1. Name and describe the function of each structure included on the human body.

Adjustments in endocrine, or hormonal, activity are triggered by the requirements of body tissues for changes in various physiologic processes. The adjustments of many endocrine glands are regulated by the anterior part of the pituitary gland, or hypophysis. The anterior pituitary is connected with the central nervous system by neurohormonal pathways via the hypothalamus; for this reason the hormonal system is ultimately under nervous control. The anterior pituitary exerts its influence on other glands by tropic hormones, which cause target glands to produce tissue-affecting hormones.

The hypothalamus (see BRAIN) is connected to the pituitary gland (hypophysis) by way of the infundibular stalk, and it secretes several factors that stimulate or inhibit various pituitary secretor cells. In some fishes the neurosecretory factors reach their target cells by diffusion. In other animals the neurons release their products into blood vessels that transport the secretions to the pituitary.

Hypothalamic neurons also send processes into a pituitary region where the antidiuretic hormone vasopressin and oxytocin or other chemically related substances are stored for release into general circulation. These substances stimulate kidney water retention, vascular and uterine smooth muscle contraction, and milk let-down. Hypothalamic neurosecretory factors may function as neurotransmitter substances in other parts of the brain and the nervous system.

The pituitary gland produces several hormones. Growth hormone promotes muscle and bone growth and affects general metabolism. Prolactin's effects range from hydromineral metabolism in fish to milk production in mammals. Thyroid-stimulating hormone (TSH) stimulates thyroid tissue growth and the production of thyroid hormones. Adrenocorticotropic hormone has a similar effect on the adrenal cortex, and also influences metabolism in adipose tissues. Gonadotrophins stimulate the production of male and female sex hormones, spermatogenesis, and ovarian development. Intermedin, melanophore-stimulating hormone, influences skin pigmentation.

The Thyroid, ultimobranchial, and Parathyroid glands are closely associated in their location and development. Thyroid glands are composed of microscopic units called follicles. Each follicle consists of a layer of secretory epithelium surrounding a hormone-storing colloid. The follicles extract iodine from the blood and concentrate it for in-corporation into the hormones thyroxine and triiodothyronine. These hormones play a major role in general metabolism, including calorigenesis, protein turnover, hydromineral balance, and growth and maturation of the individual.

Parafollicular cells, which form ultimobranchial glands in the nonmammalian vertebrates, secrete calcitonin in response to excess blood calcium levels. Parathyroid hormone (PTH) is secreted by glands that are found only in terrestrial vertebrates. PTH elevates blood calcium levels. Calcitonin and PTH help to maintain homeostatic levels of electrolytes in the blood. Their action influences bone integrity, intestinal calcium absorption, and renal electrolyte excretion.

The mammalian adrenal gland is composed of two endocrine tissues, a medullary region and a surrounding cortex. In other vertebrates, the tissues may be separated. The adrenal medulla, a nervous system derivative, secretes epinephrine and norepinephrine in response to neural stimulation (see ADRENALINE). Norepinephrine is also a neurotransmitter substance. The hormones are released in emergency or emotional situations and stimulate the heart and the vascular system. Epinephrine also stimulates various metabolic activities and elevates blood glucose levels.

Cortical tissue produces numerous steroid hormones of two general types, whose properties overlap and whose distribution varies among different animals. Glucocorticoids are principally metabolic hormones and are secreted in response to ACTH. Elevated levels of glucocorticoids exert a negative feedback on ACTH secretion, play a role in adjustment to stress, and raise blood sugar levels. They also have antiinflammatory properties in pharmacologic dose levels. Mineralocorticoid secretion, principally aldosterone, is stimulated by the renin-angiotensin system; aldosterone increases the retention of body salt by reducing renal sodium excretion.

