Flashcards in Menstruation/Menopause Deck (39):
What hormonal changes occur in the follicular phase?
slow rise and fall of FSH with a spike leading to ovulation, LH gradual rise with spike at ovulation, E2 gradual rise with a peak prior to the peak in LH and FSH, Progesterone fall at the beginning and remains low, inhibin B- same as FSH, Inhibin B gradual rise but still pretty low
What are the hormonal changes in the luteal phase?
FSH falls slowly with a slight rise at the end, LH falls more rapidly and remains low, E2 falls after surge then levels off and falls before onset of menstruation, Progesterone- rapid rise with a high plateau then falls low prior to menstruation, inhibin A- similar to progesterone, inhibin B similar to LH
What changes occur in the uterus, oviducts and vagina during the follicular phase?
endometrial proliferation, columnar oviductal and vaginal epithelium proliferation and stratification; mitosis of glandular epithelium, tortuous glands, elongation of spiral arteries, watery cervical mucus, myriad of channels in cervix for sperm movement, ciliary movement and mucus secretion in oviduct,
What is ovulation?
action of LH, progesterone, PGF2a and follicular proteolytic enzymes
How does ovulation occur?
LH via cAMP stimulates P and PGF2a production by theca cells, PGF2a induces contraction of smooth muscles within the theca, P induces matrix metalloproteinases (breakdown follicle wall
With the oocyte what occurs at ovulation?
germinal vessicale breakdown, complete first meiotic division, extrusion of first polar body, and enter metaphase II
What changes in the ovary during the luteal phase?
follicle transformed into corpus luteum secreting progesterone and inhibin; CYP17 synthesis and activity is mostly inhibited, some CYP19 activity persists in luteal cells mid-luteal,- allows androgen to estrogen conversion
What changes in the uterus, oviducts and vagina during the secretory phase?
progesterone induced shrinkage of endometrium; tortuous glands-> synthesis of glycogen, glycoproteins and glycolipids-> appearance of basal vacuoles; mid-luteal vacuoles move towards lumen, glands secrete mucus containing nutrients to support an embryo
What is the progestin challenge test?
used for diagnosing amenorrhea, in case of no estrogen there will be no primed endometrium to respond to progesterone, no breakthrough bleeding following withdrawal of progesterone; if breakthrough bleeding problem is progesterone
What is the function of the corpus luteum?
secretion of high levels of progesterone-(prepare endometrium for pregnancy), low amount of estradiol-(assist progesterone), secrete inhibin (prevent FSH and LH secretion to prevent new follicular development)
What is the process of menstruation?
withdrawal of CL 7-8 days after ovulation-> P fall-> vascular support withdrawn-> arteriole constriction->ischemia-> leukocyte infiltration-> production of PGF2a by uterine endometrium->vasoconstriction->leakage of vessels at juncture of basal and spongy zones->accumulation of blood btwn layers-> separation of top layers->liquefaction of clot by endometrium plasminogen activator, plasmin and metalloproteinases-> PGF2a induced contractions-> expulsion of blood
What are common causes for amenorrhea?
pregnancy, menopause, congenital anomalies (imperforate hymen), disorders of sexual development, endometrial destruction, gonadal dysgenesis/testicular feminization, premature ovarian failure, PCOS, Stress/athleatic endeavor/low body fat/severe systemic illness/kallman syndrome
What is the pathophysiological mechanism, diagnostic test, and intervention for pregnancy?
sustained P and E; serum B-hCG or history; prenatal care
What is the pathophysiological mechanism, diagnostic test, and intervention for menopause?
lack of E; clinical diagnosis; recommendation for osteoporosis prevention
What is the pathophysiological mechanism, diagnostic test, and intervention for congenital anomalies? On which level is the disorder?
structural issue; physical exam; surgical treatment; uterus and outflow track
What is the pathophysiological mechanism, diagnostic test, and intervention for disorders of sexual development? On which level is the disorder?
excessive androgen exposure; physical exam; surgical treatment; uterus and outflow track
What is the pathophysiological mechanism, diagnostic test, and intervention for endometrial destruction? On which level is the disorder?
recurrent infection, vigorous curettage; lack of response to E-P trial, direct visualization of endometrium; none; uterus and outflow track
What is the pathophysiological mechanism, diagnostic test, and intervention for gonadal dysgenesis/testicular feminization? On which level is the disorder?
