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Pharm 3: Reproductive Medications > pharmacology of gonadal hormones and inhibitors > Flashcards

pharmacology of gonadal hormones and inhibitors Flashcards

1
Q

What are the estrogen medications

A

estradiol
estrone
ethinyl estradiol

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2
Q

what are the SERMS

A

clomiphene
raloxifene
tamoxifen

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3
Q

What are the progesterone agonist/antagonists

A

ulipristal acetate

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4
Q

what are the anti-progestin meds

A

mifepristone

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5
Q

what is the major hormone active during the follicular phase of the menstraul cycle

A

estradiol

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6
Q

what is the dominant estrogen in postmenopausal women

A

estrone

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7
Q

what is the common synthetic estrogen

A

ethinyl

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8
Q

what are steroid hormones

A

progestogens

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9
Q

why use estrogen + progesterone

A

estrogen: potentiates progesterone so lower doses can be used, allows for endometrial growth, so less break-through bleeding
progesterone: protects against estrogen-induced endometrial hyperplasia

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10
Q

What is the MOA of estrogens

A

agonist to the estrogen receptor

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11
Q

what is the clinical use of estrogens

A

oral contraceptive
menopausal hormone therapy
gynecologic disorders

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12
Q

what is the MOA of combination oral contraceptives

A

-suppresses LH and FSH by interfering with hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary gonadotropin secretion
-ovulation is suppressed through inhibition of mid-cycle LH surge
-suppress ovarian folliculogenesis via suppression of pituitary FSH secretion

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13
Q

what are the progestin-related mechanisms of COC

A

endometrium becomes less suitable for implantation
cervical mucus thickens and becomes less permeable to penetration by sperm
impairment of normal tubal motility and peristalsis

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14
Q

what are noncontraveptive benefits of COCs

A

abnormal or dysfunctional uterine bleeding
dysmenorrhea
PMS and PMDD
Endometriosis
adenomyosis
functional ovarian cysts
PCOS
hormone replacement in women with primary hypogonadism
hyperandrogenism

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15
Q

what are the possible AE of COC

A

HTN
Thromboembolism
changes in lipids
bleeding irregularities
nausea
mood changes
breast changes
weight gain
headache

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16
Q

what are the AE of estrogen deficiency

A

vasomotor symptoms

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17
Q

what are the AE of estrogen excess

A

chloasma (melasma)
monorrhagia and clotting
increased breast size

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18
Q

what are the AE of progestin deficiency

A

breakthrough bleeding
delayed withdrawal bleeding
dysmenorrhea
heavy flow/clots

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19
Q

what are the AE of progestin excess

A

candidiasis
appetite increase
depression
fatigue
libido decrease

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20
Q

what are the AE of androgen excess

A

Acne
hirsutism
libido increase
oily skin/scalp
edema

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21
Q

what are the contraindications for estrogen-containing contraceptions

A

thromboembolic disorders
smokers > 35yo
breast cancer
impaired liver function
abnormal vaginal bleeding
pregnancy
cardiac disease
migraine

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22
Q

what are drug interactions iwth COC

A

anticonvulsants: phenytoin, carbamazepine, barbiturates, topiramate
antibiotics: Rifampin
drugs to treat HIV

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23
Q

what is the MOA of emergency contraception

A

works by delaying/blocking ovulation
must be used within 72 hours of unprotected intercourse

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24
Q

what are options for emergency contraception

A

levonorgestrel (Plan B)
Ulipristal (high dose progestin)
COC ( higher dose hormones)
Copper IUD

25
Q

what is the MOA of levonorgestrel for EC

A

prevents ovulation or fertilization, alters endometrium

26
Q

when is levonorgestrel contraindicated

A

known of suspected pregnancy

27
Q

what are the AE of levonorgestrel

A

generally well tolerated, may cause GI upset, re-administer if vomiting within 2 hours

28
Q

what is the MOA of ulipristal (ella)

