Thyroid gland hyperthyroidism

Iodine. Of the 10—20 mg of iodine in the adult body, 70—80 wt % is in the thyroid gland (see Thyroid and antithyroid preparations). The essentiahty of iodine, present in all tissues, depends solely on utilisation by the thyroid gland to produce thyroxine [51-48-9] and related compounds. Well-known consequences of faulty thyroid function are hypothyroidism, hyperthyroidism, and goiter. Dietary iodine is obtained from eating seafoods and kelp and from using iodized salt. 

The selective uptake of iodide ion by the thyroid gland is the basis of radioiodine treatment in hyperthyroidism, mainly with although various other radioactive isotopes ate also used (40,41). With a half-life of eight days, the decay of this isotope produces high energy P-particles which cause selective destmction within a 2 mm sphere of their origin. The y-rays also emitted are not absorbed by the thyroid tissue and are employed for external scanning. 

Hyperthyroidism, that is, the overproduction of thyroid hormones, is usually treated by surgical removal of the thyroid gland. Before such a procedure is undertaken, the hyperthyroidism is usually first brought under control by treatment with so-called antithyroid agents. 

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. 

TSH-induced hyperthyroidism is diagnosed by evidence of peripheral hypermetabolism, diffuse thyroid gland enlargement, elevated free thyroid hormone levels, and elevated serum immunoreactive TSH concentrations. Because the pituitary gland is extremely sensitive to even minimal elevations of free T4, a normal or elevated TSH level in any thyrotoxic patient indicates inappropriate production of TSH. 

Diseases associated with thyroid glands are the result of either excess production of thyroid hormone (hyperthyroidism), or its insufficiency (hypothyroidism). Both cases can result in a goiter. 

In a hyperfunctioning of the thyroid gland, secretion of an excess quantity of thyroid hormones leads to a hyperthyroid condition (Basedow s disease, goiter). In this condition, drags are used that suppress production of thyrotropic hormones in the anterior lobe of the hypophysis (diiodotyrosine), in the thyroid gland (propylthiouracil, methylthiouracil,... 

Drugs used for hyperthyroidism can be classified as drugs that suppress thyroid hormone synthesis in the anterior lobe of the hypophysis, and they consist of diiodotyrosine and iodine, as well as drugs that suppress thyroid hormone synthesis in thyroid glands (propylthiouracil, methylthiouracil, methimazole, and carbimazole). 

Pretreatment with antithyroid drugs is necessary to avoid the risk of thyroid storm (exacerbation of hyperthyroidism with fever and tachycardia) in the following groups the elderly, people with cardiac disease, and people with severe hyperthyroidism. Antithyroid drugs should be stopped at least 4 days before radioactive iodine is given, and restarted no sooner than 3 days after, to permit uptake of the iodine into the thyroid gland. Antithyroid drugs can usually be stopped after 2-6 weeks as the radioactive iodine takes effect. 

Worldwide, the most common thyroid disorder is hypothyroidism resulting from dietary iodine deficiency. In iodine-replete areas of the world, most thyroid disorders are the result of autoimmune disease. The symptoms manifested in hypothyroid and hyperthyroid states are largely independent of any underlying disorder of the thyroid gland itself they are a function of the degree of hormone deficiency or excess. 

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. 

Like iodine, astatine tends to accumulate in the thyroid gland of the living animal (31). The radioactivity of the element thus concentrated seems to cause severe damage to thyroid tissue without affecting the adjacent parathyroid glands. It may therefore be useful in cases of hyperthyroidism (32). Therefore it is important to determine the amount... 

The most serious complication of hyperthyroidism is thyroid storm (thyrotoxic crisis). This is an acute exacerbation of hyperthyroidism with marked tachycardia, fever, mental status changes and haemodynamic collapse. It is usually precipitated by acute illness, trauma, parturition or surgery, especially of the thyroid gland. The mortality rate is 20-30%, even with aggressive treatment, due to cardiac failure, arrhythmias or hyperthermia. 

Her weight is 136 lb (61.8 kg), an increase of 10 lb (4.5 kg) in the last year. Her thyroid gland is not palpable and her reflexes are delayed. Laboratory findings include a thyroid-stimulating hormone (TSH) level of 14.9 pIU/mL and a free thyroxine level of 8 pmol/L. Evaluate the management of her past history of hyperthyroidism. Identify the available treatment options for control of her current thyroid status. 

The thyroid gland also regulates its uptake of iodide and thyroid hormone synthesis by intrathyroidal mechanisms that are independent of TSH. These mechanisms are primarily related to the level of iodine in the blood. Large doses of iodine inhibit iodide organification (Wolff-Chaikoff block, see Figure 38-1). In certain disease states (eg, Hashimoto s thyroiditis), this can inhibit thyroid hormone synthesis and result in hypothyroidism. Hyperthyroidism can result from the loss of the Wolff-Chaikoff block in susceptible individuals (eg, multinodular goiter). 

Therapeutic Techniques. Probably the most prominent therapeutic use of radiopharmaceuticals is radioactive iodine in the treatment of metastatic thyroid cancer. 131I has a half-life of about 8 days and emits gamma and beta rays. When iodine salts are taken into the body, most of the dose is concentrated in the thyroid gland. A dose of radioactive iodine salt similarly concentrates in the thyroid gland. When there is a cancer in the thyroid gland, or the gland is overactive (hyperthyroidism), the excessive... 

Extensive iodine absorption from povidone-iodine can cause transient hypothyroidism or in patients with latent hypothyroidism the risk of destabilization and thyrotoxic crisis (SEDA-20, 226 SEDA-22, 263). Especially at risk are patients with an autonomous adenoma, localized diffuse autonomy of the thyroid gland, nodular goiter, latent hyperthyroidism of autoimmune origin, or endemic iodine deficiency (51). 

In the treatment of hyperthyroidism the dose of 131I is usually a few millicuries and is either roughly estimated or calculated according to the size of the thyroid gland, the uptake of a tracer dose of iodine, and the type of thyroid disorder (diffuse or nodular), with doses ranging from 80 to 150 microCi (3.0-5.5 MBq) per gram of thyroid tissue (3,4). 

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