Thyroid hormones drug administration

Once a euthyroid state is achieved, tlie primary health care provider may add a thyroid hormone to tlie therapeutic regimen to prevent or treat hypothyroidism, which may develop slowly during long-term antithyroid drug therapy or after administration of 131I. 

Metaproterenol (Alupent, Metaprel) [Bronchodilator/ Beta-Adrenergic Agonist] Uses Asthma reversible bronchospasm Action Sympathomimetic bronchodilator Dose Adults. Neb 0.2-0.3 mL in 2.5-3.0 mL of NS Peds. Neb 0.1-0.2 mL/kg of a 5% soln in 2.5 mL NS Caution [C, /-] Contra Tach, other arrhythmias Disp Aerosol 0.65 mg/inhal soln for inhal 0.4, 0.6% tabs 10, 20 mg syrup 10 mg/5 mL SE Nervousness, tremors (common), tach, HTN Interactions T Effects W/ sympathomimetic drugs, xanthines T risk of arrhythmias W/ cardiac glycosides, halothane, levodopa, theophylline, thyroid hormones T HTN W/ MAOIs effects W/ BBs EMS Separate additional aerosol use by 5 min fewer 3i effects than isoproterenol longer-acting monitor lung sounds before/after administration... 

The clinical manifestations of hyperthyroidism and hypothyroidism are listed in Table 31-2. From a pharmacotherapeutic standpoint, hyperthyroidism is treated with drugs that attenuate the synthesis and effects of thyroid hormones. Hypothyroidism is usually treated by thyroid hormone administration (replacement therapy). The general aspects and more common forms of hyperthyroidism and hypothyroidism are discussed here, along with the drugs used to resolve these primary forms of thyroid dysfunction. 

Treatment of metastatic differentiated thyroid cancer requires the administration of large doses of 131I (30-200 mCi) in the presence of persistently high serum levels of TSH (see Chapter 38 Thyroid Antithyroid Drugs). Patients must withdraw from thyroid hormone replacement in order to achieve this. For treatment purposes, thyrotropin alpha administration cannot substitute for thyroid hormone withdrawal. 

Pharmacokinetics Both T4 and T3 are absorbed after oral administration. T4 is converted to T3 by one of two distinct deio-dinases, depending on the tissue. T3 combines with a receptor to stimulate subsequent protein synthesis necessary for normal metabolism. The hormones are metabolized through the microsomal P-450 system. Drugs such as phenytoin, rifampin, phe-nobarbital, etc. that induce the P-450 enzymes accelerate metabolism of the thyroid hormones. 

Administration of testosterone (C14, J4), thyroid hormones (M19), and ACTH (E5) has been shown to result in elevation of serum copper levels. The latter effect could have been due to contamination of the ACTH preparation with melanotropin (A2). Antithyroid drugs produce a fall in serum copper levels (F7). 

Increased pentose excretion has been shown to follow experimental trauma, after craniofacial injuries in man, in response to cold exposure, and following the administration of thyroid hormone or cortisone. Drug-induced pentosuria has been known for a long time, but it has not been well studied. Morphine is the best-known inducer of pentosuria antipyretics have a similar effect. Urinary pentose increases in response to fever and during allergic responses (T4). 

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. 

Food and Drug Administration, United States Food Drug and Cosmetics Third National Health and Nutrition Examination Survey Thyroid-stimulating hormone United States Department of Agriculture... 

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