Chapter 18

The Endocrine System

Endocrine system
‡ Endo = inside ‡ crine = secrete ‡ hormon = to excite
± to get ~ 1# of endocrine tissue you would need to collect ALL the endocrine tissue from ~4-5 adults

‡ Exocrine cells secrete their product into a duct

‡ Works in conjunction w/ nervous system ‡ slower to react/effects last longer ‡ endocrine glands include:
± pituitary, thyroid, parathyroid, adrenal, pineal, thymus, ORGANS pancreas, gonads, hypothalamus (neuroendocrine organ), MINOR ORGANS - sm int., stomach, kidneys, heart, adipose cells

‡ locally acting chemicals that transfer information from cell to cell within single tissue
± These are not considered hormones since hormones are long-distance chemical signals

Hormone-target cell specificity ‡ A cell can only react to a H if it has a receptor on its plasma membrane or in its interior ‡ example: radio tuned to only pick up specific signals although there are many signals in the air concurrently .

affinity (strength) of bond b/t H & receptor ± up-regulation . Blood levels of the H ‡ 2.prolonged exposure to high H [ ] desensitizes the target cell by losing receptors so they respond less vigorously to H stimulation .target cells form more receptors in response to decreased blood H levels ± down-regulation .3 factors effecting target cell activation ‡ 1. # of receptors for that H on or in target cells ‡ 3.

not causing the activity ± alters plasma membrane permeability ± alters membrane potential thru open/closing ion channels ± (+) synthesis of proteins/enzymes w/in cell ± activates/deactivates enzymes ± induces secretory activity ± stimulates mitosis .Mechanism of Hormone action ‡ Hormones have their effect by altering cell activity.

Hormones ‡ Can be divided into 3 groups: ± amino acid derivatives ± peptide hormones ± lipid derivatives .

Amino Acid Derivatives ‡ Small molecules structurally related to amino acids ‡ Synthesized from the amino acids tyrosine and tryptophan .

Peptide Hormones ‡ Chains of amino acids ‡ Synthesized as prohormones: ± inactive molecules converted to active hormones before or after secretion .

with carbohydrate side chains: ± TSH.2 Groups of Peptide Hormones ‡ Group 1: ± glycoproteins: ‡ more than 200 amino acids long. LH. FSH ‡ Group 2: ± all hormones secreted by: ‡ ‡ ‡ ‡ ‡ ‡ hypothalamus hypophysis heart thymus digestive tract pancreas .

2 Classes of Lipid Derivatives ‡ Eicosanoids: ± derived from arachidonic acid ‡ Steroid hormones: ± derived from cholesterol .

blood clotting.Eicosanoids ‡ act locally so are not always thought of as Hs b/c they are not circulating in the blood ‡ examples: ± leukotrienes . enhancement of uterine contractions. & inflammation .signaling chemicals that mediate inflammation & some allergic reactions ± prostaglandins .multiple functions including raising of BP.

& may be excreted in bile or urine .Steroid Hormones ‡ Are lipids structurally similar to cholesterol ‡ Released by: ± reproductive organs ± adrenal cortex (corticosteroids) ± kidneys (calcitriol) ‡ Remain in circulation longer than peptide hormones ‡ Are converted to soluble form. are absorbed gradually by liver.

Hormone Concentrations in the Blood ‡ Hormones circulate in the blood in two forms ± free or bound ± Steroids and thyroid hormone are attached to plasma proteins and remain in circulation much longer ± All others are unencumbered and remain functional for less than one hour ‡ These are either absorbed & broken down by liver or kidneys. are broken down by enzymes. or diffuse out of the bloodstream to bind on target cells .

Mechanism of Hormone action ‡ A hormone must bind to a receptor to exert its effect ‡ There are two ways in which this happens ± Second messenger mechanism ± Using intracellular receptor .

Catecholamines and Peptide Hormones ‡ Are not lipid soluble so unable to penetrate cell membrane ‡ Bind to receptor proteins at outer surface of cell membrane (extracellular receptors) ‡ Uses intracellular intermediary (second messenger) to exert effects .

cAMP as a second messenger .

or cofactor ± results in change in rates of metabolic reactions ‡ Important Second Messengers ± Cyclic-AMP (cAMP): ‡ derivative of ATP ± Cyclic-GMP (cGMP): ‡ derivative of GTP ± Calcium ions .Intracellular Intermediaries ‡ First messenger: ± leads to second messenger ± may act as enzyme activator. inhibitor.

