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Bloc I - Reproduction > Aug28 M3-Menstrual_cycle_PMS > Flashcards

Aug28 M3-Menstrual_cycle_PMS Flashcards

1
Q

2 divisions of menstrual cycle

A

follicular phase and luteal phase

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2
Q

follicular phase charact

A
  • follicles grow until one dominant follicle with egg to be ovulated
  • dominant follicle makes estrogen which thickens uterine lining
  • estrogen increases
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3
Q

what happens on day 14 (mid cycle)

A
  • LH peak (triggers ovulation)
  • dominant follicle becomes corpus luteum
  • CL starts making P under LH influence
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4
Q

progesterone function

A

makes the endometrium secretory and ready for implantation in case of fertilization

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5
Q

end of luteal phase: what happens if no fertilization

A

estrogen and P drop, beginning of menses

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6
Q

what happens if there is fertilization and impl

A

HCG released by embryo (and trophoblast of placenta later)

  • maintains CL of pregnancy
  • CL of pregnancy keeps making E and P
  • no periods because E and P remain
  • E and P increase as HCG increases
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7
Q

in hormone pov, what starts the follicular phase

A
  • low E and P in serum so no negative feedback on pituitary
  • increase in GnRH pulse frequency
  • serum FSH and LH increases
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8
Q

FSH function in the early follicular phase

A

will stim the growth of a dominant follicle

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9
Q

LH effect on the growing dominant follicle in early follicular phase

A

stimulates the start (step 1) of estrogen prod by the growing dominant follicle in a 2 cell, 2 step process

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10
Q

as dominant follicle grows (bc of FSH), how does it make estrogen (bc of LH, step 1, and FSH, step 2), during follicular phase

A

makes estrogen in 2 cell (2 step process)

  • under LH influence, theca interna cells make androstenedione
  • granulosa cells convert this androstenedione into estradiol using aromatase enzyme (under FSH influence)
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11
Q

FSH function in dominant growing follicle making estrogen

A

stim 2nd step of granulosa cells turning androstenedione into estradiol with aromatase enzyme

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12
Q

effect of the estrogen of the follicular phase (growing dominant follicle) on the body

A

thickens the uterine lining (makes it proliferate)

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13
Q

female parallel of LH-Leydig cells FSH Sertoli cells

A
  • LH theca interna cells

- FSH granulosa cells

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14
Q

time of peak serum estradiol

A

1 day before ovulation. is the cause of the LH surge that follows

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15
Q

time of peak serum LH

A

mid cycle (around day 14) in response to estrogen surge

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16
Q

explanation of the LH surge

A

at a specific serum concentration, estrogen causes a big rise in LH (10x increase)

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17
Q

consequence of the LH surge at midcycle

A
  • follicule rupture

- release of the mature ovum (oocyte) (ovulation)

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18
Q

feedback in the HPO (ovaries) axis

A
  1. activin and inhibin produced by the ovaries = positive or negative fb depending on conc
  2. low estrogen (and progesterone) during early follicular phase = positive feedback on HYPOTHALAMUS
  3. high E and P during luteal phase = negative fb on PITUITARY
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19
Q

consequence of the mid cycle LH surge on the oocyte

A
  • oocyte of dominant follicle completes 1st meiotic div
  • increase in local plasminogen activator (activates plasmin which does fibrinolysis) and cytokines (required for ovulation)
  • luteinization of granulosa cells of dominant follicle: make P
  • ovulation 36 hrs after LH surge (P already being made by luteinized GCs)
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20
Q

effect of P produced by GCs after LH surge, before ovulation

A

slows down the LH pulses

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21
Q

number of oocyte variation in life

A
  • highest in utero
  • goes down at birth
  • follicles become antral during puberty
  • one ovulates per month
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22
Q

primordial follicles are found where

A

cortex of ovaries

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23
Q

time from primordial to antral follicle

A

2-3 months

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24
Q

how many follicles become antral, how many dominant every month

A
  • 4-5 antral every month

- 1 dominant every month

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25
Q

how to measure ovarian reserve

A

count antral follicles

26
Q

once one follicle becomes dominant (follicular phase), how does it grow and how much

A
  • accumulates fluid

- measurable on US

27
Q

corpus luteum (theca lutein cells and granulosa lutein cells) makes what

A

estrogen and progesterone (luteinized granulosa cells can make both E and P), under the influence of LH

28
Q

what happens to the corpus luteum of the menstrual cycle if there is no pregnancy

