Thyroid hormones production

The metabolic rate is increased by several hormones including thyi oid hormone, adrenalin and male sex hormones. The increase in metabolic rate caused by male sex hormones explains why males have slightly higher average metabolic rates than females of the same size and age. Living in a cold climate increases the metabolic rate because the cold stimulates thyroid hormone production and this hormone increases heat output of the body, while living in a warm climate causes the metabolic rate to decrease. 

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. 

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 goals of treating hyperthyroidism are to relieve symptoms, to reduce thyroid hormone production to normal levels and achieve biochemical euthyroidism, and to prevent longterm adverse sequelae. 

In patients with excess thyroid hormone production, reduce hormone production with an antithyroid drug and/or radioactive iodine. Choose therapy based on patient-specific factors and preference. 

Thyroid disorders encompass a variety of disease states affecting thyroid hormone production or secretion that result in alterations in metabolic stability. Hyperthyroidism and hypothyroidism are the clinical and biochemical syndromes resulting from increased and decreased thyroid hormone production, respectively. 

Thyroid hormone production is regulated by TSH secreted by the anterior pituitary, which in turn is under negative feedback control by the circulating level of free thyroid hormone and the positive influence of hypothalamic thyrotropin-releasing hormone. Thyroid hormone production is also regulated by extrathyroidal deiodination of T4 to T3, which can be affected by nutrition, nonthyroidal hormones, drugs, and illness. 

In older patients with goiter due to iodine deficiency there is a risk of provoking hyperthyroidism by increasing iodine intake (p. 247) During chronic maximal stimulation, thyroid follicles can become independent of TSH stimulation ( autonomic tissue"). If the iodine supply is increased, thyroid hormone production increases while TSH secretion decreases due to feedback inhibition. The activity of autonomic tissue, however, persists at a high level thyroxine is released in excess, resulting in iodine-induced hyperthyroidism. 

Hypothyroidism (myxedema) results when there is a breakdown of thyroid hormone production in the thyroid gland. Treatment consists of replacing this hormone with aforementioned drugs. Treatment with levothyroxine, 3,5,3, 5 -tetraiodothyronine, is preferred. Lyothyronin, L-3,5,5 -triiodothyronine, is also used, as is lotrix, a mixture of levothyroxine and levothyronine in a 4 1 ratio. Of the drugs of animal origin, thyroidin and thy-roglobulin (proloid) are used. 

Myxedema coma - Oral thyroid hormone drug products are not recommended to treat this condition administer thyroid hormone products formulated for IV. 

Thionamides are the primary drugs used to decrease thyroid hormone production. They do not inhibit secretion of stored thyroid hormone, and therefore, when they are used alone, their clinical effects are not appar-... 

People with exposure to anti-thyroid drugs (e.g., lithium), thyroid disease, or otherwise compromised thyroid function might have a more pronounced response to PBBs and PBDEs because of their underlying limitations in thyroid hormone production. Similarly, people with compromised function of other organs, such as those with liver or kidney diseases (e g., liver cirrhosis or hepatitis B), could be considered more susceptible to health effects of PBBs and PBDEs. 

Figure 5-3 shows a strong matrix effect in the analysis of perchlorate (CIO4 ) by mass spectrometry. Perchlorate at a level above 18 p,g/L in drinking water is of concern because it can reduce thyroid hormone production. Standard solutions of C104 in pure water gave the upper calibration curve in Figure 5-3. The response to standard solutions with the same concentrations of CIO4 in groundwater was 15 times less, as shown in the lower curve. Reduction of the ClOj" signal is a matrix effect attributed to other anions present in the groundwater.

Endogenous thyroid hormone production begins when neuro-input tells the hypothalamus to synthesize an release Thyroptropin -Releasing -Hormone. (TRH)... 

T-4 drugs suppress endogenous thyroid hormone production significantly. After discontinuance, most athletes experienced a metabolic lag period of 3-15 days before thyroid function rebound occurred. Interesting fact is that most monitored athletes experienced a 120-130 % increase in endogenous thyroid hormones at that point. And some maintain that level permanently. 

The primary steps in thyroid hormone biosynthesis are shown schematically in Figure 31-2. Thyroid follicle cells take up and concentrate iodide from the bloodstream—this is significant because there must be a sufficient amount of iodine in the diet to provide what is needed for thyroid hormone production.55 Thyroid cells also manufacture a protein known as thy-... 

Thyroid hormone production is controlled by the hypothalamic-pituitary system (see Chapter 28). Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release of thyroid-stimulating hormone (TSH) from the anterior pituitary.17,63 TSH then travels via the systemic circulation to the thyroid gland to stimulate the production of thyroxine and triiodothyronine. 

Nontoxic goiter is a syndrome of thyroid enlargement without excessive thyroid hormone production. Enlargement of the thyroid gland is usually due to TSH stimulation from inadequate thyroid hormone synthesis. The most common cause of nontoxic goiter worldwide is iodide deficiency, but in the USA, it is Hashimoto s thyroiditis. Less common causes include dietary goitrogens, dyshormonogenesis, and neoplasms (see below). 

In this chapter we will first briefly describe the major parameters controlling the level of thyroid hormone production and its concentration by the target cell (see Ref. 6), i.e., biosynthesis and output from the thyroid gland, transport in the blood, conversion of the prohormone thyroxine (T4), to the active form, 3,5,3 -triiodo-... 

Thyroid hormone production, transport and uptake by the target cells... 

Which of the following best describes the effect of propylthiouracil on thyroid hormone production ... 

Q9 Secretion of T3 and T4 is normally stimulated by TSH, released from the anterior pituitary. A rise in circulating thyroid hormone concentration reduces the production of TSH by negative feedback. If the gland fails to produce adequate thyroid hormone, production of TSH is not inhibited and its secretion continues to increase. Patients with hypothyroidism generally have reduced T3 and T4 production and raised plasma TSH, which is seen in Zadie s case. 

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