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Pharm II > Female Reproductive Meds > Flashcards

Female Reproductive Meds Flashcards

1
Q

hormones of the reproductive system? where do they come from and what does this mean for them?

A

estrogens, progesterones, androgens

steroid based, thus able to pass through cell membranes and enter the cell nucleus

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2
Q

when are exogenous hormones used?

A

as HRT, for contraception and to prevent and tx osteoporosis

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3
Q

an activated steroid-receptor complex causes what downstream effects?

A

interacts w/nuclear chromatin to initiate hormone-specific RNA synthesis which results in the synthesis of specific proteins that mediate a variety of physiologic fxns

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4
Q

sex hormone are necessary for what?

A

conception, embryonic maturation, growth and development of primary and secondary sexual characteristics

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5
Q

oral absorption of sex hormones?

A

generally good b/c of their high fat solubility

also well absorbed through skin and mucous membranes

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6
Q

what is the most potent form of endogenous E in women? other major estrogen forms?

A

estradiol is the most potent

other forms include estrone, estriol (each have ~1/10 the potency of estradiol)

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7
Q

bio-availability of oral intake of naturally occurring estrogens?

A

low b/c they are subject to first-pass clearance by the liver

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8
Q

first-pass of synthesized estrogens vs naturally occurring estrogen?

A

synthesized Es are subject to less first pass hepatic metabolism

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9
Q

how is E transported in the body?

A

transported bound in the blood to albumin and sex binding hormone and broken down in the liver to inactive products that are then excreted in the urine

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10
Q

what can you expect to see in pts whom have liver damage?

A

serum E levels may be increased dt reduced metabolism which can lead to feminization in males and ssxs of excess E in women

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11
Q

when has HRT primarily been used?

A

in postmenopausal women to help mitigate ssxs of menopause and osteoporosis, atrophy of tissues or urogenital tract such as the vulva, vagina, urethra, can also help improve sleep

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12
Q

exogenous E replacement has been shown to increase the risk of what?

A

stroke, blood clots, ovarian CA, endometrial CA, breast CA

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13
Q

what is medroxyprogesterone acetate? how long is it effective? risks when combined with conjugated equine estrogens? risks for post-menopausal women?

A

form of injected birth control known as depo-provera
can reduce fertility for as long as 10 mos, taking longer for overweight or obese women
when combined with conjugated equine estrogens, has been assoc w/risk of breast CA, dementia, thrombus in the eye
in combo with Es in general, MPA increases the risk of CVD, stronger association when used by post-menopausal women also taking CEE

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14
Q

not recommended to use MPA when?

A

prior to menarche or before or during recovery from surgery

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15
Q

WHI-E+P trial arm found what? recommendations of who to use in vs who to not use in?

A

found that women taking E + P had increased risk of MI, stroke, DVT, PE, breast CA
BUT decreased risk of colorectal CA, fewer fractures
based on these studies, CEE and MPA are no longer given to women in order to try to prevent CVD in older women, but can be used in postmenopausal women seeking relief from ssxs assoc w/menopause

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16
Q

which hormone helps with sleep? which hinders sleep?

A

E helps

P hinders

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17
Q

what is BiEst?

A

combo of 2 Es: estriol and estradiol, 80:20 estriol: estradiol

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18
Q

what is TriEst?

A

combo of 3 Es: estriol, estradiol, estrone, 80:10:10 estriol: estradiol: estrone

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19
Q

which is more popular, BiEst or TriEst for pt use?

A

BiEst b/c lacks estrone

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20
Q

first pass effect on conjugated Es?

A

undergo less first pass hepatic metabolism

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21
Q

indications of conjugated E/premarin?

A

prevention and tx of osteoporosis and post-menopausal ssxs: hot flashes, vaginal dryness, itching

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22
Q

MOA of conjugated E/premarin? how to give? SEs?

