reproductive- related videos (period, hormones) Flashcards
functional unit of the ovaries
follicles (contain a single oocyte)
describe an ovarian follicle layers
oocyte
surrounded by an Antrum (fluid)
inner most layer: granulosa cells
followed by oter most layers: theca cells
NOTE: theca and granulosa synthesize estrogen to drive the growth of the follicle
-pituitary hormones (i.e FSH , LH) level during the 3 phases
-estrogen, progesterone?
sos
- initially low, spike right before ovulatio, fall after
- estrogen spike right before ovukation, fall after
- following ovulation (gentle small rise of estrogen and great rise in progesterone level)
mid-cycle surge. explain
when is the oocyte released from a follicle?
switch from -ve feedback (rem: high GnRH—> high FSH—> high estradiol —-ve feedback—> decreases FSH/LH) to +ve feedback, where
estradiol triggers increase frequency of GnRH pulses leading to LH SURGE!!
-oocyte released from follicle 36 hrs after LH surge
basis of ovulation testing (when to get pregnant) test. detects what ?
urine detection of LH (i.e when its LH surge) thus 36 hrs after an oocyte is released :)
mittelschmerz. when? due to? characteristics? resolution? mimic?
- mid-cycle pain
- d/t enlargement of follicle or rupture with bleeding :)
- mild UNILATERAL (on the side where follicle is)
- resolves in hrs to days
- mimic APPENDICITIS
when is the corpus luteum formed?
what is it? fxn?
-luteal phase
-TEMPORARY endocrine gland formed from the follicle
-produces A LOT of progesterone and some estradiol
by negative feedback this deceases FSH/LH
when does menstruation occur in term of ovulation
2 weeks after ovulation
what effect fertilization has on hormonal levels in the ovaries
embryo makes hCG
which maintains corpus luteum and progesterone production, thus will maintain suppression of LH/FSH
2 phases of uterine cycle (changes in endometrium)
- proliferative phase: follicular phase of ovary
- secretory phase: luteal phase of ovary
proliferative phases of the uterine cycle
endometrial proliferation (stimulated by estrogen)
- endometrial thickness increases (> x10)
- growth of glands, stroma, blood vessels
secretory phase of the uterine cycle
AFTER OVULATION
progesterone inhibits proliferation
-NUMEROUS SECRETIONS released to PREPARE FOR EMBRYO !
-changges in blood vessels: sososos
** vessels grow and coil
** form SPIRAL ARTERIES about 9th post ovulatory day
(critical for implantation, support of fertilized egg)
physiology of menstruation
progesterone levels fall
so vasoconstriction of spiral arteries
leads to APOPTOSIS of endometrial cells !!!!!!!
thus, collapse and desquamation of endometrium
if a women presents with secondary amenorrhea (i.e cessation of normal menses after prior normal periods)
what should we consider? (group of causes)
1- PREGNANCY (screen with HCG measurement) most common
2- Hypothalamus, pituitary, other:
—thyroid: BOTH hypo and hyper
—prolactin: prolactinoma (inhibition of GnRH release, thus decreases LH/FSH)
—cortisol: cushing syndrome (high cortisol level)
3- ovary (estrogen/progesterone problems)
4- other
—LOW BODY WEIGHT (functional hypothalamic amenorrhea)
stress plus low caloric intake leads to low GnRH levels thus low LH, FSH
patients RESPOND TO pulsatile GnRH
-can occur in arorexia
what is progestin challenge?
why not used anymore?
how is it done?
- older test for cause of amenorrhea
- many false +ve
- administration of progestin (oral/IM) + observe for menstrual bleeding within 7 days
if bleeding occurs after a progestin challenge, indicates what ?
classic cause ?
if no bleeding occurs, indicates what?
common cause ?
