Endocrine System Lecture Outline PDF

Summary

This is a lecture outline for a chapter on the endocrine system. It details learning objectives, the endocrine system's function compared to the nervous system, and various types of hormones. The document includes information on the regulation of hormones, and their functions. It also describes the anatomy of various endocrine glands.

Full Transcript

Chapter 17: Endocrine System Lecture Outline ============================================ [Chapter 17 Lecture Learning Outcomes] - Describe in detail how body function is controlled via the endocrine system versus the nervous system. - Describe the categories of hormones, hormone transpor...

Chapter 17: Endocrine System Lecture Outline ============================================ [Chapter 17 Lecture Learning Outcomes] - Describe in detail how body function is controlled via the endocrine system versus the nervous system. - Describe the categories of hormones, hormone transport in the blood, and how hormones interact with body cells. - Describe in the detail the components of the endocrine system and the methods by which it controls the body systems and maintains homeostasis. [17.1a Overview of the Endocrine System] **Endocrine system** - Composed of ductless glands that synthesize and secrete **hormones** - Hormones are released into the blood and transported throughout the body - **Target cells** have the specific receptors for a hormone - They bind hormone and respond - Hormone transport to target cells: - - - - [17.1b Comparison of the Two Control Systems] - Endocrine and nervous systems are the two control systems of the body - Both the endocrine and nervous system - Release **ligands---**chemical messengers - Ligands bind to cellular receptor on particular target cells - Unlike the nervous system, the endocrine system - Transmits hormones through the blood - Targets any cells in the body with correct receptors - Can be very widespread - Exhibits longer reaction times - Has longer-lasting effects (minutes to days and weeks) - **Nervous and Endocrine System Communication Methods (Figure 17.1)** [17.1c General Functions of the Endocrine System] - **Regulating development, growth, and metabolism** - Hormones help regulate embryonic cell division and differentiation - Hormones regulate metabolism (both anabolism and catabolism) - **Maintaining homeostasis of blood composition and volume** - Hormones regulate blood solute concentrations (for example, glucose, ions) - Hormones regulate blood volume, cellular concentration, and platelet number - **Controlling digestive processes** - Hormones influence secretory processes and movement of materials in digestive tract - **Controlling reproductive activities** - Hormones affect development and function of reproductive systems and the expression of sexual behaviors [17.2a Location of the Major Endocrine Glands] - **Endocrine glands** contain epithelial tissue that makes and releases hormones within a connective tissue framework - Some glands are **endocrine organs** with solely endocrine function - Include: pituitary, pineal, thyroid, parathyroid, and adrenal glands - Some endocrine cells are found in clusters in organs with another function - Examples in: hypothalamus, skin, thymus, heart, liver, stomach, pancreas, small intestine, adipose connective tissue, kidneys, and gonads - **Location of the Major Endocrine Glands, Organs, and Tissues Containing** **Endocrine Cells (Figure 17.2)** [17.2b Stimulation of Hormone Synthesis and Release] - Hormone release is regulated by **endocrine reflexes** - Hormonal, humoral, or nervous stimuli can initiate hormone release - **Hormonal stimulation** - A gland cell releases its hormone when some other hormone binds to it - **Humoral stimulation** - A gland cell releases its hormone when there is a certain change in levels of a nutrient or ion in the blood - **Nervous system stimulation** - A gland cell releases its hormone when a neuron stimulates it - **Types of Endocrine Stimulation (Figure 17.3)** [17.3a Circulating Hormones ] - **Steroids (Figure 17.4a)** - Lipid-soluble molecules synthesized from cholesterol - Includes gonadal steroids (for example, estrogen) - Includes steroid synthesized by adrenal cortex (for example, cortisol) - Calcitriol sometimes classified in this group, but