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