Menstruation/Menopause

Question 1

What hormonal changes occur in the follicular phase?

Answer 1

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

Question 2

What are the hormonal changes in the luteal phase?

Answer 2

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

Question 3

What changes occur in the uterus, oviducts and vagina during the follicular phase?

Answer 3

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,

Question 4

What is ovulation?

Answer 4

action of LH, progesterone, PGF2a and follicular proteolytic enzymes

Question 5

How does ovulation occur?

Answer 5

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

Question 6

With the oocyte what occurs at ovulation?

Answer 6

germinal vessicale breakdown, complete first meiotic division, extrusion of first polar body, and enter metaphase II

Question 7

What changes in the ovary during the luteal phase?

Answer 7

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

Question 8

What changes in the uterus, oviducts and vagina during the secretory phase?

Answer 8

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

Question 9

What is the progestin challenge test?

Answer 9

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

Question 10

What is the function of the corpus luteum?

Answer 10

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)

Question 11

What is the process of menstruation?

Answer 11

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

Question 12

What are common causes for amenorrhea?

Answer 12

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

Question 13

What is the pathophysiological mechanism, diagnostic test, and intervention for pregnancy?

Answer 13

sustained P and E; serum B-hCG or history; prenatal care

Question 14

What is the pathophysiological mechanism, diagnostic test, and intervention for menopause?

Answer 14

lack of E; clinical diagnosis; recommendation for osteoporosis prevention

Question 15

What is the pathophysiological mechanism, diagnostic test, and intervention for congenital anomalies? On which level is the disorder?

Answer 15

structural issue; physical exam; surgical treatment; uterus and outflow track

Question 16

What is the pathophysiological mechanism, diagnostic test, and intervention for disorders of sexual development? On which level is the disorder?

Answer 16

excessive androgen exposure; physical exam; surgical treatment; uterus and outflow track

Question 17

What is the pathophysiological mechanism, diagnostic test, and intervention for endometrial destruction? On which level is the disorder?

Answer 17

recurrent infection, vigorous curettage; lack of response to E-P trial, direct visualization of endometrium; none; uterus and outflow track

Question 18

What is the pathophysiological mechanism, diagnostic test, and intervention for gonadal dysgenesis/testicular feminization? On which level is the disorder?

Answer 18

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

Question 19

What is the pathophysiological mechanism, diagnostic test, and intervention for premature ovarian failure? On which level is the disorder?

Answer 19

lack of viable follicles, radiation damage, autoimmune disease; check gonadotropins; none; ovary

Question 20

What is the pathophysiological mechanism, diagnostic test, and intervention for PCOS? On which level is the disorder?

Answer 20

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

Question 21

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?

Answer 21

altered GnRH pulses; check serum TSH, prolactin, gonadotropins; replacement if deficient, search tumor if excessive; hypothalamus/pituitary

Question 22

What causes primary dysmenorrhea?

Answer 22

ovulatory cycle; prostaglandin induced uterine smooth muscle contractions

Question 23

What causes secondary dysmenorrhea?

Answer 23

pathological; can be endometriosis, PID, congenital defects in uterine development, uterine fibroid, or ovarian cyst

Question 24

What is the management of endometriosis?

Answer 24

several months: GnRH agonist (Lupron) or GnRH antagonist (Cetrorelix)

Question 25

What are the symptoms of PMS?

Answer 25

breast tenderness, mood swing depression, fatigue, abdominal bloating, and edema of the legs

Question 26

What are the probable causes of PMS?

Answer 26

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

Question 27

What causes abnormal uterine bleeding with ovulatory cycle?

Answer 27

pathological abnormalities of uterus (tumors)

Question 28

What causes abnormal uterine bleeding with anovulatory cycle?

Answer 28

aka dysfunctional uterine bleeding, unpredictable onset, amount and duration; due to interruption of normal maturation of endometrium, luteal phase defect, perimenopausal defect in ovulation

Question 29

What is PCOS? What are the symptoms?

Answer 29

chronic anovulation associated with infertility, hirsutism, obesity and amenorrhea

Question 30

What effect does FSH have on PCOS?

Answer 30

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;

Question 31

What effect does LH have on PCOS?

Answer 31

higher LH stimulate follicular fluid accumulation and thecal production of androstenedione and testosterone leading to hyperandrogenemia,

Question 32

What effect does hyperinsulinemia have on PCOS

Answer 32

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;

Question 33

What effect does estradiol have on PCOS? Estrone?

Answer 33

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

Question 34

How is PCOS managed?

Answer 34

OC, androgen receptor antagonists (spironolactone), GnRH agonist (Lupron), or GnRH antagonist (Centritide)

Question 35

What are the possible mechanisms of menopause?

Answer 35

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

Question 36

What are the three major physical changes associated with menopause?

Answer 36

vasomotor instability, loss of bone density, and altered lipid metabolism

Question 37

What happens to cause vasomotor instability of menopause?

Answer 37

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

Question 38

What happens to cause loss of bone density in menopause?

Answer 38

increased osteoclast activity due to lacl of estradiol-> resorption of bone and loss of bone calcium and PO4->osteoporosis

Question 39

What happens to cause altered lipid metabolism with menopause?

Answer 39

increase plasma LDL-> cholesterol deposition in the vasculature-> increased risk of atherosclerotic disease; increased androgens induce hair growth on upper lip and chin and cause thinning of scalp hair