menstrual abnormalities Flashcards

1
Q

Oligomenorrhea and secondary amenorrhea definition

A

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

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2
Q

Menstrual cycle length

A

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

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3
Q

Normal HPO axis

A

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

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4
Q

Menstruation

A

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

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5
Q

Key points of menstruation

A

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

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6
Q

Anovulation

A

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

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7
Q

Oligomenorrhea with a high FSH

AKA… Hypergondatropic Hypogonadism

A

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

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8
Q

Hypergonadotropic hypogonadism Has so many friggen names!
Primary ovarian Insufficiency
Primary Hypogonadism

But they all mean the same thing

A

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

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9
Q

Premature menopaise, primary ovarian insufficiency

A

Genetic- chromosomal number- 45 X or 45 x/xx, turners syndrome, and turners mosaic)

Fragile X

Auto immune,

Iatrogenic (chemo or radiation)

Idiopathic

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10
Q

Reproductive options in oatients with primary ovarian insufficiency

A

OOcyte or embryo donation, adoption, extremely low likelihood of spontaneous conception, typically need hormone replacement therapy due to risks of hypoestrogenism

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11
Q

Why check the TSH and prolactin

A

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)

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12
Q

Low or normal FSH,

A

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)

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13
Q

Assessment of adequate estrogen exposure

A

Progestin withdrawal (medroxyprogesterone acetate), Pelvic ultrasound to demonstrate endometrial thickness>6mm

Day 2/3 serum estradiol >40 pgmL

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14
Q

Hypogonadotropic hypogonadism, secondary hypogonadism

A

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

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15
Q

hypogonadotropic hypogonadism

A

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

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16
Q

Ovulatory dysfunction

A

Low/normal FSH, but normal circulating estradiol levels, most common cause is polycystic ovarian syndrome

These patients typically have evidence of adequate estrogen exposure, positive withdrawal bleed to progestin therapy, thicker endometrium on pelvic ultrasound, serum estradiol levels >40

17
Q

PCOS

A

The most common endocrine cause of infertility and irregular menstrual cycles, 2 of 3 symptoms:
PCOS like ovaries on ultrasound, oligomenorrhea, hyperandrogenism

lots of small follicles, not removed, small fluid filled with eggs

18
Q

PCOS hormonal control

A

High Estrogen, PCO like ovary with obesity–> menses
Hypothalamas has low GnRH, high estrogen, and high androgens

The really small follicles all have high estrogens

Rise in estradiol from the developing follicle triggers the LH surge, chronicly high estradiol from lots of follicles suppresses the GnRH- FSH and LH axis

19
Q

obestiy and anovulation

A

Obese patients more likely to have anovulatory cycles
Increased peripheral aromatixation of androgens to estrogens, hyperinsulinemia, increases androgen production

decreased hepatic sex hormone binding globulin results in increased free testosterone and estradiol

20
Q

Risks of secondary amenorrhea and anovulation

A
Infertility, hypoestrogenism (risk of osteoporosis, risk of cardiac disease) 
Normal estrogen (unopposed estrogen exposure can predispose to abnormal bleeding )
21
Q

Potential reasons for lack of withdrawal bleeding in response to progesterone therapy

A

Lack of circulating estradiol, severe endometrial adhesions, pregnancy

22
Q

Intrauterine adhesions/ Ashermans syndrome

A

can obliterate the endometrial cavity and produce secondary amenorrhea
Can result in lack of withdrawal bleed in response to progesterone if pt is amenorrheic
Most likely to result from procedures that can damage the endometrial cavity

Treatment is surgical resection

hirsutism