Endocrine Physiology PDF

1 ENDOCRINE PHYSIOLOGY Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. ...

1 ENDOCRINE PHYSIOLOGY Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc.  2 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions Describe the major functions of the endocrine system. Define the terms hormone, endocrine gland, endocrine tissue (organ) and target cell. Compare and contrast how the nervous and endocrine systems control body function, with emphasis on the mechanisms by which the controlling signals are transferred through the body and the time course of the responses and actions. List the major chemical classes of hormones found in the human body. Describe how each class is transported in the blood. Compare and contrast the types of receptors (cell membrane or intracellular) that each class binds to. Compare and contrast the mechanism of response that each class elicits (i.e., change in gene expression or change in an intracellular pathway via phosphorylation mechanism) and relate the response mechanism to the biochemical nature of the hormone molecule. List and describe several types of stimuli that control production and secretion of hormones. Describe the roles of negative and positive feedback in controlling hormone release. Define the terms paracrine and autocrine. Describe the locations of and the anatomical relationships between the hypothalamus, anterior pituitary and posterior pituitary glands. Define the terms releasing hormone, inhibiting hormone and tropic hormone. Explain the role of the hypothalamus in the release of anterior pituitary hormones. Explain the role of the hypothalamus in the production and release of posterior pituitary hormones.  3 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions Use the hormones below (grouped by organs) to perform outcomes a through d: Pituitary: growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle stimulating hormone, prolactin, adrenocorticotropic hormone, oxytocin, antidiuretic hormone Thyroid gland: thyroxine, triiodothyronine, calcitonin Parathyroid gland: parathyroid hormone Adrenal gland: glucocorticoids, mineralocorticoids, gonadocorticoids, epinephrine, norepinephrine Testis: testosterone, inhibin Ovary: estrogen, progesterone, inhibin Pancreas: insulin, glucagon Other endocrine tissues: erythropoietin, calcitriol, thymosin, atrial natriuretic peptide, gastrin, secretin, cholecystokinin, motilin, gastric inhibiting peptide, leptin, resistin Describe the stimulus for release of the hormone Identify the gland or tissue/organ and the cells within that gland/tissue/organ that produce the hormone. Name the target tissue or cells for the hormone and describe the effect(s) of the hormone on the target tissue or cells. Predict the larger effect that fluctuations in the hormone level will have on conditions (variables) within the body. Describe the three stages of the stress response (general adaption syndrome). List the hormones released during short-term stress and describe the hormonal actions. List the major hormones released during long-term stress and describe the hormonal actions. Provide specific examples to demonstrate how the endocrine organs respond to maintain homeostasis in the body. Explain how the endocrine organs relate to other body organs and systems to maintain homeostasis. Predict factors or situations affecting the endocrine organs that could disrupt homeostasis. Predict the types of problems that would occur in the body if the various endocrine organs could not maintain homeostasis. Figure 16.1 Location of selected endocrine organs of the body. 4 Pineal gland Hypothalamus Pituitary gland Thyroid gland Parathyroid glands (on dorsal aspect of thyroid gland) Thymus Adrenal glands Pancreas Gonads Ovary (female) Testis (male)  5 Endocrine System: Overview Endocrinology - Study of hormones and endocrine organs Acts with nervous system to coordinate and integrate activity of body cells  Response slower but longer lasting than nervous system Influences metabolic activities via hormones transported in blood Controls and integrates Reproduction Growth and development Maintenance of electrolyte, water, and nutrient balance of blood Regulation of cellular metabolism and