A

binds to progesterone receptor. inhibitors/delays ovulations, alters endometrium.
selective progesterone receptor modulator

29
Q

when is ulipristal contraindicated

A

known of suspected pregnancy

30
Q

what are the AE of ulipristal

A

generally well tolerated, may cause headache, nausea, dysmenorrhea, dizziness, fatigue

31
Q

What is mifepristone

A

medical abortion - synthetic steroid compound
anti-progesterone used for medical abortion

32
Q

what is the MOA of Mifepristone

A

competitively binds to progesterone receptor (blocks progesterone receptor). antagonizing endometrial and myometrial effects, leads to contraction-inducing activity. disrupts implanted embryo

33
Q

when can Mifepristone be used

A

less than 49 days (7 weeks) pregnant

34
Q

what medication do you take after mifepristone

A

misoprostol (prostaglandin) for expulsion of products of conception

35
Q

what are the goals of HRT

A

decrease symptoms which may include vasomotor symptoms (hot flashes), mood lability, vaginal atrophy, sleep disturbances

36
Q

What are the risks of HRT

A

prematurely stopped because of increased incidence of cardiovascular events and breast cancer

37
Q

what is HRT protective against

A

osteoporosis
colon cancer

38
Q

what are the contraindications of HRT

A

history of breast cancer
history of coronary heart disease
previous hx of DVT/PE
history of CVA or TIA
acute liver disease
unexplained vaginal bleeding
risk of endometrial cancer

39
Q

what does SERMs stand for

A

Selective estrogen receptor modulators

40
Q

What are the SERM medications

A

Tamoxifen
Raloxifene
Clomiphene

41
Q

What is Tamoxifen

A

breast cancer tx: antagonists in breast, agonists at bone and endometrium

42
Q

what is Raloxifene

A

osteoporosis treatment: antagonists in breast and endometrium, agonist at bone (less risk of endo ca vs tamo)

43
Q

what is Clomiphene

A

ovulation induction: antagonists at hypothalamus, weak agonists in other tissues (prevent E neg feedback loop).

44
Q

what are the AE of SERMs

A

flushing, hot flashes
mood changes, depression
GI upset
vaginal bleeding
bone marrow suppression (rare)

45
Q

what are the contraindications of SERMs

A

warfarin therapy
hx DVT/PE
hx CVA/TIA
endometrial cancer

46
Q

what is ospemifene

A

antagonist s in breasts, agonists in vaginal tissue and endometrium

47
Q

what is toremifene

A

antagonists in breast, agonists in bone and endometrium (very similar to tamoxifen)

48
Q

What does prostate cancer rely on

A

testosterone

49
Q

what reduces the levels of androgen hormones with drugs to prevent the prostate cancer cells from growing

A

ADT

50
Q

what is ADT

A

androgen deprivation therapy - reduces levels of androgen hormones

51
Q

what are the ADT types

A

surgical castration
continuous GnRH agonists (leuprolide) and antagonists
anti-androgens (flutamide)

52
Q

What is LHRH

A

Luteinizing hormone - releasing hormone

53
Q

What is the MOA of Leuprolide

A

inhibitor of gonadotropin secretion. results in transient increase in LH/FSH which leads to transient increase in testosterone and estrogen BUT continuous GnRH agonist use results in decrease in LH/FSH and suppression of testosterone production in males and estrogen production in females

54
Q

what is the ASE of leuprolide

A

HA
depression
GI
decreased libido

55
Q

what are the indications of leuprolide

A

prostate CA
endometriosis
uterine fibroids
used for some IVF protocols

56
Q

What is flutamide

A

synthetic, nonsteroidal anti-androgen

57
Q

what are the AE of Flutamide

A

GI distress
gynecomastia
impotence
hot flashes
liver failure

58
Q

what is the MOA of flutamide

A

competes with natural hormone for binding to the androgen receptor. blocks effects of androgens on target organs

59
Q

what are the contraindications of flutamide

A

severe hepatic impairment

Pharm 3: Reproductive Medications (2 decks)

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