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121 Cards in this Set
- Front
- Back
Endocrine Glands
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Glands that secrete hormones into the bloodstream
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Target Cells
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Cells with receptor proteins for certain hormones
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Neurohormones
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Specialized neurons secrete these into the bloodstream
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What do hormones affect?
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The metabolism of the target cells
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Amine
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Hormones from tyrosine, tryptophan:
NE, Epi, thyroxin, melatonin |
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Polypeptide/protein hormones
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AA chains: ADH, GH, Insulin, Oxytocin, Glucagon, ACTH, PTH
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Glycoprotein (hormones?)
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LH, FSH, TSH
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Steroids
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lipids from cholesterol: testosterone, estrogen, progesterone, aldosterone, cortisol
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lipids
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thyroid hormones, steriod hormones: can diffuse into target cells, have receptors in cytoplasm/nucleus
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hormones
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either proteins, steriods, (or thyroid?)
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prehormones
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inactive precursors of hormones (T4)
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how does tissue respond to hormones?
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more hormones=more response, usually
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synergistic hormones
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hormones work together to produce a bigger effect than alone (norep and eph: both raise HR)
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antagonistic hormones
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one hormone inhibits another (insulin=fat making & glucagon=fat breakdown)
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priming effect/upregulation
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All hormones CAN do this, aka increase # of receptor sites on target membrane, which increases the cell's response
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desensitization/downregulation
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after much POLYPEPTIDE HORMONE exposure, exposure creates a lesser response, there are less receptors on target membrane
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water soluble hormones
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-receptors are on the surface of the target cell membrane
-mediated via 2nd msnger syst. |
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how do lipid hormones travel in the blood?
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attached to carrier proteins
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Nuclear Hormone Receptors
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where gene transcription is activated, mRNA is made
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HRE
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hormone response element, what binds to the target gene on the DNA
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what does the thyroid secrete?
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80% T4, 10% T3
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T4
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has 2x 2 units attached to tyrosine (2 DIT)
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T3
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has 1x 1 unit attached to tyrosine (1 MIT)
has 1x 2 units attached to tyrosine (1 DIT) |
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TBG
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Thyroid binding globulin: the carrier protein for T4 in the blood. Inside T4-->T3, T3 binds to a receptor protein in the nucleus.
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2nd msngr syst
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carries signal from receptor to inside cell
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adenylate cyclase
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an enzyme in the membrane, which mediates the effects of polypeptide/glycoprotein hormones
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inhibitory protein kinase
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what cAMP binds to
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adenylate cyclase, cAMP
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binds to g protein subunit
(=ATP-->cAMP) |
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when the inhibitory subunit breaks
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protein kinase is activated
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when protein kinase is activated
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enzymes are phosphorylated, hormones have their effects
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what inactivates cAMP?
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phosphodiesterase
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with the IP3 2nd msngr, step 1:
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hormone-->receptor, g-protein activated, which activates the Phospholipase C in the membrane
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phospholipase-c
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membrane phospholipid-->2 messengers: IP3 and DAG
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IP3
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to cytoplasm to ER=Ca 2+ channels open, in cytoplasm, bindss to&activates calmodulin
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Ca2+ and calmodulin
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activate protein kinases=phosphorylate enzymes=hormone's effects
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2nd msnger that involves a surface receptor
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tyrosine kinase
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tyrosine consists of
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2 inactive units, which, when bonding to insulin-->active dimer of tyrpsine kinase=phosphorylates molecules=hormone/growth effects
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effects of tyrosine kinase
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hormonal growth
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Location of pituitary gland
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under hypothalamus, base of forebrain
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structure of pituitary gland
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two lobes
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infundibulum
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what pituitary gland hangs from
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anterior pituitary
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gets a signal from the hypothalamus, and makes its own hormones
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posterior pituitary
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stores, releases hypothalamus' hormones: antidiuretic hormone (ADH) and oxytocin
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what do the anterior pituitary's 6 hormone's control?
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size of targets: hypertrophy/atrophy
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GH
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a polypeptide/protein hormone
growth hormone hypothal, ant. p, cells absorb AAs at muscle, bone, fat |
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GHRH
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from hypothalamus
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TSR
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a glycoprotein hormone
thyroid stimulating hormone thyroid makes lots of T4, and some T3 |
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TRH
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from hypothal
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ACTH
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a polypeptide/protein hormone that causes steroid secretion
adrenocorticotrophic hormone adrenal cortex-->cortisol, aldosterone secretion |
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LH
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a glycoprotein hormone
Lutenizing hormone causes estrogen/testost production |
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FSH
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a glycoprotein hormone
Follicle stimulating hormone egg and sperm production |
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PRL
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inhibited by PIH, released by PRH
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TRH
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thyroid releasing hormone
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hypothalmic releasing&inhibiting factors, feedback from target hormone glands
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controll A. Pit. hormone release
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Short feedback loop
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bkwd flow of hormones from a.pit. to the hypothal.= inhibits the hormone release
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negative feedback
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GnRH ihibits secretion and responsiveness
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positive feedback
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more estrogen, more LH
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higher brain fxn
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controls hypothalamus
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Adrenal gland's medulla
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secretes amine hormones: epi and ne, and is controlled by the symp ns, the MEDulla MEDiates under stress
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when is the adrenal medulla activated?
