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Endocrine E3,2
Endocrine E3 hormones of reproduction
Question | Answer |
---|---|
sexual differentiation is determined by | 1)development of the gonads 2)development of the internal genital tract 3)development of the external genitalia |
maleness or femaleness can be characterized in what 3 ways | 1)genetic sex(male XY, female XX) 2)gonadal sex(male testis, female ovaries) 3)phenotypic sex(external genitalia) |
genetic sex is determined by what | sex chromosomes, male XY, female XX |
when does the development of the testes begin | 6-7 weeks |
when do the ovaries start to develop | week 9 |
genetic sex usually determines | gonadal sex |
gonadal sex is determined by what | what gonads are present male=testes, female=ovaries |
what are the 3 cell types for the testes | 1)germ cells 2)sertoli cells 3)leydig cells |
what are the 3 cell types for the ovaries | 1)germ cells 2)theca cells 3)theca+granulosa cells |
what do germ cells of the testes produce | spermatogonia |
what do sertoli cells do | synthesize antimullerian hormone & inhibin |
what do leydig cells do | syntesize testosterone |
what do germ cells of the ovaries produce | oogonia |
what do theca cells do | synthesize progesterone |
what do theca+granulosa cells do | syntesize estrogen |
what is phenotypic sex defined by | physical characteristics of the internal genital tract & external genitalia |
males internal genital tract consists of | 1)prostate 2)seminal vesicle 3)vas deferens 4)epididymis |
the male external genitalia consists of | 1)scrotum 2)penis |
the female internal genital tract consists of | 1)fallopian tubes 2)uterus 3)upper 1/3 of the vagina |
the female external genitalia consists of | 1)clitoris 2)labia majora 3)labia minora 4)lower 2/3 of vagina |
the male testes secrete | antimullerian hormone and testosterone |
in the embryo the wolffian ducts lead to | 1)epididymis 2)vas deferens 3)seminal vesicles 4)ejaculatory ducts |
testosterone stimulates what in the embryo | growth and differentiation of wolffian ducts |
antimullerian hormone causes what in the embryo | atrophy of mullerian ducts |
growth and development of the external genitalia depend on conversion of testosterone which leads to | dihydrotestosterone and androgen receptors |
gonadal female ovaries secrete | estrogen |
since ovaries don't produce testosterone or antimullerian hormone what happens | wolffian ducts aren't stimulated and mullerian ducts aren't suppressed |
mullerian ducts lead to | 1)fallopian tubes 2)uterus 3)upper 1/3 of vagina |
growth of female structures require what to reach normal size | estrogen |
androgen insensitivity syndrome is classified as | male genotype but a female phenotype |
a female who at puberty shows breast development but no menstruation, tests show | 1)pelvic exam shows presence of testes & short vagina 2)androgen binding studies show no binding of testosterone or dihydrotestosterone leading to receptors defective 3)elevated testosterone levels and LH |
androgen insensitivity syndrome shows | 1)no fallopian tubes, uterus, or upper vagina(no menstrual cycle) 2)testes secreted both antilullerian hormone & testosterone in utero -suppression of mullerian ducts -targets unresponsive to testosterone |
androgen insensitivity syndrome: breast development at puberty due to | testes producing estradiol from testosterone, stimulated by the high circulating levels of LH |
what is the treatment for androgen insensitivity syndrome | 1)removal of testes to prevent neoplasm -source of estrogen gone 2)intermittent estrogen replacement therapy |
in both male and female gonadal function is driven by | hypothalamic pituitary axis |
what is the timeline for hormonal secretion to determine gender | 1)GnRH secretion begins at week 4 2)FSH/LH secretion begins at 10-12 weeks 3)FSH/LH low until puberty 4)LH>FSH during puberty and become pulsatile 5)in old age FSH>LH gonadotropin secretion rates continue to rise |
what is the primary hormonal event | initiation of pulsatile secretion of GnRH which drive secretion of FSH/LH, stimulate gonads to produce hormones -large nocturnal pulses of LH -GnRH up regulates it own ant. pituitary receptor |