A

becomes the corpus albicans

29
Q

what happens to the ovum after ovulation

A
  • passes in the Fallopian tube

- swept down to the uterus by the cilia lining the tube (3-4 days)

30
Q

lifespan of ovum if no fertilization

A

24 hours

31
Q

time between fertilization and implantation if there is fertilization

A

5-6 days

32
Q

HPO axis during the luteal phase

A
  • LH stims CL to make E and P

- E and P feedback negatively on the pituitiary

33
Q

effect of P from CL on the body

A

stimulates endometrium to become more glandular and secretory in prep for implantation of fertilized ovum

34
Q

factors needed for proper egg implantation

A

interaction between egg, granulosa cells around it (some GCs are around egg, not all stay to make CL) and endometrium properly timed

35
Q

HPO axis in case of fertilization

A

the trophoblast (cells of the embryo that keep it in the placenta) makes HCG.

36
Q

function of HCG

A
  • replaces LH (from HPO axis during luteal phase)

- becomes the stimulation of the CL of pregnancy to keep making E and P to support the endometrium

37
Q

when does the corpus luteum of pregnancy stop making P and E

A

at week 8-10 of gestation. placenta becomes developed and makes E and P by itself

38
Q

E and P and HCG during pregnancy

A

keep rising during all pregnancy

39
Q

Rs for HCG are where

A

are the LH-Rs, because HCG and LH have a similar subunit

40
Q

management of a pregnant patient in early pregnancy with a cyst

A
  • cyst may be a corpus luteum cyst

- give E and P replacement (CL supposed to make them but cyst formed) otherwise will miscarry

41
Q

what happens at the end of the luteal phase

A
  • CL not maintained by HCG
  • E and P fall
  • PGs and leukocytes increase in the endometrium + constriction of spiral aa + desquamation and ischemia of endometrium + arterior relaxation and bleeding and tissue breakdown
  • FSH levels start rising bc of no negative feedback (from E and P on hypothalamus)
42
Q

fixed length of the luteal phase

A

14 days.

follicular phase IS NOT constant

43
Q

mean duration of menstrual cycle (MC)

A

28 days (21-35)

44
Q

average duration of menses

A

3-8 days

45
Q

average blood loss during menses

A

30 ml

46
Q

usual time of ovulation

A

midcycle (approx 14 days). 36 hrs after LH surge

47
Q

main risk of tampons use

A

toxic shock syndrome

keep them max 8 hours

48
Q

alternatives to tampons

A
  • menstrual cups (less TSS risk, 12 hours, boil after every use)
  • Instead (worn on cervix, like diaphragm)
  • cloth pads (wash and reuse)
  • period underwear (wash and reuse)
  • sea sponges (TSS risk)
49
Q

woman with heavy period: workup

A

hemoglobin and iron

50
Q

meaning of shorter menstrual cycle long term

A

no meaning. can still have any time of menopause.

-time of menopause has to do with aging and oxidative stress, follicles will undergo atresia

51
Q

(imp?) most common affective or behavioral symptom of PMS

A

mood swings

52
Q

(imp?) most common physical manifestation of PMS

A

abdominal bloating and extreme sense of fatigue

53
Q

PMS def

A
  • recurrent
  • during luteal phase
  • resolves by end of menstruation
  • interferes with function
54
Q

PMDD def

A

premenstrual dysphoric disorder (PMDD).

  • more severe PMS
  • meets DSM-V criteria
55
Q

ddx of PMDD

A
  • psychiatric disorder (mood and anxiety disorder)

- medical condition (dysmenorrhea = painful periods, hypo or hyperT, etc.)

56
Q

rx for mild to moderate PMS

A
  • lifestyle changes (exercise, stress reduction)

- supplements not shown to be better than placebo (vitB6 and E, vitex agnus castus, Ca, Mg)

57
Q

2 medical approaches for management of mild to moderate PMS

A
  1. SSRIs and SNRIs (selective serotonin and NE reuptake i)
  2. suppress the HPO axis (OCP, GnRH-R agonist = binds the R on pit continuously compared to pulsatile GnRH so pit doesn’t make LH and FSH)
58
Q

SSRIs used for what

A

depression

59
Q

SNRIs used for what

A

hot flushes and menopausal syndrome

60
Q

certain medical approaches to moderate to severe PMS

A
  • drospirenone (4th gen progesterone that is anti-androgenic + diuretic)
  • alprazolam (benzo for anxiety + suppresses ovulation)
  • cyclic OCP
61
Q

early menopause explanation

A

born with less eggs (NOT that they lost their eggs more before menopause)

Bloc I - Reproduction (57 decks)

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