deletion of genetic material from the X chromosome; kayotype; remove streak gonads if y chromosome present in view of high risk germ cell cancer; ovary
What is the pathophysiological mechanism, diagnostic test, and intervention for premature ovarian failure? On which level is the disorder?
lack of viable follicles, radiation damage, autoimmune disease; check gonadotropins; none; ovary
What is the pathophysiological mechanism, diagnostic test, and intervention for PCOS? On which level is the disorder?
altered intraovarian hormone relationships; clinical diagnosis in patients with chronic anovulation and higher androgen levels; decrease ovarian androgen secretion (wedge resection, OC) or increase FSH secretion; ovary
What is the pathophysiological mechanism, diagnostic test, and intervention for Stress/athleatic endeavor/low body fat/severe systemic illness/kallman syndrome? On which level is the disorder?
altered GnRH pulses; check serum TSH, prolactin, gonadotropins; replacement if deficient, search tumor if excessive; hypothalamus/pituitary
What causes primary dysmenorrhea?
ovulatory cycle; prostaglandin induced uterine smooth muscle contractions
What causes secondary dysmenorrhea?
pathological; can be endometriosis, PID, congenital defects in uterine development, uterine fibroid, or ovarian cyst
What is the management of endometriosis?
several months: GnRH agonist (Lupron) or GnRH antagonist (Cetrorelix)
What are the symptoms of PMS?
breast tenderness, mood swing depression, fatigue, abdominal bloating, and edema of the legs
What are the probable causes of PMS?
P increases turnover of serotonin in brain, plasma serotonin levels fall in late luteal phase-> irritability and behavioral alterations (social withdrawl); P metabolites (allopregnenolone and pregnenolone) potentiate GABA transmission inducing anxiety; GABA receptor anagonist provides 50% improvement
What causes abnormal uterine bleeding with ovulatory cycle?
pathological abnormalities of uterus (tumors)
What causes abnormal uterine bleeding with anovulatory cycle?
aka dysfunctional uterine bleeding, unpredictable onset, amount and duration; due to interruption of normal maturation of endometrium, luteal phase defect, perimenopausal defect in ovulation
What is PCOS? What are the symptoms?
chronic anovulation associated with infertility, hirsutism, obesity and amenorrhea
What effect does FSH have on PCOS?
LH is often 2-3x the level of FSH (10-20% are normal); low FSH poorly supports granulosa cell hyperplasia and function; abnormal LH:FSH ratio disrupts ovulation;
What effect does LH have on PCOS?
higher LH stimulate follicular fluid accumulation and thecal production of androstenedione and testosterone leading to hyperandrogenemia,
What effect does hyperinsulinemia have on PCOS
hyperinsulinemia (50-70%) exacerbates LH effect on theca cells and suppresses production of SHBG-> increasing free androgens-> insulin also causes premature arrest f follicular growth (anovulation), cystic follicles retain granulosa cells;
What effect does estradiol have on PCOS? Estrone?
Estradiol low to normal tonic production with out increase, estrone increase due to conversion from androstenedione in adipose, further stimulates LH and inhibits FSH, more androstenedione produced and aromatized and cycle continues
How is PCOS managed?
OC, androgen receptor antagonists (spironolactone), GnRH agonist (Lupron), or GnRH antagonist (Centritide)
What are the possible mechanisms of menopause?
premenopausal- very few follicles poorly respond to gonadotropins, ovulation infrequent, menses at variable intervals due to irregular E peaks and low progesterone- breakthrough bleeding, menses stops when ovary devoid of functional large or preantral or antral follicles and fibrous; androstenedione converted to estrone (E1 by liver and adipose-> major weak estrogen
What are the three major physical changes associated with menopause?
vasomotor instability, loss of bone density, and altered lipid metabolism
What happens to cause vasomotor instability of menopause?
altered central thermoregulatory mechanism and sympathetic tone in skin vasculature causes vasodilation, increased skin temp, and pulse rate, followed by perfuse sweating (Hot flash)-> hypothalamus resetting to low drop in E can affect thermoregulatory center which is nearby
What happens to cause loss of bone density in menopause?
increased osteoclast activity due to lacl of estradiol-> resorption of bone and loss of bone calcium and PO4->osteoporosis