Thyroidal hypothyroidism

Thyroid hormones are still available, with a prescription, for patients with an underactive thyroid (hypothyroidism). These drugs are never given for weight loss. 

Thyroiditis/hypothyroidism 4600 83 % 17 alpha-hydroxylase, thyroid peroxidase Iodine... 

The physiology of amyloid pleural effusions is complex. AL amyloidosis can alter the function of several organs that could contribute to effusion formation including the heart (infiltrative cardiomyopathy—48% cases), kidneys (nephrotic syndrome—65% cases), and thyroid (hypothyroidism—4% cases) (20). 

Thyroid-stimulating hormone can be used clinically to test thyroid function but has not found practical apphcation in the treatment of human thyroid insufficiency. Direct replacement therapy with thyroid hormone is easy and effective, owing to a simple molecular stmcture. TSH has been used in the veterinary treatment of hypothyroidism, and preparations of TSH ate produced by Cooper Animal Health, Inc. and Armour Pharmaceuticals. 

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. 

Myxedema and goiter are the main conditions for which thyroid preparations are indicated. The treatment of cretinism is difficult because it is recognized only at or after birth. Even if this disease could be diagnosed m utero, thyroid hormones do not readily cross the placental barrier. In addition, the fetus, as does a premature infant, rapidly deactivates the thyroid hormones. The halogen-free analogue DlMlT [26384-44-7] (3), which is resistant to fetal deiodinases, may prove useful for fetal hypothyroidism (cretinism). 

The thyroid gland, located in the base of the neck, exerts i key role on growth and metabolism. In contrast with that of some of the other endocrine glands, this control is effected Ihrough a pair of relatively simple molecules, thyroxine, and its close congener, triiodothyronine. Cases of thyroid deficien-cy (hypothyroidism) are common enough to warrant the production... 

Decreased activity of the thyroid gland results in hypothyroidism and, in severe cases, myxoedema. It is often of immunological origin and the manifestations are low metabolic rate, slow speech, lethargy, bradycardia, increased sensitivity to cold, and mental impairment. Myxoedema includes a characteristic thickening of the skin. Therapy of thyroid tumours is another cause of hypothyroidism. Thyroid deficiency... 

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... 

Thyroid hormones are used as replacement therapy when the patient is hypothyroid. By supplementing the decreased endogenous thyroid production and secretion with exogenous thyroid hormones, an attempt is made to create a euthyroid (normal thyroid) state Levotliyroxine (Synthroid) is the drug of choice for hypothyroidism because it is relatively inexpensive, requires once-a-day dosages, and lias a more uniform potency than do other thyroid hormone replacement drugs. 

These drugp are contraindicated in patients with known hypersensitivity to the drug or to any constituents of the drug, after a recent myocardial infarction (heart attack), or in patients with thyrotoxicosis. When hypothyroidism is a cause or contributing factor to a myocardial infarction or heart disease, the physician may prescribe small doses of thyroid hormone... 

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. 

Use of measurement of blood thyroxine or thyroid-stimulating hormone (TSH) in the neonatal diagnosis of congenital hypothyroidism. 

Figure 42-11. Model of iodide metabolism in the thyroid follicle. A follicular cell is shown facing the follicular lumen (top) and the extracellular space (at bottom). Iodide enters the thyroid primarily through a transporter (bottom left). Thyroid hormone synthesis occurs in the follicular space through a series of reactions, many of which are peroxidase-mediated. Thyroid hormones, stored in the colloid in the follicular space, are released from thyroglobulin by hydrolysis inside the thyroid cell. (Tgb, thyroglobulin MIT, monoiodotyrosine DIT, diiodotyro-sine Tj, triiodothyronine T4, tetraiodothyronine.) Asterisks indicate steps or processes that are inherited enzyme deficiencies which cause congenital goiter and often result in hypothyroidism.

Assess possible correctable etiologies, including myocardial ischemia, serum potassium concentration (for hyperkalemia), and thyroid function tests (for hypothyroidism). 

Thyroid-stimulating hormone (TSH) should be ordered when thyroid dysfunction is suspected. Hypothyroidism may be responsible for constipation and related symptoms. 

Lithium is concentrated in the thyroid gland and can impair thyroid hormone synthesis. Although goiter is uncommon, as many as 30% of patients develop at least transiently elevated thyroid-stimulating hormone values. Lithium-induced hypothyroidism is not usually an indication to discontinue the drug. Patients can be supplemented with levothyroxine if continuation of lithium is desired.30... 

IVday, monitor urinalysis, osmolality, and specific gravity every 3 months. Thyroid function tests should be obtained once or twice during the first 6 months, then every 6-12 months monitor for signs and symptoms of hypothyroidism if supplemental thyroid therapy is required, monitor thyroid function tests and adjust thyroid dose every 1-2 months until thyroid function indices are within normal range, then monitor every 3-6 months. 

Discuss the prevalence of thyroid disorders, including subclinical (mild) and overt (typical signs and/or symptoms present) hypothyroidism and hyperthyroidism. 

O In most patients with thyroid hormone disorders, the measurement of a serum thyroid-stimulating hormone (TSH) level is adequate for the diagnosis of hypothyroidism and hyperthyroidism. The target TSH for most patients being treated for thyroid disorders should be the mean normal value of 1.4 milliunits/L or 1.4 microunits/mL (target range 0.5-2.5 milliunits/L or 0.5-2.5 microunits/mL). 

Despite the availability of a wide array of thyroid hormone products, it is clear that synthetic levothyroxine (LT4) is the treatment of choice for almost all patients with hypothyroidism. LT4 mimics the normal physiology of the thyroid gland, which secretes mostly T4 as a prohormone. As needed, based on metabolic demands, peripheral tissues convert thyroxine (T4)... 

The most common causes of hypothyroidism are listed in Table 41-2. Up to 90% of patients with autoimmune thyroiditis have circulating anti-TPOAbs. The autoimmune inflammatory response results in a lymphocytic infiltration of the thyroid gland and its eventual destruction. 

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