big points of repro physio Flashcards
male differentiation
SRY gene –> TDF protein –> SOX 9 protein.
TDF, SOX9 develop indeterminate gonads into testes.
Testosterone develops the Wolffian ducts.
AMH degenerates Mullerian ducts.
Testosterone –> DHT for development of external genitalia
DAX-1
Expresses proteins that cause female sexual reproduction.
Suppress expression of proteins that lead to male differentiation
female differentiation
DAX-1 triggers female proteins, suppresses male proteins.
Without SRY/TDF/testosterone, Wolffian ducts degenerate.
Without AMH, Mullerian ducts persist.
Without DHT, no male external genitalia.
body transitions during puberty, and hormone that accomplishes it
- external genital development (T, E)
- growth spurt (E)
- increased musculature, beard, deep voice (T)
- breast development, increased fat deposits (E)
kisspeptin
POTENT STIMULATOR OF GnRH.
secreted within hypothalamus
leptin
Increases GnRH secretion.
Enhances kisspeptide secretion.
secreted from fat cells
effect of estradiol in pubertal growth
Estradiol acts directly on growth plate.
Triggers pituitary to increase release of GH.
GH causes liver to secrete IGF-1, further stimulating growth.
After accelerated growth, estrogen causes closure of growth plates.
MALES:
testosterone is converted to estrogen by aromatase.
theca cells
Outside BM.
LH stimulates theca cells to produce androgens.
granulosa cells
Inside BM.
FSH stimulates granulosa cells to convert androgens (from theca) to estrogens by aromatase.
FSH stimulates granulosa cells to produce inhibin –> negative feedback on FSH.
FSH levels during menstrual cycle
Initially an increase in FSH due to a loss of negative feedback from previous cycle. (FSH rises in follicular phase)
Drives development of follicles.
Causes increase of estrogen.
Increased estrogen –> negative feedback on FSH.
Inhibin also causes decrease.
LH levels during menstrual cycle
LH surge causes ovulation (triggered by peak estrogen level).
Follicle forms corpus luteum –> produces progesterone.
Estradiol levels during menstrual cycle
Rises in follicular phases, peaks just before ovulation.
Increased levels after increase in FSH (delayed).
Negative feedback causes FSH levels to fall.
GROWTH OF ENDOMETRIUM to get ready for luteal phase.
PEAK LEVEL OF ESTROGEN CAUSES LH SURGE (estrogen –> kisspeptin –> GnRH –> LH surge)
progesterone levels during menstrual cycle
Low during follicular phase.
Rises during luteal phase.
Prepares uterus for implantation/pregnancy.
inhibin levels during menstrual cycle
Rise at same time as estradiol (follicular phase).
Another factor to drive FSH down.
process of fertilization
Sperm makes contact –> releases enzymes to burrow through ZP
Once thru ZP, releases enzymes to activate cortical granules –> release enzymes that change ZP so no more sperm can enter
hCG
First hormone made after implantation.
Tells mom she is pregnant, keeps baby inside.
- Mild immunosuppression (dad’s genes are foreign)
- stimulates progesterone production by corpus luteum (for 6-8 wks until placenta does)
- triggers fetal growth
- triggers uterine growth
- stop uterus from contracting
- keep cervix closed
progesterone effects/functions in pregnancy
1) development/function of placenta
2) decrease estrogen response, prostaglandins, oxytocin receptor (decrease things that cause uterus to contract)
3) stable cervix
4) immunosuppression
5) mild insulin resistance (so glucose remains available in blood for baby to use)
ACTIONS VIA PRB (progesterone receptor B)
estrogen effects/functions in pregnancy
1) increased vasculature to the uterus
2) breast development
3) cervical ripening
4) increase oxytocin receptors
5) increase prostaglandins
cervical ripening
Caused by estrogen.
Prevented by progesterone.
Progesterone keeps cervix stiff/thick.
Oxytocin, prostaglandins, estrogens –> soften cervix.
Baby’s head pushes against cervix –> thinning, broadening, opening (ripe)
HPL
Human Placental Lactogen.
Only produced by placenta.
1) anti-insulin in mother (increase glucose availability for baby)
2) breast development
3) fetal growth
4) increased gluconeogenesis in mother
5) increased lipolysis in mother
ENSURES BABY GETS ENOUGH NUTRIENTS
placental cholesterol
Placenta cannot make cholesterol, must get from mom.
Takes cholesterol –> pregnenlone –> progesterone.
Placenta can’t use progesterone, so it is exported to mom and fetus.
DHEA (mom, placenta, fetus)
Steroid pathway precursor of estrogens needed for pregnancy maintenance.
DHEA comes from mom and fetus.
DHEA –> testosterone/estradiol
HUGE amounts of estrogen.
change of progesterone receptors near end of pregnancy
PRB promotes uterine quiescence.
PRA inhibits uterine quiescence.
Near paturition:
- decrease progesterone production
- decrease PRB
- increase PRA
prostaglandins (stimulation, causes)
Produced locally in uterus.
Decrease progesterone –> no longer blocks estradiol effect –> increases prostaglandins
Increase estrogen/cortisol –> increases prostaglandins.
Rupture membranes, cervical stimulation –> increases prostaglandins
PROSTAGLANDINS CAUSE:
- increased cervical ripening
- increased contractions
oxytocin
Does NOT initiate pregnancy.
Does ENHACE/CONTINUE delivery.
STIMULATION:
1) decreased progesterone action
2) increased cervical stretch
ACTION:
1) increase contractions
2) cervical dilatation
cortisol in fetal system
acts as positive regulator on CRH (net: increase in prostaglandins from many pathways bc trying to deliver baby as fast as possible)
causes increased SURFACTANT production in lungs
adrenal axis hormones in delivery of baby
CRH –> cervical dilatation
CRH –> increased prostaglandins
CRH –> ACTH –> DHEA/E –> prostaglandins
ACTH –> cortisol –> prostaglandins
Basically everything increases prostaglandins to complete delivery as fast as possible.
Breast is developed during pregnancy, but do not lactate DURING pregnancy. Why?
Estrogen and progesterone block last step in milk production.
Ready to lactate right after delivery due to fall in estrogen/progesterone.
prolactin
Triggered by suckling.
Allows milk production.
oxytocin (lactation)
Triggered by suckling.
Causes milk let down.
May increase maternal-infant bonding.
Causes progression of contraction midlabor.
nursing vs crying (lactation triggers)
Nursing triggers prolactin and oxytocin production.
Crying just triggers oxytocin production.