Under the complex control of gonadotrophins, the gonads produce steroid sex hormones that stimulate reproductive processes, maintain secondary sex characteristics, and influence growth, development, and behavior. Testes produce androgens and ovaries produce estrogens, progesterone, and a peptide hormone called relaxin. Relaxin conditions the reproductive tract and birth canal during pregnancy and parturition. The placenta, as a temporary endocrine organ, secretes a lactogenic hormone, gonadotrophins, estrogens, progesterone, and relaxin.

B. Discuss how each system works. Follow materials through a system, or show how signals, impulses, or substances are controlled, secreted and used.

The endocrine system consists of glands tha transmit chemical messages throughout the body. These chemical messages are called hormones. Hormones are substances that are produced in one part of the body and specifically influence the activity of cells in another part of the body and specifically influence the activity of cells in another part of the body. The glands secrete tiny amounts of these hormones into the blood. The blood then carries them to every part of the body. However, each hormone affects only specific cells, called target cells, that are supplied with receptors for that hormone.

Most endocrine glands have a self-regulating system of checks and balances. This system depends on a feedback mechanism. This is a mechanism in which the end product of a series of steps controls the first step in series. If the end product promotes the first step, the mechanism is called positive feedback. If the end product inhibits the first step, the mechanism is called negative feedback.

Most endocrine glands have negative feedback mechanisms. To understand how negative feedback works, we should think of the thermostat that controls the temperature in our homes. When the temperature drops below a set level, the thermostat helps turn on the furnace. The furnace then produces heat, which warms the hair. The end product - higher air temperature - is detected by the thermostat, which then turns off the furnace.

The first step in an endocrine feedback mechanism is the secretion of a hormone by a gland. The end product is a change in the concentration in the blood of the products controlled by that hormone. Look at the chart below. When the blood glucose level in the body goes up, cells in the pancreas are stimulated and produce insulin. This insulin causes muscles and the liver to absorb glucose and store it in the form of glycogen. The reduced glucose level in the blood causes the cells to stop secreting insulin. Many negative feedback mechanisms help maintain homeostasis in the human body.

3. Discuss diseases and dysfunctions relayed to each system.

Diseases of the endocrine system primarily result in excess release (hypersecretion) or insufficient release (hyposecretion) of hormones by one or more glands. Hypersecretion of hormones, usually associated either with tumors or above-normal cell proliferation (hyperplasia), occurs because of overstimulation of endocrine glands by factors such as tropic hormones from the pituitary gland. Hyposecretion results from several causes, including: surgical or radiation destruction of glands; glandular atrophy; congenital defects in the enzymes involved in hormone synthesis; and dietary conditions such as low iodine intake that may result in insufficiency of the thyroid hormones.

Hypothalamus And Pituitary Gland

The hypothalamus and the pituitary gland are closely related. The hypothalamus modulates the activity of the anterior portion of the pituitary through release or release-inhibitor hormones, which travel through a portal venous system to the anterior pituitary. These neurohormones regulate the release of such hormones as growth hormone (GH), adrenocorticotrophin (ACTH), follicle-stimulating hormone (FSH), prolactin, luteinizing hormone (LH), and thyroid-stimulating hormone (TRH). Secretion of the neurohormones is triggered by neurotransmitters such as dopamine and acetylcholine, and affected by such mechanisms as stress, plasma levels of corticosteroid, time of day, and estrogen levels.

Decreased secretion in the hypothalamus results in decreased secretion in the pituitary, a state called secondary hypopituitarism. This undersecretion is usually caused by tumors, encephalitis, or inflammatory lesions.

Oversecretion of GH, usually caused by a pituitary tumor, leads to gigantism or acromegaly. If oversecretion occurs before the closure of the epiphyses of the long bones (maturity), an individual can reach a height of 2.1 to 2.4 m (7 to 8 ft), a condition termed pituitary gigantism. If oversecretion occurs after the closure (in adults), the resulting condition, called acromegaly, is characterized by overgrowth of the mandible, causing protrusion of the jaw (prognathism); bone overgrowth and thickening of soft tissue, resulting in coarsening of the facial features; wide hands and broad fingers; and, often, soreness of joints. GH excess may induce signs of deficiency of other hormones, resulting in such disorders as hypogonadism accompanied by menstrual disturbance in women. Treatment consists of heavy particle irradiation or surgical removal of the tumor or lesion.

