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55 Cards in this Set

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what does estrogen do bone growth?
at puberty, it is responsible for linear bone growth and later for closure of the epiphyses
describe the effects of cervical mucus with estrogen vs. progesterone.
estrogen causes a thinning of cervical mucus; progesterone causes a thick cervical mucus
what are estrogen's effects of the liver's production?
estrogen decreases total serum proteins, but stimulates hepatic production of sex hormone-binding globulin (SHBG), thyroid-binding globulin, blood-clotting factors (VII - X), plasminogen and HDL; estrogen DECREASES or inhibits antithrombin III, protein C, protein S, and LDL formation
what is the greatest risk factor for breast CA?
lifetime exposure to estrogens
estrogen also increases the retention of ________ and _________, possibly causing _____________.
Na+, H2O, edema
continuous exposure of unopposed estrogen may result in:
endometrial hyperplasia, episodes of breakthrough bleeding, and increased risk of endometrial CA
what is the difference in progestin and progesterone?
progestin include all synthetic progesterones (progesterone is what the body makes and progestin is what the pharm company makes)
what is necessary for progesterone receptor expression in almost all progesterone-responsive tissues?
what is progesterone's job on the endometrium?
progesterone slows the mitotic activity of the estrogen-stimulated uterus; it causes vascularization and induces a more glandular appearance and function of the endometrium. it is responsible for preparing the uterus for implantation of a blastocyst and maintaining the pregnancy; Progesterone also inhibits uterine contraction
what causes an increase in basal body temperature in the luteal phase and is important in mammary gland development?
progesterone increases the elimination of ________ and _________ by competing with aldosterone for binding to the mineralocorticoid receptors.
Na+ and H2O
estrogens and progesterones are produces in various tissues. what is the predominant source for nonpregnant, premenopausal women?
in the production of steroid hormones from cholesterol, what is the rate limiting step?
P450 Side chain Cleavage Enzyme (SCC)
Describe the steps of steroid synthesis from cholesterol to progesterone to 17B-estradiol.
cholesterol (scc) -> pregnenolone -> progesterone (21Carbons) -> 17a-hydroxyprogesterone -> androstenedione (androgens have 19 carbons) (aromatase) -> estradiol (18 carbons)
Describe the steps of steroid synthesis from cholesterol to 17- Hydroxypregnenolone to estradiol.
cholesterol (SCC) -> pregnenolone -> 17-hydroxypregnenolone -> DHEA (dehydroepiandrosterone) -> androstenedione -> testosterone (aromatase) -> estradiol
describe how the female fetus gets it's estrogen.
hCG stimulates essential DHEA-sulfate in the fetal adrenal gland -> the DHEA-s goes to the placenta and converts to DHEA by sulfatase -> then aromatase converts DHEA to estradiol and estrone; if the DHEA-S goes to the fetal liver instead of straight into the placenta it will get converted to 16a-OH-DHEA-S (then converted to 16-OH-DHEA by a sulfatase in the placenta); from the placenta it gets converted to the estrogen of pregnancy, estriol. (THE MORAL OF THE STORY: progesterone is synthesized in the placenta, but direct conversion from cholesterol to estrogen does not occur)
explain the relationship and pathway of GnRH and LH/FSH starting with the hypothalamus.
GnRH is released from the arcuate nucleus of the hypothalamus -> it travels down the pituitary portal vasculature to the gonadotrope cells of the anterior pituitary; -> the AP releases LH and FSH that travels through the body to stimulate (LH-estrogen/progesterone and FSH - follicle formation); it is released in a pulsatile fashion and is under negative feedback.
what will inhibit GnRH release? what will stimulate release?
too much LH and FSH; opioids, dopamine, and GABA: not enough LH or FSH; NorEp
what are estrogen and progesterone bound to?
estrogen is bound by SHGB (sex hormone-binding globulin) and progesterone is bound by CBG (corticosteroid-binding globulin); estrogen causes an increase of production of SHBG and CBG
since estrogen is hydrophobic (lipophilic) it will bind to intracellular receptors. what are the two types of receptors and where are they located?
