Chapter 16 Endocrine System Notes PDF

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Chapter 16 Endocrine System Overview - Endocrine system acts with nervous system to coordinate and integrate activity of body cells - Influences metabolic activities via hormones transported in blood - Responses slower but longer lasting than nervous system responses - Endocrinology: study of hormones and endocrine organs 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 Exocrine glands: - Produce nonhormonal substances (examples: sweat, saliva) - Have ducts to carry secretion to membrane Endocrine glands: - Produce hormones, lack ducts Chemical Messengers of Endocrine System - 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 Hormone Chemical Structure Two main classes of hormones: - Amino acid-based hormones: amino acid derivatives, peptides and proteins - Steroids: Synthesized from cholesterol, gonadal and adrenocortical hormones Action of Hormones - Though hormones circulate systemically, only cells with receptors for that hormone are affected - Target cells: tissues with receptors for a specific hormone - Hormones alter target cell activity - Hormones act in one of two ways, depending on their chemical nature and receptor location o Water-soluble hormones (all amino acid-based hormones except thyroid hormone)  Act on plasma membrane receptors o Lipid-soluble hormones (steroid and thyroid hormones)  Can enter cell - Hormone Action on Target Cell May Be To: o Alter plasma membrane permeability and/or membrane potential by opening or closing ion channels o Stimulate synthesis of enzymes or other proteins o Activate or deactivate enzymes

o Induce secretory activity o Stimulate mitosis - Plasma Membrane Receptors and Second-Messenger Systems o Cyclic AMP (cAMP) signaling mechanism 1. Hormone (1st messenger) binds receptor 2. Receptor activates G protein 3. G protein activates adenylate cyclase 4. Adenylate cyclase converts ATP to cAMP (2nd messenger) 5. cAMP activates protein kinases that phosphorylate (add a phosphate) other proteins - Intracellular Receptors and Direct Gene Activation 1. Lipid-soluble steroid hormones and thyroid hormone can diffuse into target cells and bind with intracellular receptors 2. Receptor-hormone complex enters nucleus and binds to specific region of DNA 3. Helps initiate DNA transcription to produce mRNA 4. mRNA is then translated into specific protein a. Protein synthesized have various functions b. Ex: metabolic activities, structural purposes or exported from cell Hormone Release - Blood levels of hormones controlled by: o Negative feedback systems  Increased hormone effects on target organs can inhibit further hormone release o Levels vary only within narrow, desirable range - Endocrine Gland Stimuli o Hormone release is triggered by:  Endocrine gland stimuli  Nervous system modulation o Endocrine glands are stimulated to synthesize and release hormones in response to one of three stimuli:  Humoral stimuli  Changing blood levels of ions and nutrients directly stimulate secretion of hormones  Example: Ca2+ o Declining blood Ca2+ concentration stimulates parathyroid glands to secrete PTH (parathyroid hormone) o PTH causes Ca2+ concentrations to rise and stimulus is removed  Neural stimuli  Nerve fibers stimulate hormone release o Sympathetic nervous system fibers stimulate adrenal medulla to secrete catecholamines  Hormonal stimuli  Hormones stimulate other endocrine organs to release their hormones o Hypothalamic hormones stimulate release of most anterior pituitary hormones

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Anterior pituitary hormones stimulate targets to secrete still more hormones Hypothalamic-pituitary-target organs inhibit release of anterior pituitary hormones

Nervous System Modulation o Nervous system can make adjustments to hormone levels when needed  Can modify stimulation or inhibition of endocrine glands  Nervous system can override normal endocrine controls  Ex: under severe stress, hypothalamus and sympathetic nervous system override insulin to allow blood glucose levels to increase Target Cell Specificity Target cells must have specific receptors to which hormone binds - Ex: ACTH receptors are found only on certain cells of adrenal cortex, but thyroxin receptors are found on nearly all cells of body Target cell activation depends on three factors: - Blood levels of hormone - Relative number of receptors on/in target cell - Affinity (strength) of binding between receptor and hormone Amount of hormone can influence number of receptors for that hormone - Up-regulation: o Target cells form more receptors in response to low hormone levels o Target cells have greater affinity to hormones - Down-Regulation: o Target cells lose receptors in response to prevent them from overreacting to persistently high levels of hormone (lower affinity) Half-Life, Onset and Duration of Hormone Activity - Concentration of circulating hormone reflects: o Rate of release o Speed at which it is inactivated and removed from body - Release o Hormones circulate in blood either free or bound o Steroids and thyroid hormone are attached to plasma proteins (mainly albumin) o All others circulate without carriers - Removal o Hormones can be removed from body by:  Degrading enzymes or  Kidneys or liver  Half-life: time required for level of hormone in blood level to decrease by half - Hormones have different responses times: o Some responses are immediate o Some, especially steroid, can take hours to days o Some are inactive until they enter target cells - The duration of response is usually limited