Cushing's disease is caused by an ACTH-secreting tumor that leads to excess secretion of steroid hormone, particularly cortisol, from the adrenal cortex. The syndrome is characterized by a "moon" face, thin skin, muscle wasting and weakness, and high blood pressure.

Hypersecretion of prolactin due to a pituitary tumor or secondary hypopituitarism (removal of hypothalamic inhibitory influence) is associated with galactorrhea, amenorrhea, and infertility.

Decreased production of all pituitary hormones simultaneously is termed panhypopituitarism. GH deficiency leads to growth retardation, or dwarfism, most often appearing in childhood. Loss of TSH results in hypothyroidism, evidenced by intolerance of cold, slow speech, and anemia. ACTH loss leads to secondary hypoadrenocorticism--in particular, the loss of cortisol secretion. Symptoms include weakness, low blood pressure, and diminished blood sugar. Loss of FSH and LH leads to amenorrhea, atrophy of the genitals, absence of libido, absence of sperm and ova production, and infertility. The absence of prolactin inhibits lactation. Treatment of panhypopituitarism consists of replacing the lost hormones; however, fertility cannot be restored in this manner.

The hypothalamus synthesizes antidiuretic hormone (ADH, vasopressin) and oxytocin, which are stored in the posterior pituitary and are released in response to stress and suckling. A deficiency in ADH, called diabetes insipidus, causes large volumes of water to be lost in urine. This state, characterized by thirst, results from either tumors or disease in the nuclei of the hypothalamus, where ADH is produced, or unresponsiveness of the kidney tubules. If the cause centers in the hypothalamus, the disease can be corrected with animal or synthetic ADH molecules. If untreated in newborn infants, it results in mental retardation or death by dehydration.

A deficiency of the hormones thyroxine and triiodothyronine (hypothyroidism) originates either in the thyroid (primary) or in the controlling pituitary of hypothalamus (secondary). Undersecretion of these hormones in fetal or infant life results in cretinism. Symptoms include dry, wrinkled skin, an enlarged tongue, a drooling mouth, and a broad face. Infants are apathetic and have a slow heart rate and subnormal temperature. As children, they are small for their age; as adults, they are dwarfs. Children are minimally to severely mentally retarded. If the condition is recognized and treated early, these growth defects can be prevented.

The reaction to the deficiency of thyroid hormone in adults is called myxedema. Characteristics include severe edema of the face, extremities, and body cavities, as well as gradual personality changes, hoarse speech, yellowish skin, mental apathy, and slowed brain waves. Treatment consists of administration of thyroid hormone, usually for the lifetime of the patient. Myxedema can affect other endocrine glands, and ACTH and GH may be decreased. The condition interferes with reproduction.

Various conditions can cause GOITER, an enlargement of the thyroid gland. Overproduction of hormone in the thyroid gland, which may follow emotional or physical stress, results in toxic diffuse goiter (Grave's disease) or toxic nodular goiter (Plummer's disease), both of which are characterized by nervousness, sweating, weight loss, and hyperactivity. If goiter is caused by low dietary intake of iodine, it is termed endemic (colloid) goiter. Endemic goiter is treated with iodine. Drugs such as lithium that can block synthesis of thyroid hormone are called goitrogens. The hypothalamus-pituitary responds to goitrogens with increased TSH secretion and resulting goiter formation, which is most likely to occur at puberty and during pregnancy.

Addison's disease, a progressive disorder, results from atrophy of the adrenal cortex and the subsequent decrease in the amount of hormones produced by this gland, particularly aldosterone (a mineralocorticoid) and cortisol (a glucocorticoid). Early symptoms include weakness and fatigue; later, brown spots appear on the skin because of hyperpigmentation. Weight loss, low blood pressure, nausea, and diarrhea also occur. Secondary adrenocorticoid insufficiency, the lack of glucocorticoids (cortisol), results from abnormalities in pituitary or hypothalamic function, leading to a lack of ACTH.

