RPM Pharm Quiz Flashcards

1
Q

List SERMs (2)

A

tamoxifen, raloxifene

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2
Q

MOA and use of SERMs

A

competes with estrogen for receptor binding (competitive antagonist)
for breast cancer treatment

(tamoxifen, raloxifene)

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3
Q

Toxicity of Tamoxifen

A

increased risk of VTE (inhibits anti-thrombin while increasing fibrinogen VII and X)

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4
Q

List Aromatase inhibitors (3)

A

letrozole, anastrozole, exemestane

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5
Q

aromatase inhibitor MOA and use

A

inhibit conversion of androgens into estrogens
(prevents androstenedione to estrone and testosterone to estradiol)
for breast cancer treatment

(letrozole, anastrozole, exemestane)

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6
Q

What population is aromatase inhibitors effective in? which is it not?

A

effective in post-menopausal women
not effective in pre-menopausal

(letrozole, anastrozole, exemestane)

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7
Q

What types of drugs can be used in overactive voiding dysfunction?

A

M3 antagonist and B3 agonist

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8
Q

What types of drugs can be used in urinary retention or incomplete voiding?

A

M3 agonists and alpha 1 antagonist

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9
Q

M3 agonist and MOA

A

bethanechol

contraction of detrusor muscle

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10
Q

M3 antagonist and MOA

A

oxybutynin

relaxation of detrusor muscle

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11
Q

B3 agonist and MOA

A

mirabegron

relaxation of detrusor muscle

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12
Q

alpha antagonist and MOA

A

tamsulosin

relaxation of urethral smooth muscle

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13
Q

Oxybutynin has what type of side effects?

A

anti-cholinergic
blurred vision, pupil dilation, constipation, xerostomia, sedation

(M3 antagonist)

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14
Q

Mirabegron side effects

A

constipation, xerostomia, hypertension

B3 agonist

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15
Q

tamsulosin side effect

A

hypotension (vasorelaxation), somnolence

alpha 1 antagonist

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16
Q

What medication can cause ED?

A

beta blockers due to decreased BP

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17
Q

List PDE5 inhibitors (4)

A

Avanafil, tadalafil, sildenafil, vardenafil

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18
Q

What is unique about Tadalafil?

A

Very long half-life (17 hrs)

PDE5 inhibitor

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19
Q

What side effect is specific to vardenafil?

A

prolonged QT

PDE5 inhibitor

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20
Q

What is a side effect specific to PDE5 inhibitors?

A

cyanopsia

Avanafil, tadalafil, sildenafil, vardenafil

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21
Q

What drug interaction must be avoided with PDE5 inhibitors?

A

nitrates-huge risk for hypotension

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22
Q

Can you mix PDE5 inhibitors and alpha 1 antagonists?

A

yes, but use 3rd generation alpha 1 antagonists that are selective for alpha1a receptors (tamsulosin and silodosin)

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23
Q

What drugs can also be used to treat pulmonary arterial hypertenstion?

A

tadalafil and sildenafil

PDE5 inhibitors

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24
Q

What is the opium derived PDE5 inhibitor?

A

papaverine (delivered IC) for ED

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25
Q

What alpha 1 antagonist can be used alone to treat ED?

A

phentolamine-vasorelaxation, increased penile blood flow

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26
Q

PGE1 analog and what it treats

A

alprostadil to cause vasodilation for ED treatment

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27
Q

What enzyme converts testosterone to dihyrotestosterone

A

5 alpha reductase

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28
Q

5 alpha reductase inhibitor? what does it treat?

A

finasteride for BPH

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29
Q

Other uses for finasteride

A

decrease risk for prostate cancer, prevent/reverse androgenic alopecia

(5 alpha reductase inhibitor)

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30
Q

Tadalafil is a possible treatment for? (although unconfirmed)

A

BPH

PDE5 inhibitor

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31
Q

Ketoconazole MOA and use

A

inhibits androgen synthesis

part of androgen deprivation therapy (ADT) in prostate cancer

32
Q

Leuprolide MOA and use

A

downregulates GnRH receptor and inhibits testosterone synthesis as part of ADT for prostate cancer

33
Q

androgen receptor antagonists (2)

A

flutamide and spironolactone

34
Q

PDE5 inhibitor MOA and use

A

inhibit the breakdown of cGMP, leading to vasodilation/vascular smooth muscle relaxation
for ED

35
Q

androgen receptor antagonist MOA

A

antagonize the binding of DHT to androgen receptor

flutamide, spironolactone

36
Q

List natural estrogens (3)

A

estradiol (E2), estrone (E1), estriol (E3)

37
Q

List synthetic estrogens (3)

A

ethinyl estradiol, diethylsilbestrol, mestranol

38
Q

List synthetic progestins (3)

A

etonogestrel, levonorgestrel, norethindrone

39
Q

What is the MOA of combine OCPs?

A

maintain high levels of estrogen and progestin, “mimicking pregnancy”

-inhibit maturation, ovulation, fertilization and implantation

40
Q

What are progestin’s effects on endometrial development and cervical mucus?

A

inhibits endometrial development-inhibiting implantation

increases cervical mucus-blocking sperm from fertilization

41
Q

What does the progestin mini pill prevent?