more accurately called a *sterol* - **Biogenic amines (*monoamines*) (Figure 17.4b)** - Modified amino acids - Includes: catecholamines, thyroid hormone, melatonin - Water-soluble except for thyroid hormone (TH) - TH is nonpolar (made from a pair of tyrosines) and lipid soluble - **Proteins (Figure 17.4c)** - Most hormones are in this category - Water-soluble chains of amino acids [17.3b Local Hormones] - **Local hormones** - Signaling molecules that don't circulate in blood - They bind to the cells that release them (**autocrine stimulation**) or neighboring cells (**paracrine stimulation**) - **Eicosanoids:** a type of local hormone formed from fatty acids within phospholipid bilayer of membrane - Synthesized through an enzymatic cascade - **Eicosanoid Formation (Figure 17.5)** - **Prostaglandins** are eicosanoids - Stimulate pain and inflammatory responses - Aspirin and other nonsteroidal anti-inflammatory drugs block prostaglandin formation [17.5a Lipid-Soluble Hormones] - **Lipid-soluble hormones** can diffuse across target cell membrane - Such hormones are small, nonpolar, and **lipophilic** - Their receptors are *inside* the cytosol or nucleus - Once hormone enters cell it binds to *intracellular receptor* and forms **hormone-receptor complex** - Results in synthesis of a new protein - **Lipid-Soluble Hormones and Intracellular Receptors (Figure 17.6)** [17.5b Water-Soluble Hormones] - **Water-soluble hormones** use *extracellular* membrane receptors - Such hormones are polar and can't diffuse through membrane - **Initiate series of biochemical events, signal transduction pathway** - initiated by the hormone, the **first messenger** - - termed **second messenger (e.g., cAMP)** - modifies some cellular activity - Multiple results possible with different signal transduction pathways - Activation or inhibition of enzymatic pathways - Growth through cellular division - Release of cellular secretions - Changes in membrane permeability - Muscle contraction or relaxation [17.6b Hormone Interactions on a Target Cell] - Different hormones can simultaneously bind to a cell, and their effects may interact - **Synergistic** interactions - One hormone reinforces activity of another hormone - For example, estrogen and progesterone effects on a target cell - **Permissive** interactions - One hormone requires activity of another hormone - For example, oxytocin's milk ejection effect requires prolactin's milk generating effect - **Antagonistic** interactions - One hormone opposes activity of another hormone - For example, glucagon increases blood glucose while insulin lowers it - **Hormone Interactions (Figure 17.9b)** [17.7a Anatomic Relationship of the Hypothalamus and the Pituitary Gland] - Hypothalamus controls pituitary, which controls several other endocrine organs: - **Pituitary gland** (*hypophysis*) - - - - - **Posterior pituitary** (*neurohypophysis*) - Smaller, neural part of pituitary gland - Hypothalamic neurons project through infundibulum and release hormones in posterior pituitary - Somas in **supraoptic nucleus** and **paraventricular nucleus** - Axons in **hypothalmo-hypophyseal tract** of infundibulum - Synaptic knobs within posterior pituitary - **Hypothalamo-Hypophyseal Tract (Figure 17.11a)** - **Anterior pituitary** - **Hypothalamo-hypophyseal portal system** of blood vessels connects hypothalamus to anterior pituitary - **Primary plexus** - Porous capillary network associated with - **Secondary plexus** -- Capillary network associated with anterior - **Hypophyseal portal veins** - Drain primary plexus and transport to secondary plexus - **Hypothalamo-Hypophyseal Portal System (Figure 17.11b)** [17.7b Interactions Between the Hypothalamus and the Posterior Pituitary Gland] - Posterior pituitary is storage and release site for **antidiuretic hormone ADH** & **oxytocin OT** - ADH and OT are hormones made in hypothalamus by **neurosecretory cells** - - - **Antidiuretic hormone** (*vasopressin*) - Made in supraoptic nucleus - Functions: decrease urine production, stimulate thirst, constrict blood vessels - **Oxytocin** - Made in paraventricular nucleus - Functions: uterine contraction, milk ejection, emotional bonding [17.7c Interactions Between the Hypothalamus and the Anterior Pituitary Gland] - Hypothalamus hormonally stimulates anterior pituitary