Together with the nervous system, the endocrine system regulates and integrates the body’s metabolic activities. The endocrine system meets the nervous system at the hypothalamus. The hypothalamus, the main integrative center for the endocrine and autonomic nervous systems, controls the function of endocrine organs by neural and hormonal pathways. A hormone is a chemical transmitter released from specialized cells into the bloodstream, which carries it to specialized organ-receptor cells that respond to it.
Neural pathways connect the hypothalamus to the posterior pituitary, or neurohypophysis. Neural stimulation to the posterior pituitary provokes the secretion of two effector hormones: antidiuretic hormone (ADH) and oxytocin, and influences thyroid-stimulating hormone (TSH), corticotropin, prolactin, and gonadotropin-releasing hormone.
The hypothalamus also exerts hormonal control at the anterior pituitary through releasing and inhibiting factors, which arrive by a portal system. Hypothalamic hormones stimulate the pituitary to release trophic hormones, such as corticotropin, TSH, luteinizing hormone (LH), and follicle-stimulating hormone (FSH), and to release or inhibit effector hormones, such as the growth hormone and prolactin.In turn, secretion of trophic hormones stimulates the adrenal cortex, thyroid, and gonads. In a patient whose clinical condition suggests endocrine pathology, this complex hormonal sequence requires careful evaluation at each level to identify the dysfunction; dysfunction may result from defects of releasing, trophic, or effector hormones or of the target tissue. Hyperthyroidism, for example, may result from an excess of thyrotropin-releasing hormone, TSH, or thyroid hormone.
In addition to hormonal and neural controls, a negative feedback system regulates the endocrine system. (See Feedback mechanism of the endocrine system.) The mechanism of feedback may be simple or complex. Simple feedback occurs when the level of one substance regulates secretion of a hormone. For example, low serum calcium levels stimulate parathyroid hormone (PTH) secretion; high serum calcium levels inhibit it. Complex feedback occurs through the hypothalamic-pituitary-target organ axis; for example, secretion of the hypothalamic corticotropin-releasing hormone (CRH) releases pituitary corticotropin, which, in turn, stimulates adrenal cortisol secretion. Subsequently, a rise in serum cortisol level inhibits corticotropin by decreasing CRH secretion. Steroid therapy disrupts the hypothalamic-pituitary-adrenal (HPA) axis by suppressing hypothalamic-pituitary secretion. Because abrupt withdrawal of steroids doesn’t allow time for recovery of the HPA axis to stimulate cortisol secretion, it can induce a life-threatening adrenal crisis.
In response to the hypothalamus, the posterior pituitary secretes oxytocin and ADH. Oxytocin stimulates contraction of the uterus and is responsible for the milk let-down reflex in lactating females. ADH controls the concentration of body fluids by altering the permeability of the distal convoluted tubules and collecting ducts of the kidneys to conserve water. The secretion of ADH depends on plasma volume and osmolality as monitored by hypothalamic neurons. Circulatory shock and severe hemorrhage are the most powerful stimulators of ADH; other stimulators include pain, emotional stress, trauma, morphine, tranquilizers, certain anesthetics, and positive-pressure breathing.
The syndrome of inappropriate ADH secretion is a disorder that produces hyponatremia with water overload. Generally, however, overhydration suppresses ADH secretion (as does alcohol). ADH deficiency causes diabetes insipidus, a condition of high urine output.
The anterior pituitary secretes prolactin, which stimulates milk production, and human growth hormone (hGH), which stimulates growth by increasing protein synthesis and fat mobilization and by decreasing carbohydrate utilization. Hyposecretion of hGH results in dwarfism; hypersecretion causes gigantism in children and acromegaly in adults.
The thyroid gland secretes the iodinated hormones thyroxine and triiodothyronine. Thyroid hormones, necessary for normal growth and development, act on many tissues to increase metabolic activity and protein synthesis. Deficiency of thyroid hormone causes varying degrees of hypothyroidism, from a mild, clinically insignificant form to life-threatening myxedema coma. Congenital hypothyroidism causes cretinism. Hypersecretion causes hyperthyroidism and, in extreme cases, thyrotoxic crisis. Excessive secretion of TSH causes thyroid gland hyperplasia, resulting in goiter.