increase circulating levels of sex steroids are responsible for | secondary sexual characteristics |
what can play a role in onset of puberty | 1)CNS and nutritional status -extreme stress or caloric deprivation may delay 2)melatonin -decrease melatonin, increases GnRH |
what is the timeline for events of puberty for males | 1)pubic hair (12-16 yrs) 2)penile growth (13-15 yrs) 3)growth spurt (13-16 yrs) |
what is the timeline for events of puberty for females | 1)breast development (11-15 yrs) 2)pubic hair (9-15 yrs) 3)menarche (10-16 yrs) 4)growth spurt (11-14 yrs) |
puberty of boys: activation of hypothalamic-pituitary axis timeline | 1)leydig cell proliferation increases secretion of testosterone 2)growth of testes (increase of seminiferous tubules) 3)growth of accessory sex organs 4)linear growth spurt 5)pubic hair growth 6)growth of penis 7)lowering of voice |
puberty of girls: activation of hypothalamic-pituitary axis timeline | 1)drives synthesis of estradiol by ovaries-1st sign is budding of breast followed by menarche within 2 years 2)growth spurt & closure of epiphyseal plates 3)pubic hair precedes menarche and dependent on adrenal androgens |
what is testosterone synthesized and secreted by | leydig cells of testes |
what are the major differences of testosterone and biochemical pathway of adrenal cortex | 1)lack 21 beta-hydroxylase and 11 beta-hydroxylase 2)have additional enzyme 17 beta-hydroxysteroid dehydrogenase |
in some target tissues testosterone is converted to dihydrotestosterone by what enzyme | 5alpha-reductase |
sex steroid binding globulin is stimulated and inhibited by what | estrogens, androgens |
what are the functions of the testes controlled by | hypothalamic-pituitary axis |
FSH stimulates what | spermatogenesis & sertoli cell function |
LH stimulates what | secretion of testosterone |
what are the 2 paths of negative feedback that control HPA | 1)testosterone inhibits both anterior pituitary LH & hypothalamic GnRH secretion 2)sertoli cells also secrete a glycoprotein called inhibin which inhibits anterior pituitary FSH secretion |
testosterone has a paracrine effect on the sertoli cells to do what | stimulate release of inhibin |
what is the use of 5alpha-reductase | 1)block the conversion of testosterone to dihydrotestosterone 2)blocks production of active androgens in some targets 3)finasteride-used to treat benign prostatic hyperplasia & male pattern baldness |
mechanism of action of androgens | binding of testosterone or dihydrotestosterone to androgen receptor protein in the cells of target tissues |
"sally" is a genotypic male with testes but no ovaries, what is the explanation for what happened during fetal development | 1)testes secrete test. but lacks 5A-reductase, can't convert test. to dihydrotesterone 2)external male genitalia fail to develop 3)antimullerian hormone suppressed development of mullerian duct 4)fetal test. caused internal male reproductive tract |
"sally" is a genotypic male with testes but no ovaries, what is the explanation for what happened during puberty | 1)clitoris grew & became more penis like because of high circulating levels of test., may activate DHT receptors 2)voice deepening & increased skeletal muscle mass mediated by test. 3)no body hair 4)no ovaries=no estrogen=no breast development |
what is the treatment for "sally" who is a genotypic male with testes and no ovaries | 1)women -removal of testes & estrogen replacement=breasts -surgical correction of vaginal opening -never have kids 2)man -treated with androgenic compounds that do not require 5A-reductase to complete masculinization |
what converts cholesterol to pregnenolone | cholesterol desmolase (theca cells), stimulation of LH |
what converts pregnenolone to progesterone | 3B-hydroxysteriod dehydrogenase |
what converts pregnenolone to 17-hydroxypregnenolone | 17A-hydroxylase |
what converts 17-hydroxypregnenolone to dihydroepiandrosterone | 17,20-lyase |
what converts dihydroepiandrosterone to androstenedione | 3B-hydroxysteroid dehydrogenase |
what converts androstenedione to testosterone | 17B-hydroxysteriod dehydrogenase (granulosa cells) |
