Hormones Pharm part I, Linger Flashcards
What are the estrogens we have for drugs
conjugated E- premarin
estradiol valerate
ethinyl estradiol
mestranol
what are the progestin drgus
desogestrel(inactive etonogestrel(active)
drospinenone
medroxyprogresterone, norethindrone, norgestimate
norgestrel (L-norgestrel, levonorgestrel)
what are the E and P inhibitors
Mifepristone
what are the selective E R modulators
raloxifene
tamoxifen
toremifene
what are the selective E R downregulators
clomiphene
fulvestrant
what are the aromatase inhibitors
anastrazole
exemestane
letrozole
how do synthetic E work
bind to the SHBG and lower affinity to albumin so there is more unfound E around
why are vaginal and transdermal modes for effective for giving E
because avoid the first pass metabolism of the liver
MOA E
binds ER and activates gene transcription
how do E Receptros work
homodimerize and bind promoter regions or bind to other transcription factors which bind to the promoter regions
endometrial effects of E
bleeding and shedding
continuous exposure will lead to hyperplasia of the endometrium leading to abnormal bleeding patterns
metabolic effects of E
decrease rate of bone resoprtion because promotes apoptosis of osteoclasts
stimulate adipose tissude production of letpin
stimulates increase production of the cortisol globulin, thyroxine binding globulin, sex hormone binding protein
increase HDL and TG, reduce LDL
vascular effects of E
enhance coagulability of blood
increases factors II CII IX and X, decrease antithrombin III
icnrease plasminogen
When do we use E for Tx
primary hypogonadism
postmenopausal hormone replacement
suppress ovulation in patients with intractable dysmenorrhea or suppress ovarian function in cases of hirsutism and excessive ovary androgen secretion
E and P replacement decreases risk of what
osteoporotic fractures of hip vertebrae, and wrist
adverse effects estrogens
uterine bleeding, breast and endometrial cancer
nausea, breast tenderness, hyperpigmentation, increased migraine frequency, cholestasis, gallbladder disease and HTN
how is endometrial hyperplasia from administration of E prevented
give progestin too
does adding P to E Tx prevent breast cancer
not, may actually increase risk of breast cancer
Contraindications to E
patients with E dependent neoplasms (endometrial carcinoma and breast cancer)
patients with unDx genital bleeding, liver disease, history of thromboembolic disorder and heavy smokers
what sideeffects are decreased in transdermal preparations of e
does not increase renin levels, corticosteroid binding substrate and thyroxine binding substrate
Where is P naturally made
in ovary (corpus luteum), testis and adrenal Cx
how are pharmacokinetics of P different than E
rapid regardless of PO or IM
MOA progesterone
activates gene transcription via nuclear R
isoforms of Progesterone R
A and B
physiologic effects of progesterone
- dec frequency of GnRH pulses
- onset menstruation with its abrupt decline
- maintains pregnancy and mammary gland development
- stimulates lipoprotein lipase and favors fat deposition
- increases basal insulin levels and insulin response to glucose
- promotes glycogen storage and ketogenesis
- can compete for mineralocorticoid R (dec in Na reabsorption)
clincal uses of progestins
HRT and hormone contraception
long term ovarian suppression
how are progestins used for Dx testing
can be used to test E secretion
causes bleeding after 5-7 days progesterone if endometrium has been stimulated by E
dosage and drug used for long term ovarian suppression
150mg medroxyprogesterone acetate IM every 90 days
adverse effects of progestins
breakthrough bleeding
increase BP
reduce HDL in women
2 types of oral contraception preparations
combinations E and P or just P without E
what is monophaseic? bi? tri?
mono is constant dose of both E and P in pills
biphasic changes once
triphasic changes twice
what hormones are in the transdermal preparation of contraception
ethinyl estradiol and norelgestromin
adverse effects with ransdermal patch
breast discomfort, dysmenorrhea, nausea, vomiting and skin irritation
What drugs are in the NuvaRing
ethinyl estradiol and etonogestrel
adverse effects for injectable preparations for contraceptin
unpredictable spotting or bleeding
return of fertility can take 18 mo after last injection
increased risk atherosclerosis
What drug is in IUD and how long is it effective
levonorgestrel
effective for 5 years
with IUD at increased risk for
ovarian cyst
what drug is in the implantable contraceptions
eronogestrel
good for 3 years
bleeding abnormalities are common
what drugs are in the day after pills
E alone
P alone
E and P
P R modulators
adverse effects of day after pills
nausea, vomiting, HA, dizziness, breast tenderness, abdominal and leg cramps
what is in plan B
levonorgestrel
how does plan B work
not sure
cannot reverse pregnancy that has already occurred (post implantation)
What is Ella and how does it work
Ulipristal acetate, partial agonist at P R, inhibits ovulation when taken up to 5 days after intercourse, may block implantation
adverse effects Ella
HA and abdominal pain
main MOA E and P contraceptive pills
selective inhibition of pituitary function (negative feedback)
change cervical mucus, uterine endometrium and motility of uterine tubes
effects of E and P on ovary
depress ovarian function
effects oe E and P on uterus
prolonged use may cause hypertrophy of cervix and polyp formationl
glandular atropy and decreased bleeding are common depending on preparation
E and P contraception effects on breast
stimulate enlargement and suppress lactation
other effects of E and P contraception
mood changes
increased urinary exretion of free cortisol, increased renin, increased aldosterone
increased coagulability of blood
increase certain lipids
