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Physiology Test II

Endrocrinology and Reproduction

what is a key clinical presentation of Graves disease? atrial fibrillation
what are the 2 types of receptors that hormones bind to? cell surface receptors and intracellular receptors
what are the different types of surface receptors? ligand-gated channel, receptor region (activates enzyme), G-protein coupled receptor, and integrin receptors (alters cytoskeleton)
describe the adenylate cyclase pathway (1) adenylate cyclase activates cAMP; (2) cAMP activates PKA; (3) PKA activates CREB (adding P); (4) recruitment of CREB-BP; (5) altered transcription
describe the G-protein exchanging pathway (1) hormone binds to receptor; (2) GDP is exchanged for GTP on a; a and By dissociate and work on effectors
describe the G-protein hydrolysis pathway (1) GTP is hydrolyzed to GDP on a; a joins back with By; (3) aBy binds back to receptor
how is PKA activated? PKA is blocked and when cAMP binds it unblocks PKA
what amino acids do kinases phosphorylate? serine, threonine, and tyrosine
rates of change are determined by what? rates of degradation
what are the ways the G-protein turns off its signals? (1) a is programmed to hydrolyse itself after a certain time; (2) PDE degrades cAMP; (3) phosphatases dephosphorylate nuclear proteins turned on by PKA
what is the mechanism by which cholera acts? pertussis? cholera activates a, locking it in the ON position; pertussis inhibits a-inhibitor, locking it in the OFF position
describe the guanylate cyclase pathway (1) GC activates cGMP; (2) cGMP activates PKG; (3) PKG phosphorylates enzymes
describe the PLC pathway (1) PLC breaks PI into IP3 and DAG; (2) DAG activates PKC; IP3 open Ca channel to release Ca; (3) Ca and DAG are needed to activate PKC (Ser/Thr phosrylation leading to growth and differentiation)
where did calmodulin come from and what does it do? calmodulin is activated by Ca and it activates calmodulin kinase
what are some examples of tyrosine kinase receptors and what do you think with them? examples are EGF, FGF, VEGF, and IGF receptors; think GROWTH and think CANCER
describe the Ras/MAPK pathway (1) ligand binds and receptor dimerizes; (2) auto tyrosine phosphorylation of receptor; (3) SH2 docking; (4) activation of Ras (GDP for GTP); (5) MAPKKK to MAPKK to MAPK (Ser/Thr phosphorylation) to changes in gene expression
describe the NO production pathway (1) in response to high BP, endothelial cells make NO from arginine and activated NO synthase; (2) NO diffuses across membranes; (3) NO binds to GC; (4) causes smooth muscle relaxation
what drugs treat angina prectoris function by producing NO? nitroglycerin and nitroprusside
what types of hormones bind to intracellular receptors? steroid hormones and thyroid hormones
what is something important to know about steroid hormones? they must also act on plasma membrane receptors
what is cross-talk? must have groups of signals to tell the cell to survive, divide, or differentiate
why is fluidity in the cell important? if fluidity is off, the aBy can't swim to its effectors
what is the function of PDE? it makes sure that cAMP stays in the right location for AC to activate it; without PDE, cAMP is not able to be activated
how is specificity achieved? (1) the right receptor must be present; (2) the right response machinery must be present; (3) the response machinery must be in the right location
how are receptor number, sensitivity, and max response related? receptor number changes sensitivity but preserves the max response
what is homologous receptor regulation? homologous receptor regulation: phosphorylation causes uncoupling (PKA turns off receptor by binding arrestin- sec/min), sequestration (separates machinery from receptor- takes some time), internalization of recepors (LDL- hours)
what is heterologous receptor regulation? when hormones deregulate each other; THE mechanism in pituitary feedback
how do you change receptor number physiologically? homologous and heterologous receptor regulation
why must signal mechanisms be turned on and off rapidly? it reduces the error signal
where did the anterior pituitary develop from? the posterior pituitary? AP- roof of mouth; PP- from the brain
what are the hormones in the anterior pituitary? posterior pituitary? AP- growth hormone, thyroid hormone, cortisol, FSH, LH, prolactin; PP- ADH, oxytocin
when there is elevated blood T3, what happens to sensitivity? reduced blood T3? elevated- less sensitivity because of fewer receptors are present; reduced- increased sensitivity because more receptors are present
what is the critical thyroid function test? give a test dose of TRH and measure the blood TSH
what does GH do to carbohydrates? (1) peripheral utilization decreased; (2) tendency for hyperglycemia increased; (3) glucose-sparing
