Lecture 18-20 - Female Reproduction Flashcards

1
Q

Steps of gametogenesis (oogenesis)

A
  1. oogonia (germ cells)
    mitosis and differentiation
  2. primary oocytes
    meiosis starts
  3. meiotic arrest until puberty
  4. 1st meiotic division completed at ovulation -> secondary oocyte
  5. 2nd meiotic division completed after fertilization
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2
Q

steps of follicle

A
  1. primordial follicle
  2. primary follicle
  3. preantral follicle
    steps 1-3 all before puberty
  4. early antral follicle
    acted on by GnRH/FSH/LH/estrogens
  5. mature or graafian follicle
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3
Q

function of kisspeptin

A
  • neuropeptide released from hypothalamic nuclei that constitute the pulse generator system
  • the PGS integrates information on the metabolic-health status of body and responds releasing appropriate amounts of kisspeptin
  • kisspeptin regulates the amplitude and frequency of pulsatile release of GnRH
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4
Q

low frequency pulse favors

A

FSH release

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5
Q

high frequency pulse favors

A

LH release

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6
Q

non-pulsatile GnRH

A

used in case of:
precocious pubtery (too early)
endometriosis
fibroids (benign tumors of uterus)
* continous GnRH stimulation causes decrease in LH and FSH bc body think its overstimulation so it downreguates receptors

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7
Q

LH and FSH function

A
  • develop follicle
  • FSH receptors located on granulosa cells
  • LH receptors located on theca cells only during follicular phase while during luteal phase they appear also on the granulosa cells
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8
Q

FSH and Lh coordinate granulosa and theca cells in the production of

A

estrogen

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9
Q

during the luteal phase, LH stimulates synthesis of

A

progesterone in granulosa cells

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10
Q

inhibin is released by

A

granulosa cells

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11
Q

local effects of estrogen on follicle

A
  • stimulates proliferation of granulosa cells
  • increase FSH receptors (important for select of dominant)
  • increase LH receptors (stim syn of proges during luteal)
  • increase estrogen receptors

these all promote conversion of preantral follicles into antral follicles

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12
Q

effects of estrogen on reproductive tract: facilitates fertilization

A
  • makes thin cervical mucus
  • stimualtes contract of SM in uterus and fallopian
  • growth of epithelial cilitated cells in fallopian
  • stimulates peg cells in fallopian to produce nutrients for ovum
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13
Q

effects of estrogen on reproductive tract: facilitates implantation

A
  • induces proliferation of endometrium
  • favors growth of uterine smooth muscle
  • stimulates synthesis of progesterone receptors in preparation for luteal phase
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14
Q

systemic effects of estrogen

A
  • 2nd sex characteristics
  • fat deposition
  • stimualtes GH release
  • promtoes bone deposition and closure of epiphyseal plates
  • stimulates hepatic synthesis of plasma proteins
  • favor good cholesterol
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15
Q

the positive feedback mode of estrogens happens

A

right before ovulatory phase
* rise in E induces LH surge that precipitates ovulation

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16
Q

local effects of progesterone on corpus luteum

A
  • decrease activiy of aromatase on granulosa cells which decreases estrogen synthesis
17
Q

global effects of progesterone

A
  • inhibits hypothalamus pituitary axis
  • increase body temp
  • increase food intake
  • decrease immune response
18
Q

progesterone effects on reproductive tract

A
  • decrease estrogen receptors in uterus
  • inhibits estrogen induced proliferation of endometrium
  • turns the endometrium into secretory tissue
  • increase vascularization
  • decrease PG synthesis in uterus
  • stimulates viscous and thick cervical secretions
19
Q

the follicle with the most … becomes the dominant follicle

A

FSH receptors

20
Q

the LH surge leads to ovulation: follicle maturation

A
  • LH stimulates proliferation of theca and granulosa cells
  • LH inhibits release of OMI by granulosa cells
  • first meiotic division resumes
21
Q

the LH surge leads to ovulation: rupture of graafian follicel

A
  • proteases causes ECM and connective tissue breakdown and loss of wall integry so the follicle breaks and ovum is released
  • increase blood flow and increase LH and immune cells access to follicle causes the release
  • increase GFs, cytokines, PGE/PGF which cause follicle remodeling which lead to release
22
Q

corpus luteum after ovulation

A
  • LH converts the graafian follicle into corpus luteum
  • it produces progesterone, estrogen, and inhibin
  • maximal CL activity is achieved 5 days after ovulation
23
Q

luteolysis

A
  • LH keeps corpus luteum alive for 13-14 days
  • if no fertilization, corpus luteum undergoes luteolysis
  • decrease progesterone synthesis
  • increase prostaglandins
  • vascular supplies regress
  • decrease nutrients and ischemia and necrosis
24
Q

corpus albicans

A

white body due to luteolysis leaves scar

25
Q

menstruation

A
  • drop in P and E
  • increae uterine prostaglandins
  • constrict vessels
  • fibrinolysin prevents clot formation
  • leukocytes strengthen uterus against infection
26
Q

during endometrial cycle, estrogen stimulates production of

A

progseterone-R (important)
promotes growth of endometrium and glands

27
Q

contraceptives

A

estrogen in negative feedback mode (suppress GnRH release and LH and FSH secretion)
* follicles do not mature
* estrogen does not reach critical level to have positive feedback switch so NO LH SURGE occurs and thus no ovulation