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AIM 2.2 > Reproductive Physio > Flashcards

Reproductive Physio Flashcards

1
Q

at what week does a fetus reach full sexual differentiation?

A

week 12

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2
Q

where do germ cells migrate to?

A

genital ridge

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3
Q

SRY gene encodes

A

TDF/SRY protein

causes male sexual differentiation

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4
Q

TDF makes

A

SOX 9 protein –> turns indeterminate gonad into testes

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5
Q

what is needed to turn indeterminate gonads into male?

A

TDF makes SOX9 (forms testes).
Testosterone develops Wolffian ducts.
AMH makes Mullerian ducts disappear.

Testosterone–>DHT (by 5-a-reductase) : formation of external genetalia

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6
Q

5-a-reductase

A

converts testosterone to DHT

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7
Q

where is TDF expressed?

A

somatic cells of testes

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8
Q

SOX9

A

Transcription initiated by TDF.
Initially works with TDF, then takes over to complete the differentiation of testes when TDF expression ceases.
Acts as a transcription factor.

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9
Q

hormones directing male sexual differentiation

A

TESTOSTERONE
Maintencance of Wolffian duct structures.
Critical for normal male external genitalia.

AMH
Regression of Mullerian duct structures.

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10
Q

Testosterone is secreted from?? AMH?

A

Testosterone secreted from Leydig cells.

AMH secreted from Sertolic cells.

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11
Q

DAX-1 actions

A

Expression of proteins that cause female sexual differentiation.

Supression of expression of proteins leading to male sexual differentiation.

[DAX-1 : Dosage sensitive sex reversal // on x chromosome]

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12
Q

which structures persist in female sexual development?

A

Mullerian duct.

Wolffian duct degenerates w/o testosterone

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13
Q

effect of lack of testosterone in female development

A

No testosterone –> no DHT –> female pathway

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14
Q

are genes from both X chromosomes expressed in human cells?

A

Yes and no. One of the X chromosomes is partially deactivated in each cell of a woman.

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15
Q

what happens if a person has XX genotype, but due to a mistake in crossing over, has an SRY gene?

A

Klinefelter-like (XXY).

Male gonads/genetalia.
Wolffian ducts.

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16
Q

androgen insensitivity syndrome (XY)

[gonads, mullerian/wolffian ducts, external genitalia.

A

Androgen receptor is not functional.
No axillary/pubic hair.
Testes bc SRY present.
Testes secrete AMH, so no Mullerian duct.
No Wolffian duct bc no testosterone action.
Vagina bc no DHT.
No periods bc no uterus (blind vaginal pouch bc no mullerian ducts)

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17
Q

what causes ambiguous external genitalia?

A

Male fetus exposed to too little androgen effect.

Female is exposed to too much androgen effect.

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18
Q

partial androgen insensitivity

A

ambiguous genitalia.

Perineal hypospadias/bifid scrotum.

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19
Q

describe body transitions that occur in pubertal development

A
  • external genital development (T, E)
  • growth spurt (E)
  • increased musculature, beard, deep voice in boys (T)
  • breast development, increased fat deposits in girls (E)
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20
Q

age of pubertal onset: US males

A

9-10 years old

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21
Q

age of pubertal onset: US females (caucasian, Afr.-Am.)

A

Caucasian: 8-9 years old

African-American: 7-8 years old

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22
Q

delayed puberty

A

Age 13 in females (lack of onset of menses)

Age 14 in males (absent testicular development)

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23
Q

tanner stages of male puberty

A

1) pre-pubertal
2) testes/scrotal enlargement, early pubic hair growth
3) growth of glans penis
4) completion of appearance of adult genitalia

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24
Q

adrenarche/pubcarche

A

appearance of pubic/axillary hair

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25
Q

thelarche

A

breast development

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26
Q

menarche/gonadarche

A

Period onset.

Activation of GnRH secretion.

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27
Q

tanner stages of female puberty

A

1) pre-pubertal
2) early thelarche, early pubarche
3) further development of breast tissue
4) continued development of breast tissue
5) adult female breast and pubic escutcheon (shape)

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28
Q

kisspeptin

A

Secreted from hypothalamus.

Potent stimulator of GnRH secretion.

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29
Q

leptin

A

Secreted by adipose.

Leptin causes GnRH secretion.