to release its hormones - Hypothalamus secretes **regulatory hormones** - Travel via portal blood vessels to pituitary - Anterior pituitary secretes hormones into general circulation - **Hormones of the hypothalamus** - **Releasing hormones** - Increase secretion of anterior pituitary hormones - Thyrotropin-releasing hormone (TRH) - Prolactin-releasing hormone (PRH) - Gonadotropin-releasing hormone (GnRH) - Corticotropin-releasing hormone (CRH) - Growth hormone-releasing hormone (GHRH) - **Inhibiting hormones** - Decrease secretion of anterior pituitary hormones - Prolactin-inhibiting hormone (PIH) - Growth-inhibiting hormone (GIH) - **Hormones of the anterior pituitary** - **Thyroid-stimulating hormone (TSH**; *thyrotropin***)** - Release triggered by TRH from hypothalamus - Causes release of thyroid hormone (TH) from thyroid gland - **Prolactin (PRL)** - Release triggered by PRH, inhibited by PIH from hypothalamus - Causes milk production, mammary gland growth in females - **Adrenocorticotropic hormone (ACTH;** *corticotropin***)** - Release triggered by CRH from hypothalamus - Causes release of corticosteroids by adrenal cortex - - Release triggered by GnRH from hypothalamus - - In male: sperm development and secretion of testosterone - **Growth hormone (GH;** *somatotropin***)** - Causes liver to secrete **insulin-like growth factors 1** and **2** - GH and IGFs function synergistically to stimulate cell growth and division - **Anterior Pituitary Hormones (Figure 17.12)** [17.7d Growth Hormone: Its Regulation and Effects ] - Regulation of growth hormone release - Release controlled through hormonal stimulation (GHRH and GHIH) from - - - Amount of GHRH released from hypothalamus impacted by: - A person's age, time of day, nutrient levels, stress and exercise - Effects of growth hormone - Stimulates release of IGFs from liver - Similar functions as GH but longer half-life - All cells have receptors for GH, IGFs, or both - Hormone stimulates increased protein synthesis, cell division, cell - Also stimulates release of nutrients from storage - **Glycogenolysis** (breakdown of glycogen into glucose) stimulated - **Gluconeogenesis** (conversion of nutrients to glucose) stimulated - **Glycogenesis** (synthesis of glycogen) inhibited - **Lipolysis** (breakdown of triglycerides) stimulated - **Lipogenesis** (formation of triglycerides) inhibited - **Regulation and Action of Growth Hormone (Figure 17.13)** - **Variables That Influence Growth Hormone Levels (Figure 17.14)** [17.8a Anatomy of the Thyroid Gland] - Inferior to thyroid cartilage of larynx, anterior to trachea - **Left** and **right lobes** - Connected at midline by narrow **isthmus** - Rich vascularization gives it reddish color - Composed of microscopic follicles - **Follicular cells---**cuboidal epithelial cells that surround a central lumen, synthesize **thyroglobulin (TGB)** - Produce and release **thyroid hormone (TH)** - Follicle lumen houses **colloid---**a viscous, protein-rich fluid - **Parafollicular cells---**cells between follicles, make **calcitonin** - Hormone that decreases blood calcium levels - **Thyroid Gland, Anterior View (Figure 17.15a)** - **Microscopic View of Thyroid Gland (Figure 17.15b)** - **Thyroid Hormone: Synthesis, Storage, and Release (Figure 17.16)** [17.8b Thyroid Hormone: Its Regulation and Effects ] - Regulation of thyroid hormone release - **Hypothalamic-pituitary-thyroid axis** - Cold temperature, pregnancy, high altitude, hypoglycemia, or low TH - TRH causes anterior pituitary to release TSH - TSH binds receptors of follicular cells, triggers release of TH - Follicular cells release two forms of TH to blood: T~3~, T~4~ - T~3~ = triiodothyronine; T~4~ = tetraiodothyronine - T~3~ and T~4~ are transported within blood by carrier molecules - **Regulation and Action of Thyroid Hormone (Figure 17.17)** - Effects of Thyroid Hormone - Cellular transport brings TH into target cells, binds receptor - T~3~ versus T~4~ - Thyroid gland produces more T~4~ but T~3~ is more active form - Most target cells convert T~4~ to T~3~ - TH increases metabolic rate and protein synthesis in targets - Stimulates synthesis of sodium-potassium pumps in neurons - **Calorigenic:** generates heat, raises temperature - Stimulates increased amino acid and glucose uptake - Fosters energy (ATP) production - Hepatocytes stimulated to increase blood glucose - TH causes increases in glycogenolysis and gluconeogenesis, and a decrease in glycogenesis - Adipose cells stimulated to increase blood glycerol and fatty acids - TH causes increase in lipolysis and decrease in lipogenesis - This saves glucose for the brain (**glucose-sparing effect**) - TH increases respiration rate - To meet additional oxygen demand - TH increases heart rate and force of contraction - Increased blood flow to deliver more nutrients and oxygen - Causes heart to increase receptors for epinephrine and *[Clinical View: Disorders of Thyroid Hormone Secretion ]* - **Hyperthyroidism** - Results from excessive production of TH - Increased metabolic rate, weight loss, hyperactivity, heat intolerance - Caused by T~4~ ingestion, excessive stimulation by pituitary, or loss of feedback control in thyroid (**Graves disease**) - Treated by removing the thyroid (then giving hormone supplements) - **Hypothyroidism** - Results from decreased production of TH - Low metabolic rate, lethargy, cold intolerance, weight gain - Caused by decreased iodine intake, loss of pituitary stimulation of thyroid, postsurgical, or immune system destruction of thyroid (**Hashimoto thyroiditis**) - Treated with thyroid hormone replacement - **Goiter** - Enlargement of thyroid - Typically due to insufficient dietary iodine - Lack of dietary iodine preventing thyroid from producing thyroid hormone - Once relatively common in United States, but no longer now that iodine added to table salt [17.8c Calcitonin: Its Regulation and Effects] - **Calcitonin** - Synthesized and released from parafollicular cells of thyroid gland - Stimulus for release is high blood calcium or stress from exercise - Acts to decrease blood calcium levels by - Inhibiting osteoclast activity - Stimulate kidneys to increase excretion of calcium in urine [17.9a Anatomy of the Adrenal Glands] - Located on superior surface of each kidney - Retroperitoneal; embedded in fat and fascia - Two regions: - **Adrenal medulla** - Forms inner core of each adrenal gland - Red-brown color due to extensive blood vessels - Releases **epinephrine** and **norepinephrine** with sympathetic stimulation - **Adrenal cortex** - Synthesizes more than 25 corticosteroids - Yellow color due to lipids within cells - Three regions producing different steroid hormones: zona glomerulosa, zona fasciculata, and the inner zona reticularis - **Adrenal Gland Location (Figure 17.18a)** - **Adrenal Gland Sectional Anatomy and Histology (Figure 17.18b)** - Hormones of the Adrenal Cortex - **Mineralocorticoids:** hormones that regulate electrolyte levels - Made in **zona glomerulosa:** thin, outer cortical layer - **Aldosterone** fosters Na^+^ retention and K^+^ secretion - **Glucocorticoids:** hormones that regulate blood sugar - Made in **zona fasciculata:** larger, middle cortical layer - **Cortisol** increases blood sugar - **Gonadocorticoids:** sex hormones - Made in **zona reticularis:** thin, inner cortical layer - **Androgens** are male sex hormones made by adrenals - Converted to estrogen in females - Amount of produced by adrenals is less than amount from testes [17.9b Cortisol: Its Regulation and Effects ] - Regulation of cortisol release - **Cortisol** and **corticosterone** increase nutrient levels in blood - To resist stress and repair injured tissue - Release regulated by **hypothalamic-pituitary-adrenal axis** - Stress, late stages of sleep, and low levels of cortisol stimulate hypothalamus to release CRH - CRH stimulates anterior pituitary to release ACTH - ACTH stimulates adrenal cortex to release cortisol and corticosterone - Cortisol travels through blood attached to carrier proteins - Small amounts of cortisol dissociate from carrier and leave bloodstream - Cortisol levels are regulated by negative feedback - Cortisol inhibits release of CRH from hypothalamus and ACTH from anterior pituitary - **Regulation and Action of Cortisol Hormone (Figure 17.19)** - **Variables That Influence Blood Levels of Cortisol (Figure 17.20)** - Effects of Cortisol - Cortisol causes target cells to increase blood nutrient levels - Liver cells increase glycogenolysis and gluconeogenesis; decrease glycogenesis - Adipose cells increase lipolysis and decrease lipogenesis - Many body cells break down proteins