what converts testosterone to 17B-estradiol | aromatase (granulosa cells), stimulation of FSH |
theca cells syntesize and secrete what | progesterone and androstenedione |
LH stimulates what in theca cells | cholesterol desmolase |
FSH stimulates what in granulosa cells | aromatase |
what are the 2 major functions of the ovaries | 1)oogenesis 2)synthesis/secretion of female sex hormones |
regulation of the ovaries is controlled by what | hypothalamic-pituitary axis |
what stimulates the anterior pituitary to secrete FSH/LH to the ovaries | GnRH |
what is the function of FSH and LH in the ovaries | 1)follicular development for ovulation 2)syntesize/secrete progesterone & 17B-estradiol |
follicular development--->___________---->________ | ovulation, formation & degeneration of corpus luteum |
1st 14 days of the menstrual cycle | follicular phase 1)development of follicle 2)dominated by estrogen(17B-estradiol) |
last 14 days of menstrual cycle | 1)luteal phase 2)dominated by corpus luteum |
midpoint of menstrual cycle | ovulation |
granulosa cells are the only ovarian cells with | FSH receptors |
what does FSH do | 1)stimulate the growth of granulosa cells in primary follicles 2)stimulate estradiol synthesis |
what does LH do | 1)intiate ovulation -just prior to ovulation LH rises & causes rupture of mature follicle 2)stimulates formation of the corpus luteum and maintains progesterone production corpus luteum during luteal phase |
what phase in menstrual cycle: hypothalamus--->GnRH--->ant. pit.--->FSH,LH--->ovary--->estradiol--->inhibit ant. pit. | follicular phase |
what phase in menstrual cycle: hypothalamus--->GnRH--->ant. pit.--->FSH,LH--->ovary--->estradiol--->stimulate ant. pit. | midcycle |
what phase in menstrual cycle: hypothalamus--->GnRH--->ant. pit.--->FSH,LH--->ovary--->progesterone--->inhibit ant. pit. | luteal phase |
what is the ovarian feedback during the follicular phase of menstruation | FSH & LH stimulate synthesis/secretion of estradiol by follicular cells causing negative feedback on ant. pit. inhibits secretion of FSH/LH |
what is the ovarian feedback during midcycle of menstruation | estradiol levels increase sharply & when critical threshold is reached estradiol upregulates ant. pit. GnRH receptors increasing secretion of FSH/LH (positive feedback) |
what is the ovarian feedback during the luteal phase of menstruation | progesterone secretion by corpus luteum causes negative feedback on ant. pit. to inhibit secretion of FSH/LH |
estrogen and progesterone work together to support what reproductive activity | 1)development of the ovum 2)maintenance of the corpus luteum 3)maintenance of pregnancy 4)lactation |
what are the hormonal effects on the uterus | 1)estrogen causes cell proliferation, cell growth, increased contractility 2)progesterone increases secretory activity and decreases contractility |
what are the hormonal effects on the fallopian tubes | 1)estrogen stimulates ciliary activity and contractility(sperm movement toward uterus) 2)progesterone increases secretory activity and decreases contractility |
what are the hormonal effects on the cervix | 1)estrogen causes cervical mucous to become copious, watery, elastic 2)progesterone decreases the quantity of cervical mucous and it becomes thick, nonelastic |
what are the hormonal effects on the vagina | 1)estrogen stimulates proliferation of epithelial cells 2)progesterone stimulates differentiation but inhibits proliferation of epithelial cells |
what are the hormonal effects on the mammary glands | 1)estrogen stimulates growth of lobular ducts, enlargement of areolar, increases amount of adipose tissue 2)progesterone stimulates secretory activity in lobular ducts, lined with milk-secreting epithelium |
implantation depends on what | low estrogen and progesterone ratio |
when is the highest progesterone output by the corpus luteum | 5 days after ovulation |
what are the events of early pregnancy days after ovulation | 1)fertilization(day 1) 2)entrance of blastocyst to uterus (day 4) 3)implantation(day 5) 4)attachment of endometrium (day 6) 5)secretion of human chorionic gonadotropin(day 8) 6)HCG rescue of corpus luteum(day 10) |
