Endrocrinology and Reproduction
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| what is a key clinical presentation of Graves disease? | atrial fibrillation
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| what are the 2 types of receptors that hormones bind to? | cell surface receptors and intracellular receptors
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| what are the different types of surface receptors? | ligand-gated channel, receptor region (activates enzyme), G-protein coupled receptor, and integrin receptors (alters cytoskeleton)
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| 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
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| 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
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| 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
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| how is PKA activated? | PKA is blocked and when cAMP binds it unblocks PKA
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| what amino acids do kinases phosphorylate? | serine, threonine, and tyrosine
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| rates of change are determined by what? | rates of degradation
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| 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
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| 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
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| describe the guanylate cyclase pathway | (1) GC activates cGMP; (2) cGMP activates PKG; (3) PKG phosphorylates enzymes
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| 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)
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| where did calmodulin come from and what does it do? | calmodulin is activated by Ca and it activates calmodulin kinase
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| 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
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| 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
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| 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
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| what drugs treat angina prectoris function by producing NO? | nitroglycerin and nitroprusside
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| what types of hormones bind to intracellular receptors? | steroid hormones and thyroid hormones
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| what is something important to know about steroid hormones? | they must also act on plasma membrane receptors
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| what is cross-talk? | must have groups of signals to tell the cell to survive, divide, or differentiate
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| why is fluidity in the cell important? | if fluidity is off, the aBy can't swim to its effectors
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| 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
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| 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
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| how are receptor number, sensitivity, and max response related? | receptor number changes sensitivity but preserves the max response
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| 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)
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| what is heterologous receptor regulation? | when hormones deregulate each other; THE mechanism in pituitary feedback
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| how do you change receptor number physiologically? | homologous and heterologous receptor regulation
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| why must signal mechanisms be turned on and off rapidly? | it reduces the error signal
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| where did the anterior pituitary develop from? the posterior pituitary? | AP- roof of mouth; PP- from the brain
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| what are the hormones in the anterior pituitary? posterior pituitary? | AP- growth hormone, thyroid hormone, cortisol, FSH, LH, prolactin; PP- ADH, oxytocin
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| 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
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| what is the critical thyroid function test? | give a test dose of TRH and measure the blood TSH
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| what does GH do to carbohydrates? | (1) peripheral utilization decreased; (2) tendency for hyperglycemia increased; (3) glucose-sparing
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| 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
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| what does GH do to fat? | (1) fat mobilization; (2) blood FA increased; (3) FA synthesis decreased
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| what does GH do to protein? | (1) anabolism: both transcription and translation increased
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| what is GH? | it is an insulin antagonist for carbs and fat; it is an insulin agonist for protein
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| 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
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| what are the key phrases for GH? | growth promoter, fat mobilizer, glucose sparer
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| what stimulates and inhibits GH? | stimuli- hypoglycemia, amino acids, exercise, sleep; inhibitors- hyperglycemia, fatty acids, somatomedins (IGF)
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| 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)
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| what does T3/T4 do to carbs? | gastrointestinal glucose uptake increased (appetite), increased gluconeogenesis
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| what does T3/T4 do to protein? | required for normal growth, increased levels cause catabolism, especially muscle leading to net loss
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| what does T3/T4 do to fat? | fat mobilization, blood cholesterol decreased, blood phospholipids decreased
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| what are the key phrases for TH? | development, BMR, synergy with the ANS (causes many of the effects of lipid metabolism)
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| 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)
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| in hyperthyroidism, how do you treat symptoms? | give a Beta blocker like propanolol to block Gs
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| 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
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| 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
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| 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
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| what is calcium's main function? | to stabilize nerves
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| what are the symptoms in hypercalcemia and hypocalcemia? | hypercalcemia- muscle weakness, constipation, neurological disorders, loss of bone; hypocalcemia- increased neuromuscular excitability, muscle cramps, seizures
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| 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
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| 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
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| what are the effects of PTH in the kidney? | (1) activates Vit D3; (2) elevates blood Ca; (3) lowers blood phosphate
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| what are the effects of PTH on bone resorption? | it inhibits osteoblasts and stimulates osteoclasts and osteocytes
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| what are the key phrases of Vit D? | provide calcium, preserve bone structure
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| what are the effects of Vit D excess and deficiency? | excess- mimic elevated PTH (hypercalcemia); deficiency- failure of GI Ca uptake, hypocalcemia, bone loss
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| how does bone loss occur in the absence of Vit D3? | absence of Vit D3 blocks Ca absorption so more in secreted out
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| 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
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| what cells make calcitonin? | parafollicular cells (C cells)
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| what is the key phrase of calcitonin? | lowers blood calcium
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| what happens in excess or deficit of calcitonin? | excess or deficit- no signs or symptoms
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| what are the effects of calcitonin on bone? | it inhibits resorption by reducing the number of osteoclasts, blocks PTH action
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| how are stress, cortisol, and catecholamines related? | stress increases cortisol and catecholamines, and cortisol also increased catecholamines
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| 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
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| what is the effect of cortisol on carbs? | increased gluconeogenesis from protein, increased appetite, reduced glucose uptake by muscle
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| what is the effect of cortisol on fat? | peripheral mobilization, central fat deposition, increased appetite
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| what is the effect of cortisol on protein? | increased muscle protein breakdown (muscle wasting), increased synthesis of liver gluconeogenic enzymes (glycogen-big livers)
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| what are the key phrases of cortisol? | emergency/stress, energy provider, glucose sparer, permissive
