Endocrinology
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BairNiseOtter on April 11, 2012
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ch 74, ch 75, ch 76
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96 terms
Terms | Definitions |
|---|---|
 endocrine glands secrete directly into the blood | ... |
| proteins and peptides | synthesized from amino acids soluble in water stored in vesicles, dissolved in plasma (free, unbound) bind to membrane receptor of target tissue short half life (min) |
| proteins and peptides | FLATPG oxytocin vasopressin calcitonin PTH insulin glucagon HCG |
| proteins and peptides summary | fast short half-life not protein bound activating hormone that's already made |
| steroids | synthesized from cholesterol lipid soluble diffuse out of production site, bind to plasma carrier protein, diffuse into target cell receptors are in the nucleus of target cell effects occur at membrane and in cytoplasm half life (hr) |
| steroids | corticosteroids estrogens progesterone androgens |
| steroid storage | synthesized as needed, exception: thyroid hormone protein bound, exception: adrenal androgens, DHEA long half-life (hr) |
| steroids summary | slow long half-life (hr) protein bound goes into the nucleus make new proteins |
| amines | synthesized from tyrosine |
| amines | thyroid hormones -bound to macromolecules, in thyroid, in plasma, and in target cells -bind to receptors in target cell nucleus -half-life (days) |
| amines | catecholamines -stored in vesicles and released by exocytosis -water soluble -bind to receptors on cell membrane |
| pituitary hormones and hypothalamic control | brain does not make steroid hormones all pituitary hormones are peptide hormones water soluble stored in vesicles |
| anterior pituitary/adenohypophysis | GH-growth hormone ACTH- adrenocorticotropic hormone TSH- thyroid-stimulating hormone FSH & LH- follicle-stimulating hormone and luteinizing hormone PRL- prolactin |
| posterior pituitary hormone | ADH antidiuretic hormone/vasopressin (supraoptic nuclei) Oxytocin (paraventricular nuclei) |
| anterior pituitary hormones | GH- stimulates body growth, lipid, and carb metabolism ACTH- glucocorticoids from adrenal cortex TSH- production of thyroid hormones, maintenance of thyroid cell size FSH- ovarian follicles and spermatogenesis LH- steroidogenic effect on gonads Prolactin- stimulates milk production |
| hypothalamic control of anterior pituitary | hypothalamic inputs include: internal homeostasis limbic system responses (stress, fear, strong emotion) circadian rhythyms olfactory sensations |
| hypothalamic output to the anterior pituitary | hypothalamic releasing hormones (or factors) hypothalamic inhibitory hormones |
| hypothalamic-hypophyseal portal system | the artery to the base of the pituitary breaks up into capillaries, receives releasing hormones from the hypothalamus, forms back into a small vein, then breaks up again into capillaries in the anterior lobe |
| anterior and posterior pituitary gland | hypothalamic neurons end on blood vessels to the anterior lobe hypothalamic neuron endings form the posterior lobe |
| releasing hormones | formed in neurons of the hypothalamus and released like nt from the axon terminals |
| stimulatory hormones | TRH GnRH CRH GHRH these are all small peptides |
| inhibitory hormones | Somatostatin (inhibits GH)- a small peptide PIH (Prolactin-inhibitoring hormone)- dopamine |
| board question | if you cut the stalk how come GH does not go up? b/c somatostatin only has a minor effect, GHRH has major effect |
| board question | if cut stalk, then prolactin goes up b/c of PIH |
| Posterior Pituitary Hormones Secretion | Secretion from the posterior pituitary is controlled by nerve signals that originate in the hypothalamus and terminate in the posterior pituitary. |
| Posterior Pituitary Hormones Are Synthesized by Cell Bodies in the Hypothalamus | The bodies of the cells that secrete the posterior pituitary hormones are not located in the pituitary gland itself but are large neurons, called magnocellular neurons, located in the supraoptic and paraventricular nuclei of the hypothalamus. The hormones are then transported in the axoplasm of the neurons' nerve fibers passing from the hypothalamus to the posterior pituitary gland. |
