Term
| 90% of Thyroid Hormone secretion is of which type? |
|
Definition
|
|
Term
| Thyroid Hormone receptors have a much higher affinity for which type? |
|
Definition
|
|
Term
| How does thyroid hormone cause cretinism? |
|
Definition
| thyroid hormone is necessary for optimal human growth hormone production and neuronal cell growth. |
|
|
Term
|
Definition
| enlargement of the thyroid gland |
|
|
Term
|
Definition
| hypothyroidism caused by autoimmune reactions that destroy parts of the thyroid |
|
|
Term
| what is the tx for hypothyroidism? |
|
Definition
| (iodine deficiency --> increase iodine intake) otherwise orally administered T4 |
|
|
Term
|
Definition
| most common form of hyperthyroidism caused by an autoimmune response in which antibodies directed against the TSH receptor continually bind to the TSH receptor in the thyroid cell membranes causing excessive thyroid gland growth and increased thyroid hormone production |
|
|
Term
|
Definition
| antithyroid drug therapy (targets thyroid peroxidase), surgery, radioactive iodine therapy (very active Na/I transporter will bring in LOTS of iodine to overproduce TH, if we administer radioactive iodine, it will kill some thyroid hormone cells) |
|
|
Term
| how does thyroid hormone mediate its effects on peripheral body systems in hyperthyroidism? |
|
Definition
| increases # of beta adrenergic receptors |
|
|
Term
| what % of T3 and T4 are in free form? |
|
Definition
|
|
Term
| which form of thyroid hormone is the one that ultimately has biological effects? |
|
Definition
|
|
Term
| describe the 3 domains of a thyroid hormone receptor (nuclear hormone receptor) |
|
Definition
| central DNA binding domain w/2 zinc fingers; carboxy terminal region important for ligand binding and heterodimeration with RXR; n-terminal transactivation domain |
|
|
Term
| which thyroid receptor is inactive? |
|
Definition
| alpha-2 bc unable to bind T3 |
|
|
Term
| generalized thyroid hormone resistance syndrome caused by? |
|
Definition
| point mutations in the ligand binding domain region of human T3 receptor beta gene --> defective receptor that fails to bind T3 |
|
|
Term
| where do thyroid hormone receptors bind on the DNA? |
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Definition
| thyroid hormone response elements (2 hexameric half-sites, most commonly a heterodimer of thyroid hormone receptor and retinoid X receptor occupy these sites) |
|
|
Term
| what happens in positively regulated target genes in the absence of T3? |
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Definition
| thyroid hormone receptor/RXR heterodimer bound to TRE and interacts with corepressors (nuclear receptor co-repressor and silencing mediator). Histone deacetylase interadcts with corepressor complex --> repression of gene expression |
|
|
Term
| what happens in positively regulated target genes when thyroid hormone IS present? |
|
Definition
| corepressor complexes released, T3-bound thyroid hormone receptor associates with co-activators (steroid receptor activator, vit D receptor interacting protein, thyroid hormone receptor associated protein). SRC has histone acetylase activity, and DRIP/TRAP recruit RNA polymerase II --> increase in transcription |
|
|
Term
| what are the 2 models to describe how TSH alpha and beta subunit gene transcription are negatively regulated by T3? |
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Definition
| thyroid hormone receptor MONOMOER binds to single hexameric half-site; T3-receptor-RXR-heterodimer binding to unique negative TRE |
|
|
Term
| Negative regulation of TH in absence of T3? |
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Definition
| T3-receptor-NCor-GAF complex --> increase in transcription d/t co-activator activity of NCoR |
|
|
Term
| negative regulation of TH in presence of T3 |
|
Definition
| T3 receptor undergoes conformational change that facilitates recruitment of chromatin remodeling proteins --> condense chromatin & dissociation of T3 receptor from negative TRE |
|
|
Term
| [ionized calcium] in plasma? |
|
Definition
| 1.0 - 1.3 mM (tightly regulated w/in range of 1-2%) |
|
|
Term
| resting intracellular [free ca] |
|
Definition
| 100nM (can increase from 10-100 fold) |
|
|
Term
| total serum calcium concentration |
|
Definition
| 2.1-2.6 mM (daily variation <10%) |
|
|
Term
| concentration of free, ionized ca regulated in extracellular component by what 2 hormones? |
|
Definition
| PTH and 1,25 dihydroxy vit D |
|
|
Term
