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Reproductive Phys

Constanzo-Reproductive Physiology

QuestionAnswer
cell types of testes germ cells-->spermatogonia (stem cells) Sertoli cells-->support development sperm and make antimullerian hormone Leydig cells-->testosterone
cell types of ovaries germ cells-->oogonia granulosa cells-->estradiol theca cells-->progesterone & estradiol
oogonia meiotic cells surrounded by graulosa cells and stroma-->oocytes
gonadal development testes develop 6-7wks gestation ovaries develop 9wks gestation
male internal/external genital tract internal: prostate, seminal vesicles, vas deferens, epididymis external: scrotum, penis *development DEPENDENT on testosterone and antimullerian hormone
female internal/external genital tract internal: fallopian tubes, uterus, upper 1/3 vagina external: clitoris, labia majora, labia minora, lower 2/3 vagina *development NOT dependent on hormones
required hormones for male phenotype testosterone-->stimulates growth/differentiation of wolffian ducts antimullerian hormone-->causes atrophy of mullerian ducts
wolffian ducts gives rise to epididymis, vas deferens, seminal vesicles, ejaculatory ducts
mullerian ducts gives rise to fallopian tubes, uterus, upper 1/3 vagina
pulsatile secretion of GnRH primary event at puberty drives pulsatile secretion of FSH and LH
pulsatile secretion of FSH and LH stimulates secretion of gonadal steroid hormones: testosterone and estradiol increasing circulating levels responsible for secondary sex characteristics
puberty-boys Leydig cell proliferation-->increased synthesis/ secretion of testosterone growth of sex accessory organs-->prostate growth spurt, pubic & axillary hair, growth of penis and testes, lowering of voice, initiation of spermatogenesis
puberty-girls ovaries produce estradiol budding of breasts, menarche, growth spurt, pubic and axillary hair (precedes menarche) starts earlier than boys growth spurt ends earlier than boys
seminiferous tubules composes 80% of testes-->produces sperm
Sertoli cells line seminiferous tubules fxns: 1)provide nutrients to differentiating sperm 2)form tight junctions w/ each other-->creates barrier between testes and bloodstream 3)secrete fluid into lumen of seminiferous tubules-->helps transport sperm to epididymis
blood-testes barrier formed by Sertoli cells-->selective permeability: stops noxious substances from crossing that might damage developing sperm
Leydig cells composes 20% of testes-->makes testosterone
spermatogenesis occurs continuously from puberty along seminiferous tubules phases: 1)mitotic division-->spermatocytes 2)meiotic division-->haploid spermatids 3)spermiogenesis-->spermatids mature: lose cytoplasm and development flagella *one full cycle 64 days
spermatogenic wave ensures mature spermatozoa produced continuously *128 million sperm produced daily
epididymis primary location for maturation and storage of sperm-->viable for several months
seminal fluid nourishes sperm with fructose, citrate, prostaglandins, fibrinogen
prostaglandins in seminal fluid assist in fertilization: 1)react w/ cervical mucus to make it more penetrable by sperm 2)induce peristaltic contractions in female reproductive tract to propel sperm up the tract
prostate fluid adds to ejaculate rich in citrate, calcium, and enzymes slightly alkaline-->adds to sperm motility and aids in fertilization-->neutralizes acid secretions from vas deferens and vagina
ejaculate composition 90% semen 10% sperm
capacitation process of inhibitory factors in seminal fluid washed free, cholesterol withdrawn from sperm membrane, and surface proteins redistributed Ca2+ influx into sperm increases motility *occurs 4-6hrs after sperm inside
acrosomal reaction acrosomal membrane fuses with outer sperm membrane-->creates pores that hydrolytic and proteolytic enzymes escape from acrosome and create path for sperm to penetrate ovum
sex steroid-binding protein fxns as reservoir for circulating hormone-->98% of testosterone bound to plasma proteins and only unbound testosterone is biologically active synthesis stimulated by estrogens and inhibited by androgens
5alpha-reductase converts testosterone to dihydrotestosterone
reproductive hypothalamic-pituitary axis hypothalamic hormone: GnRH pituitary: FSH and LH