to amino acids - Liver cells use the amino acids for gluconeogenesis - Most cells decrease their glucose uptake, sparing it for brain - Therapeutic doses of Corticosterone - Corticosterone is used as a treatment for inflammation - It inhibits inflammatory agents and suppresses immune system - At high doses it has side effects - Increases risk of infections, cancer - Increases retention of sodium and water - Inhibits connective tissue repair *[Clinical View: Disorders in Adrenal Cortex Hormone Secretion ]* - **Cushing syndrome** - Chronic exposure to excessive glucocorticoid hormones in people taking corticosteroids for therapy - Some cases when adrenal gland produces too much hormone - Obesity, hypertension, **hirsuitism** (excess male-pattern hair growth), kidney stones, and menstrual irregularities - **Addison disease** - Form of adrenal insufficiency - Develops when adrenal glands fail - Chronic shortage of glucocorticoids and sometimes mineralocorticoids - May develop from lack of ACTH or lack of response to ACTH - Weight loss, fatigue and weakness, hypotension, and skin darkening - Therapy of oral corticosteroids - **Adrenogenital syndrome (congenital adrenal hyperplasia)** - Begins in embryo or fetus - Inability to synthesize corticosteroids leads to overproduction of ACTH - High ACTH causes increased size of adrenal gland and production of hormones with testosterone-like effects - Masculinizes newborn *[Clinical View: Stress Response]* - Stressors elicit a **stress response** - Hypothalamus initiates neuroendocrine response - Three stages - **Alarm reaction** - Initial response involving sympathetic nervous system activation, epinephrine, norepinephrine - **Stage of resistance** - After depletion of glycogen stores, adrenal secretes cortisol to raise blood sugar and help meet energy demands - **Stage of exhaustion** - After weeks or months, depletion of fat stores results in protein breakdown for energy leading to weakening of the body and illness [17.10a Anatomy of the Pancreas] - Located posterior to stomach, between duodenum and spleen - Pancreas has endocrine and exocrine functions - **Acinar cells** generate exocrine secretions for digestion - They make up vast majority of pancreas as saclike **acini** - **Pancreatic islets** (of Langerhans) contain clusters of endocrine cells - **Alpha cells** secrete **glucagon** - **Beta cells** secrete **insulin** - Delta cells (secrete somatostatin) and F cells (secrete pancreatic polypeptide) also present - **Pancreas (Figure 17.21)** [17.10b Pancreatic Hormones ] - Pancreatic hormones help maintain blood glucose - Normal range is 70 to 110 mg of glucose/deciliter - High levels damage blood vessels and kidneys - Low levels cause lethargy, mental and physical impairment, death - **Lowering high blood glucose levels with insulin** - After food intake, beta cells detect rise in blood glucose and respond by secreting insulin - Insulin travels through blood and randomly leaves bloodstream to encounter target cells - Insulin binds to receptors and initiates 2^nd^ messenger systems - Once blood glucose falls, beta cells stop secreting insulin - **Lowering high blood glucose levels with insulin** (*continued*) - Hepatocytes remove glucose from blood; store it as glycogen - Glycogenesis stimulated; glycogenolysis and gluconeogenesis inhibited - Adipose cells decrease fatty acid levels in blood; store fat - Lipogenesis stimulated and lipolysis inhibited - Most body cells increase nutrient uptake in response to insulin - Increased amino acid uptake, protein synthesis (especially in muscle) - Increased glucose uptake by incorporating more glucose transport proteins into plasma membrane - With less alternate fuels available (for example, less fatty acids) more body cells use glucose - Some cells do not require insulin to take in glucose - Including: neurons, kidney cells, hepatocytes, red blood cells - **Regulation and Action of Insulin (Figure 17.22)** *[Clinical View: Conditions Resulting in Abnormal Glucose Levels ]* - **Diabetes mellitus** - Inadequate uptake of glucose from blood - Chronically elevated glucose, blood vessels damaged - Leading cause of retinal blindness, kidney failure, and nontraumatic amputations in the United States - Associated with increased heart disease and stroke - **Type 1 diabetes** - Absent