energy balance Mobilization of body defenses  6 Chemical Messengers Hormones: long-distance chemical signals; travel in blood or lymph Autocrines: chemicals that exert effects on same cells that secrete them Paracrines: locally acting chemicals that affect cells other than those that secrete them Autocrines and paracrines are local chemical messengers; not considered part of endocrine system  7 Mechanisms of Hormone Action Though hormones circulate systemically, only cells with receptors for that hormone are affected Target cells Tissues with receptors for specific hormone Hormones alter target cell activity Hormone action on target cells may be: Alter plasma membrane permeability and/or membrane potential by opening or closing ion channels Stimulate synthesis of enzymes or other proteins Activate or deactivate enzymes Induce secretory activity Stimulate mitosis  8 Mechanisms of Hormone Action Hormones act at receptors in one of two ways, depending on their chemical nature and receptor location 1. Water-soluble hormones (all amino acid–based hormones except thyroid hormone) Act on plasma membrane receptors Act via G protein second messengers Cyclic AMP PIP2-Calcium Cannot enter cell 2. Lipid-soluble hormones (steroid and thyroid hormones) Act on intracellular receptors that directly activate genes Can enter cell  9 Plasma Membrane Receptors and Second-Messenger Systems Cyclic AMP (cAMP) signaling mechanism 1. Hormone (first messenger) binds to receptor 2. Receptor activates a G protein 3. G protein activates or inhibits effector enzyme adenylate cyclase 4. Adenylate cyclase then converts ATP to cAMP (second messenger) 5. cAMP activates protein kinases that phosphorylate (add a phosphate) other proteins Phosphorylated proteins are then either activated or inactivated cAMP is rapidly degraded by enzyme phosphodiesterase, stopping cascade Cascades have huge amplification effect Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones. 10 Slide 1 Recall from Chapter 3 that G protein signaling mechanisms are like a molecular relay race. Hormone Receptor G protein Enzyme 2nd 1 Hormone (1st messenger) binds (1st messenger) messenger receptor. Adenylate cyclase Extracellular fluid G protein (Gs) cAMP 5 cAMP activates GTP protein kinases. Receptor GTP ATP Inactive Active GDP GTP protein protein kinase kinase Triggers responses of target cell (activates enzymes, stimulates cellular secretion, opens ion channel, etc.) Cytoplasm 2 Receptor 3 G protein 4 Adenylate activates G activates cyclase converts protein (Gs). adenylate ATP to cAMP (2nd cyclase. messenger).  11 Plasma Membrane Receptors and Second-Messenger Systems PIP2-calcium signaling mechanism Hormone-activated G protein activates a different effector enzyme: phospholipase C Activated phospholipase C splits membrane protein, PIP2, into two second messengers: Diacylglycerol (DAG) activates protein kinases Inositol trisphosphate (IP3) causes Ca2+ release from intracellular storage sites Calcium ions act as another second messenger Ca2+ alters enzyme activity and channels, or binds to regulatory protein calmodulin Calcium-bound calmodulin activates enzymes that amplify cellular response  12 Intracellular Receptors and Direct Gene Activation Steroid hormones and thyroid hormone 1. Diffuse into target cells and bind with intracellular receptors 2. Receptor-hormone complex enters nucleus; binds to specific region of DNA 3. Prompts DNA transcription to produce mRNA 4. mRNA directs protein synthesis 5. Promote metabolic activities, or promote synthesis of structural proteins or proteins for export from cell Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones. 13 Slide 1 Steroid Extracellular hormone Plasma fluid membrane 1 The steroid hormone diffuses through the plasma membrane and binds an intracellular Cytoplasm receptor. Receptor Receptor- protein hormone complex 2 The receptor- hormone complex enters the nucleus. Receptor Nucleus Binding region 3 The receptor- hormone complex binds a specific DNA region. DNA 4 Binding initiates transcription of the gene to mRNA. mRNA 5 The mRNA directs protein synthesis. New protein  14 Target Cell Activation Target cell specificity Target cell activation depends on three factors 1. Blood levels of hormone 2. Relative number of receptors on or in target cell 3. Affinity of binding between receptor and hormone Hormones influence number of their receptors Up-regulation—target cells form more receptors in response to low hormone levels Down-regulation—target cells lose receptors in response to high hormone levels  15 CONTROL OF HORMONE RELEASE Figure 16.4a Three types of endocrine gland stimuli. 