Aug28 M3-Menstrual_cycle_PMS Flashcards
2 divisions of menstrual cycle
follicular phase and luteal phase
follicular phase charact
- follicles grow until one dominant follicle with egg to be ovulated
- dominant follicle makes estrogen which thickens uterine lining
- estrogen increases
what happens on day 14 (mid cycle)
- LH peak (triggers ovulation)
- dominant follicle becomes corpus luteum
- CL starts making P under LH influence
progesterone function
makes the endometrium secretory and ready for implantation in case of fertilization
end of luteal phase: what happens if no fertilization
estrogen and P drop, beginning of menses
what happens if there is fertilization and impl
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
in hormone pov, what starts the follicular phase
- low E and P in serum so no negative feedback on pituitary
- increase in GnRH pulse frequency
- serum FSH and LH increases
FSH function in the early follicular phase
will stim the growth of a dominant follicle
LH effect on the growing dominant follicle in early follicular phase
stimulates the start (step 1) of estrogen prod by the growing dominant follicle in a 2 cell, 2 step process
as dominant follicle grows (bc of FSH), how does it make estrogen (bc of LH, step 1, and FSH, step 2), during follicular phase
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)
FSH function in dominant growing follicle making estrogen
stim 2nd step of granulosa cells turning androstenedione into estradiol with aromatase enzyme
effect of the estrogen of the follicular phase (growing dominant follicle) on the body
thickens the uterine lining (makes it proliferate)
female parallel of LH-Leydig cells FSH Sertoli cells
- LH theca interna cells
- FSH granulosa cells
time of peak serum estradiol
1 day before ovulation. is the cause of the LH surge that follows
time of peak serum LH
mid cycle (around day 14) in response to estrogen surge
explanation of the LH surge
at a specific serum concentration, estrogen causes a big rise in LH (10x increase)
consequence of the LH surge at midcycle
- follicule rupture
- release of the mature ovum (oocyte) (ovulation)
feedback in the HPO (ovaries) axis
- activin and inhibin produced by the ovaries = positive or negative fb depending on conc
- low estrogen (and progesterone) during early follicular phase = positive feedback on HYPOTHALAMUS
- high E and P during luteal phase = negative fb on PITUITARY
consequence of the mid cycle LH surge on the oocyte
- 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)
effect of P produced by GCs after LH surge, before ovulation
slows down the LH pulses
number of oocyte variation in life
- highest in utero
- goes down at birth
- follicles become antral during puberty
- one ovulates per month
primordial follicles are found where
cortex of ovaries
time from primordial to antral follicle
2-3 months
how many follicles become antral, how many dominant every month
- 4-5 antral every month
- 1 dominant every month
how to measure ovarian reserve
count antral follicles
once one follicle becomes dominant (follicular phase), how does it grow and how much
- accumulates fluid
- measurable on US
corpus luteum (theca lutein cells and granulosa lutein cells) makes what
estrogen and progesterone (luteinized granulosa cells can make both E and P), under the influence of LH
what happens to the corpus luteum of the menstrual cycle if there is no pregnancy
becomes the corpus albicans
what happens to the ovum after ovulation
- passes in the Fallopian tube
- swept down to the uterus by the cilia lining the tube (3-4 days)
lifespan of ovum if no fertilization
24 hours
time between fertilization and implantation if there is fertilization
5-6 days
HPO axis during the luteal phase
- LH stims CL to make E and P
- E and P feedback negatively on the pituitiary
effect of P from CL on the body
stimulates endometrium to become more glandular and secretory in prep for implantation of fertilized ovum
factors needed for proper egg implantation
interaction between egg, granulosa cells around it (some GCs are around egg, not all stay to make CL) and endometrium properly timed
HPO axis in case of fertilization
the trophoblast (cells of the embryo that keep it in the placenta) makes HCG.
function of HCG
- 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
when does the corpus luteum of pregnancy stop making P and E
at week 8-10 of gestation. placenta becomes developed and makes E and P by itself
E and P and HCG during pregnancy
keep rising during all pregnancy
Rs for HCG are where
are the LH-Rs, because HCG and LH have a similar subunit
management of a pregnant patient in early pregnancy with a cyst
- cyst may be a corpus luteum cyst
- give E and P replacement (CL supposed to make them but cyst formed) otherwise will miscarry
what happens at the end of the luteal phase
- 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)
fixed length of the luteal phase
14 days.
follicular phase IS NOT constant
mean duration of menstrual cycle (MC)
28 days (21-35)
average duration of menses
3-8 days
average blood loss during menses
30 ml
usual time of ovulation
midcycle (approx 14 days). 36 hrs after LH surge
main risk of tampons use
toxic shock syndrome
keep them max 8 hours
alternatives to tampons
- 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)
woman with heavy period: workup
hemoglobin and iron
meaning of shorter menstrual cycle long term
no meaning. can still have any time of menopause.
-time of menopause has to do with aging and oxidative stress, follicles will undergo atresia
(imp?) most common affective or behavioral symptom of PMS
mood swings
(imp?) most common physical manifestation of PMS
abdominal bloating and extreme sense of fatigue
PMS def
- recurrent
- during luteal phase
- resolves by end of menstruation
- interferes with function
PMDD def
premenstrual dysphoric disorder (PMDD).
- more severe PMS
- meets DSM-V criteria
ddx of PMDD
- psychiatric disorder (mood and anxiety disorder)
- medical condition (dysmenorrhea = painful periods, hypo or hyperT, etc.)
rx for mild to moderate PMS
- lifestyle changes (exercise, stress reduction)
- supplements not shown to be better than placebo (vitB6 and E, vitex agnus castus, Ca, Mg)
2 medical approaches for management of mild to moderate PMS
- SSRIs and SNRIs (selective serotonin and NE reuptake i)
- 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)
SSRIs used for what
depression
SNRIs used for what
hot flushes and menopausal syndrome
certain medical approaches to moderate to severe PMS
- drospirenone (4th gen progesterone that is anti-androgenic + diuretic)
- alprazolam (benzo for anxiety + suppresses ovulation)
- cyclic OCP
early menopause explanation
born with less eggs (NOT that they lost their eggs more before menopause)