| secretion by the anterior pituitary is controlled by | secretion by hormones called hypothalamic releasing and hypothalamic inhibitory hormones (or factors) secreted within the hypothalamus and then conducted to the anterior pituitary through minute blood vessels called hypothalamic- hypophysial portal vessels. In the anterior pituitary, these releasing and inhibitory hormones act on the glandular cells to control their secretion. |
| hypothalamus, median eminence, releasing/inhibiting hormones, transport: blood vessels-->ant. pit gland | All or most of the hypothalamic hormones are secreted at nerve endings in the median eminence before being transported to the anterior pituitary gland. |
| growth hormone | increased rate of protein synthesis increased mobilization of fatty acids decreased rate of glucose utilization increased growth of bone |
| metabolic effects of growth hormone | enhances body protein, uses up fat stores, and conserves carbohydrates |
| growth promoting effects on bone | increased deposition of protein & rate of mitosis of chrondrocytes and osteocytes conversion of chrondrocytes into osteocytes strong stimulation of osteoblasts |
| GH secretion | strenous exercise increases GH secretion most of the daily GH release is during deep sleep glucose is saved for the brain |
| GH deficiency | extremely short stature most dwarfism is caused by ADA genetic; GH has no effect |
| gigantism | tumor of cells producing GH, prior to epiphyseal plate closure |
| acromegaly | GH cell tumor in adult bones of jaw, cranium, hands, and feet thicken tongue, liver, and kidney are enlarged also |
| side effects of exogenous GH | type 2 diabetes, from hyperglycemia induced by GH ketosis, from excessive mobilization and usage of FAs, result in fatty liver carpal tunnel syndrome edema, joint pain, gynecomastia |
| sources of posterior pituitary hormones | paraventricular nucleus: oxytocin supraoptic nucleus: ADH |
| cont. | both are: peptides with 9 a.a. produced in neuron cell bodies released from axon terminals in the post. pit./neurohypophysis |
| paraventricular nucleus | in dorsal hypothalamus |
| supraoptic nucleus | dorsal to optic nerve rostral to suprachiasmatic nucleus |
| ADH | released by hypothalamic neurons sensitive to plasma osmotic concentration (osmoreceptors) high osmolality plasma (after dehydration)--> increased firing rate, increased release of ADH low osmolality plasma, decrease release, diuresis |
| ADH | primary fx is to open pores for water retention in kidney collecting ducts ADH digs holes it also contracts glomerular cells, reducing filtration |
| Increased Extracellular Fluid Osmolarity Stimulates Antidiuretic Hormone Secretion. | When a concentrated electrolyte solution is injected into the artery that supplies the hypothalamus, the ADH neurons in the supraoptic and paraventricular nuclei immediately transmit impulses into the posterior pituitary to release large quantities of ADH into the circulating blood, sometimes increasing the ADH secretion to as high as 20 times normal. |
| osmoreceptors | When extracellular fluid too concentrated cause additional ADH secretion |
| ADH | concentrated body fluids stimulate the supraoptic nuclei, whereas dilute body fluids inhibit them. |
| high osmolality plasma | increase release of ADH |
| low osmolality plasma | decrease release of ADH |
| Low Blood Volume and Low Blood Pressure Stimulate ADH Secretion | Vasoconstrictor Effects of ADH |
| decrease blood volume/low blood pressure | cause intense ADH secretion |
| vasopressin | high concentrations of ADH constrict arterioles |
| Decreased stretch of the baroreceptors of the carotid, aortic, and pulmonary regions | stimulates ADH secretion |
| The atria have stretch receptors that are excited by overfilling | when excited, send signals to brain to inhibit ADH secretion |
| unexcited/underfilling | stimulate ADH secretion |
| Oxytocin | Causes Contraction of the Pregnant Uterus. |
| Oxytocin | Milk Ejection |
| oxytocin | contracts cells around the alveoli of the mammary gland-causing milk ejection suckling by infant induces oxytocin secretion and subsequent milk release |
| plasma oxytocin levels | highest during sexual excitement-facilitating sperm transport in the uterus and have been correlated with reduction of anxiety |
| ADH and Oxytocin effects within the CNS | ADH release into the CNS affects pair-bonding behavior and agression toward non-mates -released into CNS in circadian rhythm by supraoptic nucleus oxytocin release into CNS can increase sexual arousal, maternal behavior, and empathy -oxytocin receptors are abundant in the amygdala -human studies utilize intranasal absorption |
