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67 Cards in this Set
- Front
- Back
autocrine
paracrine endocrine |
-effects on same cell
-effect on cell next to it -effect at distant target |
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-hormones varieties (2)
-activity controlled by (2) |
-peptide, steroid
-hormone release, receptors on target |
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hypothalmus
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-in forebrain
-paracrine to pituitary -many neural inputs/negative feedback affect hypo |
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describe hypothalamus to ant pit
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-release hormones into hypophyseal portal system-->pit stalk-->receptors of ant pit and stimulate release of hormones here
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all hypo hormones causing release of ant pit hormones
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-GnRH-->FSH/LH
-TRH-->TSH -GHRH-->GH -CRF-->ACTH -PIF-->prolactin *ant pit release 7 things: FSH/LH/GH/TSH/ACTH/PROLACTIN/ENDORPHINS FLAT PEG |
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most hormones from ant pit need release factor except
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-prolactin
-hypo release prolactin inhibitory hormone ie DOPAMINE =no prolactin release -no PIF= prolactin release |
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describe hypo to post pit
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-hypo neurons down pit stalk-->post pit
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post pit hormones
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oxytocin and ADH
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of ant pit have
direct and tropic hormones |
-direct: bind target receptor have direct effect
-tropic: bind target receptor, release another hormone |
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direct hormones of ant pit (3)
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-GH, prolactin, endorphins
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GH
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-increase growth muscle/bone
-inhibits glucose uptake in some cells -stimulate fatty acid breakdown - |
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gigantism
dwarfism acromegaly |
-excess GH before epiphyseal plate closes in childhood
-lack of GH -adulthood after closure, GH effects short bones *direct hormone |
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prolactin
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-females: stimulates milk production
if milk in males=BAD *direct hormone |
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endorphins
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-decrease pain perception ie affects pain modulation
*direct hormone |
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-ACTH
-TSH -LH/FSH |
-adrenal cortex-->glucocorticoids (affect glucose balance)
-thyroid to absorb iodine and release thyroid hormone -affect ovaries/testes *tropic hormones |
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post pit
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-gets oxytocin/ADH from hypo and stores
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oxytocin
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-increase uterine contraction
-stimulated by suckling-->increase milk production |
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ADH
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-released when osmolarity increase (osmoreceptors sense)
or BV low (baroreceptors sense) -act at collecting duct -increase permeabilityto water |
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thyroid gland
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-via T3/T4 affects basal metabolic rate
-via calcitonin affects calcium homeostasis |
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-T3/T4
-how affects metabolic rate -increased t3/t4 |
-made by adding iodine to tyrosine residue of thyroid follicular cells
-affect metabolic rate by: affecting glucose/fatty acid utilization and making energy production more/less efficient -increase cell respiration/protein/fatty acid turnover (more synthesis and degradation) |
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hypothyroidism
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-deficiency of iodine or inflammation of thyroid
-low T3/T4 levels -lethargy, decrease temp, slow respiratory rate/HR, weight gain |
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crentinism
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-T3/T4 deficiency=mental retardation during early development after birth
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hyperthyroidism
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-too much T3/T4
-more activity, increased HR/respiratory rate, weight loss, increase temp |
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goiter
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-swelling/enlargement due to either hypo or hyperthyroidism
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in thyroid:
follicular cells make___ c cells make___ |
-T3/T4
-calcitonin |
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calcitonin
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-decreases calcium in plasma 3 ways
1) increase excretion by kidneys 2)decrease absorption in gut 3)increase storage in bone |
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calcium (6) important function
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-bone
-muscle contraction regulator -cofactor for clotting -cell movement -exocytosis -neurotransmitter release |
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parathyroid glands
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-sit on thyroid
-4 of them -makes PTH--> increase calcium levels -PTH: antagonist of calcitonin actions opposite of calcitonin AND activates vitamin D |
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adrenal cortex
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-release corticosteroids (all under control of ACTH)
include glucocorticoids, mineralicorticoids, cortical sex hormones -all steroid hormones |
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glucocorticoids
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-regulate glucose levels
-affect protein metabolism include: cortisol and cortisone |
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cortisol and cortisone
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-decrease protein synthesis
-increase gluconeogenesis -decrease inflammation/immune response -cortisol=stress hormone |
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mineralicorticoids
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-control salt balance
- ex) aldosterone |
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aldosterone
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-increase sodium reabsorption therefore also waters
-increase H/K secretion into tubule and therefore increase excretion -secretion controlled by renin angiotensin aldosterone system |
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renin angiotensin aldosterone system
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-decrease BV-->juxtaglomerular cells of kidney secrete renin -->cleaves inactive protein angiotensinogen-->active angiotensin 1-->angiotensin 2-->adrenal cortex-->aldosterone
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cortical sex hormones:
describe men vs female |
-men testes make most androgen (sex hormone) so do adrenal but insignificant