Ranges from 10 seconds to several hours Effects may disappear rapidly as blood levels drop, but some may persist for hours at low blood levels - Half-life, onset and duration of hormone activity are dependent on whether the hormone is water or lipid soluble The Hypothalamus Hypothalamus is connected to pituitary gland via stalk called infundibulum Pituitary Gland Pituitary secretes at least eight major hormones It has two major lobes: - Posterior pituitary composed of neural tissue that secretes neurohormones o Posterior lobe, along with infundibulum make up the neurohypophysis - Anterior pituitary: (adenohypophysis) consists of glandular tissue Posterior Pituitary: 1. Hypothalamic neurons synthesize oxytocin or antidiuretic hormone (ADH) 2. Oxytocin and ADH are transported down the axons of the hypothalamic-hypophyseal tract to the posterior pituitary 3. Oxytocin and ADH are stored in axon terminals in the posterior pituitary 4. When associated hypothalamic neurons fire, action potentials arriving at the axon terminals cause oxytocin or ADH to be released into the blood Pituitary-Hypothalamic Relationships - Maintains neural connection to hypothalamus via hypothalamic-hypophyseal tract o Tract arises from neurons in paraventricular and supraoptic nuclei in hypothalamus o Runs through infundibulum - Secretes two neurohormones (oxytocin and ADH) o Hormones are stored in axon terminals in posterior pituitary and are released into blood when neurons fire - Oxytocin o Strong stimulant of uterine contractions released during childbirth o Also acts as hormonal trigger for milk ejection - Antidiuretic hormone (ADH) o Hypothalamus contains osmoreceptors that monitor solute concentrations and sodium o If concentration too high, posterior pituitary triggered or prevent urine formation o Release also triggered by pain, low blood pressure and drugs o Inhibited by alcohol, diuretics o High concentrations cause vasoconstriction, so also called vasopressin Clinical Homeostasis Imbalance 16.1 - Diabetes insipidus o ADH deficiency due to damage to hypothalamus or posterior pituitary o Must keep well hydrated - Syndrome of inappropriate ADH secretion (SIADH) o Retention of fluid, headache disorientation o Fluid restriction; blood sodium level monitoring Anterior Pituitary Hormones o o

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All six hormones are peptide hormones All but growth hormone (GH) activate target cells via cAMP second-messenger system All but two are tropic hormones (tropins) that regulate secretion of other hormones o Growth Hormone (GH) o Thyroid-stimulating hormone (TSH) (tropic) o Adrenocorticotropic hormone (ACTH) (tropic) o Follicle-stimulating hormone (FSH) (tropic) o Luteinizing hormone (LH) (tropic) o Prolactin (PRL) Growth Hormone (somatotropin) o Produced by somatotropic cells o Has direct actions on metabolism and direct growth-promoting actions o Direct actions on metabolism  Glucose-sparing actions decrease rate of cellular glucose uptake and metabolism (anti-insulin effects)  Triggers liver to break down glycogen into glucose  Increases blood levels of fatty acids for use as fuel and encourages cellular protein synthesis o Indirect actions on growth  GH triggers liver, skeletal muscle, and bone to produce insulin-like growth factors (IGF)  IGFs then stimulate:  Cellular uptake of nutrients used to synthesize DNA and proteins needed for cell division  Formation of collagen and deposition of bone matrix  GH stimulates most cells to enlarge and divide, but major targets are bone and skeletal muscle o Regulatory of Secretion  GH release or inhibition chiefly regulated by hypothalamic hormones on somatotropic cells  GH-Releasing Hormone (GHRH) – simulates GH release o Triggered by low blood GH or glucose or high amino acid levels  GH-Inhibiting Hormone (GHIH) – inhibits release o Triggered by increase in GH and IGF levels o Clinical – Homeostatic Imbalance 16.2  Hypersecretion of GH is usually caused by anterior pituitary tumor  In children by anterior pituitary tumor o In children results in gigantism  Can reach heights of 8 feet o In adults results in acromegaly  Overgrowth of hands, feet and face  Hyposecretion of GH  In children results in pituitary dwarfism o May reach height of only 4 feet

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 In adults usually causes no problems Thyroid-stimulating hormone (TSH) o Tropic hormone that is also called thyrotropin as it is produced by thyrotropic cells o Stimulates normal development and secretory activity of thyroid (T3 and T4) o Release triggered by thyrotropin-releasing hormone (TRH) from hypothalamus