what does GH do to bone? (1) growth at epiphyseal plates in kids; (2) thickening of bone if epiphyseal plates are closed in an adult
what does GH do to fat? (1) fat mobilization; (2) blood FA increased; (3) FA synthesis decreased
what does GH do to protein? (1) anabolism: both transcription and translation increased
what is GH? it is an insulin antagonist for carbs and fat; it is an insulin agonist for protein
what are signs of excess or deficit in GH? excess- postitive nitrogen balance, increased incidence of DM, acromegaly, giantism; deficit- negative nitrogen balance, body lean mass decreased, insulin sensitivity increased
what are the key phrases for GH? growth promoter, fat mobilizer, glucose sparer
what stimulates and inhibits GH? stimuli- hypoglycemia, amino acids, exercise, sleep; inhibitors- hyperglycemia, fatty acids, somatomedins (IGF)
what controls somatomedin production? GH, paracrine- locally promotes compensatory organ growth, calorie balance- when fasting, bone and muscle won't grow because it wastes calories (GH will still be high though)
what does T3/T4 do to carbs? gastrointestinal glucose uptake increased (appetite), increased gluconeogenesis
what does T3/T4 do to protein? required for normal growth, increased levels cause catabolism, especially muscle leading to net loss
what does T3/T4 do to fat? fat mobilization, blood cholesterol decreased, blood phospholipids decreased
what are the key phrases for TH? development, BMR, synergy with the ANS (causes many of the effects of lipid metabolism)
what ties the ANS and TH together? (1) reduced blood T3 makes the epi receptors less sensitive thus needing more epi; (2) T3 reduces levels of Gi (epi is Gs)
in hyperthyroidism, how do you treat symptoms? give a Beta blocker like propanolol to block Gs
how do you test the feedback loop? (1) signs and symptoms; (2) key measurements (TSH and T3); (3) tweak the feeback loop by challenging the system
what happens to TSH, T3, TSH response to TRH, and gland size in primary hyper and hypothyroidism? hyper- decreased TSH, increased T3, little TSH response to TRH, decreased gland size; hypo- increased TSH, decreased T3, larger TSH response, increased gland size
what happens to TSH, T3, TSH response to TRH, and gland size in secondary hyper and hypothyroidism? hyper- increased TSH, T3, and gland size, large TSH response; hypo- decreased TSH, T3, and gland size, little TSH response
what is calcium's main function? to stabilize nerves
what are the symptoms in hypercalcemia and hypocalcemia? hypercalcemia- muscle weakness, constipation, neurological disorders, loss of bone; hypocalcemia- increased neuromuscular excitability, muscle cramps, seizures
what are the functions of osteoblasts, osteocytes, and osteoclasts? osteoblasts- builds up bone; osteocytes- maintains bone and traffic Ca in and out; osteoclasts- breaks down bone
what is the concept of the bone cell membrane? bone cells are interconnected by membrane structures so Ca must cross the cell membrane to get into bone
what are the effects of PTH in the kidney? (1) activates Vit D3; (2) elevates blood Ca; (3) lowers blood phosphate
what are the effects of PTH on bone resorption? it inhibits osteoblasts and stimulates osteoclasts and osteocytes
what are the key phrases of Vit D? provide calcium, preserve bone structure
what are the effects of Vit D excess and deficiency? excess- mimic elevated PTH (hypercalcemia); deficiency- failure of GI Ca uptake, hypocalcemia, bone loss
how does bone loss occur in the absence of Vit D3? absence of Vit D3 blocks Ca absorption so more in secreted out
what are the effects of Vit D on bone and intestine? bone- promotes bone differentiation (cause bone cells to work well, without it, they don't); intestine- increased absorption of calcium and phosphate
what cells make calcitonin? parafollicular cells (C cells)
what is the key phrase of calcitonin? lowers blood calcium
what happens in excess or deficit of calcitonin? excess or deficit- no signs or symptoms
what are the effects of calcitonin on bone? it inhibits resorption by reducing the number of osteoclasts, blocks PTH action
how are stress, cortisol, and catecholamines related? stress increases cortisol and catecholamines, and cortisol also increased catecholamines
what are the effects of an excess or deficit in cortisol? excess- suppression of immune and inflammatory responses, breakdown of tissue and bone, increased incidence of DM; deficit- body cannot respond to stresses
what is the effect of cortisol on carbs? increased gluconeogenesis from protein, increased appetite, reduced glucose uptake by muscle
what is the effect of cortisol on fat? peripheral mobilization, central fat deposition, increased appetite
what is the effect of cortisol on protein? increased muscle protein breakdown (muscle wasting), increased synthesis of liver gluconeogenic enzymes (glycogen-big livers)
