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Biology 219 – Human Physiology Clemens Endocrine System 2 Text: Ch. 7 A. Summary of Endocrine Glands and Hormones 1a. Primary endocrine organs Hormones hypothalamus trophic hormones (releasing and inhibiting hormones) pituitary gland ( = hypophysis) anterior pituitary TSH, ACTH, FSH, LH, GH, prolactin posterior pituitary ADH, oxytocin pineal gland melatonin thyroid gland thyroxine (T4), triiodothyronine (T3); calcitonin parathyroid gland PTH thymus thymosin, thymopoietin adrenal gland adrenal cortex aldosterone, cortisol, androgens adrenal medulla epinephrine & NE 1b. Primary endocrine glands in other organs pancreas (pancreatic islets) insulin, glucagon ovaries / testes ♀: estrogen & progesterone / ♂: androgens (testosterone) placenta estrogen & progesterone, hCG 2. Secondary endocrine organs GI organs, heart, kidneys, liver, skin GI hormones, ANP, erythropoietin, vitamin D3, etc. B. Hypothalamus and Pituitary Gland hypothalamus - part of the brain (diencephalon), controls the pituitary gland pituitary gland - major endocrine gland; infundibulum attaches to hypothalamus 1. Posterior pituitary (neurohypophysis) - direct neural connection to hypothalamus - neurosecretory cells originate in hypothalamus, axons in infundibulum, axon terminals in posterior pituitary secrete neurohormones - ADH (vasopressin) and oxytocin 2. Anterior pituitary (adenohypophysis) - circulatory connection to hypothalamus via hypothalamic-hypophyseal portal system - neurosecretory cells in the hypothalamus secrete releasing hormones into portal system which control anterior pituitary secretion - anterior pituitary secretes trophic hormones that control other endocrine glands and tissues Hypothalamus-Anterior Pituitary Axis hypothalamus TRH CRH GnRH GHRH somatostatin PRH dopamine + + + + – + – → → → → → anterior pituitary TSH ACTH FSH & LH growth hormone “ prolactin “ → → → → target endocrine gland/tissue thyroid gland adrenal cortex ovaries/testes liver, bone, muscle, etc. → breasts C. Thyroid Gland 1. Production of thyroid hormones T3 and T4 (thyroxine) 2. Effects of thyroid hormones - increase basal metabolic rate - stimulate protein synthesis - developmental effects: nervous and reproductive systems 3. Feedback control of thyroid hormone secretion D. Adrenal Gland 1. Adrenal cortex a) mineralocorticoids (aldosterone) - promotes Na+ retention and K+ excretion by kidneys b) glucocorticoids (cortisol) - “stress hormones”, promote gluconeogenesis, anti-inflammatory c) androgens (testosterone, etc.) 2. Adrenal medulla - connection to sympathetic ANS - chromaffin cells secrete epinephrine (E) and norepinephrine (NE) - Epi and NE act via adrenergic receptors on target cells a. alpha-adrenergic receptors α1 → constriction of blood vessels b. beta-adrenergic receptors β1 → increase in heart rate and contractility β2 → bronchodilation E. Pancreas - endocrine portion consists of pancreatic islets (islets of Langerhans) beta cells - secrete insulin alpha cells - secrete glucagon - insulin and glucagon are major actors in the maintenance of glucose homeostasis 1. Insulin - secreted during absorptive state when blood glucose and a.a. levels are high - stimulates glucose uptake (facilitated diffusion) into most body cells - stimulates synthesis of glycogen, protein, and lipids (energy storage) - decreases plasma glucose concentration 2. Glucagon - secreted during postabsorptive state when blood glucose levels are low - stimulates glycogenolysis and gluconeogenesis in liver (releases glucose into blood) - stimulates lipolysis in adipose tissue (mobilizes energy stores, spares glucose) - increases plasma glucose concentration 3. Diabetes mellitus – insulin deficiency disease a. Type 1 diabetes - insulin dependent (IDDM), “juvenile onset” b. Type 2 diabetes - non-insulin dependent (NIDDM), “adult onset” Effects and complications: - hyperglycemia - high blood glucose levels - glycosuria - excretion of glucose in the urine osmotic effect results in excessive urinary water loss (diuresis) - elevated ketones and ketoacidosis cells are “glucose starved” because of insufficient glucose uptake → increased fat and protein catabolism → excess production of ketone bodies - vascular degeneration