Female Reproductive Flashcards

1
Q

In the female, what cell type is homologous to: Leydig cells? Sertoli cells?

A

Leydig cells ~ Theca cells (LH → androgen producing)

Sertoli cells ~ granulosa cells ( both stimulated by FSH (earlier follicular phase))

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2
Q

What is the role of ovarian granulosa cells in a 2-9mm diameter non-dominant, antral follicle?

A
  • under the influence of FSH → produce estradiol from androstenedione from theca cells
  • FSH stimulates inhibin B synthesis and release → inhibits granulosa cell proliferation
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3
Q

What is the role of ovarian granulosa cells in a 15-20 mm diameter dominant, antral follicle?

A
  • under the influence of FSH and LH → produce estradiol from androstenedione and testosterone from theca cells and directly from cholesterol
  • LH stimulates inhibin A and FSH stimulates inhibin B synthesis and release → inhibits granulosa cell proliferation
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4
Q

What is the role of theca cells in terms of steroid production in ovarian antral follicles females in the follicular phase in both non-dominant and dominant follicles?

A

Under the influence of LH, theca cells produce progesterone, androstenedione (main output) and some testosterone

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5
Q

What is the role of ovarian luteal cells in a corpus luteum (in terms of steroid hormone and inhibin production, and gonadotropin receptor expression) in the early luteal phase?

A

in response to LH surge → progesterone synthesis, LH still stimulates inhibin A synthesis

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6
Q

What is the role of ovarian luteal cells in a corpus luteum in terms of steroid hormone in the mid-to-late luteal phase

A

LH stimulates progesterone and estrodiol production, LH still stimulates inhibin A synthesis

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7
Q

granulosa cells

A
  • produce estradiol (from androgen precursor)

- stimulated by FSH (in early follicular phase) and by LH and FSH (mid-late follicular phase)

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8
Q

theca cells

A

produce progesterone, androstenedione, and some testosterone

  • provides androgen precursors to ovarian follicle granulosa cells
  • stimulated by LH
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9
Q

luteal cells

A
  • from granulosa and theca cells

- produce progesterone, estradiol, inhibin A

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10
Q

LH receptors

A

located on theca cells, located on granulosa cells in mid-late follicular phase and thereafter

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11
Q

FSH receptors

A

located on granulosa cells in follicular phase

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12
Q

List reproductive actions of estrogen and progesterone in females

A
  1. Development of genitalia & breast, female fat distribution
  2. Growth of follicle, endometrial proliferation, increase myometrial excitability
  3. Upregulation of estrogen, LH, & progesterone receptors; feedback inhibition of FSH & LH then LH surge; stimulation of prolactin secretion
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13
Q

AMH regulation of ovarian follicle growth

A
  • produced by primary, secondary, and non-dominant follicles
  • diminishes onset of follicle growth at primordial stage
  • diminishes FSH action on non-dominant follicles
  • *circulating AMH levels good biomarker for number of follicles growing
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14
Q

follicular phase

A
  • days 1-14
  • fall in progesterone, estradiol, inhibin A from corpus luteum –> increase in FSH, LH
  • onset of menstrual bleed
  • FSH –> 6-20 follicles to grow
  • follicles secrete estradiol and inhibin B (estradiol stimulates proliferation of endometrium)
  • inhibin B inhibits FSH (neg feedback) so FSH levels fall
  • BUT largest follicle (dominant) develops LH receptors on mural granulosa cells, so LH supports survival
  • dominant follicle produces estradiol (positive feedback)
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15
Q

Ovulation

A
  • dominant follicle releasing estradiol –> gene transcription in hypo
  • -> GnRH surge
  • ->causes LH surge
  • -> ovulation (day 14) from enzymes dissolving matrix around oocyte
  • stimulates oocyte meiosis from Prophase I to Metaphase II
  • *LH surge converts follicle cells into luteal cells secreting progesterone
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16
Q

Luteal Phase

A
  • days 14-28
  • LH receptors on luteal cells, so supports progesterone and estradiol secretion
  • corpus luteum secretes progesterone
  • -> matures endometrium (secretory phase), negative feedback on GnRH/LH & FSH
  • *Inhibin A contributes negative feedback on FSH
  • early decrease in estradiol, then rise
  • -days 26-28: luteal cells unresponsive to LH, endometrium will shed without progesterone support
17
Q

