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29 Cards in this Set
- Front
- Back
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How are steroids inactivated?
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conjugation to sulfate esters or glucuronic acids, mostly in the liver, oxidative, excreted in the urine
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What proteins transport estrogens?
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Sex hormone binding globulin (high affinity, low capacity, carries most) and albumin (low affinity, high capacity). 5 % is unbound. Decreased SHBG causes increased unbound circulating estrogens and androgens.
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How to steroids act on cells?
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Diffusion through the membrane
Bind the receptor in the cytoplasm/nucleus Induction of transcription, via dimerization and DNA binding |
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What are the systemic effects of estrogens?
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female: secondary sex characteristics, growth spurt, increased HDL, decreased LDL and TG and thyroxine, suppresses cellular immunity, increases coagulation factors, represses bone resorption, regulates menstrual cycle, makes cervical fluid less viscous.
males: stimulates prostatic stromal cell growth, essential for spermatogenesis. |
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What are the systemic progesterone effects?
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Decr HDL, increases LDL, regulates the menstrual cycle, increases uterine vascularity, maintains pregnancy, smooth muscle relaxant, increased basal insulin levels, increased insulin response, increased basal body temperature, decreased Na resorption.
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How are steroids used for oral contraceptives?
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synthetic (naturals are inactive orally). act on hypothalaus and pituitary to decrease GnRH realease.
progestin --> no LH, no ovulation, increased cervical mucus and decreased tubal motility. estrogen --> decreased FSH, no dominant follicle |
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What steroids are in oral contraception?
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an estrogen (ethinyl estradiol or mestranol) and a progestin (norethindrone, norethindrone acetate, ethynodiol diacetate, norgestrel levonorgesterl, desogestrel, drospirenone, norgestimate
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What's the difference between monophasic and biphasic and extended cycle OC?
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monophasic: same pill all month long.
bi/tri phasic: different pills with different amounts of progesterone for different weeks. extended cycle: withdrawal bleed every twelve weeks instead of every 3 weeks. |
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Why would you use progestin-only OC?
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norgestrel and norethindrone.
For breastfeeding women or those with contraindications to estrogen. Need consistent administration. |
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What's the metabolism for estrogen and progesterone?
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Estrogen: good absorption, 60% renally excreted in 24 hours, needs to be converted to ethinyl estradiol, then converted to estrone and estriol in the livier.
Progestins: more complex, many metabolites, metabolized in the liver. |
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What are absolute contraindications for OC?
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history of DVT/PE
vasular disease hyperlipidemia significant cardiac disease estrogen-dependent cancer pregnancy active liver disease/tumor unexplained uterine bleeding uncontrolled hypertension |
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What are "relative" contraindications for OC?
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well-controlled HTN, diabetes, seizures, smoking, factor V Leiden deficiency, gallbladder disease, breast feeding, prolonged immobilization, immediate post-partum period
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What are the side effects (minor and major) of OC?
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minor: weight gain, breakthrough bleeding, nausea, breast discomfort, changes in carb metabolism, mood changes
serious: throboembolism, CVA, MI, change in coagulation profile, HTN, headache, hepatic adenoma, gallbladder disease, changes in lipid profile |
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What are the benefits of OC?
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decrease in pregnancy, anemia, dysmenorrhea, endometrial carcinoma, ovarian neoplasia, rheumatoid arthritis, PID, benign breast disease
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What are some other ways to get hormonal contraception?
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NuvaRing: ethinyl estradiol and etonogestrel, ring inserted in the vagina.
OrthoEvra: ethinyl estradiol and norelgestromin, path. DepoProvera: progestin-only, IM every 12 weeks, inhibits ovulation, impairs sperm transport, produces endometrial atrophy. Implanon: implanted rod, gives progestin for 3 years |
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What is emergency contraception?
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Plan B, Preven. decrease the chance of pregnancy by 74 %. delay/inhibit ovulation, alter endometrium. Usually progesterone (Plan B is 1.5 mg of Levonorgestrol). Can also insert an IUD within 72 hours of unprotected intercourse.
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How do you perform a medical abortion?
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1. Mifepristone (progesterone-antagonist) then misoprostol (softens cervix, induces contractions): 96% efficacy at < 49d gestation.
2. Methotrexate (antimetabolite) and misoprostol: more toxic, better for ectopics. |
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What can be used to control menorrhagia or dysmenorrhea if OC can't be tolerated?
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GnRH analogues (eg leuprolide)--> feedback on pituitary to increase LH/FSH then decrease its secretion to menopausal levels --> amenorrhea.
AE: hot flashed, decreased bone density, urogenital atrophy. Usually used short-term. |
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What are the different types of estrogen receptors?
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alpha and beta. Work with coactivators.
alpha: more common in reproductive system, increases estrogen response. beta: bone brain, urinary system. dampens the response to estrogen. |
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What are the different types of progesterone receptors?
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alpha and beta, different transcription, promoter-specific.
alpha represses beta and estrogen signaling. uterus: PR opposes ER stimulation. breast: PR enhances ER stimulation. |
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What are the clinical applications for estrogen?
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hormone therapy for post-menopausal women.
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What are the clinical applications for progesterone?
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prophylaxis against endometrial hyperplasia/carcinoma in estrogen-treated women,
w/drawal bleed in women with amenorrhea, contraception, inhibit gonadotropin secretion in girls with precocious puberty/endometriosis |
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What are the FDA-approved indications for post-menopausal hormone therapy?
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mod/severe vasomotor symptoms
mod/severe vaginitis prevent post-menopausal osteoporosis |
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What are the guiding principles for ET/EPT use? (estrogen/estrogen+progestin therapy)
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Use at the lowest effective dose for as short a time as possible and individualize the risks, benefits and patient satisfaction
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What are contraindications to ET/EPT?
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hormone-sensitive cancer, unexplained uterine bleeding, active liver disease, history of DVT/PE
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What are SERMs?
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Selective ER modulators, eg site-specific anti-estrogens. Tamoxifen, Raloxifen and Fulvestrant are in the lecture.
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What's tamoxifen?
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nonsteroidal SERM for metastatic breast cancer.
Can also prevent breast cancer for high risk women, adjuvant tx for breast cancer, DCIS, protect from bone loss, decreases LDL. AE: hot flashes, vaginal bleeding, endometrial hyperplasia, polyps. CI: coumadin, hx of DVT/PE |
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What's raloxifen?
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SERM, tissue-specific estrogen antagonist/agonist. Like tamoxifen w/ a high binding affinity.
For post-menopausal osteoporosis prevention, decreases LDL, decreases breast cancer and uterine epithelium. CI: hx of DVT/PE no indication for premenopausal women, may increase hot flashes. |
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What's fulvestrant?
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estrogen-R antagonist, competitive -->downregulation of ER protein in breast cancer cells.
tx for ER/PR + metastatic breast cancer in post-menopausal women with disease progression after antiestrogen therapy |