The parathyroid glands secrete PTH, which regulates calcium and phosphate metabolism. PTH elevates serum calcium levels by stimulating resorption of calcium and phosphate from bone, reabsorption of calcium and excretion of phosphate by the kidneys and, by combined action with vitamin D, absorption of calcium and phosphate from the GI tract. PTH also stimulates conversion of vitamin D to its metabolically active form. Thyrocalcitonin, a secretion from the thyroid, opposes the effect of PTH and therefore decreases serum calcium levels. Hyperparathyroidism results in hypercalcemia, and hypoparathyroidism causes hypocalcemia. Altered calcium levels may also result from nonendocrine causes such as metastatic bone disease.
The endocrine part of the pancreas produces glucagon from the alpha cells and insulin from the beta cells. Glucagon, the hormone of the fasting state, releases stored glucose to raise the blood glucose level. Insulin, the hormone of the nourished state, facilitates glucose transport, promotes glucose storage, stimulates protein synthesis, and enhances free fatty acid uptake and storage. Absolute or relative insulin deficiency causes diabetes mellitus. Insulin excess can result from an insulinoma (a tumor of the beta cells).
The adrenal cortex secretes mineralocorticoids, glucocorticoids, and sex steroids. Aldosterone, a mineralocorticoid, regulates the reabsorption of sodium and the excretion of potassium by the kidneys. Although affected by corticotropin, aldosterone is regulated by angiotensin II, which in turn, is regulated by renin and plasma volume. Together, aldosterone, angiotensin, and renin may be implicated in the pathogenesis of hypertension. An excess of aldosterone (aldosteronism) can result primarily from hyperplasia or from adrenal adenoma or secondarily from many conditions, including heart failure and cirrhosis.
Cortisol, a glucocorticoid, stimulates gluconeogenesis, increases protein breakdown and free fatty acid mobilization, suppresses the immune response, and provides for an appropriate response to stress. Hyperactivity of the adrenal cortex results in Cushing’s syndrome; hypoactivity of the adrenal cortex causes Addison’s disease and, in extreme cases, adrenal crisis. Adrenogenital syndromes may result from overproduction of sex steroids.
The adrenal medulla is an aggregate of nervous tissue that produces the catecholamines epinephrine and norepinephrine, both of which cause vasoconstriction. Epinephrine also causes the fight-or-flight response — dilation of bronchioles and increased blood pressure, blood glucose levels, and heart rate. Pheochromocytoma, a tumor of the adrenal medulla, causes hypersecretion of catecholamines and results in characteristic sustained or paroxysmal hypertension.
The testes synthesize and secrete testosterone in response to gonadotropic hormones, especially LH, from the anterior pituitary gland; spermatogenesis occurs in response to FSH. The ovaries produce sex steroid hormones, primarily estrogen and progesterone, in response to LH and FSH.
Chronic endocrine abnormalities are common health problems. For example, deficiencies of cortisol, thyroid hormone, or insulin may require lifelong hormone replacement for survival. Consequently, these conditions make special demands on your skills during ongoing patient assessment, acute illness, and patient teaching.
Common dysfunctions of the endocrine system are classified as hypofunction and hyperfunction, inflammation, and tumor. The source of hypofunction and hyperfunction may originate in the hypothalamus or in the pituitary or effector glands. Inflammation may be acute or subacute, as in thyroiditis, but is usually chronic, commonly resulting in glandular hypofunction. Tumors can occur within a gland — as in thyroid cancer or adrenal pheochromocytoma — or in other areas, resulting in ectopic hormone production. Certain lung tumors, for example, secrete ADH, PTH, or structurally similar substances that have the same effects on target tissues.
The study of endocrine function focuses on measuring the level or effect of a hormone. Radioimmunoassay, for example, measures insulin levels; a fasting blood glucose test measures insulin’s effects. Sophisticated techniques of hormone measurement have improved diagnosis of endocrine disorders.
Diagnostic tests confirm endocrine disorders but clinical data usually provide the first clues. Nursing assessment can reveal such signs and symptoms as excessive or delayed growth, wasting, weakness, polydipsia, polyuria, and mental changes. The quality and distribution of hair, skin pigmentation, and the distribution of body fat are also significant.
Nurses are also responsible for patient preparation, including instruction and support during testing, and for specimen collection, particularly of timed blood and urine specimens.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
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