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Pharm 2014 Unit 1 > Reproductive Pharm > Flashcards

Reproductive Pharm Flashcards

1
Q

lecture objectives?

A
  1. understand the pharmacology of the reproductive process
  2. understand the mechanism of contraceptive and erectile dysfunction drugs
  3. understand the clinical indications for the use of these drugs
  4. understand the relevant side effects of the use of contraceptive and erectile dysfunction drugs
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2
Q

what are the three major estrogens produced by female body?

A
  1. estradiol
  2. estrone
  3. estriol
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3
Q

what is the primary source of estradiol in premenopausal women?

A

the ovary

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4
Q

what cells are responsible for making estrogen?

A

granulosa cells of ovarian follicle

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5
Q

estradiol can be converted to estrone and estriol in

A

the liver

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6
Q

estrogens are converted from androstenedione and testosterone

A

in ovaries or in other tissues (eg - adipose tissue, bone, and brain)

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7
Q

estrogens can also be produced in other tissues such as

A
  1. adipose tissue

2. adrenal gland in men and post-menopausal women

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8
Q

during pregnancy, large quantities of estriol are produced by

A

the placenta

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9
Q

what is the major circulating estrogen in premenopausal women?

A

estradiol

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10
Q

for men and postmenopausal women what is the major circulating estrogen?

A

estrone

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11
Q

aromatase in involved in the production of

A

estrogen

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12
Q

aromatase converts testosterone to

A

estradiol

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13
Q

aromatase converts androstenedione to

A

estrone

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14
Q

where is aromatse expressed in our body?

A

ovaries, placenta, adrenal gland, adipose tissue, testicles, brain

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15
Q

synthetic estrogens include

A

steroidal and nonsteroidals forms

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16
Q

what are the 3 synthetic steroidal estrogens in therapeutic use?

A
  1. estradiol esters
  2. conjugated estrogens
  3. alkyl estrogens
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17
Q

nonsteroidal synthetic estrogens

A

are less commonly used in the clinic

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18
Q

diethylstilbestrol (DES) was reported to increase the risk of

A

clear cell adenocarcinoma in the vagina and cervix

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19
Q

when does positive feedback on gonadotropin happens?

A

occurs at high concentrations near the end of the follicular phase, estrogen positively regulated pituitary to trigger the release of FSH and LH that causes the ovary to produce more estrogen.

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20
Q

what is responsible for ovulation?

A

high levels of estrogen and LH

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21
Q

what are the cardiovascular effects of estrogen

A

whether estrogens reduce cardiovascular dz is still under debate

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22
Q

what are the effects of estrogen on lipoprotein?

A

increase HDL and decrease LDL

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23
Q

what is the effect of estrogen on bone?

A

decrease bone resorption, thus used for the treatment of osteoporosis

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24
Q

what are the uses of estrogen for contraception?

A

synthetic estrogen, such as Ethinyl estrodiol is frequently used along with Progestin for prevention of pregnancy

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25
Q

what is the other use of estrogen?

A

primary hypogonadism (reduced or absent secretion of hormones from the sex glands, eg- ovaries)

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26
Q

how is estrogen used for postmenopausal hormone therapy?

A

used to reduce postmenopause symptoms such as “hot flashes”, atrophic vaginitis, also for the prevention of osteoporosis

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27
Q

what are the other physiological effects of estrogen?

A

decrease bone resorption –> thus, used for the osteoporosis

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28
Q

side effects of estrogen?

A

increase body fat, salt, and fluid retention

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29
Q

what are the 3 therapeutic uses of estrogen?

A
  1. contraception
  2. primary hypogonadism
  3. postmenopausal hormone therapy
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30
Q

what type of estrogen is used for contraception?

A

synthetic estrogen, such as ethinyl estrodiol, is frequently used along with progestin for prevention of pregnancy

31
Q

what is primary hypogonadism?

A

reduced or absent secretion of hormones from the sex glands (eg - ovaries)

32
Q

why is estrogen used for postmenopausal symptoms?

A

reduce postmenopause symptoms such as hot flashes, atrophic vaginitis, also for the prevention of osteoporosis

33
Q

what are the common adverse effects of estrogen?

A

nausea, breast tension/pain, vaginal bleeding, headache, weight gain, hypertension

34
Q

what are some less common adverse effects of estrogen?

A
  1. breast cancer (controversial)
  2. 2-3 fold increase in the incidence of DVT and pulmonary embolism
  3. increase risk of heart attach, stroke, gallbladder dz
  4. may increase the risk of cervical and endometrial cancers
35
Q

what are two contradictions of estrogen?