16 Slide 1 Humoral Stimulus Hormone release caused by altered levels of certain critical ions or nutrients. Capillary (low Ca2+ in blood) Thyroid gland (posterior view) Parathyroid glands Parathyroid glands PTH Stimulus: Low concentration of Ca2+ in capillary blood. Response: Parathyroid glands secrete parathyroid hormone (PTH), which increases blood Ca2+. Figure 16.4b Three types of endocrine gland stimuli. 17 Slide 1 Neural Stimulus Hormone release caused by neural input. CNS (spinal cord) Preganglionic sympathetic fibers Medulla of adrenal gland Capillary Stimulus: Action potentials in preganglionic sympathetic fibers to adrenal medulla. Response: Adrenal medulla cells secrete epinephrine and norepinephrine. Figure 16.4c Three types of endocrine gland stimuli. 18 Slide 1 Hormonal Stimulus Hormone release caused by another hormone (a tropic hormone). Hypothalamus Anterior pituitary gland Thyroid Adrenal Gonad gland cortex (Testis) Stimulus: Hormones from hypothalamus. Response: Anterior pituitary gland secretes hormones that stimulate other endocrine glands to secrete hormones.  19 Hormones in the Blood Hormones circulate in blood either free or bound Steroids and thyroid hormone are attached to plasma proteins All others circulate without carriers Concentration of circulating hormone reflects Rate of release Speed of inactivation and removal from body Hormones removed from blood by Degrading enzymes Kidneys Liver Half-life—time required for hormone's blood level to decrease by half Varies from fraction of minute to a week  20 Interaction of Hormones at Target Cells Multiple hormones may act on same target at same time Permissiveness: one hormone cannot exert its effects without another hormone being present Example: reproductive hormones need thyroid hormone to have effect Synergism: more than one hormone produces same effects on target cell, causing amplification Example: glucagon and epinephrine both cause liver to release glucose Antagonism: one or more hormones oppose(s) action of another hormone Example: insulin and glucagon  21 Comparison between Lipid- and Water-Soluble Hormones Table 16.2 Comparison between Lipid- and Water- Soluble Hormones.  22 HYPOTHALAMUS & PITUITARY  23 The Pituitary Gland (Hypophysis) Corpus callosum Thalamus Pineal Hypothalamus Mammillary body Brain stem Pituitary (hypophysis) Posterior Anterior lobe lobe Optic chiasma Mammillary Median eminence body Chromophobe of hypothalamus Tuber cinereum cells Anterior lobe Posterior lobe Basophil Pars tuberalis Infundibulum cells Pars intermedia Pars nervosa Acidophil Pars distalis cells Pituicytes (neuroglia)  Figure 16.5b The hypothalamus controls release of hormones from the pituitary 24 gland in two different ways. Slide 1 Hypothalamus Hypothalamic neurons synthesize GHRH, GHIH, TRH, Anterior lobe CRH, GnRH, PIH. of pituitary Superior hypophyseal artery 1 When appropriately stimulated, 2 Hypothalamic hormones travel hypothalamic neurons secrete through portal veins to the anterior releasing or inhibiting hormones into pituitary where the primary capillary plexus. they stimulate or inhibit Hypophyseal release of hormones made in the anterior pituitary. portal system Primary capillary 3 In response to releasing plexus A portal hormones, the anterior pituitary Hypophyseal system is secretes hormones into the two portal veins secondary capillary plexus. This capillary in turn empties into the general Secondary plexuses circulation. capillary plexus (beds) connected GH, TSH, ACTH, by veins. FSH, LH, PRL Anterior lobe of pituitary  25 The Hypothalamus Controls Release of Hormones from the Pituitary Gland in Two Different Ways Posterior Pituitary: Nerve impulses travel down the axons of hypothalamic neurons, causing hormone release from their axon terminals in the posterior pituitary. Paraventricular