Polycystic ovarian syndrome

A

Diagnosed from at least 2 criteria:

  • clinical (hirsutism, Ferriman-Gallwey >8) or biochemical (high testosterone) hyperandrogenism
  • intermittent (3 months w/o pregnancy) menstrual cycles
  • polycystic ovaries
  • *need to eliminate mimics: congenital adrenal hyperplasia, Cushing’s syndrome, hyperprolactemia, hypothyroidism, androgen-secreting tumors, and hypothalamic amenorrhea

commonly accompanied with metabolic syndrome, type 2 diabetes, obesity, and sleep apnea

  • theca cell proliferation, excess androgen secretion
  • increased AMH from having more non-dominant follicles
  • increased circulating testosterone and androstenedione levels
  • infrequent/no ovulation
  • increased LH, so decreased negative feedback of estradiol/progesterone
18
Q

Oral contraceptives

A
  • combined: estrogen and progestins
  • progestin only pills
  • *use negative feedback to prevent ovulation (like luteal phase)
19
Q

Premature ovarian failure

A
  • loss of sufficient numbers of follicles to maintain negative feedback regulation before age 40
  • low estradiol (and other ovarian hormones), leads to high FSH/LH, absent menstrual cycles
  • replacement hormone therapy
20
Q

Functional hypothalamic amenorrhea

A
  • low LH and FSH (and GnRH?) leading to low ovarian hormones and absent menstrual cycles
  • treat with GnRH pump or recombinant gonadotropin treatment
  • also treat with cognitive behavioral therapy
  • *can occur due to weight loss or excessive exercise
21
Q

Primary Amenorrhea

A
  • after girl is 16 years and has undergone other normal changes with puberty (just not menarche)
  • LH and FSH low/high with low ovarian hormones
  • causes: many, including Kallmann and Turner (XO) syndromes
22
Q

Secondary Amenorrhea

A
  • when previously menstruating woman stops having periods
  • most likely from pregnancy
  • also could be from oral contraceptives, stress, eating disorders, PCOS, excessive exercise, & more.
23
Q

Menopause stages

A

1) initial signs (ages 38-45 years)
- monotropic rise in FSH in early-mid-follicular phase
- no elevation in LH, but falling AMH levels (from decreased inhibin B rise from less growing follicles)
- estradiol-responsive follicles have increased estradiol secretion due to elevated FSH

2) Menopause transition
- elevated FSH (possibly LH)
- lower estradiol in follicular phase
- intermittent cycles

3) Menopause
- elevated FSH (usually LH too)
- no cycles
- low estradiol, androgens, AMH

24
Q

Abortion pill

A
  • post-ovulatory contraception
  • progesterone receptor antagonist plus a prostaglandin E1 analogue for muscle contraction
  • induces miscarriage before 8 weeks (afterwards, placenta takes over)
25
Placenta endocrine action
-converts cholesterol to progesterone (progesterone inhibits -LH receptors on luteal cells, so supports progesterone and estradiol secretion contractions)
26
Describe the important role that hCG plays in the early stages of pregnancy.
hCG binds to LH receptors on luteal cells, rescues corpus luteum, allowing it to continue to produce progesterone unt0l the placenta takes over
27
What is the “luteoplacental shift”, and when does it occur?
Shift in the responsibility of synthesizing progesterone. They mutually contribute in weeks 6-8 of pregnancy, then placenta takes over.
28
Describe the hormonal processes that initiate parturition, including positive feedback loops
**placenta → CRH → fetal cortisol → additional CRH etc **placenta → CRH → fetal adrenal DHEAS → increased estradiol to progesterone ratio → increased oxytocin receptors at uterus → increased contraction proteins at uterus → increased prostoglandin E2 and F2alpha at placenta → myometrial contractions → labor onset **uterine contractions → stretch receptors → induce oxytocin release from posterior pituitary → oxytocin reinforces prostaglandin induced contractions → cycle ends when birth relieves pressure on cervix