-females: increase in adrenal sex hormone=masculinizing effects |
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adrenal medulla
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-epinephrine and norepinephrine
-above=flight or fight sympathetic hormones, peptides, belong to catecholamines |
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islets of langerhans
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-endocrine pancreas, 3 cell types
-alpha cell:glucagon -beta cells:insulin -delta cells:somatostatin |
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glucagon
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-antagonistic to insulin
-glycogen-->glucose -degrades proteins/fatty acids -increases gluconeogenesis -secreted by low glucose, GI hormones (gastric/CCK) |
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insulin
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-glucose-->glycogen
-high during high glucose -stimulates anabolic processes (fat/protein synthesis) |
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hypoglycemia
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-too much insulin =low blood glucose
- |
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diabetes mellitus
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-not enough insulin
-aka hyperglycemia -type 1: autoimmune destroy beta cells -type 2: receptor not responding well to insulin |
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diabetic report (2)
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-polyurea and polydypsia
-more glucose in filtrate increase water reabsorption=more urinating/more thirsty |
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somatostatin
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-inhibits glucagon and insulin
-stimulated by high blood glucose and amino acid conc |
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what hormones increase plasma glucose (4)
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-GH
-Glucagon -epinephrine -glucocorticoids |
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testes:
FSH act on __Cells LH on__cells Testosterone for (4) Testosterone negative feedback on (3) Androgen insensitivity syndrome |
-sertoli (for sperm maturation)
-interstitial (makes testosterone-->main male androgen) -spermatogenesis, embryonic differentiation,puberty, secondary sex characteristics -FSH,LH,GnRH -lack test receptors, XY male have female secondary sex characteristics |
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ovaries make (2)
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-estrogen
-progesterone |
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estrogen
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-increase FSH/LH release it
-secondary sex characteristics -thicken endometrium -stimulate development female reproductive track in embryo -secreted by follicles and corpus luteum |
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progesterone
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-LH stimulates release
-from corpus luteum -develops/maintain endometrium -end of 1st trimester progesterone from placenta, corpus luteum stops |
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menstrual cycle
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-endometrium grows then sheds
-estrogen/progesteron control -4 phases 1)follicular 2)ovulation 3)luteal 4)menstruation |
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follicular phase
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-follicles made from increasing FSH/LH
-mature -follicles secrete estrogen |
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ovulation
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LH surge triggers it (due to estrogens positive feedback effect)
release ovum |
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luteal phase
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-LH+ruptured follicle=corpus luteum
-corpus-->estrogen+progesterone -->build lining/inhibit GnRH,FSH and LH |
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menstruation
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-no fertilization=no hCG=decrease estrogen/progesterone from corpus=lining sheds
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estrogen peaks around
progesterone LH FSH |
-before ovulation/before menses
-before menses -ovulation -ovulation |
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if implantation occurs
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-hCG maintain corpus
-estrogen/progesterone keep lining up -hCG declines, but placenta takes over and keeps progesterone/estrogen high - |
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menopause
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-decreased responsiveness of ovaries to FSH/LH
-less follicles -decrease estrogen/progesterone -FSH/LH high levels (no neg feedback in them) |
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pineal gland
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-secrete melatonin-->maybe for circadian rhythm
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are there endocrine organs in GI
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yes
-stomach/intestine have glandular tissues -ex) secretin,cck,gastrin -stimulation for release=food intake |
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erythropoietin
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-kidneys make
-stimulate marrow-->increase RBC -secreted when low oxygen levels in blood |
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does heart have endocrine function
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yes
-release atrial natriuretic peptide (ANP) -ANP: regulate salt/water balance |
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does thymus have endocrine function
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yes
-release thymosin -thymosin: T-cell development/differentiation |
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3 major hormone group
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peptides,steroids, amino acid derived
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peptide hormone synthesis
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-made up of aa
-come from large precursor-->cleaved posttranslational -->modification in golgi activate hormone-->packed in vesicle-->exocytosed |
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peptide hormones charged therefore___so they
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-cant cross membrane
-so bind to receptors ie 1st messengers -stimulate 2nd messenger production |
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explain peptide hormone action
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-bind receptor
-activate 2nd messenger ex)cAMP -cAMP binds intracellular targets ex)DNA -above= signalling cascade -cAMP action ended by phosphodiesterase -can have amplification of effect -short lived, faster, need constant stimulation though |
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steroid hormone action
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-easily cross membrane (nonpolar, made from cholesterol)
-bind intracell receptors-->dimerize-->bind DNA-->alter transcription -longer lived but take longer to see effect |
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amino acid derivative hormone
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-one or two aa with modifications
-use 2nd messengers(like peptide) or enter cell (like steroid) depends on polarity |