Adrenocorticotropic hormone (ACTH) o Also called corticotropin as it is secreted by corticotropic cells o ACTH stimulates adrenal cortex to release corticosteroids (mainly cortisol) o Regulation of ACTH release  Triggered by hypothalamic corticotropin-releasing hormone (CRH) in daily rhythm  Highest levels in morning Gonasotropins (FSH and LH) o Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are secreted by gonadotropic cells of anterior pituitary o FSH stimulates production of gametes (egg or sperm) o LH promotes production of gonadal hormones  In females, LH helps mature follicles of egg, triggers ovulation and release of estrogen and progesterone  In males, LH stimulates production of testosterone Prolactin (PRL) o Secreted by prolactin cells of anterior pituitary o Stimulates milk production in females; role in males not well understood o Regulation primarily controlled by prolactin-inhibiting (PIH), which is dopamine Clinical – Homeostatic Imbalance 16.3 o Hyposecretion of PRL not a problem in anyone except women who choose to nurse o Hyperprolactinemia (abnormally high levels of PRL is the most frequent abnormality o Clinical signs include:  Inappropriate lactation  Lack of menses  Infertility in females

 Impotence in males Thyroid Gland Location: butterfly-shaped gland in anterior neck of the trachea, just interior to larynx, that consists of: - Isthmus: median mass connecting two lateral lobes - Colloid: Fluid of follicle lumen containing thyroglobulin plus iodine and is precursor to thyroid hormone - Parafollicular cells: produce hormone calcitonin Synthesis of Thyroid Hormone: - Thyroglobulin is synthesized and discharged into follicle lumen - Iodide is trapped: iodide ions (I-) are actively taken into cell and released into lumen - Iodide oxidized: electrons are removed, converting it to iodine (I2) - Iodine is attached to tyrosine: o Monoiodotyrosine (MIT): formed if only one iodine attaches o Diiodotyrosine (DIT): formed if two iodines attach - Iodinated tyrosines link together to form T3 and T4 o If one MIT and one DIT link, T3 is formed o If two DITs link, T4 is formed - Colloid is endocytosed by follicular cells - Lysosomal enzymes cleave T3 and T4 from thyroglobulin o Hormones are secreted into bloodstream o Mostly T4 secreted, but is also secreted Thyroid Gland Functions - Body’s major metabolic hormone - Found in two forms o T4 (thyroxine): major form that consists of two tyrosine molecules with four bound iodine atoms o T3 (triiodothyronine): form that has two tyrosines with three bound iodine atoms  Must be converted to T4 at tissue level - Both are iodine-containing amine hormones - TH affects virtually every cell in body - Enters target cell and binds to intracellular receptors within nucleus o Triggers transcription of various metabolic genes - Effects of thyroid hormone include: o Increases basal metabolic rate and heat production  Referred to as calorigenic effect - Regulates tissue growth and development o Critical for normal skeletal and nervous system development and reproductive capabilities - Maintains blood pressure o Increases adrenergic receptors in blood vessels - Transport and Regulation o T4 and T3 transported by thyroxine-binding globulins  Both bind to target receptors, but T3 is 10 times more active than T4  Peripheral tissues have enzymes needed to convert T4 to T3

 Enzyme removes one iodine Clinical – Homeostatic Imbalance 16.4 o Hyposecretion of TH in adults can lead to myxedema  Symptoms include low metabolic rate, thick and/or dry skin, puffy eyes, feeling chilled, constipation, edema, mental sluggishness, lethargy  If due to lack of iodine, a goiter may develop  Lack of iodine decreases TH levels, which triggers increased TSH secretion, triggering thyroid to synthesize more and more unusable thyroglobulin  Thyroid enlarges o Hyposecretion in infants leads to cretinism  Symptoms include intellectual disabilities, short and disproportionately sized body, thick tongue and neck o Hypersecretion of TH: most common type of Graves’ disease  Autoimmune disease: body makes abnormal antibodies directed against thyroid follicular cells  Antibodies mimic TSH, stimulating TH release  Symptoms include elevated metabolic rate, sweating, rapid and irregular heartbeats, nervousness and weight loss despite adequate food  Exophthalmos may result: eyes protrude as tissue behind eyes becomes edematous and fibrous  Treatments include surgical removal of thyroid or radioactive iodine to destroy active thyroid cells - Calcitonin o Produced by parafollicular cells in response to high Ca2+ levels o No known physiological role in humans at normal physiological levels, but at higherthan-normal doses:  Inhibits osteoclast activity and prevents release of Ca2+ from bone matrix  Stimulates Ca2+ uptake and incorporation into bone matrix Parathyroid Gland Functions: - PTH is most important hormone in Ca2+ homeostasis o Secreted in response to low blood levels of Ca2+ o Inhibited by rising levels of Ca2+ - Target organs are skeleton, kidneys and intestine - Healthy Ca2+ blood levels necessary for nerve transmission, bone health, muscle contraction -

