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Transcript
An Introduction to Endocrinology Chapter 18 & 19 Human Physiology by Sherwood BROWN-SEQUARD - Bull testicle extracts - Rejuvination - Organotheraphy - Placebo - Success in 1891 STARLING & BAYLISS X Cannula X - pancreatic duct Pancreatic secretions Drops out of pancreas Addition of an extract of jejunal mucosa (acidic) into the blood Defined “hormone”…… “THESE CHEMICAL MESSENGERS, HOWEVER, OR “HORMONES” (FROM THE GREEK, I EXCITE OR AROUSE), AS WE MIGHT CALL THEM, HAVE TO BE CARRIED FROM THE ORGANS WHERE THEY ARE PRODUCED TO THE ORGAN WHICH THEY AFFECT BY MEANS OF THE BLOODSTREAM AND THE CONTINUALLY RECURRING PHYSIOLOGICAL NEEDS OF THE ORGANSISM MUST DETERMINE THEIR REPEATED PRODUCTION AND CIRCULATION THROUGH THE BODY…” Endocrine system - A chemical communication system in body - Hormone-secreting ductless glands - Hormones : chemical messenger carried by blood from endocrine gland to target tissue Hormones 1. Amines (melatonin, thyroid hormones, catecholamines) 2. Peptides/Proteins (insulin) 3. Steroids (cortisol, androgens, oestrogen) Endocrine System Major endocrine glands Physiological Functions • Regulation of salt and water balance • Regulation of calcium balance • Regulation of energy balance/metabolism • Coping with a hostile environment (induce adaptive changes) • Co-ordination of growth • Reproduction and lactation • Regulation of circulation and digestion Hormone: is a chemical secreted by a cell or group of cells into the blood for transport to a distant target, where it exerts its effect at very low concentrations. Receptors in target organ Target organ - hormone influences function of target Endocrine gland - releases hormone into blood Tropic Hormones • Regulates hormone secretion by another endocrine gland • Stimulates and maintains their endocrine target tissues • Example – Thyroid-stimulating hormone (TSH) secreted from anterior pituitary stimulates thyroid hormone secretion by thyroid gland Termination of action • Allows body to adapt to changes in it’s internal state MECHANISMS OF CONTROL - limit secretion - remove/inactivate (metabolites are excreted) - terminating activity in target cells Plasma Concentration of Hormones is influenced by: • 1. The hormone rate of secretion • 2. The rate of Metabolic Activation or Conversion • 3. Transport • 4. Inactivation • 5. Excretion Endocrine Dysfunction • Can arise from a variety of factors • Most commonly result from abnormal plasma concentrations of a hormone caused by inappropriate rates of secretion – Hyposecretion • Too little hormone is secreted – Hypersecretion • Too much hormone is secreted Hyposecretion • Primary hyposecretion – Too little hormone is secreted due to abnormality within gland – Causes • Genetic • Dietary • Chemical or toxic • Immunologic • Other disease processes such as cancer • Secondary hyposecretion – Gland is normal but too little hormone is secreted due to deficiency of its tropic hormone Hypersecretion • Causes – Tumors that ignore normal regulatory input and continuously secrete excess hormone – Immunologic factors • Primary hypersecretion – Too much hormone is secreted due to abnormality within gland • Secondary hypersecretion – Excessive stimulation from outside the gland causes oversecretion 1. Pituitary Gland Anatomy of the Pituitary Gland epithelial tissue nervous tissue Chapter 18 The Central Endocrine Glands Human Physiology by Lauralee Sherwood ©2007 Brooks/Cole-Thomson Learning Pituitary Gland • Hypophysis • Small gland located in bony cavity just below hypothalamus – Thin stalk connects pituitary gland to hypothalamus • Consists of two anatomically and functionally distinct lobes – Posterior pituitary (neurohypophysis) • Composed of nervous tissue – Anterior pituitary (adenohypophysis) • Consists of glandular epithelial tissue Pituitary Gland • Posterior pituitary – Along with hypothalamus forms neuroendocrine system – Does not actually produce any hormones – Stores and releases two small peptide hormones: • Vasopressin - Conserves water during urine formation • Oxytocin - Stimulates uterine contraction during childbirth and milk ejection during breast-feeding Pituitary Gland Anterior Pituitary – Secretes 6 different peptide hormones • Tropic hormones – Thyroid-stimulating hormone (TSH) » Stimulates secretion of thyroid hormone – Adrenocorticotropic hormone (ACTH) » Stimulates secretion of cortisol by adrenal cortex – Growth hormone (GH) » Primary hormone responsible for growth • Not a tropic hormone – Prolactin (PRL) » Enhances breast development & milk production 2. Hypothalamus Releasing/inhibiting Releasing Gonadotrophin releasing hormone - stimulates FSH/LH release by A.pituitary Corticotrophin releasing hormone - response to stress Inhibiting Prolactin inhibiting hormone Growth hormone inhibiting hormone Dopamine Act locally as neurotransmitters Growth Hormone (P.P.) • Primarily promotes growth indirectly by stimulating liver’s production of somatomedins – Primary somatomedin is insulin-like growth factor (IGF-1 -2) • Acts directly on bone and soft tissues to bring about most growthpromoting actions • Stimulates protein synthesis, cell division, and lengthening and thickening of bones - Exerts metabolic effects not related to growth – Increases fatty acid levels in blood by enhancing breakdown of triglyceride fat stored in adipose tissue – Increases blood glucose levels by decreasing glucose uptake by muscles Growth Hormone Abnormalities • Growth hormone deficiency – Due to pituitary defect or hypothalamic dysfunction – Hyposecretion of GH in child is one cause of dwarfism – Deficiency in adults produces relatively few symptoms Growth Hormone Abnormalities • Growth hormone excess – Most often caused by tumor of GH-producing cells of anterior pituitary – Symptoms depend on age of individual when abnormal secretion begins • Gigantism – Caused by overproduction of GH in childhood before epiphyseal plates close • Acromegaly – Occurs when GH hypersecretion occurs after adolescence Acromegaly Giantism 3. Thyroid Follicular cells Synthesise Thyroglobulin - exocytosed into colloid Iodine - transferred from blood to colloid Bind together (Storage) Reuptake by follicular cells degraded & secreted Thyroxine (T4) Tri-iodothyronine (T3) Thyroid follicles Effects of thyroid hormone – Main determinant of basal metabolic rate – Influences synthesis and degradation of carbohydrate, fat, and protein – Increases target-cell responsiveness to catecholamines – Increases heart rate and force of contraction – Essential for normal growth – Plays crucial role in normal development of nervous system Hypothyroidism • Causes – Primary failure of thyroid gland – Secondary to a deficiency of TRH, TSH, or both – Inadequate dietary supply of iodine • Cretinism – Results from hypothyroidism from birth • Myxedema – Term often used for myxedema in adults • Treatment – Replacement therapy – Dietary iodine Hyperthyroidism • Most common cause is Graves’ disease – Autoimmune disease – Body erroneously produces thyroid-stimulating immunoglobulins (TSI) – Characterized by exopthalmos • Treatment – Surgical removal of a portion of the over-secreting thyroid – Administration of radioactive iodine – Use of antithyroid drugs 4. Adrenal Glands Adrenal Glands • Embedded above each kidney in a capsule of fat • Composed of two endocrine organs – Adrenal cortex • Outer portion • Secretes steroid hormones (aldostrone, cortisol) – Adrenal medulla • Inner portion • Secretes catecholamines Cortisol – Secretion - Regulated by the pituitary through Adrenocorticotropic hormone (ACTH) – Displays a characteristic diurnal rhythm – Stimulates hepatic gluconeogenesis – Inhibits glucose use by many tissues (except brain!) – Stimulates protein degradation in many tissues, especially muscle also facilitates lipolysis – Plays key role in adaptation to stress – At pharmacological levels, can have anti-inflammatory and immunosuppressive effects • Long-term use can result in unwanted side effects Cortisol Hypersecretion – Cushing’s syndrome Cushing – Causes • Overstimulation of adrenal cortex by excessive amounts of CRH and ACTH • Adrenal tumors that uncontrollably secrete cortisol independent of ACTH • ACTH-secreting tumors located in places other than the pituitary – Signs and symptoms • Hyperglycemia and glucosuria (adrenal diabetes) • Abnormal fat distributions – “buffalo hump” and “moon face” Addison’s Disease Adrenocortical insufficiency Autoimmune disease Aldosterone deficiency Hyperkalemia and hyponatremia Cortisol deficiency Hypoglycemia Lack of permissive action for many metabolic activities Poor response to stress ‘Addisonian crisis’ 5. Pancreas – Endocrine cells – Islets of Langerhans • Β (beta) cells – Site of insulin synthesis and secretion • Α (alpha) cells – Produce glucagon • D (delta) cells – Pancreatic site of somatostatin synthesis • PP cells – Least common islet cells – Secrete pancreatic polypeptide • Insulin and glucagon – Most important in regulating fuel metabolism Insulin Important after meal Secretion is increased during absorptive state • Primary stimulus for secretion is increase in blood glucose concentration • Promotes cellular uptake of glucose, fatty acids, and amino acids and enhances their conversion into glycogen, triglycerides, and proteins, respectively Lowers blood concentration of these small organic molecules Glucagon – Mobilizes energy-rich molecules from storage sites during postabsorptive state – Secreted in response to a direct effect of a fall in blood glucose on pancreatic α cells – Generally opposes actions of insulin Diabetes mellitus Describes several syndromes of abnormal carbohydrate metabolism that are characterised by hyperglycaemia. Impairment in insulin secretion Varying degrees of peripheral resistance to the action of insulin. Diabetes mellitus • Type I (insulin-dependent, juvenile-onset) – Lack of insulin secretion by ß-cells in pancreas – Require exogenous insulin for survival • Type II (non insulin-dependent, adult onset) – Normal insulin levels produced – Target cells less responsive to insulin Diabetes insipidus (DI) not related to the above Diabetes is NOT a mild disease Stroke Diabetic retinopathy Leading cause of blindness in working-age adults1 2- to 4-fold increase in cardiovascular mortality and stroke3,4 Cardiovascular disease 75% diabetic patients die from CV events4 Diabetic nephropathy Leading cause of end-stage renal disease2 Diabetic neuropathy Leading cause of non-traumatic lower extremity amputations5 Worldwide prevalence of TII diabetes in 2030 (projected) Number of persons < 5,000 5,000–74,000 75,000–349,000 350,000–1,499,000 1,500,000–4,999,000 > 5,000,000 No data available Total cases > 300 million adults World Health Organization Diabetes Programme Facts and Figures. www.who.int/diabetes/facts/world_figures/en. Accessed 21/07/2005. Central obesity contributes to hyperglycemia Obesity Visceral Fat Liver Glucose output Free fatty acids Insulin Resistance Muscle Glucose uptake