone. [Pg.1568]

Thyrotoxicosis A state caused by an excess of thyroid hormone. [Pg.1578]

In individuals who took thyroid hormones, 80% of the weight lost was lean body mass (muscle and bone) rather than excess fat. People taking these extracts experienced muscle weakness and bone breakdown, which led to a condition called osteoporosis, in which bones are weakened and the risk of bone fractures or breaks is increased. Thyroid hormone extracts also made the heart work harder by increasing metabolism, which led to problems such as increased heart rate, palpitations, and irregular heartbeat. These problems were potentially life threatening When the heart beats abnormally (or not at all), it is unable to pump blood and oxygen to the brain and body. Individuals die suddenly from this condition because the brain can only function for a few minutes without oxygen and nutrients. [Pg.41]

The adult brain is endowed with nuclear as well as cytosolic and membrane T3 receptors that have been visualized by autoradiography and studied biochemically [30-33]. Both neurons and neuropil are labeled by [ 1251]T3, and the labeling is selective across brain regions. Functionally, one of the most prominent features of neural action of thyroid hormone in adulthood is subsensitivity to norepinephrine as a result of a hypothyroid state [27], These changes may be reflections of loss of dendritic spines in at least some neurons of the adultbrain. Clinically, thyroid hormone deficiency increases the probability of depressive illness, whereas thyroid excess increases the probability of mania (Ch. 52) in susceptible individuals [27],... [Pg.854]

Thyrotoxicosis factitia is hyperthyroidism produced by the ingestion of exogenous thyroid hormone. This may occur when thyroid hormone is used for inappropriate indications, when excessive doses are used for accepted medical indications, or when it is used surreptitiously by patients. [Pg.241]

Amiodarone may induce thyrotoxicosis (2% to 3% of patients) or hypothyroidism. It interferes with type I 5 -deiodinase, leading to reduced conversion of T4 to T3, and iodide release from the drug may contribute to iodine excess. Amiodarone also causes a destructive thyroiditis with loss of thyroglobulin and thyroid hormones. [Pg.241]

An elevated 24-hour radioactive iodine uptake (RAIU) indicates true hyperthyroidism the patient s thyroid gland is overproducing T4, T3, or both (normal RAIU 10% to 30%). Conversely, a low RAIU indicates that the excess thyroid hormone is not a consequence of thyroid gland hyperfunction but is likely caused by thyroiditis or hormone ingestion. [Pg.242]

General supportive measures, including acetaminophen as an antipyretic (aspirin or other nonsteroidal antiinflammatory drugs may displace bound thyroid hormone), fluid and electrolyte replacement, sedatives, digoxin, antiarrhythmics, insulin, and antibiotics should be given as indicated. Plasmapheresis and peritoneal dialysis have been used to remove excess hormone in patients not responding to more conservative measures. [Pg.247]

Excessive doses of thyroid hormone may lead to heart failure, angina pectoris, and myocardial infarction. Allergic or idiosyncratic reactions can occur with the natural animal-derived products such as desiccated thyroid and thyroglobulin, but they are extremely rare with the synthetic products used today. Excess exogenous thyroid hormone may reduce bone density and increase the risk of fracture. [Pg.250]


See other pages where Thyroid hormone excess is mentioned: [Pg.352]    [Pg.68]    [Pg.292]    [Pg.2057]    [Pg.778]    [Pg.778]    [Pg.172]    [Pg.678]    [Pg.352]    [Pg.68]    [Pg.292]    [Pg.2057]    [Pg.778]    [Pg.778]    [Pg.172]    [Pg.678]    [Pg.398]    [Pg.386]    [Pg.566]    [Pg.46]    [Pg.48]    [Pg.52]    [Pg.65]    [Pg.97]    [Pg.533]    [Pg.338]    [Pg.268]    [Pg.80]    [Pg.292]    [Pg.669]    [Pg.130]    [Pg.29]    [Pg.41]    [Pg.279]    [Pg.478]    [Pg.95]    [Pg.54]   
See also in sourсe #XX -- [ Pg.481 ]




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