menstrual abnormalities Flashcards
Oligomenorrhea and secondary amenorrhea definition
Oligomenorrhea- menstrual cycles greater than 35 days apart
Secondary amenorrhea those who previously menstruated byt have had no menses for at least 3 previous cycles or 6 months
the median menstrual cycle is 28 days but can ranges from 21- 35 days
Menstrual cycle length
Can vary in an individual women
Most variable in the first few years following menarcche and preceding menopause
times of life during which anovulatory cycles are most frequent, typically menses can last 7-9 days
Normal HPO axis
hypothalamus releases GnRH–> pituitary FSH and LH–> Ovary–> Estrogen and prgesterone–> uterus–> menses
In the ovary there are cells containing maturing folliciles and eggs and make estradiol whcih act on a uterus
Estrogen and progesterone inhibit both pituitary and hypothalamus
Menstruation
Early in the menses the pituitary makes FSH (after pulsatile GnRH from hypothalamus), this stimulates a follicle to develop in the ovary which has granulosa cells to make estaradiol–> endometrium to make the endometrium a proliferative endometrium, the increase in estradiol stimulates an LH surge from pituitary
LH surge acts to induce ovulation from the follicle, and the follicle becomes a corpus luteum, the CL which make estrogen and a lot of progestrone to make the endometrium secretory (where implantation is possible)
If no pregancny the CL dies, progesterone falls, and the endometrium sheds, (the lowered progesterone stimulates GnRH pulsatility) to start the cycle all over
Key points of menstruation
Estradiol exposure results in a proliferatie endometrium, Estradiol exposure leads to inductiong of progesterone receptors
The Fall in progesterone levels results in menstruation this concept is used clinically and describes as progesterone withdrawal
Anovulation
No follicle that develops, no estradiol increase, no LH surge, no ovulation, no production of estrogen and endometrim does not become secretory
can lead to realy wierd menstrual cycle
Oligomenorrhea with a high FSH
AKA… Hypergondatropic Hypogonadism
confirm the high FSH then could be premature ovarian failure or if <40 look for chromosomal and Autoimmune disorders
The ovaries arent makeing E and P to reduce the FSH and LH
So the hypothalamus makes GnRH increase, and FSH and LH, But the ovary and Egg reserve is low and they dont make estrogen and progesterone so theres no effect on the uterus–> no menses
Hypergonadotropic hypogonadism Has so many friggen names!
Primary ovarian Insufficiency
Primary Hypogonadism
But they all mean the same thing
Premature ovarian Failure, hypergonadotropic hypogonadism before age 40 –> elevated FSH /LH
Affects approximately 1% of all women, 90% of cases occuring between ages 30 and 40
Premature menopaise, primary ovarian insufficiency
Genetic- chromosomal number- 45 X or 45 x/xx, turners syndrome, and turners mosaic)
Fragile X
Auto immune,
Iatrogenic (chemo or radiation)
Idiopathic
Reproductive options in oatients with primary ovarian insufficiency
OOcyte or embryo donation, adoption, extremely low likelihood of spontaneous conception, typically need hormone replacement therapy due to risks of hypoestrogenism
Why check the TSH and prolactin
Standard and the two homones can affect the menstrual cycle
Hypothalamus makes TRH, Pituitary makes TSH, Thyroid makes T3 and T4
dopamine inhibits TRH and Prolactin release
Thyroid hormone - metabolism, development, steroidogenesis
Prolactin supresses GnRH expression (from prolactinoma)
Low or normal FSH,
it is essential to assess estrogen status in patients with amenorrhea or oligomenorrhea
Estradiol exposure leads to induction of progesterone receptors, we can treat patients with progestins which act on the progesterone receptor to assess degree of estrogen exposure
Only if the endometrium has been exposed to estrogen will there be withdrawal bleeding following cessation of progestin therapy, (progestin withdrawal or progestin challenge)
Assessment of adequate estrogen exposure
Progestin withdrawal (medroxyprogesterone acetate), Pelvic ultrasound to demonstrate endometrial thickness>6mm
Day 2/3 serum estradiol >40 pgmL
Hypogonadotropic hypogonadism, secondary hypogonadism
Low or abnormally normal FSH, Low estrogen
Low circulating estradiol level lack of withdrawal bleed to progestin–> there was very low estrogen exposure, thin endometrial lining on pelvic ultrasound
you need to determin why the estradiol is so low, if the hypothalamus senses a low E it should be increasing GnRH levels
Usually environmental factors that mess up Hypothalamic activity
hypogonadotropic hypogonadism
Normal feedback relationship between ovarian estrogen production and pituitary gonadotropin secretion ( a low estrogen level should cause a compensatory increase in FSH release)
Low estrogen and low FSH indicates that basic central feedback mechanisms in the HPO axis are not functioning
Common etiologies- physical, nutritional, emotional stress, hyperprolactinemia (meds),
Brain MRI imaging to exclude tumors when there is no clear explanation (pituitary adenoma, benign or malignant tumors, cysts, sarcoidosis)
If MRI is normal, the diagnosis is functional hypothalamic amenorrhea, treatment involves measures to decrease stressors or involves ovulation induction or HRT