Thyroid gland consequences

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. 

Half-lives span a very wide range (Table 17.5). Consider strontium-90, for which the half-life is 28 a. This nuclide is present in nuclear fallout, the fine dust that settles from clouds of airborne particles after the explosion of a nuclear bomb, and may also be present in the accidental release of radioactive materials into the air. Because it is chemically very similar to calcium, strontium may accompany that element through the environment and become incorporated into bones once there, it continues to emit radiation for many years. About 10 half-lives (for strontium-90, 280 a) must pass before the activity of a sample has fallen to 1/1000 of its initial value. Iodine-131, which was released in the accidental fire at the Chernobyl nuclear power plant, has a half-life of only 8.05 d, but it accumulates in the thyroid gland. Several cases of thyroid cancer have been linked to iodine-131 exposure from the accident. Plutonium-239 has a half-life of 24 ka (24000 years). Consequently, very long term storage facilities are required for plutonium waste, and land contaminated with plutonium cannot be inhabited again for thousands of years without expensive remediation efforts. 

Reports of the effects of Li+ upon the thyroid gland and its associated hormones are the most abundant of those concerned with the endocrine system. Li+ inhibits thyroid hormone release, leading to reduced levels of circulating hormone, in both psychiatric patients and healthy controls [178]. In consequence of this, a negative feedback mechanism increases the production of pituitary TSH. Li+ also causes an increase in hypothalamic thyroid-releasing hormone (TRH), probably by inhibiting its re-... 

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. 

Goiter enlargement of the thyroid gland as a consequence of inadequate dietary iodine. 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

CN intoxication may result in morphological and functional adverse effects in specific organ systems or tissues as a consequence of acute or repeated exposure to CN. These include both direct adverse reactions to and lesions of the respiratory, cardiovascular and central nervous systems. Secondary toxic effects, from SCN, may occur with the thyroid gland. These organ and tissue effects are summarized below. 

The drug fails to cause interference with the release or usage of accumulated thyroid hormone and the time-gap that essentially elapses between the very initial stage of medication together with the manifestations of its antithyroid activity entirely depends upon the quantum of thyroid hormone present in the gland (thyroid). The resulting marked and pronormced hyperplasia of the thyroid gland which follows soonafter its administration, in fact, is a consequence of a compensatory enhancement of thyroprotein release as a result in the thyroid hormone titer value of the blood. 

Iodine deficiency with impairment of thyroid hormone production may have severe consequences. To compensate for the low iodine supply that was previously highly prevalent in the world, complex mechanisms have been developed in the thyroid gland. On the one hand, mechanisms are able to accumulate and utilize even very small supplies of iodine. On the other hand, the thyroid immediately reacts to a sudden load of iodine to avoid overproduction of thyroid hormone. As usual when complex mechanisms are involved, this leads to a risk of malfunction — and disease. To minimize such a risk at the level of the population, iodine intake is best kept within a relatively narrow range around the recommended level. 

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