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Reproduction > Female Reproduction Biochem > Flashcards

Female Reproduction Biochem Flashcards

1
Q

What cells in the woman produce estrogens and what hormone signals their release?

A

FSH signals for estrogen release from granulosa cells, lutein cells, fat cells and the placenta

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2
Q

What is the effect of estrogen on the brain?

A

inhibits release of GnRH, FSH, LH, and stimulates production of GH, PRL, and OT

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3
Q

What is the effect of estrogen on the myometrium and endometrium?

A

increases contractility stimulating parturition and causes growth of the epithelia

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4
Q

What cells in the woman produce progesterone and what stimulates their release?

A

theca lutein cells of the corpus lutein, granulosa cells and the placenta stimulated by LH

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5
Q

What are the effects of progesterone on the brain?

A

inhibits GnRH and OT

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6
Q

What are the effects of progesterone on the breast?

A

growth and differentiation of the alveolus

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7
Q

What does progesterone do to the myometrium and endometrium?

A

Decrease contractility and activate secretory glands of endometrium to prepare the uterus for implantation of the egg

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8
Q

What is the effect of estrogen on bone?

A
  1. causes the growth plates to fuse 2. inhibits bone erosion 3. pubertal growth spurt (increases GH)
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9
Q

What produces androgens in the females and what stimulates androgen release?

A

LH stimulates the thecal cells and lutein cells to secrete androgens. ACTH stimulates the adrenal to secrete androgens.

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10
Q

What are the effects of androgens on the brain?

A

regulates GnRH release and libido (testosterone)

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11
Q

What are the effects of androgens on muscles?

A

Increases muscles mass, pectorals and larynx

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12
Q

What are the effects of androgens on the kidney and skin?

A

causes erythropoeitin production and acne and hair production.

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13
Q

What are the effects of androgens on the placenta?

A

androgens act as a precursor for estrogen production

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14
Q

What happens to any primordial follicles that develop prior to puberty?

A

primordial cells can develop to secondary follicles and then will undergo atresia

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15
Q

What hormones are considered the androgens?

A
  1. testosterone 2. androstenedione 3. DHT
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16
Q

What hormones are the gonadotropins?

A

FSH, LH and hCG (acts very similarly to LH)

17
Q

How is follicle development regulated in the reproductive years?

A

a cohort of follicles are selected to grow when they acquire FSH receptors. They grow slowly and FSH prevents apoptosis. The granulosa cells also proliferate under the influence of FSH/estrogen/growth factors. Only 1 follicle is selected to ovulate and the remaining follicles become atretic.

18
Q

Where do gap junctions exist in the ovary?

A

between the granulosa cells and the ovum

19
Q

What is the best indicator of ovulation?

A

high progesterone levels that occur after ovulation has taken place.
high body temp also signals that ovulation occurred

20
Q

Describe stimulation pathway for estradiol production during follicular/proliferative phase?

A
  1. GnRH is released from hypothalamus in pulsatile manner
  2. FSH (non-pulsatile) and LH (pulsatile)
  3. LH binds to theca interna cells and stimulates them to take up cholesterol and make androstenedione
  4. androstenedione transported to the granulosa cells where they are converted to estradiol with FSH and LH stimulation.
21
Q

What enzyme converts androstenedione to estradiol?

A

CYP19

22
Q

What are the effects of 17B estradiol (E2)?

A
  1. proliferation of GC
  2. ovum development
  3. LH receptors on GC (requires FSH)
  4. proliferation of the endometrium
23
Q

What do high and low E2 levels stimulate?

A

high levels: stimulates KiSS-1 neurons which releases GnRH and thus increases FSH and LH release
low levels: inhibits FSH and LH release

24
Q

What is the feed back regulation in the follicular phase?

A
  1. FSH stimulates production of Inhibin B which inhibits FSH release from the anterior pituitary.
  2. Low levels of estradiol inhibit GnRH release from the KiSS-1 neuron in the hypothalamus, thus inhibiting FHS/LH release
  3. Also, estradiol can simply inhibit the AP inhibiting FSH/LH release
25
Q

What causes ovulation and formation of corpus luteum?

A

Surge in LH that is created from the drastic increase in granulosa cells that are thus producing net more estradiol. At high levels estradiol stimulates even more release of LH/FSH allowing for the huge surge in LH to cause ovulation.

26
Q

What prevents progesterone from being secreted in large amounts during follicular/proliferative phase?