Cascade Effect ‡ When the binding of a small number of hormone molecules to membrane receptors leads to thousands of second messengers in cell ‡ Magnifies effect of hormone on target cell .

G Protein ‡ Enzyme complex coupled to membrane receptor ‡ Involved in link between first messenger and second messenger ± Binds GTP ‡ Activated when hormone binds to receptor at membrane surface ‡ Changes concentration of second messenger cyclic-AMP (cAMP) within cell ± Increased cAMP level accelerates metabolic activity within cell .

Levels of cAMP decline 3. Adenylate cyclase activity is inhibited 2.Lower cAMP Levels 1. cAMP breakdown accelerates & cAMP synthesis is prevented .

activating or inactivating specific genes ‡ Alter rate of DNA transcription in nucleus: ± change patterns of protein synthesis ‡ Directly affect metabolic activity and structure of target cell .Eicosanoids & Steroid Hormones ‡ Are lipid soluble ‡ Diffuse across membrane to bind to receptors in cytoplasm or nucleus.

³tropic´ Hs from Ant.SNS to adrenals. As a result of the target gland raising H levels in blood .Endocrine reflex Triggers ‡ NEGATIVE FEEDBACK SYSTEM ± humoral . insulin.PTH raises blood Ca. oxytocin/ADH release from post. aldosterone ± neural . pituitary due to hypothalamic (+) ± hormonal . Pit.

Contains autonomic centers: ± Exert direct neural control over endocrine cells of adrenal medullae .a neuroendocrine organ 1. Secretes regulatory hormones: ± Special hormones control endocrine cells in pituitary gland 2.Hypothalamus .

Pituitary gland aka Hypophysis ‡ Found in sella turcica ‡ pea sized & connected to hypothalamus via infundibulum ‡ secretes at least 9 Hs ± Master gland ‡ anterior (glandular) & posterior (neural)lobes .

Neurohypophysis ‡ Derived from hypothalamic tissue ‡ Connected to the hypothalamus via the infundibulum ‡ Does not synthesize its own hormones ± Stores those made in the hypothalamus ‡ Oxytocin & ADH Adenohypophysis ‡ Formed from epithelial tissue originating from Rathke¶s pouch (oral mucosa) ‡ No neural connection to hypothalamus ‡ Synthesizes its own hormones ‡ Communicates via a vascular connection ± Primary capillary plexus in hypothalamus ± Secondary capillary plexus in ant. pituitary .

Hypophyseal secretory effectors .

Activity of the Adenophypophysis ‡ The hypothalamus sends a chemical stimulus to the anterior pituitary ± Releasing hormones stimulate the synthesis and release of hormones ± Inhibiting hormones shut off the synthesis and release of hormones .

Adenohypophyseal Hormones ‡ Tropic hormones ± 4 out of 6 are tropic (turn on/stimulatory) ± TSH. ACTH. LH ± All adenohypophyseal Hs affect their target cells via a second messenger system . FSH.

Thyroid stimulating hormone ‡ TSH«thyrotropin ‡ Release triggered by thyrotropin-releasing hormone (TRH) ‡ Somatostatin is released by hypothalamus w/ increasing TSH levels to block release .

specifically those that help the body resist stressors .Adrenocorticotropic hormone ‡ ACTH«corticotropin ‡ Release triggered by corticotropin-releasing hormone (CRH) ‡ (+) adrenal cortex to release corticosteroid Hs.

Gonadotropins ‡ Follicle stimulating hormone (FSH) ± AKA follitropin ± Stimulates gamete production (sperm & egg) ‡ Luteinizing hormone (LH) ± AKA lutotropin ± Promotes production of gonadal hormones ± Stimulates maturation of the ovarian follicle and then triggers ovulation ± Stimulates interstitial cells of testes to produce testosterone«AKA interstitial cell stimulating hormone (ICSH) ‡ Virtually non-existant in prepubescents ‡ Release regulated by gonadotropin-releasing hormone (GnRH) & suppressed by rising levels of gonadal Hs .

