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Repro II Exam I > Physiology Review Repro > Flashcards

Physiology Review Repro Flashcards

1
Q

the proliferative/follicular phase is predominated by what hormone

what other hormones are elevated during this phase?

A

estrogen

-estrogen stimulates proliferation of endometrial cells, increase in length and number of endometrial glands, and increased blood flow to the uterus

FSH is also elevated during the follicular phase (causes proliferation of granulosa cells and increased estrogen secretion within a cohort of follicles)

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2
Q

ovulation occurs b/c of surge of what

A

LH

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3
Q

luteal phase/secretory phase is predominated by what hormone

A

progesterone

endometrial cell hypertrophy, increased vascularity, edema

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4
Q

after ovulation occurs what do the theca cells and the granulosa cells start secreting

A

theca cells– estrogen

granulosa cells – progesterone

they form the corpus luteum

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5
Q

theca cells have receptors for what gonadotropin. how does this gonadotropin exert its effect/what does the theca cell produce

A

LH

cholesterol is transported into the cell –> production of androgens –> androgens enter the adjacent granulosa cells and are converted to estrogen

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6
Q

after estrogen is produced in the granulosa cell (b/c of conversion of androgen to estrogen by aromatase) where does this estrogen go?

A

goes to the anterior pituitary to inhibit release of LH and fSH

acts locally on granulosa cells to increase sensitivity to FSH and proliferation of these cells

estrogen is increasing BUT also putting an inhibitory effect on FSH release

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7
Q

what cells release inhibin B

A

granulosa cells

inhibin B inhibits the secretion of FSH by the pituitary

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8
Q

circulating estrogen during the follicular phase has what effect on cervical mucus

A

thin and water! easy for sperm to transverse

slightly alkaline

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9
Q

how do estrogen levels change at the end of the follicular phase and how does this affect ovulation

A

at the end of the follicular phase estrogen levels increase dramatically

when estrogen rises above a certain level they no longer inhibit the release of LH and FSH but instead stimulate the release of LH and FSH

causes surge in release of LH –> ovulation (follicular rupture occurs 24-36 hours after the onset of the LH surge

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10
Q

in the pre-ovulatory follicle, what changes are happening ?

A

Estradiol and FSH cause the granulosa cells to produce LH receptors

metabolic pathways then are altered to favor progesterone production

there is also a decrease in aromatase activity resulting in a decrease in estrogen

after the LH surge, the granulosa and theca cells are turned into luteal cells –> increase in secretion of progesterone

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11
Q

effects of progesterone on cervical mucus and body temp

A

thick
sealing off the uterus from further entry of sperm or bacteria

makes it slightly acidic - sperm don’t like this

increase in body temp during the secretory/luteal phase

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12
Q

urine:

low progesterone metabolites and low but slowly rising estrogen metabolites

A

early follicular phase

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13
Q

urine:

low progesterone metabolites, rapidly rising estrogen metabolites

A

latter part of follicular phase just before ovulation

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14
Q

urine:

elevated progesterone

A

luteal phase and pregnancy

early luteal phase- progesterone rising
late luteal phase- progesterone falling

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15
Q

why does menses occur’>

A

corpus luteum is initially very responsive to LH

over time the corpus luteum becomes less functional, less responsive to LH

progesterone exerts negative feedback on LH which contributes to the demise of the corpus luteum

then progesterone and estradiol fall to levels that are unable to support the endometrial changes and menses begins

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16
Q

what substance rises slightly and initiates the next cycle of follicular growth

A

FSH

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17
Q

source of HCG

A

trophoblastic cells of the fetus

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18
Q

HCG functions

A

by the 10th day of after ovulation, HCG stimulates corpus luteum to secrete progesterone and estrogen

19
Q

what is the source of progesterone and estrogen in the third month to term of pregnancy

A

placenta

20
Q

rising serum or urinary estriol is considered an excellent index of what

A

both placental and fetal well - being

enzymatic action by the fetal liver and placenta convert androgens into estrogens which then enter the maternal circulation