30
Q

the two nuclei in the hypothalamus that both make GnRH

A

ARC : arcuate nucleus

AVPV : anteroventral periventricular nucleus

31
Q

Leptin _______ kisspeptide secretion.

Leptin _______ negative feedback by testosterone

A

Leptin ENHANCES kisspeptin secretion –> increases GnRH secretion

Leptin DECREASES negative feedback by testosterone –> permits more GnRH secretion.

32
Q

three spikes in FSH/LH in males’ lives

A

1) in utero
2) newborn
3) puberty

33
Q

role of estradiol in growth

A

Estradiol acts on growth plate directly to stimulate growth.

Triggers pituitary to increases release of GH.
GH triggers liver to secrete more IGF-1, further stimulating growth.

After accelerated growth, estrogen closes growth plates.

MEN: testosterone is converted to estrogen by aromatase.

34
Q

inhibin

A

Secreted by ovary.

Decreases FSH secretion (triggered by GnRH)

35
Q

theca cells

A

Outside basement membrane.

Stimulated by LH to produce androgens.

36
Q

granulosa cells

A

Inside basement membrane.
Stimulated by FSH to convert androgens (from theca cells) to estrogen, by aromatase.

Produce inhibin –> negative feedback on FSH

37
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.

38
Q

LH levels during menstrual cycle

A

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

39
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)

40
Q

progesterone levels during menstrual cycle

A

Low during follicular phase.
Rises during luteal phase.

Prepares uterus for implantation/pregnancy.

41
Q

inhibin levels during menstrual cycle

A

Rise at same time as estradiol (follicular phase).

Another factor to drive FSH down.

42
Q

male hormone cycles

A

Not cyclical.

GnRH (hypothalamus) triggers release of FSH and LH (pituitary).

LH –> testis –> testosterone –> negative feedback on GnRH

Testosterone in testes triggers sperm production

43
Q

testosterone in testes triggers ______

A

testosterone in testes triggers SPERM PRODUCTION

44
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

45
Q

blastocyst contact with endometrium causes

A

Converts trophoblast cells into syncytiotrophoblast cells.

Syncytiotrophoblast cells invade endometrium for nutrients.

46
Q

embryonic hypoblast develops into _______

A

fetus

47
Q

syncytiotrophoblast develops into ________

A

placenta

48
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
49
Q

chorionic villi

A

Structures in placenta that allow for maximal exchange of nutrients.
Blood returns to baby via umbilical cord.

50
Q

hormones from placenta

A 
Estrogen
Progesterone
hPL (human placental lactogen)
hCG
CRH (corticotrophic releasing hormone) --> ACTH --> cortisol
51
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)

52
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

53
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)

54
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

55
Q

adrenal steroid pathways

A

CRH (hypothalamus) –> ACTH (pitutary) –> pregnenolone

Pregnenolone –> DHEA
Pregnenolone –> Progesterone

DHEA/Progesterone –> testosterone –> E2

56
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.

57
Q

DHEA (mom, placenta, fetus)

A

DHEA comes from mom and fetus.

DHEA –> testosterone/estradiol

HUGE amounts of estrogen.

58
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
59
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
60
Q

where are prostaglandins produced?

A

Myometrium of uterus.
Cause local actions to increase muscle contractions.

LOCAL

61
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

62
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

63
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.

64
Q

breast development during pregnancy is mediated by

A 
Prolactin.
hPL.
Estrogens.
Progesterone.
GH.
Thyroid hormone.

Mammary ducts develop, precursors for milk are synthesized.

65
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.

66
Q

colostrum (production date, importance)

A

Start production in 3rd trimester.

  • High fat content.
  • Minerals, solutes, carbs, vitamins.
  • IgA.
  • Active lymphocytes, monocytes.
  • Interferon (facilitates meconium passage).
  • Bifidus Factor (stimulates lactobacillus bifidus colonization of GI tract)
67
Q

importance of breast milk

A
  • Maintenance of proper gut flora through antimicrobial factors/bifidus factor.
  • low casein content facilitates digestion
  • lipase
  • immunologic factors
  • vitamin A/C/D
  • growth factor (GI growth, barrier function, overall growth)
68
Q

prolactin

A

Triggered by suckling.

Allows milk production.

69
Q

oxytocin (lactation)

A

Triggered by suckling.
Causes milk let down.

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

70
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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