Pituitary gland hypothyroidism

Damage and destruction of the pituitary gland may result in secondary hypothyroidism, hypogonadism, adrenal insufficiency, growth hormone deficiency, hypoprolactinemia, or... 

Prolactin is an essential hormone for normal production of breast milk following childbirth. It also plays a pivotal role in a variety of reproductive functions. Prolactin is regulated primarily by the hypothalamus-pituitary axis and secreted solely by the lactotroph cells of the anterior pituitary gland. Under normal conditions, secretion of prolactin is predominantly under inhibitory control by dopamine and acts on the D2 receptors located on the lactotroph cells. Increase of hypothalamic thyrotropin-releasing hormone (TRH) in primary hypothyroidism can stimulate the release of prolactin. 

Thyroid disorders may be divided into over- and underproduction of the thyroid hormones. These may be caused by thyroid gland disorders or disorders of the pituitary gland (TSH production) or hypothalamus (thyrotropin-releasing hormone release). Thyroid hormone deficiency in infancy may cause mental retardation if it is not corrected immediately after birth. For this reason, many states require thyroid function tests in all newborns. In adults, thyroid deficiency may be caused by Hashimoto s thyroiditis, an immune disorder, or dietary iodine deficiency, in which case it is called simple goiter. The term "myxedema" has been used to refer to hypothyroidism of whatever cause. Myxedemas may... 

Although Brian is tired and weak, with a puffy face and significantly increased body weight, all of which may be observed in myxoedema (a severe form of adult hypothyroidism), his thyroid hormones and TSH concentration are normal. In hypothyroidism T3 and T4 concentrations are usually low, which leads to an increase in TSH because of reduced negative feedback between the thyroid hormones and the anterior pituitary gland. 

Secondary hypothyroidism Either the hypothalamus is unable to release sufficient quantities of thyrotropin-releasing hormone or the anterior pituitary gland is unable to release sufficient thyroid-stimulating hormone. 

Three possible causes of hypothyroidism are the decreased secretion of thyrotropin-releasing hormone (TRH) by the hypothalamus gland, decreased secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, and decreased secretion of thyroid hormones by the thyroid gland. 

Destruction of the pituitary gland may result in secondary hypothyroidism, hypogonadism, adrenal insufficiency, growth hormone deficiency, and hypoprolactinemia. The formation of certain types of pituitary tumors may result in pituitary hormone excess. Pituitary tumors may also physically compress the pituitary and prevent the release of the trophic hypothalamic factors that regulate pituitary hormones. In this chapter, the pathophysiology and role of pharmacotherapy in the treatment of acromegaly, short stature, hyperprolactinemia, and panhypopituitarism will be discussed. 

Thyroid Hypofunction Hypothyroidism is the most common disorder of thyroid function. It can be divided into patients who have a failure of the thyroid gland to produce sufficient thyroid hormone (primary hypothyroidism) and patients in which pituitary or hypothalamic disease is associated with impaired TSH stimulation (central or secondary hypothyroidism). Worldwide, primary hypothyroidism is caused most often by iodine deficiency. In areas where iodine is sufficient, chronic autoimmune thyroiditis (Hashimoto s thyroiditis) accounts for most cases. Other causes include postpartum thyroiditis, surgical removal, or radioactive iodine ablation of the gland. Hypothyroidism present at birth (cretinism) is the most common preventable cause of mental retardation in the world. 

Figure 84.1 Showing a huge goiter of a femaie inhabitant aged 78 years, who lived for a long time in an iodine-deficient area in Austria. Hypothyroidism caused by iodine deficiency led to an increase in thyroid-stimulating hormone produced in the pituitary gland leading to such an enlargement of the thyroid gland.

Rats in an altered metabolic condition, particularly with an increased metabolic load and a stimulated pituitary gland, would be likely candidates for thyroid follicular tumors [19, 23, 24, 25, 26, 27]. Furthermore, unlike rats, hypothyroidism in humans, associated with increased TSH, is not related to an increased risk of thyroid cancer. The only recognized human thyroid cancer-inducing agent is radiation. 

TSH, or thyrotropin, is a glycosylated protein of two subunits, a and p. TSH stimulates the thyroid gland to produce thyroid hormones. Deficiencies are treated by giving thyroxine itself rather than TSH, but TSH is available for diagnostic purposes to differentiate between pituitary and thyroid gland failure as causes of hypothyroidism (see Chapter 65). 

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. 

As mentioned in Chapter 1, perhaps the purest form of drug therapy is the replacement of inadequate amounts of an endogenous substance such as a hormone. Any gland that normally secretes a hormone is a potential target for hypofunctioning. Classical examples include Addison s disease (adrenal cortex), dwarfism (anterior pituitary), juvenile-onset insulin-dependent diabetes (pancreas), and hypothyroidism (thyroid). 

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. 

Iodide is well absorbed from the intestine, is distributed like chloride in the body and is rapidly excreted by the kidney. It is selectively taken up and concentrated (about x 25) by the thyroid gland, but more in hyperthyroidism and less in hypothyroidism. A deficiency of iodide reduces the amount of th)T oid hormone produced, which stimulates the pituitary to secrete TSH. The result is hyperplasia and increased vascularity of the gland, with eventual goitre formation. 

Many structural or functional abnormalities of the thyroid gland can lead to thyroid hormone deficiency (Box 52-2). Primary hypothyroidism is frequently caused by diseases or treatments that directly destroy thyroid tissue or interfere with thyroid hormone biosynthesis. Secondary hypothyroidism occurs as a result of pituitary or hypothalamic disease and/or disorders. 

Hypothyroidism is caused by a deficiency of thyroid hormones. Primary hypothyroidism is failure of the thyroid gland itself and is one of the mo.st commonly encountered endocrine problems. The demonstration of an elevated T.SH concentration is usually diagnostic. Secondary hypothyroidism, failure of the pituitary to secrete TSH, is much less common. Isolated pituitary deficiency of TSH is rare, but impairment of the hypothalamic-pituitary-thyroid axis may happen as a result of any pituittu y disca.se or damage. 

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