A

2 cell hypothesis! In early follicular steroidogenesis, only the theca interna cell has LDL receptor and the enzymes necessary for converting cholesterol to progesterone. Within the theca cell, cholesterol can be taken up when under LH stimulation, leading to increased expression of StaR/P450scc and 3BHSD producing pregnenolone, progesterone and androstenedione. Since the granulosa cell doesn’t have StAR/P450scc or 3BHSD/CYP17 they can’t make progesterone. Instead they take the androstenedione from the theca cell and convert that to testosterone then to estradiol since the granulosa cells do have the CYP19 and 17BHSD.

27
Q

What causes progesterone to be released in such drastic amounts in pre-ovulatory phase?

A

FSH/E2 now stimulates the granulosa cells to express LH receptors which stimulates the granulosa cells to express LDL receptors, StAR/P450scc, 3BHSD which allows uptake of cholesterol and conversion to progesterone. The intermediate on the way to progesterone, pregnalone is still made and can be transferred to theca cell where it can be fully converted to androstenedione with CYP17 (still not made in granulosa cells so they cannot convert progesterone to androstenedione) and then androstenedione can be returned to the granulosa cell where it is converted to estradiol via 17BHSD and CYP19

28
Q

When is the general effect of progesterone?

A

Creates a quiescent environment and proper endometrium for implantation and development of the fetus

29
Q

Why is there a huge estrogen surge prior to LH surge?

A

estrogen causes the granulosa cells to proliferate and thus there are more granulosa cells secreting even more estradiol when there is FSH stimulation. Estradiol has positive feedback and stimulates the hypothalamus via KiSS-1 neuron to produce even more GnRH leading to increased production of LH

30
Q

What happens to the hormone levels in the absence of fertilization?

A
  1. LH/FSH decline
  2. corpus luteum is not maintained
  3. not more progesterone to maintain the endometrium
31
Q

When does the corpus luteum die and what takes over its role?

A

corpus luteum is important for the first two months. The synsytiotrophoblast takes over and produces estrogen and progesterone under stimulation of hCG which acts in the same manner as FSH/LH causing secretion of estradiol and progesterone.

32
Q

What is the role of hCG in the male?

A

hCG stimulates differentiation of the leydig cells so they can produce testosterone which is important for development of the duct system and male genitalia

33
Q

What is hCS?

A

placental lactogen that is responsible for gestation diabetes, breast development and mobilization of nutrients for the fetus

34
Q

What happens to levels of hCG, hCS, estriol and progesterone during pregnancy?

A
  • hCG starts decreasing at 70 days and ceases at 140 days.

- hCS, estriol and progesterone gradually increase until birth (increase due to the increasing size of the placenta)

35
Q

What precursors does the mother have to provide to the placenta for steroid biosynthesis?

A

cholesterol and androstenedione. Can convert cholesterol to progesterone using 3BHSD. Can convert androstenedione to estradiol using CYP19. Doesn’t have CYP17 so cannot convert progesterone to androstenedione therefore need androgens from the mother

36
Q

What is the pathway in estrogen biosynthesis in pregnancy?

A
  • Maternal adrenal provides DHEA and testosterone. Testosterone is converted to estriol by CYP19 in the synsytiotrophoblast and DHEA to estrone.
  • Fetal adrenal cortex makes DHEA-SO4 which is converted to 16-OH-DHEA-SO4 at the fetal liver and that is converted to estriol by the synsytiotrophoblast. Estriol is a good measure for fetal development
37
Q

How is cortisol produced in the fetus and what is its role?

A

the placenta secretes CRH which acts on fetal AP and adrenal cortex causing production of cortisol and DHEA. Cortisol is important for fetal lung maturation and GI tract maturation

38
Q

What happens to hormonal levels during parturition?

A

Normally, progesterone inhibits CRH release from the placenta, prostaglandin release and myometrium contraction (reduced the number of OT receptors in the myometrium and prevents OT release). CRH does the opposite. When progesterone decreases and CRH increases, the inhibition of progesterone is released and there is increased cortisol, estrogens and prostaglandins. Increased cortisol further increases CRH release and more prostaglandins leading to more myometrium contractions, more OT release and more OT receptors on the myometrium and gap junctions leading to more excitation.

39
Q

How do oral contraceptives work?

A
  • prevent ovulation by preventing LH surge
  • the pill provides low amounts of estradiol that are low enough to maintain negative feedback on the hypothalamus and AP preventing release of LH/FSH. Without FSH/LH, the theca and granulosa cells are unable to make estradiol therefore the granulosa cells are not stimulated to proliferate and we do not see the LH surge you would normally.

Reproduction (11 decks)

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