Oversecretion of one or more of the hormones of the adrenal cortex results in distinct syndromes. Overproduction of androgens results in adrenal virilism or precocious development of male sex characteristics. This condition is caused by the production of steroids with androgenic properties by a tumor. Virilization depends on sex and age. It is more marked in women, and is caused by a tumor and characterized by such signs as baldness, acne, deep voice, decreased breast size, and increased masculinity. Feminizing adrenal tumors are rare.

Hypersecretion of glucocorticoids, particularly cortisol, produces Cushing's syndrome, and excessive aldosterone results in aldosteronism. Signs of primary aldosteronism, which is caused by a tumor, include high blood pressure, normal to high serum sodium, and low serum potassium. Secondary aldosteronism results from a stimulus originating outside the adrenal gland. Its symptoms mimic those of primary aldosteronism, and it is related to high blood pressure and disorders characterized by edema, such as cardiac failure. If multiple tumors must be removed in primary aldosteronism, permanent corticosteroid therapy may be necessary.

Pheochromocytoma is a condition characterized by excess epinephrine secreted by an adrenal medullary tumor. It results in high blood pressure and metabolic problems.

Deficiency of parathyroid hormone (PTH) leads to a tendency for chronic tetany, or increased neuromuscular excitability (TETANY). Chemically, hypoparathyroidism is characterized by low serum calcium and high serum phosphorus. The disease is caused either by accidental removal or by damage during removal of the thyroid gland, or by a form of autoimmune disease.

Oversecretion of parathyroid hormone results from a tumor, enlargement, or cancer of the glands. Primary hyperparathyroidism is characterized by high serum calcium, low levels of inorganic phosphate, and abnormal bone metabolism. Many patients with hypercalcemia, usually mild, show no symptoms. Others exhibit weakness, nausea, constipation, abdominal pain, and thirst among their symptoms. Emotional problems may also ensue. Hypercalcemia can result in irreversible kidney damage due to calcium deposits. Many patients suffer from bone disease, such as the occurrence of cysts. Kidney failure is the most common cause of secondary hyperparathyroidism. The increases in serum inorganic phosphorus and decreases in serum calcium that develop in uremia stimulate an increase in secretion of parathyroid hormone.

Premature development of the ovaries and testes through early but normal hypothalamus-pituitary maturation, without apparent cause, accelerates body growth but ultimately results in stunting due to premature fusing of the growing ends of bones. This condition is called true sexual precocity; reproduction is possible as early as age 6. Brain tumors and encephalitis can also result from premature development of the ovaries and testes.

The development and functioning of the male reproductive organs and related structures and characteristics depend on the pituitary gonadotrophins. LH stimulates the cells of the testes to produce androgen. FSH stimulates the sperm-producing cells of the sex glands. Primary male hypogonadism consists of a failure to synthesize androgens (testosterone) due to defective enzymes. Secondary male hypogonadism is caused by a lack either of LH, which inhibits androgen production, or of FSH, which leads to a failure of spermatogenesis. A deficiency of FSH and LH prior to or during puberty delays the development of genitalia and secondary sex characteristics. Dwarfism occurs if GH is also deficient.

Primary Amenorrhea, the failure of a women to begin menstruation, may be due to pituitary dysfunction (such as tumors) or to other endocrine disorders (such as hypothyroidism). Secondary amenorrhea halts the menstrual cycle.

Juvenile Diabetes mellitus (Type 1) results from both hereditary and environmental factors and is characterized by insulin deficiency and a high blood-sugar (glucose) level. In the absence of insulin treatment, the disease rapidly causes dehydration, ketoacidosis, low blood volume, hypotension, coma, and death.