Estrogens and Progestins Flashcards
(50 cards)
Hormone domino for estrogen release
At puberty: hypothalamus GnRH –> anterior pituitary FSH/LH –> estrogen from ovaries
Pharm use of estrogens/progestins
for contraception - supression of HPO axis via negative feedback
Physiologic use of estrogens/progestins
Menopausal hormone therapy (MHT)
granular cells secrete
estradiol - allows endometrium to proliferate
leuteal cells secrete
progesterone - early, with estrogen, suppress LH/FSH. later at higher levels, has anti-estrogen effects to halt proliferation of endometrium
clinical use of synthetic GnRH
Test for delayed puberty
Replacement (pulsatile) therapy: male and female infertility or abnormal function of hypothalamus
Continuous administration: prostate cancer, endometriosis, idiopathic precocious puberty
Pulsatile GnRH agonist administration
Increases LH and FSH release from pituitary
Continuous GnRH agonist administration
blocks release of gonadotropins after 3-4 weeks (downregulation of receptors) after an initial rise of gonadotropin release
Continuous GnRH antagonist administration
reduces testosterone levels in one week without initial rise
SIde effects of GnRH
vasodilation, headache, multiple pregnancies, hypoestrogenic SSX. If using continuously, can have “flare symptoms” secondary to surge in testosterone. NO flare symptoms with antagonists
Exogenous FSH MOA
stimulates gametogenesis and follicular development in women and spermatogenesis in men
Exogenous LH MOA
stimulates testosterone production in testicular Leydig cells and (w/FSH) stimulates follicular developement in ovary
Gonadotropin clinical uses
hypogonadism with infertility. FSH used with LH sequentially in women and together in males
Side effects of exogenous gonadotropin use
ovarian enlargement, multiple births, spontaneous abortion, gynecomastia
Human Chorionic Gonadotropin (from urine of preggos) MOA
Stimulates corpus luteum to produce and maintain placenta.
Stmulates Leydig cells to produce testosterone
hCG uses
action similar to LH, some FSH action. For infertility in M and F
hCG Side Effects
H/A, depression, edema, gynecomastia, Ab production
Estrogen MOA
diffuse through PM, enter nucleus and bind estrogen receptor (ERa, ERb) to ultimately initiate gene transcription
Estrogen antagonist MOA
Will enter cells and bind ER, but reduce transcription of genes.
Estrogen Physiologic Effect
Maintain CT structure, alter liver metabolism, enhance blood coagulability, alter plasma lipid composition (cardioprotective)
Estrogen menopausal hormonal therapy - symptomatic TX
Treats the vasomotor symptoms and vulvovaginal/urogenital complaints. Use for a short period of time at lowest possible dose
Non-hormonal therapy for hot flashes is an alternative for women with E+ breast cancer or history of blood clots
:)
Estrogen menopausal hormonal therapy - Prevention of osteoporosis
ONLY for patients at significant risk of osteoporosis. Worry for breast cancer risk, MI, blood clots.
Selective estrogen receptor modulators (SERMs) have less risks
Raloxifene (Evista) SERM
Estrogen like activity on bone (increase mineral density) and liver (decrease LDL and total cholesterol)
Lack agonist activity (growth) in breast and uterine tissue.
Retain risk of clots d/t increase in hepatic clotting factor synthesis