| how does our body compensate for a low level of calcium concentration in ECF? |
|
Definition
| PTH works on bone and kidney; binding of PTH in kidney cells --> produce active form of vit D --> facilitates efficient absorption of ca from intestine |
|
|
Term
| what is the cellular mechanism by which an increased level of [ca] causes downregulation of PTH? |
|
Definition
| high ca--> ca-sensing receptor activated (in plasma membrane) --> stimulation of PLC & simultaneous inhibition of adenylate cyclase --> increase in intracellular ca and decerase in cAMP --> block PTH secretion |
|
|
Term
| how does PTH work in bone? |
|
Definition
| binding of PTH to receptors in osteoblasts stimulates release of cytokines that cause osteoclasts to adhere to bone matrix |
|
|
Term
| how does PTH work in kidney? |
|
Definition
| direct stim effect on ca reabsorption in thick ascending limb and distal tubule; inhibits phosphate reabsorption in prox tubule; increases activity of 1alpha-hydroxylase, enz responsible for active form of vit D |
|
|
Term
| whats the 3 step process to make active vit D? |
|
Definition
| 7-dehydrocholesterol + uv light (in skin) --> cholecalciferol (in liver) --> 25-hydroxycholecalciferol (in kidney + PTH) --> 1, 25 dihydroxycalciferol |
|
|
Term
| 3 points of vit D action to increase ca absorption? |
|
Definition
| increase # of ca channels; increase calbindin (more binding of ca when it gets within the cell); increase ca-ATPase (get rid of ca from IC to blood stream) |
|
|
Term
| describe the cleaving of pro-opiomelanocortin |
|
Definition
| into ACTH and B-lipotropin. ACTH --> alpha-melanocyte stimulating hormone and corticotropin-like intermediate peptide. B-lipotropin --> B-endorphin + y-lipotropin |
|
|
Term
|
Definition
| granulosa cells and sertoli cells (inhibit FSH synthesis) |
|
|
Term
| PRL secretion is positively regulated by? |
|
Definition
| TRH, estrogen, and angiotensin II |
|
|
Term
| PRL secretion is negatively regulated by? |
|
Definition
| dopamine and somatostatin |
|
|
Term
| describe the long-loop negative feedback on growth hormone secretion |
|
Definition
| GH causes liver and other tissues to produce IGF-1 --> IGF-1 inhibits GH secretion at hypothalamic level (increases somatostatin release and decreases GHRH release) and pituitary level (interferes with GHRH action) |
|
|
Term
| inhibitory signals for gastric ghrelin production |
|
Definition
| somatostatin, interleukin 1B, GH, high-fat diet |
|
|
Term
| stimulatory signals for gastric ghrelin production |
|
Definition
| fasting, low-protein diet |
|
|
Term
|
Definition
| GH resistant (high GH levels, no IGF-1 production) |
|
|
Term
|
Definition
| problem with GH receptor, IGF-1 levels do not rise normally after GH administered, but do not totally lack IGF-1 reponse |
|
|
Term
| Supraoptic nuclei produce what hormone |
|
Definition
|
|
Term
| paraventricular nuclei produce what hormone |
|
Definition
|
|
Term
| what is the purpose of neurophysins |
|
Definition
| (seq attached to all hormones stored in neurohypophysis) stabilizes the structure of prohormone during passage in the granule (ADH - neurophysin II, oxytocin - neurophysin I) |
|
|
Term
| 3 parts of seminiferous tubules |
|
Definition
| epithelium (closest to lumen); basal lamina; tunica propria (myoid cells) |
|
|
Term
| describe spermatocytogenesis |
|
Definition
| mitotic cell division of spermatogonia to form primary spermatocytes. in response to testosterone (produced by leydig cells, under control of LH), type A spermatogonia (pale nucleus) become type B spermatogonia, which undergo a last phase of mitosis and double their DNA content --> enter meiotic prophase (now called primary spermatocytes) |
|
|
Term
| describe DNA content of secondary spermatocytes |
|
Definition
| haploid (23 chromosomes), DNA content of 2N (after first meiotic division of primary spermatocytes) |
|
|
Term
| describe dna content of spermatids |
|
Definition
| after 2nd meiotic division --> haploid (23 chromatids), DNA content 1N |
|
|
Term
| what are the 3 steps of spermiogenesis |
|
Definition
| development of flagellum, development of acrosome, nuclear condensation (histones replaced by arginine and lysine rich protamines which stabilize and protect the sperm genomic dna) |
|
|
Term
| what happens in the golgi phase of acrosomal development |
|
Definition
| formation of acrosomal granules, granules fuse to form acrosmal vesicle, acrosomal vesicle binds to one pole of nucleus, centriole at other end produces flagella |