| thyroid metabolic hormones | thyroxine and triiodothyronine, T4 and T3 the production of T4/T3 is increased by TSH from ant pit calcitonin is also produced by thyroid gland, involved in regulation of calcium |
| thyroid follicles | thyroid gland composed of 100-300 um in dia, closed follicles lined with epithelial cells and filled with a protein colloid |
| colloid | The major constituent of colloid is the large glycoprotein thyroglobulin, which contains the thyroid hormones. |
| C-cells in between follicles | C-cells secrete calcitonin |
| production of thyroid hormones | thyroid epithelial cells produce glycoprotein, thyroglobulin each contain about 70 tyrosine residues secreted into follicle center, where they are combined with iodine (released as T4, T3) iodinated thyroglobulin can be stored for months |
| Iodine, thyroglobulin, and thyroxine | iodide ion is pumped into the cell thyroglobulin is produce and secreted into the follicle, where it is iodinated to contain T4 & T3 iodinated thyroglobulin is brought back inot the cell and cut by proteases, which releases T4 and T3 to diffuse into the blood |
| release of T4/T3 into the blood | almost all the T4/T3 released is T4 T4/T3 are immediately bound to plasma proteins (thyroxine-binding globulin) witihin a few days, about half of the T4 is deiodinated to T3 |
| uptake of T4/T3 by tissue cells | T4/T3 are slowly released from the plasma proteins and diffuse into tissue cells almost all T4 is now T3, binds to receptor in/on DNA strand gene transcription increased/decreased and cellular effects follow |
| Thyroid Hormones Have Slow Onset and Long Duration of Action. | After injection of a large quantity of thyroxine, essentially no effect on the metabolic rate can be discerned for 2 to 3 days, thereby demonstrating that there is a long latent period before thyroxine activity begins. |
| Most of the T4 Secreted by the Thyroid Is Converted to T3 | more than 90 percent of the thyroid hormone molecules that bind with the receptors is T3 |
| Thyroid Hormones Increase metabolic rate | mitochondria increase in size and # increase activity of Na-K-ATPase cell membranes leak more Na+ resultant increase heat production can increase met rate up to 60-100% |
| general tissue actions | carbohydrate metabolism increases fat metabolism increases body wt decreases (w/ increased thyroid hormone) heart rate and cardiac output increases respiratory rate and GI motility increases |
| regulation of thyroid secretion | TSH directs growth and secretion increased T4/T3 inhibits TSH release |
| iodine deficiency goiter | iodine deficiency in the diet thus, low production of T4/T3 lack of feedback inhibition causes gland enlargement (goiter) |
| Grave's Disease | hyperthyroid autoimmune disease antibodies form to TSH receptor stimulate the receptor, form goiter, produce excess T4/T3, which inhibits natural TSH release exophthalmos (protrusion of eyeballs) due to antibody rxn with TSH receptors on extraocular muscles |
| Hashimoto's thyroiditis | a hypothyroid autoimmune disease antibodies form against thyroglobulin or thyroid peroxidase these antibodies gradually destroy the follicles the decreased T4/T3 increases TSH, a goiter can form from the remaining undamaged tissue most common form of hypothyroidism in N.America more common in women |
| Hashimoto's thyroiditis | Hypothyroidism, autoimmunity against the thyroid gland (Hashimoto disease), but immunity that destroys the gland rather than stimulates it. The thyroid glands of most of these patients first have autoimmune "thyroiditis," which means thyroid inflammation. This causes progressive deterioration and finally fibrosis of the gland, with resultant diminished or absent secretion of thyroid hormone. |
| adrenal gland | outer cortex: epithelial cells central medulla: neuron-like cells |
| cell layers | salt sugar sex |
| cell layers | zona glomerulosa- aldosterone zona fasciculata- cortisol zona reticularis- androgens |
| zona glomerulosa | secretes aldosterone in response to increased K and Angiotensin II |
| zona fasciculata | secretes mostly cortisol, some corticosterone, some androgens & estrogens in response to ACTH from the pituitary |
| zona reticularis | secretes mostly androgens, some estrogens, some corticosteroids in response to ACTH from the pituitary |
| circulation to the adrenal cortex and medulla | several arteries enter the outer capsule form plexua, go thorough the different layers, joins a vein draining into the central vein within the medulla the medullary arterioles traverse the cortex directly to the medulla, thus medulla has direct access to arterial blood, exposed to the secretions of the cortex |