A

MOA: alters gene transcription
give orally or as a topical cream; P should be added to E HRT in any woman who has not undergone a hysterectomy
SEs: vaginal bleeding, breast tenderness, increased risk of DVT, increased risk of atherosclerosis, CAD, increased risk for uterine and breast CA

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23
Q

rule of thumb for giving HRT to a women w/a uterus?

A

have to give E+P b/c if give just E will cause endometrial hyperplasia which can lead to CA

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24
Q

2 MC uses of progestins?

A

hormonal contraception (either alone or w/E) and to prevent endometrial hyperplasia from unopposed E in HRT

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25
Q

two families of progestins?

A

estrane and gonane

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26
Q

estrane family consists of what drugs?

A

norethindrone and other progestins that metabolize to norethindrone

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27
Q

further subdivision of gonane family?

A

2nd gen progestins which have varying degrees of androgenic and estrogenic activities; levonorgestrel and norgestrel
newer/3rd gen progestins which have the least androgenic effects, desogestrel and norgestimate

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28
Q

4th gen progestin? derived from what?

A

drospirenone

derived from 17a-spirolactone

29
Q

progestins can be used to tx what?

A

secondary amenorrhea, dysfxnal uterine bleeding, endometriosis, palliative tx of endometrial CA, renal cell carcinoma, breast CA, prostate CA

30
Q

describe the monophasic method

A

E+P are administered for 20-21 d and stopped for 7-8 d period that includes the 5 d menstrual period
st a 28 d regiment w/6-7 inert tablets is used

31
Q

describe bi or triphasic methods?

A

instead of mixing E+P the whole time, start with E, then move to P

32
Q

class of medroxyprogesteron/provera? indications? MOA? how to give? why is progestin added?

A

class: synthetic variant of progesterone
indications: contraceptive, HRT, dysfxnal uterine bleeding, tx endometriosis, replacement therapy for male-to-female transsexuals as well as to control inappropriate sexual behavior to chemically castrate convicted sexual offenders
MOA: alters gene transcription
can give PO or IM, progestin component of HRT is added to prevent the development of endometrial hyperplasia and endometrial CA

33
Q

SEs of medroxyprogesteron/provera? C/I when?

A

increases ratio of LDL:HDL (lowers HDL), increases risk for DVT, breast tenderness, increased facial hair, decreased scalp hair, difficulty falling asleep and staying asleep, stomach pain, dysuria, anxiety, H/A, N/V, cervicitis, may reduce bone density
C/I w/PMHx of DVT, breast, ovarian or uterine CA

34
Q

medroxyprogesterone/provera can be used at high dose to tx what? SEs of high dosing?

A

can be used at high doses to tx breast CA but can cause wt gain, worsen DM and edema with high dosing
high dosing can also decrease HPA signaling

35
Q

when MPA is used to tx BPH, SEs?

A

reduced libido, impotence, reduced ejaculate volume, chemical castration w/in 3 days

36
Q

current preparations of contraceptive pills contain what concentrations of ethinyl estradiol?

A

definitely less than 50 micrograms, most have 30-35, newer ones contain 20-25

37
Q

Es effect on fertility? Ps effect on fertility?

A

E suppresses ovulation while P prevents implantation and helps make cervical muscus impenetrable to sperm

38
Q

possible link between depression and OCP use?

A

with high levels of E as in first gen OCPs, and P, as in some progestin-only contraceptive, there can be a lowering of serotonin levels in the brain b/c the E+P cause an increase in concentration of the enzyme which breaks down serotonin

39
Q

if a woman already has depression, what kind of OCP is best?
if a woman experiences depression on OCPs, what kind of OCP is best?

A

combo E+P b/c if they already have depression, a progestin-only contraceptive will increase depression sxs
if a woman experiences depression on OCPs, first try a progestin-only contraceptive method

40
Q

potential benefits of taking OCPs? SEs, esp for women over 35 and smoke?

A

potential benefits: reduced risk of colorectal CA, may improve PID, dysmenorrhea, premenstrual syndrome and acne, reduce sxs of endometriosis, PCOS, decreased anemia
SE: CVD, DVT, HTN, stroke (esp if over 35 and smoke), acne, depression, H/A, edema, N, breast fullness

41
Q

COCPs are C/I in what populations? relation to COCPs and breast CA?