|
|
Term
| what happens during cap phase of acrosomal development |
|
Definition
| acrosomal vesicle grows, flattens, and forms cap. nucleus condenses, cell elongates, flagellum elongates, entire spermatid rotates |
|
|
Term
| what happens during the acrosomal phase of acrosomal development |
|
Definition
| manchette develops at edge of acrosomal cap (perinuclear ring with attached microtubules), axoneme continues to develop, mitochondria start migration |
|
|
Term
| what happens in the maturation phase of acrosomal development |
|
Definition
| outer dense fibers develop, mitochondria encircle tail, elongation of nucleus, elongation of spermatid |
|
|
Term
|
Definition
| process by which sperm are released into the lumen of seminiferous tubules by phagocytosis of the residual bodies by sertoli cells |
|
|
Term
| what marks the lower limit of the middle piece of sperm tail? |
|
Definition
| annulus (dense ring adjacent to mitochondria) |
|
|
Term
| how does NO mediate erection |
|
Definition
| sexual stimulation --> NO release --> No binds to guanylate cyclase --> activates guanylate cyclase in smooth muscle to produce cyclic GMP --> relaxes smooth muscle surrounding vascular spaces of corpus cavernosum, allowing more blood to fill spaces |
|
|
Term
| how does phosphodiesterase-5 work? |
|
Definition
| degrades second messengers cyclic GMP (converts it to inactive form) --> terminates effects of NO |
|
|
Term
| how does ACTH work on a molecular level to bring about increase in cortisol/corticosterone concentration? |
|
Definition
| ACTH binds plasma receptor on adrenal cortex cells --> G protein activation of adenylyl cyclase --> rise in cAMP, activates PKA, phosphorylates proteins that stimulate CHOLSTEROL ESTERASE (releases cholesterol from lipid-storing droplets in cytoplasm, translocates to inner mit) |
|
|
Term
| steroid secreting cells store the hormone itself? |
|
Definition
| no, they store the precursor, then synthesize the hormones, which diffuse thru the plasma membrane and enter the blood stream via fenestrated cap |
|
|
Term
| what is the pathway from cholesterol to corticosterone? |
|
Definition
| cholesterol --> pregnenalone --> progesterone --> 11-deoxycorticosterone --> corticosterone |
|
|
Term
| what is the pathway from cholesterol to aldosterone? |
|
Definition
| cholesterol --> pregnenalone --> progesterone --> 11-deoxycorticosterone --> aldosterone |
|
|
Term
| what is the pathway from cholesterol to cortisol? |
|
Definition
| cholesterol --> pregnenalone --> 17-hydroxypregnenalone --> 17-hydroxyprogesterone (could come from progesterone) --> 11-deoxycortisol --> cortisol |
|
|
Term
| what is the pathway from cholesterol to dihidroepiandrosterone? |
|
Definition
| cholesterol --> pregnenalone --> 17-hydroxypregnenalone --> dehydroepiandrosterone |
|
|
Term
| how does cortisol work on a molecular level? |
|
Definition
| cortisol diffuses across plasma membrane binds to glucocorticoid receptor in cytoplasm --> receptor forms complex with heat shock proteins (released upon cortisol binding) --> hormone-receptor complex translocates to nucleus binds to glucocorticoid response element --> enhances or represses gene transcription |
|
|
Term
| what is the pathway of cortisol metabolism? |
|
Definition
| cortisol --> dihydrocortisol --> tetrahydrocortisol --> tetrahydrocortisol glucuronide |
|
|
Term
| what are 2 ways cortisol raises blood glucose? |
|
Definition
| antagonizes the action of insulin on muscle and adipose tissue, sparing glucose for brain; increases liver output of glucose |
|
|
Term
| what are 3 ways cortisol promotes gluconeogenesis? |
|
Definition
1. inhibits protein synthesis and accelerates protein degradation in muscle and CT (increasing free AA, which are available to liver for GNG)
2. mobilizes fatty acids and glycerol from adipocytes (freeing them up for GNG)
3. directly activates key hepatic gluconeogenic enzymes |
|
|
Term
| what are the 2 main causes of cushings disease? |
|
Definition
1. (80%) hypersecretion of ACTH (adrenal secondarily stimulated)
2. (20%) adrenal tumors autonomously producing cortisol |
|
|
Term
| how does the rise in [K+] cause increase in aldosterone prod? |
|
Definition
| depolarizes zona glomerulosa cell membrane --> causing [ca] influx which stimulates aldosterone production |
|
|
Term
| how does a fall in sodium levels cause increase in aldosterone production? |
|
Definition