GnRH secreted by arcuate nuclei from hypothalamus secretion inhibited by testosterone-->negative feedback
FSH-male reproductive system stimulates spermatogenesis and Sertoli cell fxn-->reinforced by testosterone
LH-male reproductive system stimulates Leydig cells to synthesize testosterone-->increases activity of cholesterol desmolase-->stimulates first step in steroidogenic pathway secretion inhibited by testosterone-->negative feedback
inhibin secreted by Sertoli cells-->negative feedback inhibitor of FSH
testosterone actions on target tissues fetal differentiation of internal male genital tract puberty: increased muscle mass, growth spurt/cessation, growth of penis and seminal vesicles, deepening of voice, spermatogenesis, negative feedback to anterior pituitary, libido
dihydrotestosterone actions on target tissues fetal differentiation of external genital tract puberty: male hair pattern, male pattern baldness, sebaceous gland activity, growth of prostate
function of ovaries 1) oogenesis 2) sex steroid hormone secretion: progesterone and estrogen
ovaries-cortex zone outer and largest zone contains all oocytes
ovaries-hilum zone inner zone blood vessels and lymphatics pass thru
ovarian follicle structure germ cell surrounded by endocrine cells
ovarian follicle function fully developed: provide nutrients for developing oocyte, release oocyte at proper time, prep vagina and fallopian tubes for fertilization, prep lining of uterus for implantation, maintain steroid hormone production until fetal placenta takes over
oogenesis oogonia only produced thru mitotic divisions until gestational 20-24wk oogonia turn into oocytes thru meiosis from gestational wk 8 to 6M after birth-->remain suspended in prophase til ovulation *do not produce new oogonia-->fxn from declining pool
development of ovarian follicles-first stage lasts many years(13-50) primordial follicle-->primary follicle granulosa cells proliferate-->nurture oocyte with nutrients and steroid hormones; secrete fluid theca interna cells develop *perpubertal ovaries don't pass this stage
development of ovarian follicles-second stage takes 70-85 days; a few follicles enter per menstrual cycle granulosa and theca cells continue to grow-->antrum accumulates fluid containing steroid hormones, mucopolysaccharides, proteins, and FSH primary follicle-->graafian follicle
development of ovarian follicles-third stage final stage of follicular development; occurs 5-7 days after menses dominant follicle emerges-->ovulation occurs on day 14-->dominant follicle releases oocyte(1st meiosis complete) and enters FT-->if fertilized 2nd meiotic division completed
corpus luteum ruptured primary follicle composed of granulosa cells, theca cells, capillaries, fibroblasts synthesizes and secretes steroid hormones for implantation and maintenance of zygote until placenta takes over
corpus albicans regressed corpus luteum if fertilization doesn't occur
17beta-estradiol major ovarian estrogen converted from testosterone by aromatase supports trophic effect of FSH on follicular cells acts on anterior pituitary-->inhibit secretion of FSH and LH during follicular phase but stimulates during mid cycle
testosterone major testicular hormone product
theca cells and hormone synthesis produce progesterone and testosterone stimulated to make testosterone by LH acting on cholesterol desmolase
granulosa cells and hormone synthesis contains aromatase and produce 17beta-estradiol from testosterone produced by theca cells only ovarian cells with FSH receptors
aromatase found in granulosa cells converts testosterone to 17beta-estradiol stimulated by FSH
ovarian function and pulsatile activity of hypothalamic-pituitary axis GnRH stimulates pulsatile secretion of FSH and LH necessary for follicular development and ovulation
menstrual cycle 28 day sequence: follicular development, ovulation, formation and degeneration of corpus luteum follicular phase(varies): first 14 days-->follicular development luteal phase(constant): last 14 days-->dominated by corpus luteum
FSH-female reproductive system stimulates growth of granulosa cells in primary follicles-->stimulate estradiol synthesis
