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AIM 2.2 > big points of repro physio > Flashcards

big points of repro physio Flashcards

1
Q

male differentiation

A

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

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2
Q

DAX-1

A

Expresses proteins that cause female sexual reproduction.

Suppress expression of proteins that lead to male differentiation

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3
Q

female differentiation

A

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.

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4
Q

body transitions during puberty, and hormone that accomplishes it

A
  • external genital development (T, E)
  • growth spurt (E)
  • increased musculature, beard, deep voice (T)
  • breast development, increased fat deposits (E)
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5
Q

kisspeptin

A

POTENT STIMULATOR OF GnRH.

secreted within hypothalamus

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6
Q

leptin

A

Increases GnRH secretion.
Enhances kisspeptide secretion.

secreted from fat cells

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7
Q

effect of estradiol in pubertal growth

A

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.

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8
Q

theca cells

A

Outside BM.

LH stimulates theca cells to produce androgens.

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9
Q

granulosa cells

A

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.

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10
Q

FSH levels during menstrual cycle

A

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.

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11
Q

LH levels during menstrual cycle

A

LH surge causes ovulation (triggered by peak estrogen level).
Follicle forms corpus luteum –> produces progesterone.

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12
Q

Estradiol levels during menstrual cycle

A

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)

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13
Q

progesterone levels during menstrual cycle

A

Low during follicular phase.
Rises during luteal phase.

Prepares uterus for implantation/pregnancy.

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14
Q

inhibin levels during menstrual cycle

A

Rise at same time as estradiol (follicular phase).

Another factor to drive FSH down.

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15
Q

process of fertilization

A

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

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16
Q

hCG

A

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
17
Q

progesterone effects/functions in pregnancy

A

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)

18
Q

estrogen effects/functions in pregnancy

A

1) increased vasculature to the uterus
2) breast development
3) cervical ripening
4) increase oxytocin receptors
5) increase prostaglandins

19
Q

cervical ripening

A

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)

20
Q

HPL

A

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

21
Q

placental cholesterol

A

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.

22
Q

DHEA (mom, placenta, fetus)

A

Steroid pathway precursor of estrogens needed for pregnancy maintenance.

DHEA comes from mom and fetus.

DHEA –> testosterone/estradiol

HUGE amounts of estrogen.

23
Q

change of progesterone receptors near end of pregnancy

A

PRB promotes uterine quiescence.
PRA inhibits uterine quiescence.

Near paturition:

  • decrease progesterone production
  • decrease PRB
  • increase PRA
24
Q

prostaglandins (stimulation, causes)

A

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
25
Q

oxytocin

A

Does NOT initiate pregnancy.
Does ENHACE/CONTINUE delivery.

STIMULATION:

1) decreased progesterone action
2) increased cervical stretch

ACTION:

1) increase contractions
2) cervical dilatation

26
Q

cortisol in fetal system

A

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

27
Q

adrenal axis hormones in delivery of baby

A

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.

28
Q

Breast is developed during pregnancy, but do not lactate DURING pregnancy. Why?

A

Estrogen and progesterone block last step in milk production.

Ready to lactate right after delivery due to fall in estrogen/progesterone.

29
Q

prolactin

A

Triggered by suckling.

Allows milk production.

30
Q

oxytocin (lactation)

A

Triggered by suckling.
Causes milk let down.

May increase maternal-infant bonding.
Causes progression of contraction midlabor.

31
Q

nursing vs crying (lactation triggers)

A

Nursing triggers prolactin and oxytocin production.

Crying just triggers oxytocin production.

AIM 2.2 (26 decks)

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