| fall in sodium --> JG cells of kidney secrete renin --> ang II --> angII binding to receptor on glomerulosa cells stimulates aldosterone synthesis |
|
|
Term
| how does aldosterone work in kidney on molecular level? |
|
Definition
| aldosterone binds mineralcorticoid receptor in cytoplasm of cortical collecting tubule --> receptor-hormone complex travels to nucleus and binds to mineralocorticoid-responsive element on DNA --> increase in synthesis of epithelial Na channels and insertion into apical membrane |
|
|
Term
| what reaction(s) is 21-hydroxylase supposed to catalyze? |
|
Definition
| 17-hydroxyprogesterone --> 11-deoxycortisol; progesterone --> deoxycorticosterone |
|
|
Term
| what is a good diagnostic criteria of primary aldosteronism? |
|
Definition
|
|
Term
| what is the pathway from tyrosine to epinephrine? |
|
Definition
| tyr --> dopa --> dopamine --> norepi --> epi |
|
|
Term
| which steps of catecholamine synthesis require ACTH stimulation? |
|
Definition
| tyr --> dopa (catalyzed by tyrosine hydroxylase); dopamine --> norepi (catalyzed by dopamine-b-hydroxylase) |
|
|
Term
| which step of epinephrine synthesis requires cortisol? |
|
Definition
| norepi --> epi (phenylethanolamine N methyltransferase) |
|
|
Term
|
Definition
| neurons that produce GnRH originate in nasal epithelium and migrate along olfactory nerve into brain during embryonic development. obstruction in region of cribiform plate can prevent migration of both olfactory nerve and GnRH neruons |
|
|
Term
| what 2 things cause GnRH to be secreted? |
|
Definition
1. decreased estrogen levels (as in beginning of menstrual cycle)
2. neurotransmitters (norepi stimulates GnRH, seratonin and dopamine exert inhibitory effects) |
|
|
Term
| how does GnRH cause LH and FSH release on a molecular level? |
|
Definition
| GnRh binds (w/help from ca and prostaglandin) receptor on surface membrane of target cell --> membrane bound adenylate cyclase activated --> stimulates cAMP production --> activates protein kinase by dissoc regulatory subunit --> catalytic subunit phosphorylates membrane protein to increase ca permeability --> ca enters cell --> ca activates release of LH and FSH |
|
|
Term
| what four hormones have the same alpha subunit? |
|
Definition
|
|
Term
| which cells are LH receptors located on? |
|
Definition
| theca cells at all stages of the cycle, and on granulosa cells after the follicle matures under FSH and estradiol |
|
|
Term
| describe the 2-cell theory |
|
Definition
| LH acts on theca cell to convert cholesterol to androstenedione --> transported to granulosa cell, where FSH makes aromatase available to convert androstenedione to estrone and 17-hydroxysterodehydrogenase converts estrone to estradiol |
|
|
Term
| what 2 important things does the LH surge do? |
|
Definition
| initiates the resumption of meiosis in the oocyte and induce further luteinization of the granulosa cell to produce more progesterone that is necessary in the luteal phase |
|
|
Term
| how do estrogen and progesterone work on a molecular level to exert their effects? |
|
Definition
| bind to ligand binding domain of estrogen receptor and progesterone receptor in the cytoplasm (receptor loses chaperone proteins and changes conformation) --> when bound by their hormone ligand, they are activated, dimerize, translocated to nucleus, bind to ERE or PRE on target genes --> mRNA --> DNA |
|
|
Term
| what does mifiprex target? |
|
Definition
| endometrial progesterone receptors in uterus (supposed to enhance endometrial secretions in preparation for pregnancy. HCG supports corpus luteum which secretes the progesterone that acts on these receptors) |
|
|
Term
| what does oocyte maturation inhibitor do and where does it come from/ |
|
Definition
| comes from corona radiata. keeps primary oocyte in prophase I. |
|
|
Term
| what hormone helps regrow the stratum functionalis? |
|
Definition
|
|
Term
| what causes the rise in basal body temp during ovulation? |
|
Definition
|
|
Term
| how do estrogen and progesterone affect the cervix's mucus? |
|
Definition
| estrogen causes it to become copious and watery (facilitates and directs sperm); progesterone decreases the quantity and causes it to become moreviscous (mucus plug forms during preg) |
|
|
Term
| how is insulin synthesized? |
|
Definition
| as preprohormone in granular ER, microsomal enzymes cleave into proinsulin --> proinsulin packaged into membrane-bound secretory granules + protease that cleaves it --> on stimulation, granule cell contents released by exocytosis, reqs functional microtubular system and is Ca dependent (insulin, C peptide and proinsulin are secreted) |