nucleus Hypothalamus 1 Hypothalamic neurons synthesize oxytocin or antidiuretic hormone (ADH). Posterior lobe of pituitary Optic chiasma Supraoptic nucleus Infundibulum 2 Oxytocin and ADH are (connecting stalk) transported down the axons of the hypothalamohypophyseal tract to Inferior Hypothalamo- the posterior pituitary. hypophyseal hypophyseal artery tract Axon terminals 3 Oxytocin and ADH are stored in axon terminals in the posterior Posterior lobe pituitary. of pituitary Oxytocin Antidiuretic hormone (ADH) 4 When associated hypothalamic neurons fire, nerve impulses arriving at the axon terminals cause oxytocin or ADH to be released into the blood.  26 Posterior Pituitary and Hypothalamic Hormones Oxytocin ADH Each composed of nine amino acids Almost identical – differ in two amino acids  27 Oxytocin Strong stimulant of uterine contraction Released during childbirth Hormonal trigger for milk ejection Acts as neurotransmitter in brain  28 ADH (Vasopressin) Inhibits or prevents urine formation Regulates water balance Targets kidney tubules  reabsorb more water Release also triggered by pain, low blood pressure, and drugs Inhibited by alcohol, diuretics High concentrations  vasoconstriction  29 ADH Diabetes insipidus ADH deficiency due to hypothalamus or posterior pituitary damage Must keep well-hydrated Syndrome of inappropriate ADH secretion (SIADH) Retention of fluid, headache, disorientation Fluid restriction; blood sodium level monitoring  30 Anterior Pituitary Hormones Growth hormone (GH) Thyroid-stimulating hormone (TSH) or thyrotropin Adrenocorticotropic hormone (ACTH) Follicle-stimulating hormone (FSH) Luteinizing hormone (LH) Prolactin (PRL)  31 Anterior Pituitary Hormones All are proteins All except GH activate cyclic AMP second- messenger systems at their targets TSH, ACTH, FSH, and LH are all tropic hormones (regulate secretory action of other endocrine glands)  32 Growth Hormone (GH, or Somatotropin) Produced by somatotropic cells Direct actions on metabolism Increases blood levels of fatty acids; encourages use of fatty acids for fuel; protein synthesis Decreases rate of glucose uptake and metabolism – conserving glucose  Glycogen breakdown and glucose release to blood (anti- insulin effect)  33 Growth Hormone (GH, or Somatotropin) Indirect actions on growth Mediates growth via growth-promoting proteins – insulin-like growth factors (IGFs) IGFs stimulate Uptake of nutrients  DNA and proteins Formation of collagen and deposition of bone matrix Major targets—bone and skeletal muscle  34 Homeostatic Imbalances of Growth Hormone Hypersecretion In children results in gigantism In adults results in acromegaly Hyposecretion In children results in pituitary dwarfism Figure 16.6 Growth-promoting and metabolic actions of growth hormone35(GH). Hypothalamus secretes growth Feedback Inhibits GHRH release hormone–releasing Stimulates GHIH release hormone (GHRH), and Anterior pituitary GHIH (somatostatin) Inhibits GH synthesis and release Growth hormone (GH) Indirect actions Direct actions (growth- (metabolic, promoting) anti-insulin) Liver and other tissues Produce Insulin-like growth factors (IGFs) Effects Effects Fat Carbohydrate Skeletal Extraskeletal metabolism metabolism Increases, stimulates Reduces, inhibits Increased protein Initial stimulus Increased cartilage Increased Increased blood synthesis, and formation and fat breakdown glucose and other Physiological response cell growth and skeletal growth and release anti-insulin effects proliferation Result  36 Thyroid-stimulating Hormone (Thyrotropin) Produced by thyrotropic cells of anterior pituitary Stimulates normal development and secretory activity of thyroid Release triggered by thyrotropin-releasing hormone from hypothalamus Inhibited by rising blood levels of thyroid hormones that act on pituitary and hypothalamus Figure 16.8 Regulation of thyroid hormone secretion. 