Hyperthyroidism Thyrotoxicosis

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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. 

The symptoms of hypothyroidism and hyperthyroidism are given in Table 51-1. A severe form of hyperthyroidism, called thyrotoxicosis or tiiyroid storm, is characterized by high fever, extreme tachycardia, and altered mental status. Thyroid hormones are used to treat hypothyroidism and antithyroid... 

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. 

Iodine excess (including radiocontrast, amiodarone) Thyrotoxicosis without hyperthyroidism Subacute thyroiditis Silent (painless) thyroiditis... 

Secondary hyperthyroidism TSH-secreting pituitary tumors Trophoblastic (hCG-secreting) tumors Gestational thyrotoxicosis... 

Subclinical or mild thyrotoxicosis is defined as a low TSH with a normal FT4 level. While there may be few or no symptoms in these patients, there are several areas of concern.31,32 Many patients will progress to overt thyrotoxicosis. Patients with subclinical hyperthyroidism have been shown to suffer long-term cardiovascular and bone sequelae. In a 10-year follow-up of 2007 patients over age 60,33 patients with an undetectable TSH level had a 3.1-fold increased risk of atrial fibrillation versus those with a normal TSH. In a different 10-year follow-up study34 of... 

Treatment of thyrotoxicosis due to hyperthyroidism is similar, regardless of the underlying cause. The goals of treating hyperthyroidism are to relieve symptoms, to reduce thyroid hormone production to normal levels and achieve biochemical euthyroidism, and to prevent long-term adverse sequelae. 

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. 

Hyperthyroidism results from excess production of thyroid hormones due to various reasons. Treatment of the resulting thyrotoxicosis (Basedow s disease) consists of using... 

Thyrotoxicosis -adrenergic blockers may mask clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm. 

As the symptoms of hyperthyroidism mimic in many aspects those of sympathic stimulation propranolol, and probably also other non-selective beta blockers (see Chapter 20), give rapid relieve in thyrotoxicosis while having no effect on the underlying disease. 

The manifestations of hyperthyroidism depend on the severity of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Of the various types of hyperthyroidism, only two are common Graves disease and toxic multinodular goiter. Less common causes include toxic adenoma and postpartum thyroiditis, among others. 

Thyrotoxic crisis, thyroid storm, or accelerated hyperthyroidism is an extreme accentuation of thyrotoxicosis. Although uncommon, this serious complication of hyperthyroidism usually occurs in association with Grave s disease and occasionally with toxic multinodular goiter. 

In addition, the metabohsm of OCAs results in the release of large amounts of E into the circulation. As described for KI, I released from OCAs may have effects at the thyroid gland and if used alone to treat hyperthyroidism, OCAs carry the same potential to induce increased secretion of thyroid hormone and exacerbation of thyrotoxicosis. When an OCA is used in the treatment of hyperthyroidism, large doses of antithyroid agents are usually administered concomitantly. However, the combination of OCAs and antithyroid drugs may cause resistance to the antithyroid drugs with time, presumably because of the elevation in intrathyroidal 1 content. Thus, it is recommended that the use of OCAs be reserved for short-term treatment of patients with severe thyrotoxicosis and significant comorbidity (e.g., myocardial infarction, sepsis, stroke) for rapid control of plasma Tj concentrations. 

Beta blockers without intrinsic sympathomimetic activity (eg, metoprolol, propranolol, atenolol) are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with sympathetic stimulation. Propranolol has been the 3 blocker most widely studied and used in the therapy of thyrotoxicosis. Beta blockers cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels. Propranolol at doses greater than 160 mg/d may also reduce T3 levels approximately 20% by inhibiting the peripheral conversion of T4 to T3. 

Hyperthyroidism (thyrotoxicosis) is the clinical syndrome that results when tissues are exposed to high levels of thyroid hormone (Table 38-4). 

Dobyns BM, Sheline GE, Workman JB, Tompkins EA, McConahey WM, Becker DV. Malignant and benign neoplasms of the thyroid in patients treated for hyperthyroidism a report of the cooperative thyrotoxicosis therapy follow-up study. J Clin Endocrinol Metab 1974 38(6) 976-98. 

Potassium perchlorate is a thyrostatic drug that is still used (in a dose of 1000 mg/day or more) as an alternative to the thionamides, especially in cases of allergy. It has also been used to treat the iodine-induced form of thyrotoxicosis, such as type 1 hyperthyroidism due to amio-darone (qv). 

Patients with beta-thalassemia major have an increased risk of primary hypothyroidism. In 23 patients with beta-thalassemia amiodarone was associated with a high risk of overt hypothyroidism (33 versus 3% in controls) (43). This occurred at up to 3 months after starting amiodarone. The risk of subclinical hypothyroidism was similar in the two groups. In one case overt hypothyroidism resolved spontaneously after withdrawal, but the other patients were given thyroxine. After 21-47 months of treatment three patients developed thyrotoxicosis, with remission after withdrawal. There were no cases of hyperthyroidism in the controls. The authors proposed that patients with beta-thalassemia may be more susceptible to iodine-induced hypothyroidism, related to an underlying defect in iodine in the thyroid, perhaps associated with an effect of iron overload. 

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