|
|
Term
| describe the insulin receptor |
|
Definition
| tyrosine kinase-containing receptor. 2 alpha subunits (external to cell membrane) contain hormone binding sites. beta subunits contain tyrosine kinase on cytosolic surface --> insulin binds --> autophosphorylation of beta subunits (prolongs signal) & phosphorylation of insulin receptor substrate 1 &2 (act as intracellular docking proteins for proteins mediating insulin action) |
|
|
Term
| what helps regulate the termination of insulin signal? |
|
Definition
| when insulin binds to receptor --> increased rates of receptor internalization (eventually get recycled to surface) |
|
|
Term
| how is glucose taken up by B-cells of pancreas? |
|
Definition
| by low affinity glucose transporter GLUT2. high Km assures that amount of glucose transported into beta cells is porportional to [glu] in blood |
|
|
Term
| how does the b-cell in pancreas sense how much glucose is in the blood? |
|
Definition
| by amt of glucose that enters the cell and gets converted into G6P |
|
|
Term
| what ensures that the amount of glucose that gets converted to G6P is proportional to intracellular [glu] in beta cells of pancreas? |
|
Definition
| relatively high Km of glucokinase that converts glu to G6P |
|
|
Term
|
Definition
| secreted in same granule as insulin. eat large meal --> secrete insulin and amylin --> amylin tries to curb how much we eat via satiety |
|
|
Term
| explain how increase in glucose leads to insulin secretion. |
|
Definition
| increase in G6P --> increase ATP/ADP ratio --> ATP sensitive K channel closes, K efflux from B cell suppressed and cell depolarizes --> increase in IC [Ca] activates mechanism for secretory granule movement along microtubules and is the signal for exocytosis |
|
|
Term
| why is there always a diffusion gradient driving insulin into the blood from B cells? |
|
Definition
| blood flow thru capillaries removes insulin so fast that insulin concentrations are always higher in extracellular space than in the blood |
|
|
Term
| what are incretins and what do they do? |
|
Definition
| glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) gut peptides released from endocrine cells in intestinal mucosa following ingestion. bind cell surface, activate g-protein coupled reaction --> activate adenylate cyclase --> increase in cAMP --> cAMP amplifies signal through PKA to cause more insulin secretion @ same glucose level. (helps with excessive glucose load) |
|
|
Term
| where are GLUT4 receptors located and what is their purpose |
|
Definition
| adipose and muscle. these are insulin-dependent glucose channels that are stored in the golgi apparatus of insulin-sensitive cells. insulin binds plasma membrane --> GLUT4 receptors translocate from IC pool to plasma membrane. (this is how insulin works to increase glucose uptake in these tissues) |
|
|
Term
| where are GLUT1 receptors and how are they different from GlUT4? |
|
Definition
| brain - i think not insulin-sensitive. bc if it were like GLUT4, when there is low insulin, # of glu transporters would decrease, and too little glu would get to the brain --> death. |
|
|
Term
|
Definition
| inhibitor of insulin secretion (neuronal) |
|
|
Term
| what effect does somatostatin have on alpha and beta cells? |
|
Definition
| inhibits secretion of insulin and glucagon |
|
|
Term
|
Definition
| hormone present in adipocytes that inhibits food intake |
|
|
Term
| what 2 important things are restrained by insulin (and thus unrestrained in the diabetic) |
|
Definition
| lipolysis and fasting state levels of glucagon |
|
|
Term
| Beta cells of the pancreas are only found in the pancreas. where are alpha cells? |
|
Definition
| pancreas + throughout the gut. alpha cells in the gut secrete enteroglucagon which is functionally identical to glucagon |
|
|
Term
| 2 most important factors affecting secretion of glucagon? |
|
Definition
| plasma glucose levels and plasma AA levels (esp. glucogenic AA like alanine and arginine) |
|
|
Term
| only situation in which insulin and glucagon get secreted simultaneously? |
|
Definition
| high-protein/carb-free diet |
|
|
Term
| if you inject a person w/cortisol, what happens to [AA]? |
|
Definition
| increases, esp AA like Ile, Leu, and Val (ala will not increase for example, bc it is glucogenic and can be converted into glucose) |
|
|
Term
| what stops the continued growth of epithelial and stromal cells during the secretory phase? |