what are the key phrases of cortisol? emergency/stress, energy provider, glucose sparer, permissive
what are effects of an excess or deficit of aldosterone? excess- sodium retention, potassium loss, hypertension; deficit- sodium loss, potassium retention, death
what are the key phrases of aldosterone? volume regulation, sodium retention, potassium loss
what are the effects of epi on carbs? liver and muscle glycogen mobilization, gluconeogenesis
what are the effects of epi on fat? increased lipolysis: mobilization
what are the effects of epi on protein? little or no effect
what are the key phrases of epi? emergency/stress, energy provider/mobilizer
what other hormone regulates cell sensitivity to the catecholamines? thyroid hormone increases sensitivity to epi
what are the 2 main types of DM? type I- beta cell failure; type II- loss of insulin sensitivity, later loss of beta cell capacity to secrete insulin due to wearing out
what are the key phrases of insulin? after dinner hormone, storage hormone
what are the principal targets of insulin? liver, adipose, muscle
what are the effects of insulin on carbs? glucose uptake increased, glycogenesis increased, gluconeogenesis decreased
what are the effects of insulin on fat? triglyceride synthesis increased, triglyceride breakdown decreased
what are the effects of insulin on protein? decreased breakdown (most impt), increased synthesis
how does insulin regulate glucose transporters? when insulin is present, it causes the transporters to go to the surface to uptake glucose, when absent, the transporters stay inside cell
where does insulin work in muscle and liver? muscle- cell surface; liver- intracellularly
how are insulin and aldosterone similar? they both cause sodium retention and potassium loss (insulin does it quicker)
what is the order of insulin sensitivity in tissues? kidney is more sensitive than fat is more sensitive than muscle
why do diabetics become more obese? muscle cannot take up glucose so all the glucose gets taken up by fat since it's still sensitive
why do Type I diabetics have DKA more often than Type II diabetics? Type I diabetics have no insulin so they have lots of fat mobilization leading to DKA; type II diabetics still have fat sensitivity to insulin so it's not as likely to have fat mobilization
what are the effects of an excess or deficit of insulin? excess- hypoglycemia, convulsion, coma; deficit- DM, retinopathy and neuropathy, vascular disease
what is the key phrase of glucagon? glucose provider (glycogenolysis and gluconeogenesis)
what are the effects of glucagon on carbs and fats? hepatic glycogenolysis (secs), hepatic gluconeogenesis (hours), fat mobilization
what are the signs of excess or a deficit in glucagon? not yet described
why is insulin the number one hormone? because without it, it causes glycogenolysis, gluconeogenesis, lipolysis, inhibition of glucose uptake, and muscle protein breakdown
why is it when cortisol is added to glucagon, and epi the glucose response increases drastically? because cortisol provides the amino acids so that epi and glucagon can make it into glucose
what happens after eating a protein meal? GH (IGF) and insulin increased, growth increased, caloric balance
what happens after eating a carb meal? increased insulin, decreased GH (IGF), growth neutral, increased caloric storage
what happens during fasting? increased GH, decreased IGF and insulin, no growth, mobilization of calories
what effect does epi have on glucagon and insulin? it stimulates glucagon and inhibits insulin
what is the randle hypothesis on the fatty acid cycle? glucose promotes fat storage, fat block glucose by: FA block intracellular pathway fro glucose metabolism, FA mess up glucose transporters, and FA block insulin signaling
what does muscle use for energy? it uses fat or glucose, but ALWAYS prefers fat
what does brain use for energy? brain ALWAYS needs glucose
what does adipose tissue use for energy? it doesn't use much of anything; it's main job is to store (absorptive phase) or mobilize (postabsorptive) fat
what does the liver use for energy in the absorptive phase? it uses AAs as the energy source; glucose is stored as glycogen or shipped to the liver to be made into fat stores
what does the liver use for energy in the postabsorptive phase? it uses fats as the energy source; it exports glucose for body needs
during fasting, what happens to the hormones? glucose, protein, and insulin decreasep; glucagon and GH increase
what does fasting do to TH? fasting lowers set point and reduced BMR, making less T3, and more rT3
how does the body adapt to fasting? (1) brain uses fat for some of its energy needs; (2) BMR is reduced; (3) kidney takes over job of liver and become gluconeogenic