estrogens bind to intraNUCLEAR receptors. ERalpha is the "classic" receptor, LOCATION: repro tract, breast, mediates sexual development and repro fxn. ERbeta is highly expressed in the ovary and brain; THEY DIFFER in location and in their affinities for certain ligands
describe progesterone receptors.
they are in the nuclear receptor super family - Steroid Receptor Family; INTRANUCLEAR, only 1 gene encodes the progesterone receptor, but 2 protein isoforms are produced, progesterone receptor A and PR-B (have to have estrogen to express progesterone receptors) high concentration of progestrone decrease estrogen receptors, which will decrease progesterone receptor concentrations
in combo oral contraception name the usual estrogen components.
ethinyl estradiol or mestranol (synthetic that is metabolized to ethinyl estradiol)
in combo oral contraception, name the usual progestins.
norethindrone, norgestrel, levonorgestrel, norethindrone acetate, ethynodiol diacetate, or desogestrel or synthetic drospirenone
what is meant by monophasic, biphasic, and triphasic?
monophasic means the same levels of hormone throughout the pill pack; biphasic means there are two levels of progestins that will vary during the pill pack; triphasic- there are 3 different amounts of progestins in the pack
how do combo oral contraceptives prevent pregnancy?
they inhibit ovulation by suppressing gonadotropin synthesis and release; they lower FSH so there is decreased ovarian fxn and minimal follicular development; the endometrium is not in an appropriate state for implantation
how many missed doses will increase the risk of pregnancy?
miss 2 or more doses during a cycle increases risk substantially
how are OCP metabolized?
90% in the liver by cytochrome P450. drugs that induce CYP3A4 will decrease the amount of contraception and increase risk for pregnancy
Name some common drugs that utilize the CYP3A4 system that may decrease the efficacy of OCP.
barbs, carbamazepines (teratogen), cortiocosteroids, phenytoin (teratogen), St.Johns Wort
Name some pros to taking OCP.
controls fertility, decreases the risk for ovarian and endometrial CAs, decrease risk of fibroadenomatosis and fibrocystic breast dz, decrease risk for PID, reduce acne, reduce dysmenorrhea and ovarian cyct fxn, decrease menorrhagia
name the cons of taking OCP.
possibility of thromboembolism, DVT, stroke (esp in smokers, older women, and clotting defects); may have breast earlier than would if already going to get it anyway; possible breakthrough bleeding, nausea, breast tenderness, headache, skin pigmentation, depression,(older preps with more androgenic progestins may cause weight gain, acne and hirsutism)
name some other non-oral combination contraception.
PATCH - ethinyl estradiol and L-norgestrel (3wkson/1off); VAGINAL RING - ethinyl estradiol and desogestrel inserted and stays in for 3wks; INJECTION - estradiol cypionate and medroxyprogesterone acetate (monthly)
what are the progestin-only contraceptions' cons?
have slightly higher failure rates as well as much higher incidience of menstrual disturbances ranging from frequent, heavy, irregular bleeding to amenorrhea, often leading to discontinuing meds
Name some progestin only delivery methods.
ORAL - contains norethindrone or norgestrel (failure rate 1-3/100); SUBDERMAL silastic CAPSULES of levonorgestrel- surgically inserted and removed, goes subderm, lasts 5yrs, cons: irregular uterine bleeding; DEPOT IM INJECTION - medroxyprogesterone shot every 3 months; PROGESTIN ONLY IUD - local progestin, causes endometrial atrophy and decreases bleeding (may bleed all the time)
how do progestin only OC prevent pregnancy?
supress FSH, LH, and ovulation to variable degrees; create a thick cervical mucus that prevents sperm passage; endometrial atrophy prevents implantation;
what makes up emergency contraception?
prevent pregnancy if administered within 72 hours after unprotected intercourse. contain large doses of estrogen alone, a progestin (L-norgestrel) alone or estrogens in combo with progestins. (inhibit ovulation and implantation by making endometrium nonreceptive to blastocyst)
name the term used for the oral contraception that is used to prevent pregnancy for up to 49 days after the last menstrual period.