or diminished release of insulin by pancreas - Tends to occur in children and younger individuals - May have autoimmune component - Requires daily injections of insulin - **Type 2 diabetes** - From decreased insulin release or insulin effectiveness - Obesity major cause in development - Tends to occur in older individuals, but can occur in young adults - Treatment with diet, exercise, and medications - **Gestational diabetes** - Seen in some pregnant women - If untreated, causes risk to fetus and increases delivery complications - Increases chance of later developing type 2 diabetes - **Hypoglycemia** - Glucose levels below 60 mg/DL - Numerous causes - Insulin overdose, prolonged exercise, alcohol use, liver or kidney dysfunction - Deficiency of glucocorticoids or growth hormone, genetics - Symptoms of hunger, dizziness, confusion, sweating, and sleepiness - Glucagon given if individual unconscious and unable to eat - **Raising low blood glucose levels with glucagon** - Alpha cells detect drop in blood glucose and release glucagon - Glucagon acts through membrane receptors and 2^nd^ messengers causing body cells to release stored nutrients into blood - Hepatocytes release glucose - Glycogenolysis and gluconeogenesis stimulated; glycogenesis inhibited - Adipose cells release fatty acids and glycerol - Lipolysis stimulated, while lipogenesis inhibited - Glucagon does not affect protein composition - Glucagon can be given by paramedics to unconscious individuals with low blood sugar - Once blood glucose rises, glucagon release is inhibited - **Regulation and Action of Glucagon (Figure 17.23)** [17.11a Pineal Gland] - **Pineal gland** is a small unpaired body in the epithalamus of the diencephalon - Pineal secretes **melatonin** at night - Causes drowsiness - Regulates circadian rhythm and has effects on mood - Melatonin influences GnRH secretion [17.11b Parathyroid Glands] - **Parathyroid glands** are small structures on the posterior surface of the thyroid gland - There are between 2 and 6 of them (usually 4) - Contain **chief cells** and oxyphil cells - Chief (principal) cells make **parathyroid hormone (PTH)** - PTH increases blood calcium - Liberates it from bone, decreases its loss in urine, activates calcitriol hormone [17.11c Structures with an Endocrine Function ] - **Thymus** epithelial cells secrete **thymic hormones** - Located anterior to top of heart - Grows during childhood but shrinks during adulthood - Maturation site for T-lymphocyte white blood cells - Endocrine tissue in **heart** atria secretes **atrial natriuretic peptide (ANP)** - ANP is a hormone that lowers blood pressure - Kidneys increase urine output and blood vessels dilate - **Kidney** endocrine cells release **erythropoietin (EPO)** - Secretion occurs in response to low blood oxygen - EPO causes increased red blood cell production - **Liver** secretions include insulin-like growth factors and the inactive hormone **angiotensinogen** - Angiotensinogen is converted to active **angiotensin II** by enzymes from the kidney and lung blood vessels - Angiotensin II helps raise blood pressure when it starts to fall - Causes vessel constriction, decreases urine output, stimulates thirst - **Stomach** secretes **gastrin** - Gastrin increases secretion and motility in stomach for digestion - **Small intestine** secretes **secretin** and **cholecystokinin (CCK)** into blood - Secretin stimulates secretion of bile and pancreatic juice - CCK stimulates release of bile from gall bladder - In **skin** cells, light converts modified cholesterol to **vitamin D~3~,** which is then released into blood - Vitamin D~3~ is converted to calcidiol by a liver enzyme - Calcidiol is converted to calcitriol by a kidney enzyme - **Calcitriol** is the active hormone that raises blood calcium - Stimulates Ca^2+^ from bone, decreases Ca^2+^ loss in urine, stimulates Ca^2+^ absorption in intestine - **Adipose connective tissue** secretes **leptin** - Leptin controls appetite by binding to neurons in hypothalamus - Lower body fat is associated with less leptin and this stimulates appetite - **Adipose has other endocrine effects** - Excess adipose raises risk of cancer - Excess adipose delays male puberty - Abnormally low adipose interferes with female menstrual cycle

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