A

C/I in those w/PMHx of CVD, familial tendency to form blood clots, severe obesity and/or hypercholesterolemia and in smokers over 35 yo
COCPs and breast CA: while taking and 10 yrs after stopping taking, increased relative risk of breast CA; no significant excess risk after 10 or more years after stopping taking

42
Q

what drugs can reduce the efficacy of OCPs?

A

antibiotics such as penicillin, amoxil, tetracycline, cephalosporins, sulfa drugs, seizure drugs and St. John’s Wort

43
Q

protective effects of OCPs?

A

use of OCPs for five or more years decreases risk of ovarian CA in later life by 50%
COCPs reduced risk of endometrial CA by 50%
80% risk reduction of both ovarian and endometrial CA when used for more than 10 yrs

44
Q

effects of drospirenone? drospirenone use C/Is?

A

anti-mineralcorticoid, counteracts E-stimulated activity of RAS system, not androgenic
anti-mineralcorticoid effects reduce water retention and bloating
C/I in those w/hepatic failure, renal insufficiency, adrenal insufficiency

45
Q

first and only hormonal contraceptive that has been shown to be effective for tx of premenstrual dysphoric d/o?

A

yaz (drospirenone)

46
Q

MOA of depo-provera and other high dose forms of progestin? protective effects?

A

inhibit follicular development and prevent ovulation
protective effects: decrease GnRH release by hypothalamus which decreases release of FSH and LH which can help to decrease risk of endometrial CA

47
Q

SEs of MPA/depo-provera? how long does it take, after the last injection, to regain fertility?

A

menstrual irregularities, abd discomfort, wt changes, H/A, hair loss, fatigue, depression, nervousness
average return to fertility is 9-10 mos after last injection

48
Q

advantages of depo-provera?

A

high effective birth control
dosed only 4 times a year
No E = no increased risk of DVT, PE, stroke or MI
minimal drug interactions
decreased risk of endometrial CA
decreased risk of iron deficiency anemia, PID, ectopic PG, uterine fibroids
decreased sxs of endometriosis
decreased incidence of seizures in those w/epilepsy
decreased incidence and severity of sickle cell crises

49
Q

disadvantages of depo-provera?

A

takes one week after given to provide effective contraception
offers no protection against STDs
can affect menstrual bleeding (irregularities)
delays return of fertility (9-10 mos)
slight increased risk of breast CA
can cause birth defects if become PG while receiving shots
increases bone loss (why can’t be on for more than 2 yrs)

50
Q

implantable contraceptive?

A

implanon - can be left in for 3 yrs, in office procedure done w/or w/o local anesthesia

51
Q

transdermal patch? different layers? how to use? where can you apply the patch?

A

ortho evra
3 layers
middle contains norelgestromin and ehtinyl estradiol
inner layer is an adhesive
outer layer is protective cover
first patch should be applied w/in first 5 days of menstrual cycle and new patch should be applied every week for 3 wks followed by 1 patch-free week
can apply patch to abd, outer arm, buttocks, torso (not over the breasts) - rotate spots to reduce skin irritation

52
Q

if patch-free interval exceeds 2 days (when not in patch-free week) what do you need to do?

A

need to do a PG test, if (=) then re-apply and use back up contraceptive for next seven days

53
Q

C/I to using the patch? major SE of ortho evra patch?

A

women weighing more than 198 lbs as its effectiveness is reduced
b/c the patch has higher levels of E, there is 2x the risk of blood clots

54
Q

hormones in nuvaring? how to use? if falls out or is expelled? MC reported adverse effects?

A

contains low dose E+P
leave in for 3 wks, then remove for 1 wk
effectiveness is reduced if out for more than 3 hours, use back up method if this occurs until ring has been in place for seven days
adverse effects: vaginitis, H/A, leucorrhea, nausea, wt gain

55
Q

4 different types of IUDs?