|
Definition
|
|
Term
| what causes vasospasm during menstruation? |
|
Definition
| decreased levels of estradiol and progesterone, and released prostaglandins |
|
|
Term
| capacitation characterized by 3 accomplishments, they are? |
|
Definition
1. ability to undergo acrosome reaction (seminal plasma factors and cholesterol removed from cell membrane + modification of surface charge --> breakdown and merging of plasma membrane and membrane lying under it --> allows egress of acrosome enz contents
2. ability to bind to zona pellucida
3. hypermotility (critical for zona pellucida penetration) |
|
|
Term
| what changes does estradiol produce in the fallopian tube? |
|
Definition
| stimulates cilia production, increases rate of cilia beating, increases secretion of mucous to facilitate sperm movement against cilia beat |
|
|
Term
| what changes does progesterone produce in fallopian tube? |
|
Definition
| increases contractions of muscular wall of the fallopian tube to facilitate the fimbria drawing in the ovum from the ovary |
|
|
Term
| what are placental estrogens responsible for? |
|
Definition
| growth of myometrium, development of breast ducts glands and adipose tissue, (with relaxin) promote loosening of pelvic ligaments, increases uterine and placental blood flow |
|
|
Term
| what does placental progesterone do? |
|
Definition
| maintains uterine lining, relaxes smooth muscle, suppresses maternal immune response to fetal antigens |
|
|
Term
| how is placental progesterone created? |
|
Definition
| maternal LDL cholesterol --> pregnenolone --> progesterone |
|
|
Term
| what does human placental lactogen do? |
|
Definition
causes a lot of insulin antagonism in the mother (maternal tissue sensitivity decreases as much as 80% bc glucose being drained to fetus --> post-prandial hyperglycemia and hyperinsulimia)
in fasting state as maternal glucose decreases --> placental glucose decreases --> HPL increases --> lipolysis increases --> FFA increases --> Ketones in mother and fetus increase
post-prandial --> glucose increases --> HPL decreases --> lipolysis decreases --> FFA decreases (no ketones) |
|
|
Term
| what is the main substrate and 3 hormones important in growth of fetus? |
|
Definition
| glucose; HPL, prolactin, IGF-2 |
|
|
Term
| what stimulates bone growth in fetus? |
|
Definition
| PTH - actively transports Ca into fetal circ, calcitonin from fetal kidney, and vit D from placenta |
|
|
Term
| what hormones in what sequence are important in parturition? |
|
Definition
| fetal brain --> increased ACTH --> increased cortisol --> decreased progesterone --> withdrawal assoc w/increased elec. excitability of uterus in response to electric and oxytocic stimuli. oxytocin important in contractions and also prostaglandins |
|
|
Term
| lactogenesis is initiated by binding of prolactin to membrane receptors...then what? |
|
Definition
| tyrosine kinase receptors are associated --> they activate TF that induce gene expression of enzymes involved in synthesis of milk nutrients (i.e. milk protein, casein) |
|
|
Term
| what is the final endocrine hallmark of puberty? |
|
Definition
| development of positive estrogen feedback on pituitary and hypothalamus (stimulates LH surge req'd for ovulation) |
|
|
Term
| how does menopausal absence of bleeding actually come about? |
|
Definition
| in perimenopause lower levels of inhibin (d/t decrease in # of viable follicles and granulosa cells) --> allows FSH to be secreted at higher than normal levels --> greater secretion of estradiol --> after few months, levels of FSH not enough to stim sufficient estradiol secretion (d/t even more decreased # of follicles and granulosa cells) --> estradiol levels decline --> failure of endometrial dev |
|
|
Term
| post-menopause where do women get their estrogen? |
|
Definition
| chief source of androstenedione is the adrenal glands --> majority of androstenedione passes into circ and is aromatized peripherally in the fat to estrone |
|
|
Term
| what's an explanation for why CAD is more common in men? |
|
Definition
| estrogen inhibits proliferation of smooth muscle cells after vessel wall injury and dihydrotestosterone increases human monocyte adhesion to the endothelial cells |
|
|
Term
| what part of the placenta produces HCG? |
|
Definition
| syncytiotrophoblast cells --> diffuses into maternal circulation to keep corpus luteum functioning until placenta ready to take over |
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|