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| what are effects of an excess or deficit of aldosterone? | excess- sodium retention, potassium loss, hypertension; deficit- sodium loss, potassium retention, death
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| what are the key phrases of aldosterone? | volume regulation, sodium retention, potassium loss
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| what are the effects of epi on carbs? | liver and muscle glycogen mobilization, gluconeogenesis
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| what are the effects of epi on fat? | increased lipolysis: mobilization
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| what are the effects of epi on protein? | little or no effect
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| what are the key phrases of epi? | emergency/stress, energy provider/mobilizer
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| what other hormone regulates cell sensitivity to the catecholamines? | thyroid hormone increases sensitivity to epi
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| 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
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| what are the key phrases of insulin? | after dinner hormone, storage hormone
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| what are the principal targets of insulin? | liver, adipose, muscle
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| what are the effects of insulin on carbs? | glucose uptake increased, glycogenesis increased, gluconeogenesis decreased
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| what are the effects of insulin on fat? | triglyceride synthesis increased, triglyceride breakdown decreased
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| what are the effects of insulin on protein? | decreased breakdown (most impt), increased synthesis
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| 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
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| where does insulin work in muscle and liver? | muscle- cell surface; liver- intracellularly
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| how are insulin and aldosterone similar? | they both cause sodium retention and potassium loss (insulin does it quicker)
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| what is the order of insulin sensitivity in tissues? | kidney is more sensitive than fat is more sensitive than muscle
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| 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
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| 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
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| what are the effects of an excess or deficit of insulin? | excess- hypoglycemia, convulsion, coma; deficit- DM, retinopathy and neuropathy, vascular disease
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| what is the key phrase of glucagon? | glucose provider (glycogenolysis and gluconeogenesis)
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| what are the effects of glucagon on carbs and fats? | hepatic glycogenolysis (secs), hepatic gluconeogenesis (hours), fat mobilization
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| what are the signs of excess or a deficit in glucagon? | not yet described
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| why is insulin the number one hormone? | because without it, it causes glycogenolysis, gluconeogenesis, lipolysis, inhibition of glucose uptake, and muscle protein breakdown
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| 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
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| what happens after eating a protein meal? | GH (IGF) and insulin increased, growth increased, caloric balance
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| what happens after eating a carb meal? | increased insulin, decreased GH (IGF), growth neutral, increased caloric storage
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| what happens during fasting? | increased GH, decreased IGF and insulin, no growth, mobilization of calories
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| what effect does epi have on glucagon and insulin? | it stimulates glucagon and inhibits insulin
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| 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
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| what does muscle use for energy? | it uses fat or glucose, but ALWAYS prefers fat
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| what does brain use for energy? | brain ALWAYS needs glucose
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| 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
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| 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
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| what does the liver use for energy in the postabsorptive phase? | it uses fats as the energy source; it exports glucose for body needs
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| during fasting, what happens to the hormones? | glucose, protein, and insulin decreasep; glucagon and GH increase
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| what does fasting do to TH? | fasting lowers set point and reduced BMR, making less T3, and more rT3
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| 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
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| 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
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| what are the 3 glycoproteins in the ZP? | ZP1- structural (crosslinks); ZP2- sperm binding, block to polyspermy; ZP3- sperm binding
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| what is the acrosome reaction? | enzymes released from cap once bound to let the sperm fuse with the egg
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| what is the cortical reaction? | once fertilzed, cortical granules fuse with membrane release proteins which harden ZP from other sperm
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| what is the zona reaction? | it represents the block to polyspermy; the ZP hardens and sperm receptors are destroyed
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| what does blastocyst formation indicate? | first evidence of differentiation
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| 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
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| what is the luteal placental shift? | shift of production of progesterone and estrogen from corpus luteum to placenta, thus keeping good environment for fetus
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| 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)
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| 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
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| what factors increase uterine contractions? | increased wall tension, decreased P/E ratio, prostaglandin secretion, oxytocin receptors and secretion
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| what are 3 things that a male must have to be reproductively fertile? | (1) makes sperm; (2) produce erection; (3) ejaculation
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| describe the process of sperm motility | ATP stimulates dynein, sliding of tubules, whipping action of tail
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| describe the process of spermatogenesis | spermatogonium, primary spermatocyte, secondary spermatocyte, spermatid, spermatozoa
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| what are the basic requirement for fertility? | sufficient number/concentration, motility, ability to penetrate ovum, complete and functional genetic material
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| 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)
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| what's the difference between semen and sperm? | 5% of semen contains sperm, the rest are secretions
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| 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
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| what does a varicocele cause? | decreases efficiency of heat exchange, decreases sperm count, may contribute to male infertility
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| what are some problems of spermatogenesis? | heat, radiation, defects in genetic material
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| what are the stages of male arousal? | (1) erection; (2) lubrication; (3) ejaculation
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| what does NANC do? | NANC (non adrenergic non cholingergic) transmitter causes increased blood flow by producing NO which relaxes smooth muscle
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| 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
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| what does Viagra do? | it inhibits PDE; PDE breaks down cGMP so Viagra slows down the breakdown, leading to increased cGMP
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| what are the phases of the menstrual cycle? | ovarian phase- follicular, ovulatory, luteal phases; uterine phase- menstrual, proliferative, secretory phases
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| what hormone predominates in the first half of the cycle? second half? | first half- estrogen; second half- estrogen and progesterone
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| 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)
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| 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
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| 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
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| 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
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| 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
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