This section discusses the main endocrine glands, which include the pituitary, thyroid, parathyroid, and adrenal glands. Other organs in the body such as the pancreas (islets of Langerhans; Chapter 46: The Endocrine Pancreas (Islets of Langerhans)), ovaries (granulosa cells and luteal cells; Chapter 52: The Ovaries & Uterine Tubes), testes (interstitial cells of Leydig; Chapter 51: The Testis, Prostate, & Penis), gastrointestinal tract (pyloric antral G cells; Chapter 38: The Stomach), and placenta (chorionic gonadotropin; Chapter 55: Diseases of Pregnancy; Trophoblastic Neoplasms) have endocrine components that are discussed in those chapters.
The pituitary secretes tropic hormones that control the function of the thyroid, the cortisol-producing zones of the adrenal cortex, and the gonads. The pituitary in turn is controlled by releasing and inhibiting hormones secreted by the hypothalamus.
Hormones usually bind to receptors on target cells in the body. The receptors may be located in the cell membrane (catecholamines, polypeptide hormones), the cytoplasm (steroids), or the nucleus (thyroid hormones and steroids). The binding of the hormone to the receptor leads to a series of changes in the cell that results in the metabolic action of the hormone. In the case of catecholamines and polypeptide hormones, there is activation of adenylyl cyclase, which stimulates intracellular production of cyclic adenosine monophosphate (cAMP). cAMP acts as an internal (second) messenger, effecting the specific biochemical change dictated by the hormone on the target cell. Other hormones such as corticosteroids and thyroid hormone cause increased messenger ribonucleic acid (mRNA) synthesis, leading to protein (enzyme) synthesis.
Endocrine diseases are frequently characterized by abnormal patterns of hormone secretion:
Excessive secretion of hormones may be due to the presence of increased numbers of cells of the type that normally secrete the hormone. This may occur as primary hyperfunction, due to hyperplastic or neoplastic proliferation of the cells; or secondary hyperfunction, due to increased stimulation by increased levels of tropic hormones or decreased feedback inhibition. Excessive secretion may also be due to production of hormones by cells that do not normally secrete the hormone, resulting in what we call ectopic hormone syndromes.
Decreased secretion of hormones may be due to decreased numbers of hormone-secreting cells, which may in turn be due to primary hypofunction, from congenital absence or hypoplasia or from destruction of the gland by trauma, infection, ischemia, immunologic mechanisms, or neoplasms; or secondary hypofunction, from absence of stimulation by the tropic hormones on which the cells are dependent. Secondary hypofunction is characterized by atrophy of the hormone-secreting cells due to lack of stimulation. Diminished secretion may also be due to deficiency of enzymes required to synthesize the hormone. Decreased hormone activity may be caused by a defect in the target organ receptors, which is usually congenital. Because serum hormone levels are normal in such patients, the prefix pseudo- is attached to these hypofunctional states, eg, pseudohypoparathyroidism (see Chapter 59: The Parathyroid Glands).
Secretion of abnormal ...