A
  1. strongly contraindicated in pts with breast or endometrial cancer, endometriosis, and undiagnosed vaginal bleeding
  2. generally contraindicated in pts with pregnancy, thromboembolic dz, hypertension , hepatic dz or with family hx of breast or uterine cancer
36
Q

what are two compounds that are estrogen receptor competitive antagonist?

A
  1. tamoxifen

2. clomiphene

37
Q

tamoxifen is

A

a nonsteroidal agent

38
Q

tamoxifen has both

A

estrogenic and antiestrogenic actions

39
Q

antiestrogenic effect of tamoxifen is on

A

mammary epithelium

40
Q

pro-estrogenic effect of tamoxifen is on

A

uterine endometrium and bone

41
Q

how does tamoxifen work on breast?

A

works as a partial estrogen competitive antagonist in the breast –> blocks estrogen from binding to estrogen receptor and is commonly used for the treatment of ER-positive advanced breast cancers

42
Q

estrogen binds to

A

sex hormone binding globulin in cell

43
Q

estrogen has much higher binding affinity than

A

tamoxifen

44
Q

tamoxifen must be used in concentration much

A

higher than estrogen to maintain inhibition of breast cancer cells

45
Q

prolonged use of tamoxifen (for prevention of breast cancer)

A

increases incidence of endometrial carcinoma

46
Q

clomiphene has two isomers:

A

cis and trans

47
Q

cis clomiphene is

A

a weak estrogen agonist

48
Q

trans clomiphene is

A

a potent estrogen antagonist

49
Q

estrogen feedback on gonadotropin release can be either

A

positive or negative

50
Q

the negative feedback of estrogen occurs

A

when estrogen reaches high level –> it acts in a negative feedback loop on ant. pituitary as well as hypothalamus and thus slows down the release of FSH and estrogen itself

51
Q

the positive feedback of estrogen occurs

A

at high conc near the end of the follicular phase, estrogen positively regulates pituitary to trigger the release of FSH and LH that cause the ovary to produce more estrogen –> high level of estrogen and LH are responsible for ovulation

52
Q

what is the mech of action of clomiphene?

A

blocks estrogen binding to its receptors in the hypothalamus and inhibits estradiol’s negative feedback on the gonadotropins –> increases in the secretion of gonadotropins and LH –> leads to ovulation

53
Q

clomiphene blocks

A

E2 receptor and increases GnRH –> LH and FSH surge –> ovulation

54
Q

clomiphene is used for

A

stimulating ovulation in patients with disorder of ovulation who wish to become pregnant

55
Q

side effects of clomiphene?

A

symptoms of menopause, multiple pregnancy, hot flashes

56
Q

progestin is considered as

A

synthetic progesterone

57
Q

what are the physiological functions of progesterone?

A
  1. stimulate endometrium to develop secretory glands
58
Q

what is effect of progesterone on growth?

A

suppress growth and can prevent endometrial cancers

59
Q

prolonged use of pregesterone has

A

atrophic effect on endometrium (thus, progesterone is used to oppose estrogen effect)

60
Q

what are the clinical usages of progesterone?

A
  1. contraception
  2. hormone replacement therapy
    3.
61
Q

what is the abortion pill?

A

RU-486 (mifepristone)

62
Q

what is progesterone contraindicated?

A

similar to estrogen

63
Q

estrogen-progesteron combination contracepties are the

A

most affective, reversible contraceptive

64
Q

progestin only oral contraceptives is called

A

mini pills and less effective than combination prep

65
Q

what is the the use for pregestin only oral pill?

A

useful when estrogens are contraindicated (eg - endometrial cancer)

66
Q

what is the abortion pill?

A

mifepristeon (RU-486)

67
Q

mifepristone is the progestin

A

antagonist (indicated for the medical termination of early preg. 49 days or less)

68
Q

what are the mech of sildenafil, verdenafil, tadalafil (cialis)

A

inhibitors of PDE5

69
Q

half life for sildenafil and vardenafil

A

4 h

70
Q

half life for tadalafil

A

17.5

71
Q

what are common side effects of PDE5 inhibitor?

A

flushing and change in vision

72
Q

PDE5 inhibitors can cause sudden blood pressure drop to unsafe level when taken with other drugs such as

A

nitrates and alpha-blocker

73
Q

PDE5 inhibiros should not be used with

A

nitrates and alpha blocker

Pharm 2014 Unit 1 (13 decks)

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