Prolactin (PRL) ‡ AKA mammotropin ‡ Some people consider it a gonadotropin but structurally similar to GH ‡ Well documented to (+) milk production in breasts ‡ May enhance testosterone production in males ‡ Release controlled by both prolactin-releasing hormone (PRH)«thought to be serotonin & prolactin-inhibiting hormone (PIH)«thought to be dopamine ± PIH dominates in males ± In women PRL levels rise & fall w/ estrogen levels (low estrogen«(+) PIH release/high estrogen«(+) PRH«when just prior to menstruation accounts for breast swelling & tenderness .

Growth hormone (GH) ‡ AKA Somatotropin (STH) ‡ Major targets are bone & sk mm cells ± (+) most body cells to grow & divide ± Encourages protein synthesis & use of fat for fuel ‡ Secretion is regulated by 2 hypothalamic Hs ± Growth hormone-releasing hormone (GHRH) ± Growth hormone-inhibiting hormone (GHIH) ‡ Aka somatostatin (also (-) other ant. GI. & pancreatic secretions²both endo & exocrine) . Hs.pit.

Melanocyte Stimulating Hormone ‡ ‡ ‡ ‡ Also called melanotropin (MSH) Stimulates melanocytes to produce melanin Inhibited by dopamine Secreted during: ± fetal development ± early childhood ± pregnancy ± certain diseases .

Summary: The Hormones of the Pituitary Gland Table 18²2 .

Neurohypophyseal Hormones ‡ ADH & Oxytocin ‡ Both composed of 9 Aas & are almost identical ± Differ in only 2 of 9 AAs .

Antidiuretic hormone (ADH) ‡ Inhibits or prevents urine formation ‡ Hypothalamus has osmoreceptors to monitor blood solute [ ] ± If too [ ] ADH is released which causes kidneys to resorb more water ± Other (+) include: pain. hypotension. morphine ± (-) by alcohol & caffeine ‡ At high blood [ ] ADH has a vasoconstrictive effect«conditions such as severe blood loss cause ADH release which causes a rise in BP ± Aka Vasopressin . nicotine.

Diabetes insipidus ‡ ‡ ‡ ‡ Deficiency of ADH Leads to huge amounts of urine production Insipidus = tasteless«no glucosuria OK if thirst centers intact ± Dangerous in unconscious patients & w/head injury ± Head trauma victims must be carefully monitored .

Oxytocin ‡ A strong stimulant of uterine contraction ± Amounts higher during childbirth & w/nursing ± Stretching of the uterus & cervix sends afferent signals to the hypothalamus«release of more oxytocin ‡ Triggers milk ³letdown´ or ejection in lactating breasts ) from PRL ± Both are positive feedback mechanisms .

cont.Oxytocin. ‡ Natural & synthetic drugs (pitocin) are used to induce labor & speed it up ‡ Sometimes used to stop postpartum bleeding (compressing of ruptures blood vessels) ‡ May play role in sexual satisfaction & orgasm in males & non-lacting females ± May promote nurturing/affectionate behavior in non-sexual relationships«cuddling hormone .

Thyroid gland ‡ Butterfly shaped w/2 lobes connected by an isthmus ‡ Made up of 2 types of cells ± Follicle cells (simple cuboidal or squamous epithelium) make up the follicle & produce a glycoprotein called thyroglobulin ‡ The lumen of the follicle contains thyroglobulin w/ attached Iodine molecules ‡ Thyroid hormone (TH) is produced from the iodinated thyroglobulin ± Parafollicular cells are interspersed b/t follicular epithelium & the CT separating the follicles ‡ Calcitonin is produced here .

Thyroid Gland Figure 18²10a. b .

uterus. testes. spleen. & the thyroid gland itself .Thyroid Hormone (TH) ‡ The body¶s major metabolic hormone ‡ Actually 2 different Hs: ± T4 or thyroxin (major H secreted by follicle cells) ± T3 or triiodothyronine (most formed at target tissues by converting T4 to T3) ‡ Affects virtually every body cell except adult brain.