21
Q

what accounts for the development of gestational diabetes

A

hCS (aka HPL) which is secreted by the placenta (secretion is increased in the 2nd half of pregnancy)

has anti-insulin actions - helps increase glucose supply for the developing fetus

normal levels of hCS is a sign of placental well being

22
Q

if you see a woman post-menopausal with low FSH and LH what does this indicate

A

pituitary issue (should be high)

23
Q

estrogen effects on the oviduct

A

increase endosalpinx epitheilal size

increase blood flow

increase oviduct specific glycoproteins

increase ciliogenesis

increase mucus, muscular tone

all favorable for transport of the ovum

24
Q

progesterone effects on the oviduct

A

decrease epithelial size

cause deciliation

decrease mucus production

relax muscular tone

25
Q

during the secretory phase, progesterone inhibits what

A

further growth of the uterine endothelium and induces differentiation of epithelial and stromal cells

downregulates estrogen receptors and promoting the conversion of estradiol-17beta to less potent estrone

26
Q

what is the breakdown of the stratum functionalis due to the action of

A

Matrix metalloproteases and prostaglandins

27
Q

what is inhibin A produced by and what are its actions

A

produced by granulosa cells in the luteal phase and suppresses FSH secretion

28
Q

effects of estrogen on bone

A

promotes the closure of epiphyseal plates

29
Q

effect of estrogen on CV

A

vasodilation through NO synthesis

30
Q

what hormone causes morning sickness

A

HCG

31
Q

what are the limitations of the placenta (3)

A

1 - cant make adequate cholesterol (needs maternal supply)

  1. lacks enzymes for estrone and estradiol (lacks 17-alpha hydroxylase)
  2. Lacks enzymes for estriol (lacks 16-alpha hydroxylase)
32
Q

what does the mother lack in steroid biosynthesis

what does she contribute

A

lacks adequate synthetic capacity for progesterone and estrogens

contributes LDL cholesterol

33
Q

what does the placenta contribute in the steroid biosynthesis pathway

A

contributes progesterone (3-beta hydroxysteroid dehydrogenase)

aromatase

34
Q

what does the fetus contribute in the biosynthesis of steroids during pregnancy

A

17 alpha hydroxylase (needed to synthesize estrone and estradiolo)

16- alpha hydroxylase (needed to synthesize estriol)

35
Q

what does the fetus lack during pregnancy in terms of steroid biosynthesis

A

progesterone

36
Q

when can you detect hPL in the serum

A

3 weeks

hPL causes

  • insulin resistance- increase in glucose
  • mammary growth and development

index of placenta well being

37
Q

at 20 weeks where does the uterus hit the abdomen

A

umbilicus

38
Q

what are the changes in the pituitary of the mother during pregnancy

A

2x increase in size- increase in size of lactotrophs (estrogen and progesterone increases –> stimulates prolactin)

ADH set point is lowered
-releases ADH sooner than normal, maternal blood volume is increased

39
Q

adrenal changes in mother during pregnancy

A

cortisol and aldosterone increase

estrogen stimulates activity of the renin-ang system (but you DON”T see hypokalemia- one thing that is blocked by progesterone)

40
Q

Thyroid changes in mother during pregnancy

A

Total T4 and T3 increase but free T4 is normal (increase in thyroid binding globulin)

TSH levels decrease (HCG causes increase in T3/4 which feeds back to inhibit TSH)

41
Q 
pregnancy effects on:
vascular volume
peripheral resistance 
stroke volume
heart rate
Contractility
CO
A 
increase vv
decrease PR
increase SV
increase HR
increase Contractility
increase CO
42
Q

respiratory changes during pregnancy

A 
minute volume increase
tidal volume increase 
decrease in PCO2
decrease in FRC
decrease in IRV

resp alkalosis

43
Q

renal changes during pregnancy

A

increase in ADH, renin, ang II, aldosterone

increase in GFR

Repro II Exam I (5 decks)

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