A

implantation and fertilization

42
Q

What are the 3 combined OCP formulations

A

cyclic, extended cycle and continuous cycle

43
Q

define monophasic v. bi/triphasic OCPs

A

monophasic-every pill contains the same doses of estrogen and progestin

bi/triphasic-pills vary in dosses of estrogen and/or progestin

44
Q

Other benefits of OCPs

A

decreased bleeding, lighter periods, decreased dysmenorrhea, decreased acne, increased bone density

45
Q

OCPs effects on cancer risk

A

increased risk in breast (ER+/PR+), cervical and liver (estrogen dependent) cancer

decreased risk in ovarian endometrial and colorectal cancer

46
Q

OCPs are conraindicaetd in wha populaion

A

those with cardiovascular risk

can at time use mini pill instead

47
Q

What type of drugs can decrease effectiveness of OCPs?

A

anti-epileptic drugs by inducing metabolism

anti-bacterial drugs by reducing enterohepatic circulation (not recycled by bacteria)

48
Q

List emergency contraception and their mechanism of action

A
  • levonorgestrel, ulipristal
  • take within 24-72 hours of intercourse

MOA: inhibit LH surge and ovulation

49
Q

What medication is used for medical abortion? MOA?

A

Mifepristone (RU-486)

-disrupts the endometrium (by inhibiting progesterone effect on endometrial development), terminating the pregnancy

50
Q

What is mifepristone often paired with? why?

A

misoprostol

-induces uterine contraction

51
Q

What is estrogens effects on LDL levels?

A

estrogens reduce serum LDL levels by regulating lipid metabolism in the liver

52
Q

What is estrogens effects on bones?

A

estrogens inhibit bone resorption by inhibiting osteoclasts and stimulating osteoblasts

53
Q

Main 2 steps in treating ovulatory infertility

A
  1. downregulate GnRH receptors and inhibit gonadotropin release
  2. administer hormones that stimulate maturation and ovulation
54
Q

What drug down regulate GnRH receptors and can be used to treat ovulatory infertility?

A

leuprolide

55
Q

What hormones are administered to stimulate maturation and ovulation? and what does each do?

A
  1. rFSH- stimulates estradiol production and follicle maturation
  2. hCG- mimics LH surge and stimulates ovulation
56
Q

What drug with a different MOA may promote maturation and ovulation? how?

A

clomiphene (SERM)
disinhibits HPG axis and promotes maturation and ovulation (anti-estrogenic effect: inhibits estrogens negative feedback on axis)

57
Q

When is clomiphene administered?

A

on days 3-7 to promote FSH and LH release midcycle to induce ovulation

58
Q

Clomiphene toxicities

A

superovulation effects: abdominal pain/bloating, ectopic pregnancy, fraternal twins

menopause like symptoms: mood swings, hot flashes

increased risk of VTE

59
Q

What drug disinhibits the HPG axis and can promote spermatogenesis?

A

clomiphene

60
Q

What can directly stimulate spermatogenesis?

A

rFSH and LH/hCG

61
Q

What drug inhibits the conversion of testosterone to estradiol in obesity associated hypogonadism?

A

anastrozole (aromatase inhibitor)

62
Q

What causes PMS/PMDD?

A

sensitivity to monthly estrogen/progesterone fluctuations

63
Q

What can be used to prevent monthly fluctuation of estrogen/progesterone?

A

OCPs and leuprolide

64
Q

What can be used during menopause to mediate symptoms?

A

estradiol, progesterone and medroxyprogesterone

-to maintain non-fertility benefits

65
Q

What are non-fertility benefits of estrogen?

A

reduction of hot flashes, increase in bone mineralization

66
Q

estrogen toxicities

A

estrogen-dependent endometrial hyperplasia

67
Q

What drugs can be used to treat PCOS?

A

clomiphene, OCPs, spironolactone, flutamide, and finasteride

68
Q

anti-androgenic drugs serve what purpose in PCOS?

A

inhibit activity of androgens that can cause hirsutism

clomiphene, OCPs, spironolactone, flutamide, and finasteride (also think about how each of these would do so!!)

69
Q

What is OCPs MOA in PCOS?

A

stimulate expression of SHBG reducing free testosterone

70
Q

How do OCPs help in endometriosis?

A

inhibit the HPG axis and interrupt the growth/shrinkage cycle
this includes OCPs, levonorgestrel, and medroxyprogesterone
progestin-only pills may also be effective

71
Q

What is Danazol’s MoA

A

androgenic effects that inhibit the HPG axis, also increases levels of free testosterone in plasma by binding SHBG and kicking testosterone off (in endometriosis)
-has a lot of side effects so not really used anymore

72
Q

What is a GnRH receptor antagonist used to treat endometriosis?

A

elagolix

-blocks the receptors

73
Q

what is a GnRH receptor agonist that treats endometriosis?

A

leuprolide

-decreases number of receptors

74
Q

What role does progestin treatment play in menopause?

A

prevents estradiol induced endometrial hyperplasia

therefore not needed in individuals who have had a hysterectomy

75
Q

What is the cause of increased risk of VTE w/ SERMs?

A

estrogenic effect on liver cells that produce clotting factors