37 Hypothalamus TRH Anterior pituitary TSH Thyroid gland Thyroid hormones Stimulates Target cells Inhibits  38 Adrenocorticotropic Hormone (Corticotropin) Secreted by corticotropic cells of anterior pituitary Stimulates adrenal cortex to release corticosteroids Regulation of ACTH release Triggered by hypothalamic corticotropin-releasing hormone (CRH) in daily rhythm Internal and external factors such as fever, hypoglycemia, and stressors can alter release of CRH  39 Gonadotropins Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) Secreted by gonadotropic cells of anterior pituitary FSH stimulates gamete (egg or sperm) production LH promotes production of gonadal hormones Absent from the blood in prepubertal boys and girls Regulation of gonadotropin release Triggered by gonadotropin-releasing hormone (GnRH) during and after puberty Suppressed by gonadal hormones (feedback)  40 Prolactin (PRL) Secreted by prolactin cells of anterior pituitary Stimulates milk production Role in males not well understood  41 Prolactin (PRL) Regulation of PRL release Primarily controlled by prolactin-inhibiting hormone (PIH) (dopamine) Blood levels rise toward end of pregnancy Suckling stimulates PRL release and promotes continued milk production Hypersecretion causes inappropriate lactation, lack of menses, infertility in females, and impotence in males  42 THYROID GLAND  Figure 16.9 The thyroid gland. 43 Hyoid bone Thyroid cartilage Epiglottis Colloid-filled follicles Follicular cells Superior thyroid Common carotid artery artery Inferior thyroid artery Isthmus of thyroid gland Trachea Left subclavian artery Left lateral lobe of thyroid gland Aorta Parafollicular cells Gross anatomy of the thyroid gland, anterior view Photomicrograph of thyroid gland follicles (145x)  44 Thyroid Hormone (TH) Actually two related compounds T4 (thyroxine); has 2 tyrosine molecules + 4 bound iodine atoms T3 (triiodothyronine); has 2 tyrosines + 3 bound iodine atoms Affects virtually every cell in body Major metabolic hormone Increases metabolic rate and heat production (calorigenic effect) Regulation of tissue growth and development Development of skeletal and nervous systems Reproductive capabilities Maintenance of blood pressure Figure 16.10 Synthesis of thyroid hormone. 45 Slide 1 Thyroid follicular cells Colloid 1 Thyroglobulin is synthesized and discharged into the follicle lumen. Tyrosines (part of thyroglobulin molecule) Capillary 4 Iodine is attached to tyrosine in colloid, forming DIT and MIT. Golgi apparatus Rough Thyro- ER Iodine globulin 3 Iodide DIT MIT colloid is oxidized to iodine. Iodide (I−) 2 Iodide (I–) is trapped (actively transported in). T4 5 Iodinated tyrosines are T3 linked together to form T3 Lysosome and T4. T4 6 Thyroglobulin colloid is endocytosed and combined T3 7 Lysosomal enzymes with a lysosome. T4 Colloid in cleave T4 and T3 from lumen of T3 thyroglobulin and hormones diffuse into bloodstream. follicle To peripheral tissues  46 Transport and Regulation of TH T4 and T3 transported by thyroxine-binding globulins (TBGs) Both bind to target receptors, but T3 is ten times more active than T4 Peripheral tissues convert T4 to T3 Negative feedback regulation of TH release Rising TH levels provide negative feedback inhibition on release of TSH Hypothalamic thyrotropin-releasing hormone (TRH) can overcome negative feedback during pregnancy or exposure to cold Figure 16.8 Regulation of thyroid hormone secretion. 47 Hypothalamus TRH Anterior pituitary TSH Thyroid gland Thyroid hormones Stimulates Target cells Inhibits  48 Table 16.4 Major Effects of Thyroid Hormone (T4 and T3) in the Body Table 16.4 Major Effects of Thyroid Hormone (T4 and T3) in the Body.  49 Homeostatic Imbalances of TH Hyposecretion in adults—myxedema; goiter if due to lack of iodine Hyposecretion in infants—cretinism Hypersecretion—most common type is Graves' disease  50 Calcitonin Produced by parafollicular (C) cells No known physiological role in humans Antagonist to parathyroid hormone (PTH) At higher than normal doses Inhibits osteoclast activity and release of Ca2+ from bone matrix Stimulates Ca2+ uptake and incorporation into bone matrix  51 PARATHYROID GLANDS Figure 16.12 The parathyroid glands. 