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121 Cards in this Set

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