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Female Repro

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imissyou419's version from 2017-04-03 00:42

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Question Answer
Uterussite of implantation
Fallopian tubepassage for sperm and oocyte, where they meet
Ovariesoogenesis + hormones
Cervixentrance to uterus (PAP smear is taking swab of cervix cells)
Vaginasite of sperm deposition, removal of menstrual fluid
Fimbriaeduring ovulation, sweep ovum that leaves ovary into fallopian tube (fallopian tube and ovary is not joined together)
Does ovary have blood supply?Yes, gives nutrients (cholesterol) to theca cells for steroidogenesis
Suspensory ligaments hold reproductive organ together, if fail - prolapse where uterus moves out into vagina
OogenesisOvary makes all oocyte during fetal life (unlike spermatogonia that keeps making sperm), massive decline of number of oocytes before birth, cells arrest at prophase I (after genetic cross over) before birth until puberty
How do oogonium become egg?oogonium (2n=46) -> primary oocyte (2n=46, in prophase I from before birth to puberty) -> secondary oocyte (n=23, puberty - finish meiosis I, only 1 primary oocyte each month complete meiosis I [have polar body]- high LH for ovulation, halted in metaphase II until fertilization, if fertilized when create polar body) -> egg (finish meiosis II once sperm meets secondary oocyte)

Only 1 primary oocyte become secondary oocyte a month
How many days is oogenesis?28 days (the ovulated oocyte might have been alive longer i.e. from a previous cycle, 2 months from primary to pre-Graafian)
How many variable cells do males produce compared to femalesMales produce 4 sperm cells, females produce 1 (take cytoplasm)
What oocyte is in primordial follicle, in Graafian follicle?Primary oocyte -> primordial follicle (arrested like this in childhood); SECONDARY OOCYTE -> GRAAFIAN FOLLICLE (what you ovulate)
Primary follicleprimary oocyte, granulosa cells, Zona pellucida surrounds oocyte (glycoproteins produced by oocyte itself), NO THECA CELLS! - Gnatotrophin-independent, do not need LH & FSH
Secondary follicleprimary oocyte, granulosa layers, theca cells appear - need LH & FSH
What are preantral follicles?primordial follicle, primary follicle, secondary follicle; without fluid filled cavity
Theca cellsin contact with blood (cholsterol -> testosterone)
Granulosa cellsremoved from circulation, rely on theca cells (convert testosterone to estrogen)
Graafian folliclesecondary oocyte, atrum develops, considerable size (massive development as fluid fills spac, proteins pull fluid from circulation)
Antral folliclesGraafian follicle
LH and FSH during early/mid follicular period - negative feedback, primary oocyteLH binds to LH receptor in theca cell and increase cAMP, increasing cholesterol metabolism by upregulating rate limiting enzyme StAR (converting cholesterol -> androgens (Androstenedione, testosterone)),
FSH bind to FSH receptor increase cAMP and convert androgens -> estrogen (upregulate aromatase, 17-beta-HSD) - Estrogen drives growth and proliferation of granulosa cells, more estrogen produced and proteins pulling in fluid to increase follicle size (so FSH initiates follicle development)
Dominant Graafian FollicleLarge antrum, corona radiata (around granulosa cells)
Feedback systemnegative feedback at beginning of follicular phase (estrogen negative feedback from primary to secondary oocyte), positive feedback leading to ovulation (estrogen positive feedback), negative feedback luteal phase (progesterone negative feedback)
LH and FSH just prior to LH surge - positive feedbackDevelopment of LH receptor on granulosa cell prior to ovulation b/c of FSH, increase estrogen a lot - stimulate growth, increase progesterone, IGFs (increase cell numbers, stimulate androgen production in theca cells), and VEGF (angiogenesis in theca cells to bring more cholesterol for theca cells); LH upregulate p450 (genes involved in progesterone), shut down aromatase/17-beta-HSD to make more progesterone just prior to ovulation => facilitate follicle rupture
Corpus luteumremnant of follicle/group of granulosa cells that remain, lipid rich (promotion of lipid accumulation), greatest endocrine body, progesterone main steroid produced now, get uterus ready for implantation
Estrogen vs progesteroneEstrogen - increase layering of vaginal epithelium, prepares uterine endometrium for progesterone's (post the follicular phase) actions by INDUCING PROGESTERONE RECEPTOR SYNTHESIS, stimulate proliferation of epithelial cells/glands of uterus (spiral artery development), increase contractions and ciliary activity of fallopian tube around ovulation, contraction of smooth muscles, contraction of myometrium, decreased viscosity of mucus, (to allow sperm to move through), increased glycogen and decreased pH, invokes enzyme synthesis for zona pellucida lysis, stimulates growth of external genitalia (puberty) and breast/mammary glands (duct work), uterine enlargement
Secondary sex characteristics: stimulates female body development, narrow shoulders broad hips and female body fat distribution, stimulates breast development, particularly ducts and fat deposition during puberty, stimulates female body hair pattern
Non-sexual tissues: stimulates bone growth & ultimate cessation of bone growth, protects against osteoporosis - conserve bone mass, protect against atherosclerosis, promote blood clotting - protect CVD, reducing LDL levels

Progesterone - 10-fold rise in luteal phase, decrease contractions of fallopian tube and uterus, slow contractions (slow down cilia, flagella action as we anticipate conception), converts estrogen primed (PR action) uterine endometrium into glandular structure ready for embryo implantation (uterine milk), DECREASE UPTAKE OF EXTRACELLULAR CA2+ required for contraction of myometrial cells,
Secondary sexual characteristics: promotes mammary alveolar development during pregnancy in preparation of milk production;

Estrogen and progesterone are steroid hormones so they either act directly through steroid receptor or through transcription factor to elicit gene transcription for their corresponding phases
Endometriumlining of uterus, where fertilized egg embed into, source of bleeding associated with end of cycle
Consists of 2 layers: stratum functionalis (grows under influence of estrogen, maintained with progesterone and breaks down in menses), stratum basalis (stem cell area)
Myometriummuscle layer - involved in expanding during fetal development, critical in getting fetus out
Mensesbreakdown of endometrium through apoptosis, INHIBITION OF UTERINE CONTRACTION LIFTED and bleeding (50 mL) b/c of exposure to spiral arteries and cramps of menstruation begin; occurs during first period of follicular phase, pregnancy has not occured so estrogen & progesterone is not there to maintain it anymore (corpus luteum degraded)
Proliferative phasecells undergo growth and proliferation under estrogen
Secretory phase/luteal phaseprogesterone secrete uterine milk where blastocyte can implant to; Stimulated by LH, the Corpus luteum secretes P4; levels of estrogen & progesterone falls due to corpus luteum being degraded towards menses
If implantation occurscorpus luteum stays a bit and developing placenta takes over secreting progesterone
Follicular phase is divided intomenses and proliferative phase
Endometriosisendometrial tissue end up outside of uterus/outside ovaries/anus, it is responsive to estrogen so will grow and shed
Menopausefollicles become less responsive to LH & FSH (levels rise), follicular apoptosis accelerates, secrete less estrogen; ovulation and menstruation become irregular and finally cease; Menopause signs & symptoms: breast tenderness, decreased libido, difficulty sleeping, fatigue, hot flashes, night sweats, mood swings, poor attention span or forgetfulness, skin dryness, thinning of hair, vaginal dryness, weight gain
Mittelschmerzmiddle pain or ovulation pain, increase temp when you ovulate
memorize

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