A

ParaGard - contains copper
Skyla + Kiara - low dose hormones
Mirena - higher dose hormones
hormone containing ones contain a mix of progestin, levonorgestrel

56
Q

potential MOAs of cooper IUD? can leave in for how long?

A

copper in paragard is thought to immobilize sperm
additionally thought that it causes ongoing inflammation of the uterine lining which serve to reduce the likelihood that a fertilized ovum can attach to uterine wall
approved for 10 years of use

57
Q

MOA of hormone containing IUDs?

A

progestin, levonorgestrel diminishes frequency of ovulation and changes consistency of cervical mucus and makes it less likely for implantation to occur

58
Q

mg of levonorgestrel in mirena? release rate per day? how long can you use Mirena for? three hormone containing IUDs?

A

mirena = 52 mg of levonorgestrel and releases at 20 mcg/d
can use mirena for 5 years
three hormone containing IUDs= mirena, liletta, skyla

59
Q

dosages and time of efficacy for liletta and skyla?

A 
liletta = 52 mg of LNg and release rate of 20 mcg/d; approved for 5 yrs
skyla = 13.5 mg LNg and release rate of 14 mcg/d; approved for 3 yrs
60
Q

dosing of the “morning after pill”? MOA?

A

progestin-only method: progestin/levonorgestrel in 1.5 mg dose or two 70 microg doses, 12 hrs apart
MOA: prevent ovulation or fertilization and possibly post-fertilization implantation of a blastocyst

61
Q

how long after unprotected intercourse can the “morning after pill” be efficacious?

A

best when used 72 hrs after but effective to use up to 5 days after

62
Q

MOA of ulipristal acetate (ellaOne)?

A

MOA: should be given w/in 5 days after unprotected intercourse; delays or inhibits ovulation and inhibits follicle rupture

63
Q

can you utilize regular OCPs as a morning after pill?

A

YES

take 2 of the hormone pills every 12 hrs for 2 total doses

64
Q

what is mifepristone/mifeprex? MOA?

A

abortifacient, can be used during 1st TM
synthetic steroid compound used as an abortifacient in first 2 mos of PG and in smaller doses as an emergency contraceptive
MOA: progestin antagonist w/partial agonist activity

65
Q

MOA of mifepristone/mifeprex? often used in conjunction w/what? how does it work as an abortifacient?

A

MOA: blockade of progesterone receptors and cause decrease in Hcg which decreases progesterone production by corpus luteum
often used in conjunction w/misoprostol (prostaglandin E1 analog)
works an abortifacient by blocking P receptors which causes endometrial degeneration, cervical softening and dilation along with release of endogenous PG release and increase in sensitivity of myometrium to contractile effects of PGs

66
Q

common use of misoprostol?

A

commonly used for labor induction, causes uterine contractions and ripening of the cervix
more effective in starting labor than other drugs used for induction
can be combined with oxytocin to induce labor

67
Q

SEs of mifepristone/mifeprex? if incomplete termination of PG? C/I in what population?

A

SE: abd pain, uterine cramping, vaginal bleeding or spotting for 9-16 days, some experience bleeding for 30 d or more, N/V, diarrhea, dizziness, fatigue, fever
excessive uterine bleeding or incomplete termination of PG requires emergent medical intervention
C/I in those w/IUD, ectopic PG, pts w/known hemorrhagic d/os or anticoagulant therapy and pts on long term prednisone tx

68
Q

class of clomiphene/clomid? indications? MOA?

A

class: SERM
indications: infertility, amenorrhea
MOA: binding to E receptor sites in brain interferes w/normal (=) feedback of E on GnRH which means more GnRH which increases release of LH and FSH and stimulation of ovulation

69
Q

how to give clomiphene/clomid? SEs? potential C/Is?

A

give PO, make sure to assess potential SEs
SE: vaginal dryness, vaginal bleeding, breast tenderness, anxiety, hot flashes, multiple birth PG
potentially C/I in those w/prior hx of liver dz, breast or uterine CA

Pharm II (18 decks)

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