52 Pharynx (posterior aspect) Capillary Thyroid Parathyroid gland cells Parathyroid glands (secrete parathyroid Esophagus hormone) Trachea Oxyphil cells  53 Parathyroid Hormone Functions Stimulates osteoclasts to digest bone matrix and release Ca2+ to blood Enhances reabsorption of Ca2+ and secretion of phosphate by kidneys Promotes activation of vitamin D (by kidneys); increases absorption of Ca2+ by intestinal mucosa Negative feedback control: rising Ca2+ in blood inhibits PTH release Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine. 54 Hypocalcemia (low blood Ca2+) PTH release from parathyroid gland Osteoclast activity Ca2+ reabsorption Activation of in bone causes Ca2+ in kidney tubule vitamin D by kidney and PO43- release into blood Ca2+ absorption from food in small intestine Ca2+ in blood Initial stimulus Physiological response Result  55 Homeostatic Imbalances of PTH Hyperparathyroidism due to tumor Bones soften and deform Elevated Ca2+ depresses nervous system and contributes to formation of kidney stones Hypoparathyroidism following gland trauma or removal or dietary magnesium deficiency Results in tetany, respiratory paralysis, and death  56 ADRENAL GLANDS  Figure 16.14 Microscopic structure of the adrenal gland. 57 Hormones Capsule secreted Zona glomerulosa Aldosterone Zona fasciculata Cortex Adrenal gland Medulla Cortex Cortisol and androgens Kidney Zona reticularis Medulla Adrenal medulla Epinephrine and norepinephrine Drawing of the histology of the Photomicrograph (115x) adrenal cortex and a portion of the adrenal medulla  58 Mineralocorticoids Regulate electrolytes (primarily Na+ and K+) in ECF Importance of Na+: affects ECF volume, blood volume, blood pressure, levels of other ions Importance of K+: sets RMP of cells Aldosterone most potent mineralocorticoid Stimulates Na+ reabsorption and water retention by kidneys; elimination of K+  59 Aldosterone Release triggered by Decreasing blood volume and blood pressure Rising blood levels of K+  60 Mechanisms of Aldosterone Secretion Renin-angiotensin-aldosterone mechanism: decreased blood pressure stimulates kidneys to release renin  triggers formation of angiotensin II, a potent stimulator of aldosterone release Plasma concentration of K+: increased K+ directly influences zona glomerulosa cells to release aldosterone ACTH: causes small increases of aldosterone during stress Atrial natriuretic peptide (ANP): blocks renin and aldosterone secretion to decrease blood pressure Figure 16.15 Major mechanisms controlling aldosterone release from the adrenal cortex. 61 Primary regulators Other factors Blood volume K+ in blood Stress Blood pressure and/or blood and/or blood pressure volume Hypo- Heart thalamus Kidney CRH Direct Anterior stimulating pituitary Renin effect Initiates cascade that produces ACTH Atrial natriuretic peptide (ANP) Angiotensin II Inhibitory effect Zona glomerulosa of adrenal cortex Enhanced secretion of aldosterone Targets kidney tubules Absorption of Na+ and water; increased K+ excretion Blood volume and/or blood pressure  62 Glucocorticoids Keep blood glucose levels relatively constant Maintain blood pressure by increasing action of vasoconstrictors Cortisol (hydrocortisone) Only one in significant amounts in humans Cortisone Corticosterone  63 Glucocorticoids: Cortisol Released in response to ACTH, patterns of eating and activity, and stress Prime metabolic effect is gluconeogenesis— formation of glucose from fats and proteins Promotes rises in blood glucose, fatty acids, and amino acids "Saves" glucose for brain Enhances vasoconstriction  rise in blood pressure to quickly distribute nutrients to cells  64 Homeostatic Imbalances of Glucocorticoids Hypersecretion—Cushing's syndrome/disease Depresses cartilage and bone formation Inhibits inflammation Depresses immune system Disrupts cardiovascular, neural, and gastrointestinal function Hyposecretion—Addison's disease Also involves deficits in mineralocorticoids Decrease in glucose and Na+ levels Weight loss, severe dehydration, and hypotension  65 Gonadocorticoids (Sex Hormones) Most weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens May contribute to Onset of puberty Appearance of secondary sex characteristics Sex drive in women Estrogens in postmenopausal women  66 Adrenal Medulla Medullary chromaffin cells synthesize epinephrine (80%) and norepinephrine (20%) Effects Vasoconstriction Increased heart rate Increased blood glucose levels Blood diverted to brain, heart, and skeletal muscle Responses brief Epinephrine stimulates metabolic activities, bronchial dilation, and blood flow to skeletal muscles and heart Norepinephrine influences peripheral vasoconstriction and blood pressure  67 Adrenal Medulla Hypersecretion Hyperglycemia, increased metabolic rate, rapid heartbeat and palpitations, hypertension, intense nervousness, sweating Pheochromocytoma Benign vs Malignant Hyposecretion Not problematic Adrenal catecholamines not essential to life Figure 16.17 Stress and the adrenal gland. 