& hydration of skin . & reproductive system)also affects CV system. ‡ Stimulates enzymes concerned w/glucose oxidation«increases BMR ‡ Increases body heat production (calorigenic effect) ‡ Increases # of adrenergic receptors in BVs so it is important in maintaining BP ‡ Regulator of tissue growth & development (esp skeletal.TH. cont. mm system. nervous. GI system.

Synthesis of Thyroid Hormone .

rising levels of glucocorticoids & sex Hs (estrogens & testosterone). & remain high during the night ‡ Conditions that increase the body¶s energy requirements (pregnancy. peak just b/f sleep. pit. & excessively high blood iodide [ ] all (-) TSH release .TH regulation ‡ Falling thyroxin blood levels trigger release of TSH«thyroxin ‡ TSH levels are usually lower during the day. ± TRH overcomes the (-) feedback controls ‡ Somatostatin. prolonged cold) cause hypothalamus to release thyrotropin-releasing hormone (TRH)«TSH release from ant.

exophthalmos (from edematous accumulation b/h eyes) . sweating. thick tongue. increased BMR. weight loss. may be a genetic defect in thyroid or inadequate maternal dietary iodine intake ‡ Hyperthyroid ± Grave¶s disease ± believed to be autoimmune. constipation. feel cold. lethargy. usually mentally retarded. nervousness. rapid heart rate. mental sluggishness ‡ if it is a result of iodine insufficiency the thyroid gland enlarges to form a colloidal goiter (follicle cells produce colloid & store it but cannot iodinate it«TSH secretion increases«more colloid produced but no TH«after a while thyroid cells µburn out¶ & gland atrophies) ± Cretinism ± severe hypothyroid in infants. thick/dry skin.Thyroid disorders ‡ Hypothyroid ± Myxedema ± low BMR. edema. puffy eyes. short. disproportioned body.

Exophthalmos Colloidal goiter .

Calcitonin ‡ Produced by the parafollicular (C-clear) cells ‡ Antagonist to PTH by lowering blood calcium levels ± (+) Ca uptake & incorporation into bone matrix ± (-) osteoclast activity«bone resorption ‡ Excessive blood Ca levels (~20% above normal) (+) calcitonin release ‡ Declining blood Ca levels (-) release ‡ Seems more important in childhood w/rapidly growing bones & rapidly changing blood Ca levels ‡ In adults it is a weak hypocalcemic agent .

Parathyroid glands
‡ Usually 4 BB sized glands found on the posterior aspect of the thyroid gland ‡ Secretion of PTH is by chief cells ‡ As many as 8 glands have already been found and some have even been found in other areas of the neck & thorax

Parathyroid hormone (PTH)
‡ AKA parathormone ‡ Single most important H controlling Ca balance in the blood ‡ (+) from falling blood Ca levels ‡ (-) from hypercalcemia ‡ PTH release (+) 3 target organs«

PTH, cont.
‡ PTH release (+)
± Osteoclasts ± to digest bony matrix & release Ca & phosphates to the blood ± Kidneys ± to enhance reabsorption of Ca (& excretion of phosphates) ± Intestine ± increases absorption of Ca by intestinal mucosa cells« PTH causes conversion of vitamin D from the inactive form absorbed in the skin into its active form, calcitriol
‡ Vit D is needed to absorb Ca from ingested food

Adrenal glands
‡ AKA suprarenal glands ‡ Dual glands
± Adrenal medulla ± nervous tissue (SNS) ± Adrenal cortex ± glandular tissue derived from embryonic mesoderm; majority of gland

‡ All adrenal hormones help us cope with extreme (stressful) situations

gluconeogenesis. anti-inflammatory ± Zona reticularis ± produce gonadocorticoids ‡ Insignificant in adults.Adrenal cortex ‡ Produce over 2 dozen steroid Hs called corticosteroids ‡ 3 distinct layers or zones of cells ± Zona glomerulosa ± produce mineralocorticoids ‡ Balance of water & minerals in body ± Zona fasciculata ± produce glucocorticoids ‡ Metabolism of body cells. female libido? ‡ All corticosteroids are produced by some degree in all 3 layers .

saliva. (+) distal tubules in kidneys to reabsorb Na ions from the forming urine & return them to bloodstream (same result of Na reabsorption from perspiration. & gastric juices) ± Remember«where Na goes. hyponatremia. decreasing blood volume & decreasing BP ± (-) of secretion is due to the reverse factors ± ACTH has little to no effect on aldosterone release .Mineralocorticoids ‡ Aldosterone is the most potent (95% of total). water will follow ± (+) of aldosterone secretion: hyperkalemia.