| adrenocortical hormones are steroids | synthesized from cholesterol cortex binds and engulf plasma LDLs cholesterol is cleaved to pregnenolone in the mitochondria (rate-limiting step) pregnenolone is converted into: -mineralocorticoids: aldosterone -cortiosteroids- cortisol -androgens- DHEA and androstenedione |
| metabolism of adrenal steroids | carried in the plasma bound to protein -90% of cortisol on cortisol-bind globulin (long half-life) -60% of aldosterone (short half-life b/c 40% free) broken down in the liver -conjugated (side-chain added) for solubility -25% out in the bile -remainder excreted by kidney |
| regulation of adrenal cortex secretion | feedback inhibition by cortisol of CRF secretion from the hypothalamus, and of ACTH secretion from the pituitary |
| circadian rhythm of cortisol secretion | high in the morning and low through the day and evening |
| Co-secretion of several pituitary hormones | ACTH is produced as a prehormone, which is split in the pituitary (PC1, red) into ACTH and β-lipotropin and in the hypothalamus (PC2, blue) into MSH, γ-lipotropin, and β-endorphin |
| aldosterone MOA | ACTH is req'd for secretion to occur, but does not determine rate of secretion lipid soluble, so diffuses into target cells, binds to nuclear receptor, affects DNA transcription -particularly of the NA/K-ATpase and epithelial Na+ channel protein |
| cortisol effects: on carb metabolism | increase gluconeogenesis by liver decrease glucose availability to most body cells (by decreasing glucose transporter protein) thus increases blood glucose for brain and essential fxs |
| cortisol: protein metabolism | decrease protein synthesis, in peripheral tissue, muscle, lymph decrease amino acid transport into tissues increase protein synthesis by the live -increase plasma proteins -increase storage of A.A.s by the liver |
| Effects of Cortisol on Fat Metabolism | increase mobilization of fatty acids from adipose tissue increase plasma free F.A.s thus increase their avail for conversion to energy for stressed cells (spare glucose for brain) if in excess, will enhance conversion of preadipocytes into adipoctyes, in trunk and face (moon face) |
| Cortisol response to stress | •Secretion of cortisol will greatly increase within a few minutes of induction of a stress (via ACTH) -This stress can be pain, fear, tissue trauma, change in temperature, disease onset, et al. •Cortisol increases plasma levels of glucose, amino acids, and free fatty acids for use by stressed tissue. •Cortisol increases synthesis of erythropoietin, -and production of red blood cells •Cortisol induces Ca++ resorption from bones •When tissue damage occurs, inflammation follows |
| Inhibition of Inflammation by Cortisol | Blocks production of prostaglandins -decreases vasodilation & capillary permeability •Inhibits protein synthesis by lymph tissue -reduces T-cell reproduction and mobility •Stabilizes lysosomal membranes •Reduces release of IL-1 from leucocytes -Reduces fever -Reduces T-cell and B-cell activation/cloning •Reduces release of other inflammatory cytokines, histamine, and proteolytic enzymes |
| Abnormalities | •Addison's Disease - hypoadrenalism -Usually an autoimmune response to the adrenal cortex -treatment is replacement therapy •Cushing's Syndrome - hyperadrenalism -Usually a tumor overproducing ACTH -Can be due to long-term application of cortisol -Treatment is removal of the tumor or the cortisol •Conn's Syndrome -Tumor of the zona glomerulosa, with overproduction of aldosterone -Treatment is removal of the tumor, or blockage of the aldosterone receptor |
| Use of Cortisol for treatment | •Healing is faster -More glucose, amino acids, & FFA available -Less damage from inflammation •Particularly useful for -Rheumatoid arthritis -Acute glomerulonephritis -Allergic responses, including anaphylactic shock -Autoimmune diseases |
| Side effects of long-term exogenous cortisol | •Suppresses the immune system - thus enhances further infections •Disturbs intermediary metabolism •Muscular weakness - from reduced protein synthesis •Elevates blood glucose, increases insulin release, exhausts pancreatic B-cells •Increases osteoporosis and bone fractures •Insufficient corticosteroid secetion after steroid treatment ends - from suppressed ACTH production |
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