LH-female reproductive system induces follicular rupture when concentration rises sharply in blood stimulates formation of corpus luteum; maintains steroid hormone production during luteal phase-->luteinization stimulates cholesterol desmolase in theca cells-->testosterone
ovulatory surge of FSH and LH happens mid menstrual cycle and triggers ovulation of mature oocyte
progesterone and negative feedback major hormone secreted by ovaries during luteal phase negative feedback on anterior pituitary-->inhibit secretion of FSH and LH
actions of estrogen-development maturation and maintenance of uterus, FT, cervix, and vagina; secondary sex characteristics at puberty; thelarche; poroliferation and development of granulosa cells; up-regulation of estrogen, progesterone, and LH receptors; -/+ feedback on FSH and LH
actions of estrogen-pregnancy maintenance of pregnancy; lowering uterine threshold to contractile stimuli; stimulation of prolactin secretion; blocking action of prolactin on breast
actions of progesterone maintenance of secretory activity of uterus during luteal phase; thelarche; (-) feedback effects on FSH and LH; maintenance of pregnancy; raising uterine threshold to contractile stimuli during pregnancy
follicular phase first 14 days of menstrual cycle before ovulation AKA proliferative phase dominated by estrogen 1)stimulate endometrial lining growth 2)cervical mucus becomes copious, watery, elastic-->ferning pattern-->channels form for sperm be propelled
luteal phase last 14 days of menstrual cycle after ovulation AKA secretory phase dominated by progesterone-->decreases quantity of cervical mucus-->thick and nonelastic and does not "fern" *proliferation of endometrium slows
breast development ABSOLUTELY DEPENDENT ON ESTROGEN-->lobular ducts grow, areola enlarges, adipose tissue increases lobular ducts lined by milk-secreting epithelium-->small ducts converge onto large ducts-->nipples glandular structures embedded in adipose tissue
pregnancy- estrogen levels estrogen and progesterone reach highest levels-->synthesized by corpus luteum then placenta estrogen actions: stimulates growth of myometrium, ductal system of breasts, prolactin secretion, enlargement of external genitalia
pregnancy-progesterone levels progesterone: maintains endometrial lining, increases uterine threshold to contractile stimuli-->preserve pregnancy until fetus ready to be delivered mild thermogenic action (luteal phase)-->increases hypothalamic temp set point-->rhythm method basis
menstrual cycle-follicular/proliferative phase varying phase; day 0-day 14 primordial follicle-->graffian follicle-->dominant follicle FSH & LH receptors upregulated-->gonadotropins stimulate estradiol synthesis 17beta-estradiol increasing-->endometrial proliferation & (-) feedback on FSH & L
menstrual cycle-ovulation *always occurs 14 days prior to menses follows burst of estradiol secretion at end of follicular phase-->(+) feedback on FSH & LH secretion cervical mucus increases-->watery & penetrable by sperm estradiol levels decrease after ovulation
menstrual cycle-luteal/secretory phase constant phase; 14 days & ends w/ menses corpus luteum develops-->make estradiol & progesterone progesterone dominated-->stimulates secretory activity & vascularity of endometrium-->prep to receive fertilized ovum cervical mucus decrease and thic
menstrual cycle-late luteal/secretory phase no fertilization-->corpus luteum regresses-->luteal source of estradiol and progesterone lost-->blood levels of hormones decrease abruptly
menstrual cycle-menses regression of corpus luteum-->abrupt loss of estradiol and progesterone-->endometrial lining and blood sloughed typically lasts 4-5 days primordial follicles for next cycle recruited and begin to develop
pregnancy period of fetal development=40WKS estrogen and progesterone levels increase -sources: corpus luteum (1st trimester) placenta (2nd and 3rd trimesters) -fxn: maintain endometrium, develop breasts for lactation, suppress development of new follicles
early pregnancy-fertilization occurs within 24hrs of ovulation in ampulla sperm penetration-->2nd polar body extruded and ovum divides and becomes blastocyst 4 days later and arrives in uterine cavity
early pregnancy-implantation blastocyst floats in uterine cavity freely for 1 day and implants in endometrium 5 days after ovulation corresponds to period of highest progesterone output by corpus luteum