Glucocorticoids ‡ Cortisol is the most important. antiinflammatory ± Secretion promoted by ACTH ± Any stress will cause override of (-) feedback that normally would reduce cortisol levels ± Cortisol also enhances epinephrine¶s vasoconstrictive effects to increase BP«ensuring circulatory efficiency to help distribute nutrients . very active responding to stress. help keep blood glucose levels constant w/sporadic meal patterns.

& GI function ± Frequently are the drug of choice for chronic inflammatory diseases . ‡ Excessive levels of cortisone: ± Depress cartilage & bone formation ± (-) inflammation by preventing vasodilation ± Depresses the immune system ± Promotes changes in cardiovascular.Glucocorticoids. neural. cont.

rise in K levels«dehydration. poor wound healing«tx w/ discontinuing drugs or removal of tumor ‡ Hyposecretion ± Addison¶s disease ± usually deficits of both glucocorticoids (cortisone) & mineralocorticoids (aldosterone) ‡ Weight loss. drop of plasma glucose & Na levels. easy bruising. loss of mm/bone protein. ³buffalo hump´ from fat redistribution. also adrenal cortex tumors or tumors of pituitary causing release of ACTH ‡ Hyperglycemia. salt/water retention«´moon face´. hypotension«tx w/corticosteroid replacement .Cortisone diseases ‡ Hypersecretion ± Cushing¶s disease (syndrome) ± most often results from overmedication.

Cushing Syndrome .

testosterone is most important ‡ Minimal amounts of estrogen production ‡ Not much function in the adult«adrenal androgens seem to be related to the female sex drive (libido) ± May convert to estrogens after menopause when ovarian estrogens are no longer produced .Gonadocorticoids ‡ AKA sex hormones ‡ Most are androgens.

Adrenal medulla ‡ Chromaffin cells are modified ganglionic sympathetic neurons that secrete the catecholamines ± Epinephrine ± Norepinephrine .

20% are norepi ± Epi is more potent for (+) heart & metabolic activities ± Norepi is more potent for (+)vasoconstriction & BP ± Epi is often used clinically as a heart stimulant and a bronchioldilator during asthma attacks . vasoconstriction. heart. & skeletal mm ‡ Catecholamines released after SNS (+) prolong response. tachycardia.Catecholamines ‡ SNS fibers w/ fight or flight ± Blood sugar levels rise. diversion of blood from nonessential organs to brain. response is brief in relation to effects of adrenocortical Hs ‡ 80% of Hs released are epi.

sleep.Pineal Gland ‡ Small gland hanging from the roof of the third ventricle of the brain ‡ Secretory product is melatonin ‡ Melatonin is involved with: ± Inhibits reproductive functions ± Protects against free radical formation ± Day/night cycles & physiological processes that show rhythmic variations (body temperature. appetite) .

which has both exocrine and endocrine cells. located behind the stomach ‡ Acinar cells produce an enzyme-rich juice used for digestion (exocrine product) ‡ Pancreatic islets (islets of Langerhans) produce hormones (endocrine products) ‡ The islets contain four cell types: ± ± ± ± Alpha (E) cells that produce glucagon Beta (F) cells that produce insulin Delta ( ) cells that produce somatostatin F-cells secrete pancreatic polypeptide (PP) ± (-) g.Pancreas ‡ A triangular gland. bladder .

GH. thyroxine. or glucocorticoids²all are called into action as blood glucose levels drop . & kidney tissue--these have easy access to glucose regardless of insulin levels ‡ Main (+) is hyperglycemia ± Any hyperglycemic H can also (+) release: glucagon. epi. also affects protein & fat metabolism ‡ Insulin enhances membrane transport of glucose into body cells like mm & fat cells«not liver.Insulin ‡ Produced by beta cells (islets of Langerhans) ‡ Major effect is lowering of blood sugar. brain.