what is the difference between capacitation and decapacitation? decapacitation- during its travel, lipids attatch to sperm head to make it more rigid and resistant to trauma; capacitation- hypermotile, able to undergo acrosome reaction, fluids in female tract remove lipids to make it ready to bind the ZP
what are the 3 glycoproteins in the ZP? ZP1- structural (crosslinks); ZP2- sperm binding, block to polyspermy; ZP3- sperm binding
what is the acrosome reaction? enzymes released from cap once bound to let the sperm fuse with the egg
what is the cortical reaction? once fertilzed, cortical granules fuse with membrane release proteins which harden ZP from other sperm
what is the zona reaction? it represents the block to polyspermy; the ZP hardens and sperm receptors are destroyed
what does blastocyst formation indicate? first evidence of differentiation
what is CVS and amniocentesis? CVS- taking a tissue from uterus, can be done 9 wks but greater chance of birth defects; amnio- 15-16 wks, withdraw fluid from sac surrounding fetus
what is the luteal placental shift? shift of production of progesterone and estrogen from corpus luteum to placenta, thus keeping good environment for fetus
what are the cardiovascular and respiratory changes in the mother? increased plasma volume, RBC volume, cardiac output; decreased or unchanged BP; activation of renin-angiotensin system; increased minute volume (breathing off CO2 for self and baby)
what is abruptio placentae? placenta previa? AP- placenta separates from wall of uterus before birth; PP- implantation is low in cervix so placenta covers cervix
what factors increase uterine contractions? increased wall tension, decreased P/E ratio, prostaglandin secretion, oxytocin receptors and secretion
what are 3 things that a male must have to be reproductively fertile? (1) makes sperm; (2) produce erection; (3) ejaculation
describe the process of sperm motility ATP stimulates dynein, sliding of tubules, whipping action of tail
describe the process of spermatogenesis spermatogonium, primary spermatocyte, secondary spermatocyte, spermatid, spermatozoa
what are the basic requirement for fertility? sufficient number/concentration, motility, ability to penetrate ovum, complete and functional genetic material
what are the functions of sertoli cells? form blood-testis barrier, provide nourishment for spermatozoa, secrete luminal fluid (washes spermatozoa into epididymus), site of hormonal control, produce inhibin and ABP (soaks up T to keeps testosterone high in tubule)
what's the difference between semen and sperm? 5% of semen contains sperm, the rest are secretions
describe the function of the testes scrotal skin has evaporative cooling environment, cremasteric muscle pull testes away or to body depending on temp, countercurrent exchange mechanism
what does a varicocele cause? decreases efficiency of heat exchange, decreases sperm count, may contribute to male infertility
what are some problems of spermatogenesis? heat, radiation, defects in genetic material
what are the stages of male arousal? (1) erection; (2) lubrication; (3) ejaculation
what does NANC do? NANC (non adrenergic non cholingergic) transmitter causes increased blood flow by producing NO which relaxes smooth muscle
describe the GnRH pathway GnRH to FSH and LH; FSH to sertoli cell, spermatogenesis or produces inhibin which feedsback to FSH; LH to leydig cells, produces T which goes to sertoli cells or target tissues, T feedsback to LH or hypothalamus
what does Viagra do? it inhibits PDE; PDE breaks down cGMP so Viagra slows down the breakdown, leading to increased cGMP
what are the phases of the menstrual cycle? ovarian phase- follicular, ovulatory, luteal phases; uterine phase- menstrual, proliferative, secretory phases
what hormone predominates in the first half of the cycle? second half? first half- estrogen; second half- estrogen and progesterone
describe the GnRH pathway in females GnRH to FSH and LH; FSH to granulosa cells which facilitate oogenesis, produce inhibin (fb to FSH), and make estrogen; LH to theca cells which make androgens that go to granulosa cells to become estrogen (fb to LH and GnRH)
what happens in the ovulatory phase that benefits fertilization? the uterus produces a clear mucus that makes it easier for sperm to swim right through; estrogen causes this
what happens in the luteal phase that prevents fertilization? high progesterone makes thick mucus which makes it difficult for foreign material to enter the uterus
what are the main actions of estrogen? (1) development of female structures; (2) stimulates growth of endometrium; (3) stimulates watery secretions to facilitate sperm; (4) endocrine feedback
what are the main actions of progesterone? (1) stimulates thick secretion of endometrium; (2) stimulates gowth of myometrium in pregnancy; (3) quiets uterus; (4) stimulates breast growth
Created by: medchichi