- estrogen is present but NO PROGESTERONE
- classic cause: PCOS (corpus luteum is not forming to make progesterone)
-estrogen not present to proliferate endometrium or anatomic menstrual outflow problem
follow up: estrogen-progestin challenge
common cause: menopause (oestrogen, progesterone, ovulation are absent)
girl present with primary amenorrhea
- normal LH/FSH levels
- normal estrogen/progesterone levels
due to all hormones normal (hypothalamus, pituitary, ovaries must be normal) so:
mullerian dysgenesis (failure of mullerian duct development)
absent upper vagina and/or uterus
(i.e no lining to be shed at puberty)
why anoroxic women can get secondary amenorrhea?
tx?
—LOW BODY WEIGHT (functional hypothalamic amenorrhea)
stress plus low caloric intake leads to low GnRH levels thus low LH, FSH
-patients RESPOND TO pulsatile GnRH
MENOPAUSE IS THE —-
median age?
depletion of ovarian follicles !
median age= 51 yrs
women loses estrogen and progesterone coming from the ovaries
what is the source of esstrogen after menopause
adipose tissue
(aromatase converts androstenedione to estrone)
androstenedione: weak androgen produced by the adrenal gland
what is an early finding test in menopause?
HIGHH FSH (followed by high LH later on)
due to loss of INHIBIN production from follicles
*inhibin normally suppresses FSH release
symptoms of menopause 4
all associated with loss of estrogen levels 1- hot flashes (few mins and passes) 2- vaginal atrophy (thin, dry, friable) 3- osteoporosis 4- CV dxs (risk rises)
what tx can be used for menopause symptoms
HRT
-(oral or transdermal estradiol)
+progestin (if uterus is intact) to prevent endometrial hyperplasia :)
what is the main indication for HRT in menopause?
1- relieves HOT FLASHES
and 2- improves bone density
risk of HRT 2
- increased risk of stroke, DVT, MI
- increased risk of BREAST cancer
how can PCOS cause 2o amenorrhea?
genetics + diet/obesity —>increased LH:FSH ratio
so, LH drives production of ANDROSTENEDIONE from theca cells
will be released into serum and some of it will be converted into estrone by adipose tissue.
estrone —> decreases more FSH —> anovulation
review PCOS causes and hormones
1- genetics + die/obesity lead to:
—-increased LH: FSH ratio
—-hyperinsulinemia
2-high LH drives production of andriostenedione from theca cells
—-normally: andriostenedione should be converted to estradiol (by granulosa cells) but this cant happed d/t low FSH
—-so some of it is converted to testosterone leading to hirsutism/ acne
—-others are converted into estrone (in adipose tissue)
3- estrone further suppress FSH (so there will be anovulation and follicular cysts)
as a result progesterone will be decreased (no normal ovulation)
PCOS can lead to diabetes !!!! due to
hyperinsulinemia leading to insulin resistance
-obese female
-HIRSUTISM (facial hair)
-acne
-amenorrhea
-INFERTILITY
US shows: multiple follicular cysts
PCOS
how is PCOS diagnosed?
hormone measurements?
-clinically
-TOTAL TESTِESTERONE (most reliable indicator)
-LH and FSH normal range
but LH:FSH ratio usually >2:1 !!!!!!!!!!!!!! abnormal (characteristic feature)
tx for pcos
1- weight loss
2- ORAL CONTRACEPTIVES (suppress LH)
also, estrogen component will increase the SHBG sex hormone binding globulin which will decrease androgens
3- spironolactone blocks androgens
4- metformin/TZDs (improve insulin resistance)
not routinely used !
risk of diabetes in PCOS statistics
10% by 40 yrs
what are acanthosis nigricans?
can they be found in PCOS?
in what diseases are they common?
-plaques of darkened skin
-yes, ass with insulin resistance
1- diabetes
2-PCOS
3- gastric cancer
PCOS increases the risk of what cancer?why?
endometrial cancer (unopposed estrogen) d/t lack of progesterone
workup for amenorrhea
sososososo
RULE OUT 1- pregnancy 2- thyroid 3- cushing 4- prolactin 5- anorexia THEN measure FSH: low: PCOS (high LH: FSH ratio) high: menopause normal: mullerian dysgenesis