Glucagon ‡ Produced by alpha cells (islets of Langerhans) ‡ Major target is the liver ± Promotes glycogenolysis. fats & AAs ‡ 1 molecule of glucagon can cause the release 100 million molecules of glucose in to the blood ‡ Secretion (+) by falling blood sugar levels ‡ Secretion (-) by rise in blood sugar & somatostatin . gluconeogenesis from lactic acid.

Diabetes mellitus (DM) ‡ Hyposecretion or inactivity of insulin ‡ 3 cardinal signs ± Polyuria ± decreased blood volume & dehydration ± Polydipsia ± thirst centers (+) from dehydration ± Polyphagia ± b/c present glucose cannot be used & body starts breaking down fat & protein stores for energy metabolism .

Gonads: Male ‡ Testes located in an extra-abdominal sac (scrotum) produce testosterone & Inhibin (sperm maturation) ‡ Testosterone: ± ± ± ± Initiates maturation of male reproductive organs Causes appearance of secondary sexual characteristics and sex drive Is necessary for sperm production Maintains sex organs in their functional state Gonads: Female ‡ Paired ovaries in the abdominopelvic cavity produce estrogens and progesterone ‡ They are responsible for: ± Maturation of the reproductive organs ± Appearance of secondary sexual characteristics ± Breast development and cyclic changes in the uterine mucosa .

Thymus ‡ Lobulated gland located deep to the sternum in the thorax ‡ Major hormonal product is thymosin ‡ This hormone is essential for the development of the T lymphocytes (T cells) of the immune system .

and stimulates increased energy expenditure. which reduces blood pressure. and blood sodium concentration ‡ Gastrointestinal tract ± enteroendocrine cells release local-acting digestive hormones ‡ Placenta ± releases hormones that influence the course of pregnancy ‡ Kidneys ± secrete erythropoietin.Other Hormone-Producing Structures ‡ Heart ± produces atrial natriuretic peptide (ANP). which is involved in the sensation of satiety. the precursor of vitamin D ‡ Adipose tissue ± releases leptin. & renin which is a powerful vasoconstrictor ‡ Skin ± produces cholecalciferol. resistin ± reduces insulin sensitivity . which signals the production of red blood cells. blood volume.

Interaction of Hormones at Target Cells ‡ Four types of hormone interaction ± Permissiveness ± one hormone cannot exert its effects without another hormone being present ± Synergism ± more than one hormone produces the same effects on a target cell ± Antagonism ± one or more hormones opposes the action of another hormone ± Integration ± hormones produce different & complementary effects .

exhaustion phase Figure 18²18 .General Adaptation Syndrome (GAS) ‡ AKA stress response ‡ How bodies respond to stress-causing factors ‡ Divided into 3 phases: 1.alarm phase 2.resistance phase 3.

Alarm Phase ‡ Is an immediate response to stress directed by ANS ‡ Energy reserves mobilized (glucose) ‡ ³Fight or flight´ responses ‡ Dominant hormone is epinephrine .

2. heart rate. kidneys. 3. and respiratory rate . Drastic reduction in digestion and urine production 6. Increases in blood pressure. and digestive organs 5. 4. Increased mental alertness Increased energy consumption Mobilization of energy reserves (glycogen and lipids) Circulation changes: ± increased blood flow to skeletal muscles ± decreased blood flow to skin. Increased sweat gland secretion 7.7 Characteristics of Alarm Phase 1.

Resistance Phase ‡ ‡ ‡ ‡ Entered if stress lasts longer than few hours Dominant hormones are glucocorticoids Energy demands remain high Glycogen reserves nearly exhausted after several hours of stress .

Mobilize remaining lipid and protein reserves 2. water. Elevate and stabilize blood glucose concentrations + + 4. and loss of K . Conserve salts. Conserve glucose for neural tissues 3. H .Effects of Resistance Phase 1.

Exhaustion Phase ‡ Begins when homeostatic regulation breaks down ‡ Failure of 1 or more organ systems will prove fatal ‡ Mineral imbalance .

Interactions between Endocrine and Other Systems Figure 18²19 .

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