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By David G. Ferriman

ISBN-10: 0723602050

ISBN-13: 9780723602057

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A change in antithyroid agent is called for. (iv) Enlargement of retrosternal goitre, with pressure phenomena. c. —Acceptability. —(i) Assessment of correct dosage difficult. HYPERTHYROIDISM 39 (ii) Maximum effect not visible for 3 months, (in) High incidence of long-term hypothyroidism, caused by radioactive damage to regenerative capacity of thyroid cells. At one time it was feared that 131I therapy might predispose to carcinoma of the thyroid. This is not now considered likely. However, it is best avoided in younger subjects, and particularly in children.

The precise order in which these enzymatic actions takes place is not certain. Many compounds have been isolated from the adrenal cortex and are classified according to their principal effects:— 1. ' Glucocorticoids ' (cortisol, corticosterone). 2. 'Mineralocorticoids' (aldosterone). 3. 'Androgens' (dehydroepiandrosterone sulphate, androstendione, androsterone ; trace of testosterone—can be greatly increased in tumours). 52 T H E ADRENAL GLANDS—ADRENAL CORTEX Adrenal Cortex—Physiology, continued.

Lodothyronine derivatives such as T3 or T4 acetic acids are formed in tissues and may be the ultimately active forms of these hormones. T3 or T4 acetic acids are potent metabolic stimulants. Ultimately they are de-iodoinated and the iodine recycled. Iodothyronines appear to act by uncoupling oxidative phosphorylation, leading to dissipation of energy as heat. Biological half-life of T4 is around 6-7 days, t h a t of T3 around 2-3 days. —Thyroxine is secreted in the bile as glueuronide but this is hydrolysed in the gut and the thyroxine reabsorbed.

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A Synopsis of Endocrinology and Metabolism by David G. Ferriman

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