what is HCG | human chorionic gonadotropin |
the blastocyst consists of | inner mass cells=future fetus outer rim of cells=trophoblast |
trophoblast invades the endometrium and attaches | contributes the fetal portion of the placenta begins secreting HCG at day 8 |
HCG has similar biologic activity as what | LH |
what is the function HCG | 1)maintains the corpus luteum function which continues to produce estrogen and progesterone -high levels of estrogen & progesterone suppress follicular development 2)without HCG, CL regresses and menses occurs |
what is the purpose of increase in HCG after first few weeks of pregnancy | basis of preggo test, detectable in urine at day 9 |
what are the hormones of the 1st trimester of pregnancy | 1)HCG increases and peaks about week 9 then decreases 2)rescues corpus luteum 3)stimulates corpus luteum to produce estrogen & progesterone |
what are the hormones of the 2nd and 3rd trimester of pregnancy | 1)placenta takes over production of steroid hormones 2)estriol production requires cholesterol from mother & both fetal adrenal cortex & fetal liver 3)progesterone requires cholesterol from mother -levels rise until parturition |
what are the hormones of pregnancy | 1)prolactin 2)corticotropin releasing hormone |
what does prolactin do during pregnancy | 1)produced by ant. pituitary, stimulated by estrogen 2)levels gradually rise throughout pregnancy 3)lactation is suppressed during pregnancy by estrogen and progesterone and lactation starts after parturition when estrogen and progesterone decrease |
what does corticotropin releasing hormone do during pregnancy | 1)produced in the placenta, drives the fetal pituitary-adrenal axis to produce cortisol-maturation of the lungs to produce surfactant 2)stimulate formation of both PGF2A and PGE |
when does delivery of fetus normally occur | 40 weeks |
what acquires capacity for forceful coordinated contractions during parturition | myometrium |
what are the hormones of parturition | 1)cortisol 2)estrogen 3)relaxin 4)prostoglandins 5)oxytocin |
what does cortisol do during parturition | 1)fetal cortisol increases estrogen/progesterone ratio 2)increases sensitivity of uterus to contractile stimuli |
what does estrogen(estriol) do during parturition | stimulates production of PGE2 & PGF2alpha |
what does relaxin do during parturition | 1)produced by corpus luteum 2)relaxes the pubic ligament and softens the cervix |
what does prostaglandins do during parturition | 1)rupture of fetal membranes 2)softening of the uterine cervix 3)contraction of myometrium -increases intracellular Ca++ leads to increase uterine contractility 4)stimulates both placental production & fetal production of CRH-->ACTH-->cortisol |
what does oxytocin do during parturition | 1)stimulates slow & prolonged contractions of the uterine myometrium @ end of preg. 2)secreted as a neuroendoncrine reflex in response to stretching of uterus 3)protects against hemorrhage after expulsion of fetus-natural tourniquet |
what appears to stimulate parturition | various processes that are set in motion weeks earlier gradually build up to overwhelm progesterone dominance & unleash excitatory forces that expel the fetus |
what happens to progesterone levels during parturition | levels do not decline until after loss of placenta but there is a decrease in progesterone effectiveness prior to parturition |
what happens to hormone levels after delivery of placenta | all hormone concentrations return to pre-preggo levels except prolactin which remains high if breast feeding |
lactation is maintained by | 1)suckling 2)stimulates the secretion of both oxytocin and prolactin 3)suppresses ovulation 4)prolactin inhibits GnRH and FSH/LH |
how do oral contraceptives work | 1)combination of estrogen & progesterone -negative feedback effects pituitary gland to inhibit FSH/LH -change character of cervical mucosa to make environment hostile to sperm 2)progestins alone -effects cervical mucosa -altered tubal motility |
how does the morning after pill work | 1)higher dose combinations of estrogen/progesterone -interfere with implantation 2)mifepristone(RU 486) -antagonist to progesterone receptor to prevent implantation |