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during fight/flight response
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adrenal cortex
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controlled by ACTH adrenocorticotrophic hormone, secretes STERIOD hormones: cortisol, aldosterone, can secrete prehormones
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cortisol
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steriod that inhibits glucose using, and promotes gluconeogenesis. MINOR sug. mech, from long term stress on body
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aldosterone
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kidneys reabsorb Na+, secrete K+ (MAIN mechanism for K+, from nephron to urine)
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GAS
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general adaptation syndrom, causes acth and cortisol release from adrenal cortex
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Addison's disease
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poor secretion of cortex (steriods, perhaps adrenal gland doesn't fxn, or adrenal gland is resistant to acth.)
low blood glucose weak b/c of poor glucose useage bad Na+ & K+ balance |
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Cushings
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high ACTH secretion from cortex, (excess stimulation of adrenal gland or adrenal over pumps)
opposite Na K imbalance high blood glucose=high bp fat redistributed |
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ACTH
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secretes cortisol, aldosterone
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Thyroid gland's location
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below larynx
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thyroid gland's fxn
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secrete TH (T3, T4) and change the BMR
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outer thyroid
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follicle cells
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inner layer
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protein rich colloid (fluid)
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thyroglobulin
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attaches to oxidized iodide (iodine), stores TH, and stimulates TH hydrolysis, secretion
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tyrosines
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also bond to iodine
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Goiter
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absent dietary iodide, TH can't be made=negative feedback=TSH levels up. TSH=trophic, so thyroid gland grows
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hypothyroid
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low TH, synthroid, more in women, low CO, cold, lethargic, low BMR, wt gain, lowered immune syst
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Hyperthyroid
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high TH, lose weight, high temp, high HR, sleeplessness
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results of thyroid probs
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antibodies chew at thyroid, and then it has more holes and allows mass amounts of hormones out-->autoimmune problem
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grave's disease
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autoimmune disese: antibodies act like TSH. gland oversecretes, trophic problem=goiter-like growth.
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parathyroid glands
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secrete PTH (a polypeptide protein hormone) MAIN mech for Ca2+ level control
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PTH
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released if low blood Ca, bones, kidneys, intenstines increase Ca levels
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parathyroid hormone
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on kidney: ca reabsorp
on bone: dissolves crystals |
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calcitonin
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stores ca, does opp of parathyroid hormone
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islets of langerhans
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endocrine cells in pancreas w/ alpha and beta cells
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alpha cells
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like eating alphabet soup when hungry
secrete glucagon, stimulate glycogenolysis and lipolysis, when blood glucose is low |
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gluconeogenesis
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forms glucose from non-carbs
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gylcogenolysis
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glycogen split-->glucose
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beta cells
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secrete insulin when blood glucose is high, glucose goes into cells, glucose is turned into glycogen, fat for storage, lowers blood glucose
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when cells have enough glucose, and more uptake is needed
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enough glycogen will create fat
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Thymus
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below thyroid, produces t cells of immune system, and their stimulating hormones, produces prostaglandins
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gonads
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secrete steroid hormones: test, est, progest
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placenta
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secretes est, progest, hCG, somatomammotrophin
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prostaglandins
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(wbc-->injury)
eicosanoid family |
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prostaglandin fxn
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antagonistic to tissues
change permiability vaso constrict/dilate blood vessle maintenance change infmammation clotting/not musc contract/relax ovulation gastric secretion |
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MR
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metabolic rate= O2 consumption/min
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BMR
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MR of awake, relaxed not eating person
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what increases BMR?
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maleness/testosterone
youth fat vs muscle surface area exercise |
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PPARgamma
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activated receptors of adipocytes that secrete regulatory fxns--> muscle responds more to insulin
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adipocyte hormones
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TNF alpha, resistin, leptin, reduce the sensitivit of muscle to insulin
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leptin
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tells body that it is full, esp when fat is stored more. more leptin = more adiposity
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glucagon
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raises serum glucose, liver does glycogenolysis, alpha
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insulin
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lowers serum insulin
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normal fasting glucose
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65-105
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max glucose
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107 afer meal, or glucose dumping in urin occurs
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min glucose
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50 b/w meals
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insulin
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promotes storage of digestion products, inhibits fat/protein breakdown, inhibits glucagon secretion, puts GLUT4 (glucose tporters) in cell
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glucagon
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maintains blood glucose, stimulates glyconeolysis in liver, gluconeogenesis, liploysis, ketogenesis at other places
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diabetes mellitus
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chronic high blood glucose
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Type 1
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insulin dependant: not enough beta cells, glucose can't enter cells, ketoacidosis, high glucagon levels=glycogenolysis in liver
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type 2
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more common, insulin resistant, happens in overwt ppl, treated w/ diet, exercise
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gestational diabetes
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preggers
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cortisol changes metabolism
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lipolysis, ketogenesis, protein breakdown
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protein breakdown
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aa's for liver to gluconeogenesis
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insulin
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anabolic, but adrenal, thyroid and ant. pit. antagonize it
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protein synthesis from
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insulin, thyroxine, and GH
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somatostatin
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from hypothal, inhibs GH
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circadian pattern
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lots of GH at night, not during day
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high blood glucose
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stops GH secretion
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skeleton growth occurs @
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epiphyseal discs
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excess growth hormone
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excess before epiphyseal discs stop growing, or after
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dwarfism
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lack of GH during childhood
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acromegaly
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excess GH in adults, weird pics
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