68 Short-term stress Prolonged stress Stress Nerve impulses Hypothalamus CRH (corticotropin- releasing hormone) Spinal cord Corticotropic cells of anterior pituitary Preganglionic To target in blood sympathetic fibers Adrenal cortex Adrenal medulla (secretes steroid (secretes amino acid– hormones) based hormones) ACTH Catecholamines Mineralocorticoids Glucocorticoids (epinephrine and norepinephrine) Short-term stress response Long-term stress response Heart rate increases Kidneys retain Proteins and fats converted Blood pressure increases sodium and water to glucose or broken down Bronchioles dilate Blood volume and for energy Liver converts glycogen to glucose and releases blood pressure Blood glucose increases glucose to blood rise Immune system Blood flow changes, reducing digestive system activity supressed and urine output Metabolic rate increases  69 PANCREAS Figure 16.18 Photomicrograph of differentially stained pancreatic tissue. 70 Pancreatic islet  (Glucagon- producing) cells  (Insulin- producing) cells Pancreatic acinar cells (exocrine)  71 Glucagon Major target—liver Causes increased blood glucose levels Effects Glycogenolysis—breakdown of glycogen to glucose Gluconeogenesis—synthesis of glucose from lactic acid and noncarbohydrates Release of glucose to blood  72 Insulin Effects of insulin Lowers blood glucose levels Enhances membrane transport of glucose into fat and muscle cells Inhibits glycogenolysis and gluconeogenesis Participates in neuronal development and learning and memory Not needed for glucose uptake in liver, kidney or brain Figure 16.19 Insulin and glucagon from the pancreas regulate blood glucose levels. 73 Stimulates glucose uptake by cells Insulin Tissue cells Stimulates glycogen formationw Pancreas Glucose Glycogen Blood Liver glucose falls to normal range. IMB ALA NC Stimulus E Blood glucose level BALANCE: Normal blood glucose level (about 90 mg/100 ml) Stimulus Blood IMB ALA glucose level NC Blood E glucose rises to normal range. Pancreas Glucose Glycogen Liver Stimulates glycogen Glucagon breakdown  74 Factors That Influence Insulin Release Elevated blood glucose levels – primary stimulus Rising blood levels of amino acids and fatty acids Release of acetylcholine by parasympathetic nerve fibers Hormones glucagon, epinephrine, growth hormone, thyroxine, glucocorticoids Somatostatin; sympathetic nervous system  75 Homeostatic Imbalances of Insulin Diabetes mellitus (DM) Due to hyposecretion (type 1) or hypoactivity (type 2) of insulin Blood glucose levels remain high  nausea  higher blood glucose levels (fight or flight response) Glycosuria – glucose spilled into urine Fats used for cellular fuel  lipidemia; if severe  ketones (ketone bodies) from fatty acid metabolism  ketonuria and ketoacidosis Untreated ketoacidosis  hyperpnea; disrupted heart activity and O2 transport; depression of nervous system  coma and death possible  76 Diabetes Mellitus: Signs Three cardinal signs of DM Polyuria—huge urine output Glucose acts as osmotic diuretic Polydipsia—excessive thirst From water loss due to polyuria Polyphagia—excessive hunger and food consumption Cells cannot take up glucose; are "starving"  77 GONADS  78 Ovaries and Placenta Gonads produce steroid sex hormones Same as those of adrenal cortex Ovaries produce estrogens and progesterone Estrogen Maturation of reproductive organs Appearance of secondary sexual characteristics With progesterone, causes breast development and cyclic changes in uterine mucosa Placenta secretes estrogens, progesterone, and human chorionic gonadotropin (hCG)  79 Testes Testes produce testosterone Initiates maturation of male reproductive organs Causes appearance of male secondary sexual characteristics and sex drive Necessary for normal sperm production Maintains reproductive organs in functional state