front 1 male reproductive hormone tract | back 1 hypothalamus, GnRH, anterior pituitary, FSH and LH, Sertoli cells, inhibin, interstitial cells, testosterone |
front 2 what produces testosterone | back 2 interstitial cells between seminiferous tubules |
front 3 what supports sperm development | back 3 Sertoli cells |
front 4 what inhibin does | back 4 acts as negative feedback on the anterior pituitary |
front 5 hormone that prostate cancer and BPH are dependent on | back 5 testosterone |
front 6 mechanism that can be blocked to treat BPH | back 6 testosterone turning into DHT |
front 7 how testosterone exhibits "double negative feedback" | back 7 it inhibits anterior pituitary and GnRH secretion |
front 8 female reproductive hormone tract | back 8 hypothalamus, GnRH, anterior pituitary, FSH and LH, granulosa cells, estrogen and inhibin |
front 9 what influences amount of estrogen being produced | back 9 amount of granulosa cells |
front 10 average length of one menstrual cycle | back 10 28 days |
front 11 three phases of menstrual cycle | back 11 follicular, ovulatory, luteal |
front 12 basic function of the follicular phase | back 12 stimulate granulosa cells to divide, grow oocyte from primordial follicle to secondary follicle |
front 13 basic function of the ovulatory phase | back 13 enough estrogen builds up to stimulate LH release, causes egg release which leaves corpus luteum behind, corpus luteum takes over estrogen secretion |
front 14 effects of estrogen on the uterus | back 14 growth of myometrium, growth of endometrium |
front 15 what myometrium is | back 15 smooth muscle layer in uterus |
front 16 what endometrium is | back 16 epithelial lining in uterus |
front 17 basic function of the luteal phase | back 17 corpus luteum shifts production to favor progesterone, which stimulates angiogenesis, inhibits myometrium contraction and GnRH secretion, period begins when granulosa cells die off |
front 18 progesterone function | back 18 stimulates angiogenesis, inhibits myometrium contraction, completely inhibits GnRH secretion |
front 19 what happens if fertilization does not occur | back 19 corpus luteum dies, progesterone production stops, capillaries break and endometrium dies, myometrium contracts |
front 20 how we can stimulate hyperovulation | back 20 injections of GnRH |
front 21 what hormone puberty begins with | back 21 GnRH |
front 22 why menstrual cycle takes a long time | back 22 it is heavily dependent on cell division |
front 23 how birth control pills work | back 23 estrogen and progesterone, negative feedback to inhibit ovulation |
front 24 how plan B works | back 24 progesterone only, blocks ovulation and implantation, taken up to 72hrs after sex |
front 25 RU486/mifepristone | back 25 chemical abortion, progesterone antagonist to break down endometrium lining |
front 26 ELLA | back 26 works like mifepristone, progesterone antagonist |
front 27 IUD | back 27 copper or plastic, irritates lining of uterus to block implantation |
front 28 detected in pregnancy tests | back 28 HCG |
front 29 what must be done in order to rescue the corpus luteum | back 29 the embryo must make HCG |
front 30 "hand-off" that happens in the second trimester | back 30 HCG decreases, placenta takes over estrogen and progesterone secretion |
front 31 what the enlarged uterus pushes up against | back 31 liver, stomach, diaphragm, intestines, bladder |
front 32 changes to mammary glands | back 32 compound tubular secretory epithelium proliferate |
front 33 reason for risk of gestational diabetes | back 33 BV increases by 30-50%, so insulin must also increase |
front 34 how pregnancy affects MAP | back 34 BV increases, PR decreases, CO increases, usually MAP increases |
front 35 what the increased MAP puts a pregnant woman at risk for | back 35 hypertension, pre-eclampsia |
front 36 symptoms of pre-eclampsia | back 36 widespread edema, headache |
front 37 how pre-eclampsia is made worse | back 37 protein is taken up by the baby, decreasing osmotic pressure |
front 38 symptoms of eclampsia | back 38 cerebral edema, blurred vision, convulsions, coma, vascular spasm |
front 39 how pregnancy affects the respiratory system | back 39 increases respiratory rate |
front 40 how pregnancy affects the thyroid | back 40 gland enlarges by 40% |
front 41 what prostaglandins do | back 41 stimulate collagenase to digest collagen ropes holding cervix shut |
front 42 example of a prostaglandin used in medicine | back 42 mifeprostol |
front 43 incompetent cervix | back 43 inadequate collagen ropes, cervix dilates too early, miscarriage |
front 44 CRH hormone pathway | back 44 stress, hypothalamus, CRH, anterior pituitary, ACTH, adrenal cortex, glucocorticoids, increase glucose and estrogen, risk of premature delivery |
front 45 why stress causes risk for premature delivery | back 45 increased estrogen causes myometrium to tighten, may cause contractions to begin |
front 46 Braxton-Hicks contractions | back 46 spontaneous depolarization of the uterine smooth muscle |
front 47 treatments for braxton-hicks | back 47 bedrest, calcium channel blockers, beta adrenergic agonists |
front 48 positive feedback cycle of oxytocin | back 48 hypothalamus, posterior pituitary, oxytocin release, myometrium contracts, cervix dilates, hypothalamus is stimulated more |
front 49 reason for rest periods between contractions | back 49 allows blood flow to the baby |
front 50 epidural | back 50 sodium channel blocker injected into epidural space at L1, relatively safe but relief is not immediate |
front 51 spinal block | back 51 injected into subarachnoid space, works faster but may cause cerebral spinal fluid to leak, leading to headache |
front 52 risk of oxytocin injection to help labor along | back 52 may be too much and result in a continual contraction, causing brain damage to the baby |