CONTRAGESTATION: RU-486 or mifepristone is an oral active steroid antagonist of progesterone and glucocorticoids that is used to abort an embryo; the endometrium sheds and prostaglandins are released within 2-4 days that cause the uterus to contract (like cramps); this causes an attached fetus to detach. (effectiveness declines after 5 weeks of pregnancy b/c placenta produces enough progesterone to overcome the antagonist)
what represents 20-30% of infertility cases?
what agents are used to treat infertility/anovulation?
gonadotropins, GnRH, and Clomiphene
what are SERMs and name some.
SERMS are Selective Estrogen Receptor Modulators (serms have agonist activity in one tissue and antagonist activity in another) clomiphene is a partial agonist at estrogen receptors in the pituitary and increases the release of LH and FSH to stimulate ovulation.; EXTRA: other SERMS: tamoxifen (breast CA); raloxifene (osteoporosis); toremifene (metastatic breast CA)
Name some stages/disorders that may need hormone replacement therapy (HRT).
Menopause; Ovarian failure (primary and premature); Dysfunctional Uterine Bleeding; Luteal Phase Deficiency
Name symptoms of menopause.
hot flashes, night sweats, vaginal dryness, sleep disturbances, mood and anxiety disturbances, concentration difficulties and forgetfulness, decreased libido and sexual dysfunction, urinary incontinence and urgency, headache
what is the relationship b/w HRT and osteoporosis?
HRT protects against development of osteoporosis and hip and vertebral fractures (other agents are equally effective)
Name some HRT risks and contraindications.
may be: small increase in Breast CA (debated); as long as there is PROGESTIN in the HT regimen, the increased risk for endometrial CA is eliminated; risk for DVT
__________ estrogens have less problems with clotting.
why are progestins combined with estrogens in OCP?
progestins are combined with estrogens in oral pills to prevent endometrial hyperplasia and to minimize the risk of endometrial CA
When is it okay/usual to give progestin only contraceptives?
progestins are not necessary in women who have had a hysterectomy; some women (hereditary clotting) should be on added estrogen; if the prep is intravaginal estrogens, the systemic absorption is insufficient to cause endometrial hyperplasia
why is it important for estrogen therapy to be given continuously instead of cyclic?
oral estrogen (if given cyclically) may cause increased hot flashes or migranines when the estrogen is withheld. progestins don't have that effect and may be given cyclically
Name the 1st SERM that is used in breast CA therapy.
tamoxifen (1st generation SERM)
How does this 1st SERM work?
this nonsteroidal selective estrogen receptor modulator (tamoxifen) acts as a competitive inhibitor of estradiol in breast tissue and an agonist on endometrial tissue (thus: treats breast CA, but increases the risk of endometrial cancer)
name the 2nd generation SERM that is used to prevent osteoporosis in postmenopausal women that have a high risk for getting breast CA.
raloxifene - estrogen agonist on teh bone and has antagonist effects on breast tissue (no effects on endometrium)
name the breast CA treatmetn that is a PURE estrogen receptor antagonist that is used in pts that have become resistant to tamoxifen.
name the nonsteroidal inhibitor of aromatase. what is aromatase's purpose?
anastrozole (and related compounds) block aromatase; aromatase blocks the converstion of androgens to estrogens
name the weak partial agonist that binds to progesterone, androgens, and glucocorticoid receptors and is used to treat endometriosis and fibrocystic dz of the breast.
danazol (inhibits several P450 enzymes)
name the nonsteriodal compound with estrogen agonist activity that is no longer used b/c it caused _______________.
DES - diethylstilbestrol caused infertility, ectopic pregnancy, and most importantly vaginal adenocarcinoma in the daughters of women who were treated with large doses during pregnancy
name two GnRH analogs that were used both to stimulate and to inhibit ovarian function. how is it possible to do both?
nafarelin and buserelin; if released in pulsatile fashion, would stimulate the release of FSH and LH; if given in a continuous manner would negatively feedback and inhibit ovarian funciton