Lecture 22: Reproduction II Flashcards
(23 cards)
HPG axis to ovaries
Pulsatile GnRH -> FSH/LH -> granulosa/theca cells
Granulosa cells
Stim. by FSH to produce inhibins, develop follicles. Contain aromatase to convert A -> E -> oogenesis
Theca cells
LH stim. -> androgen production
Menstrual cycle ovarian events
- Follicles develop (oocyte w/ surrounding granulosa layers)
- Antral/Graafian follicle is ovulated (1 per month)
- Ovulation stim. by LH spike
- In ovulation corpus luteum produces E + P; no fertilization -> degen to corpus albicans
Oogenesis
Germ cell production
- Meiosis I occurs before birth, meiosis II resumes at puberty
- Only 1 cell from meiosis II becomes oocyte; other degens to polar bodies
Ovarian reserve
Depends on age, ovarian size (number of antral follicles), FSH lvls, AMH
Menstrual cycle hormonal events
- Follicular phase
- FSH -> follicle recruit. + growth; limited by inhibin B
- E synthesis; pos. fb at high levels triggers LH spike
- LH spike stims ovulation - Luteal phase
- LH promotes CL survival
- CL E + P inhibit GnRH, LH; inhibin A inhibs FSH
- If fertilized, hCG maintains CL; else CL degens. and neg fb is lost
Menstrual cycle uterine events
- Proliferative phase: functional lining grows, stim. by E from follicle
- Secretory phase: P + E from CL maintains functional layer; loss of P + E -> menstruation
- P –| myometrial contraction, stims. vascularization
Roles of inhibin A vs B
Inhibin B: follicular phase; ensures only 1 dominant follicle arises
Inhibin A: luteal phase; preps FSH receptor sensitivity for next cycle
Estrogen actions
Many; incl. inhib. GnRH, inhib. milk production during pregnancy
Progesterone actions
Stim. breast glands, increase body temp., uterine secretions
- Inhib. GnRH, contractions, inhib. PRL effects on milk
Sperm fertilization requirements
- Capacitation in female tract
- Hyperactivation (oocyte chemotaxis)
- Acrosome rxn w/ zona pellucida
Egg/endometrium fertilization requirements
- Ovulated oocyte viable only in 12-24 hr window
- Post fertilization in ampulla transport to implant in uterine lining
- Transport delay -> ectopic pregnancy in oviduct or abdomen
Implantation
Occurs ~7 days post ovulation
- P from CL maintains endomet.
- Trophoblast hCG takes over to maintain CL until 7th wk
- Then placental P maintains endomet., CL degens
Fetal/maternal interactions
Placenta = nutrient/O2 supply + waste removal
hCG functionally = LH:
- Rescues CL
- Prevents further ovulation by keeping E + P constantly high
P in implantation
CL/placental P maintains uterus through implantation; inhibs. contraction through pregnancy
- Stim. breast gland development but inhib. milk production
RU-486
Aka mifepristone; P inhib. to abort fetus (-> contractions, endomet. shedding)
Maternal-placental-fetal unit synthesis
Fetal adrenal DHEA-S -> E2 in placenta OR -> fetal liver 16alpha-OH-DHEA-S -> E3 in placenta
E -> breast develop., inhib. milk production
All sourced from mother’s cholesterol -> placental pregnenolone -> fetus
Post-partum no placenta -> P drops
Placental lactogens
~ GH or PRL
- Facilitate breast development and maintains energy availability (diabetogenic)
How is birth triggered?
Oxytocin -> uterine PGs -> increased contractility
P efficacy drops -> incr. uterine stretch sensitivity via more oxytocin/oxytocin Rs -> stretch stim. oxy release
-> uterine muscle has pos. fb stretch activation
PRL 3 functions in pregnancy/birth
- Mammogenesis (gland growth/dev)
- Lactogenesis (milk production/gene expression)
- Galactopoiesis (maintain milk production)
Inhib. GnRH (thus ovulation) in pregnancy/nursing
Lactation
PRL, placental lactogen, E, P all stim. breast development; no production occurs while E and P high
Birth -> E/P drop -> colostrum produced (init. milk)
Suckling –| dopamine release, stim. oxytocin
Oxytocin -> milk let down (ejection)
Less dopamine -> more PRL -> milk synthesis increased
Lactation amenorrhea
No menstruation occurs during lactation bc PRL + neural inputs –| GnRH during nursing (wet nurse effect; no ovulation/menses)
