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Endocrine Physiology > Female Reproductive > Flashcards

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
Q

Placenta endocrine action

A

-converts cholesterol to progesterone (progesterone inhibits -LH receptors on luteal cells, so supports progesterone and estradiol secretion contractions)

26
Q

Describe the important role that hCG plays in the early stages of pregnancy.

A

hCG binds to LH receptors on luteal cells, rescues corpus luteum, allowing it to continue to produce progesterone unt0l the placenta takes over

27
Q

What is the “luteoplacental shift”, and when does it occur?

A

Shift in the responsibility of synthesizing progesterone. They mutually contribute in weeks 6-8 of pregnancy, then placenta takes over.

28
Q

Describe the hormonal processes that initiate parturition, including positive feedback loops

A

**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

Endocrine Physiology (5 decks)

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