trophoblast fetal portion of placenta-->invades endometrium and forms attachment to maternal membranes-->proliferates to become syncytiotrophoblast-->allows blastocyst to penetrate deep into endometrium
decidual cells specialized layer of endometrium under stimulation of progesterone eventually envelop entire conceptus
early pregnancy-secretion of HCG and rescue of corpus luteum HCG secreted by trophoblasts 8 days after ovulation HCG directs corpus luteum to continue making progesterone and estrogen to maintain endometrium for implantation-->rescues CL from regression
pregnancy test HCG production increases dramatically during first weeks of pregnancy-->basis of pregnancy test HCG detectable 9 days after ovulation
hormones of pregnancy-first trimester HCG produced by trophoblasts-->levels maximal at gestational wk 9 then decline HCG continues to be produced but fxn unclear beyond 1st trimester
hormones of pregnancy-2nd and 3rd trimester placenta responsible for hormone synthesis progesterone produced from cholesterol by mother-placenta interplay estriol the major form of estrogen during pregnancy; produced from cholesterol by mother-placenta-fetal adrenal cortex-liver interplay
parturition approximately 40WKS after onset of last menstrual period
Braxton Hicks contractions uncoordinated contractions beginning 1 month before parturition
parturition-cortisol, estrogen/progesterone ratio fetal adrenal cortex produce lots of cortisol-->increases estrogen/progesterone ratio-->increases sensitivity of uterus to contractile stimuli *estrogen stimulates contractions/progesterone decreases contractions
parturition-prostaglandins estrogen stimulates local prostaglandin production-->increases intracellular calcium concentrations of uterine smooth muscle-->increase contractility
parturition-oxytocin powerful uterine contraction stimulant dilation of cervix stimulates oxytocin secretion-->maternal blood levels of oxytocin DO NOT increase near term
stages of normal labor-first stage uterine contractions originating in fundus sweeps downward-->moves fetal head toward cervix and progressively widen and thin cervix
stages of normal labor-second stage fetus forced through cervix and delivered thru vagina
stages of normal labor-third stage placenta separates from uterine decidual tissue and is delivered-->hormones return to pregnant levels except prolactin-->remains high if mother breastfeeds powerful contractions of uterus constrict uterine blood vessels and limit postpartum bleeding
lactation prepped by estrogen and progesterone development of breasts but block prolactin action-->works after parturition when levels drop estrogen stimulates prolactin synthesis maintained by suckling-->stimulates prolactin and oxytocin
lactation and suppression of ovulation prolactin inhibits GnRH, FSH and LH secretion as long as lactation continues ovulation is suppressed-->not 100% but defacto method of contraception and family spacing
oral contraceptives combination OC have (-) feedback effect on anterior pituitary and reduce fertility by changing cervical mucus so hostile to sperm penetration and decreases motility of fallopian tubes progesterone OCP based on effects on cervical mucus and tubal motili
postcoital contraceptives morning after pills-->higher dosed preparations of estrogen and progesterone interfere with implantation
mifepristone (RU 486) postcoital contraceptive-->antagonist to progesterone receptor block uterine progesterone receptor-->prevents implantation of trophoblast
menopause cessation of menstrual cycles in women at approximately 50yo preceded by years of anovulation number of functioning ovarian follicles decreases-->estrogen secretion ceases-->reduced (-) feedback on FSH and LH-->increased secretion and pulsatility
symptoms of menopause caused by loss of ovarian estrogen source: thinning of vaginal epithelium, decreased vaginal secretions, decreased breast mass, accelerated bone loss, vascular instability "hot flashes", emotional lability *obese women less symptomatic
estrogen replacement therapy replaces ovarian source of estrogen-->minimizes/prevents menopause symptoms
Created by: kphom001