Hyperparathyroidism due to parathyroid gland tumor - Calcium leaches from bones, causing them to soften and deform - Elevated Ca2+ depresses nervous system and contributes to formation of kidney stones - Osteitis fibrosa cystica: severe form resulting in easily fractued bones Hypoparathyrodism following gland trauma or removal can cause hypocalcemia - Results in tetany (seizures), respiratory paralysis and death Adrenal Gland Paired, pyramid-shaped organs atop kidneys - Also referred to as suprarenal glands Structurally and fnctionally it is two galnds in one - Adrenal cortex - Adrenal medulla Adrenal medulla produces over 24 different hormones collectively called corticosteroids Three layers of cortical cells produce the different corticosteroids 1. Zona glomerulosa – Mineralocorticoids 2. Zona fasciculata – Glusocoricoids 3. Zona reticularis – Gonadocorticoids Mineralocorticoids is a calss of steroid hormones that influence salt and water balance - Regulate electrolyte concentrations (primarily Na+ and K+) - Aldosterone: most potent mineralocorticoid o Stimulates Na+ reabsorption by kidneys  Results in increased blood volume and BP o Stimulates K+ elimination by kidneys Factors that regulate aldosterone secretion: - Renin-angiotensin-aldosterone mechanism (blood volume and blood pressure) - Plasma concentration of K+ - Atrial natriuretic peptide secretion Aldosteronism: hypersecretion usually die to adrenal tumors - Results in two major problems: o Hypertension and edema due to excessive Na+ o Excretion of K+ leading to abnormal nonresponsive neurons and muscle

Glucocorticoids is a class of steroid hormones that regulate glucose metabolism - Influence metabolism (glucose and lipids) of most cells and help us resist stressors - Maintian blood pressure by increasing action of vascocontrictors - Glucocorticoid hormones include: o Cortical; onlt glucocorticoid in significant amounts in humans o Cortisome o Corticosterone - Main Actions of Cortisol o Cortisol causes increase in blood levels of glucose, fatty acids, and amino acids o Prime metabolic effect is gluconeogenesis, formation of glucose frm fats and proteins o Enhances vascoconstriction Clinical – Homeostasis Imbalance 16.7 - Hyposecretion – Addison’s disease o Bronze Pimentation of Skin o Hypoglycemia o Changes in Distribution of body Hair o Postrual Hypotension o GI Disturbances o Weakness o Weight Loss - Hypersecretion – Cushing’s Syndrome/disease o Depresses cartilage/bone formation and immue system; inhibits inflammation; dusrupts nerual, cardiovascular and gastrointestinal function o Causes: tumors, or adrenal cortex; overuse of corticosteroids o Signs: “moon” face and “buffalo hump” Gonadocorticoids (adrenal sex hormone) is a class of steroid hormones regualting sexual characteristics development and maintenance - Weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens - May contribute to: o Onset of puberty and appearance of secondary sex charcteristics o Sex drive in women o Source of estrogens in postmenopausal women - Hypersecertion of gonadocorticoids – Adrenogenital syndrome (masculinization) o Not noticeable in adult males  Already masculinized with testosterone, so no effect o Females and prepubertal males  Boys: reproductive organs mature; secondary sex characteristics emerge early  Females: beard, masculine pattern of body hair; clitoris resembles small penis Adrenal Medulla - Medulla synthesize catecholamines: A) epinephrine (80%) and B) norepinephrine (20%) Clinical – Homeostasis 16.9

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Hyposecretion o Epinephrine and norepinephrine are not essential to life; therefore there are no problems associated with hyposecretion - Hypersecretion o Leads to symptoms of uncontrlled sympathetic nervous system, such as:  Hyperglycemia, increased metabolic rate, rapid heartbeat palpitations, hypertension, intense nervousness and sweating Pineal Gland Pinealocytes secrete melatonin Melatonin may affect - Timing of sexual maturation and puberty - Day/night cycles - Physiological processes that show rhythmic variations (body, temperature, sleep, appetite) Pancreas - Triangular gland located aprtially behind stomach - Has both exocrine and endocrine cells o Acinar (exocrine) produce enzyme rich-juice for digestion o Pancreatic islets (islets of Langerhans) contain andocrine cells  Alpha cells produce glucagon (hyperglycemic hormone)  Beta cells produce insulin (hypoglycemic...