Reproductive Flashcards

1
Q

what is leuprolide

A

GnRH analog

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2
Q

leuprolide mechanism

A

pulsatile –> GnRH agonist

continuous –> GnRH antagonist (downregulates receptor) –> decrease FSH and LH

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3
Q

clinical use of pulsatile leuprolide

A

infertility

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4
Q

clinical use of continuous leuprolide (3)

A
  1. prostate cancer (with flutamide)
  2. uterine fibroids
  3. precocious puberty
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5
Q

three types of estrogen drugs

A
  1. ethinyl estradiol
  2. DES
  3. mestranol
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6
Q

clinical use of estrogens (3)

A
  1. hypogonadism or ovarian failure
  2. HRT
  3. androgen-dependent prostate cancer
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7
Q

side effects of estrogens

A
  1. increase risk endometrial cancer

2. increase risk thrombi

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8
Q

complications in female baby from DES exposure in utero

A

clear cell adenocarcinoma of vagina

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9
Q

contraindications for estrogen administration

A

ER+ breast cancer

history of DVTs

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10
Q

clomiphene drug class

A

selective estrogen receptor modulators (SERMs)

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11
Q

tamoxifen drug class

A

selective estrogen receptor modulators (SERMs)

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12
Q

raloxifene drug class

A

selective estrogen receptor modulators (SERMs)

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13
Q

clomiphene mechanism

A

antagonist at estrogen receptors in hypothalamus

prevents feedback inhibition –> increase LH and FSH release –> stimulates ovulation

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14
Q

clinical use clomiphene

A

infertility due to anovulation (i.e. PCOS)

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15
Q

side effects clomiphene (4)

A
  1. hot flashes
  2. ovarian enlargement
  3. multiple pregnancies
  4. visual disturbances
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16
Q

tamoxifen mechanism

A

estrogen receptor antagonist in breast, agonist in bone and uterus

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17
Q

clinical use tamoxifen

A

ER+ breast cancer

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18
Q

side effects tamoxifen (2)

A
  1. endometrial cancer

2. thromboembolic events

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19
Q

raloxifene mechanism

A

estrogen receptor agonist in bone, antagonist in uterus

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20
Q

clinical use raloxifene

A

osteoporosis (decreases resorption of bone)

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21
Q

side effects raloxifene (1)

A
  1. thromboembolic events
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22
Q

clinical use hormone replacement therapy (HRT) (2)

A
  1. relief of menopausal symptoms

2. osteoporosis (increase estrogen –> decrease osteoclast activity)

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23
Q

side effects HRT (2)

A
  1. endometrial cancer (unopposed estrogen, so add progesterone)
  2. cardiovascular risk
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24
Q

what is anastrozole

A

aromatase inhibitor

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25
Q

what is exemestane

A

aromatase inhibitor

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26
Q

clinical use anastrozole

A

used in postmenopausal women with breast cancer

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27
Q

clinical use exemestane

A

used in postmenopausal women with breast cancer

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28
Q

progestin mechanism

A

bind progesterone receptors –> decrease growth and increase vascularization of endometrium

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29
Q

clinical use progestin (2)

A
  1. oral contraceptives

2. endometrial cancer

30
Q

mifepristone (RU-486) mechanism

A

competitive inhibitor of progestin (at progesterone receptors)

31
Q

clinical use mifepristone

A

termination of pregnancy (give with misoprostol – PGE1)

32
Q

side effects mifepristone (2)

A
  1. heavy bleeding

2. GI effects

33
Q

mechanism oral contraceptives

A

estrogen and progestins inhibit LH/FSH –> prevent estrogen surge –> prevent ovulation
progestins: thickening of cervical mucus (sperm can’t get in) and inhibit endometrial proliferation (can’t implant)

34
Q

contraindications for oral contraceptives (3)

A
  1. smokers > 35
  2. hx of thromboembolism or stroke
  3. hx estrogen-dependent tumor
35
Q

what is terbutaline

A

beta-2 agonist

36
Q

mechanism terbutaline

A

beta-2 agonist –> relaxes uterus –> decrease contraction frequency

37
Q

what drug decreases contraction frequency during labor?

A

terbutaline (beta-2 agonist)

38
Q

what is danazol?

A

synthetic androgen

39
Q

mechanism danazol

A

synthetic androgen, partial agonist at androgen receptors

40
Q

clinical use danazol (2)

A
  1. endometriosis

2. hereditary angioedema

41
Q

side effects danazol (5)

A
  1. weight gain
  2. edema
  3. acne, hirsuitism, masculinization
  4. decrease HDL
  5. hepatotoxicity
42
Q

mechanism testosterone

A

agonist at androgen receptors

43
Q

mechanism methyltestosterone

A

agonist at androgen receptors

44
Q

clinical use testosterone / methyltestosterone (3)

A
  1. hypogonadism
  2. promotes secondary sex characteristics
  3. anabolism for burn/injury recovery
45
Q

side effects testosterone / methyltestosterone (4)

A
  1. masculinization
  2. inhibits release LH (negative feedback) –> gonadal atrophy
  3. premature closure epiphyseal plates
  4. increase LDL, decrease HDL
46
Q

what are four antiandrogens?

A
  1. finasteride
  2. flutamide
  3. ketoconazole
  4. spironolactone
47
Q

what is finasteride?

A

5-alpha reductase inhibitor

48
Q

mechanism finasteride

A

inhibits 5-alpha reductase –> prevents conversion of testosterone to DHT

49
Q

clinical use finasteride (2)

A
  1. BPH

2. male-pattern baldness (hair growth)

50
Q

what is flutamide?

A

nonsteroidal competitive inhibitor of androgens at the testosterone receptor

51
Q

clinical use flutamide

A

prostate carcinoma

52
Q

what is ketoconazole?

A

antiandrogen, inhibits 17,20-desmolase

53
Q

ketoconazole mechanism

A

inhibits 17,20-desmolase –> inhibits steroid synthesis

54
Q

what is spironolactone?

A

antiandrogen

55
Q

mechanism spironolactone

A

inhibits steroid binding

56
Q

clinical use ketoconazole

A

PCOS (prevent hirsuitism)

57
Q

what does tamoxifen do to LDL levels?

A

normalizes LDL and cholesterol in ovarian failure from breast cancer

58
Q

clinical use spironolactone

A

PCOS (prevent hirsuitism)

59
Q

what two drugs are used in PCOS to prevent hirsuitism?

A

spironolactone and ketoconazole

60
Q

side effects spironolactone (2)

A
  1. gynecomastia

2. amenorrhea

61
Q

side effects ketoconazole (2)

A
  1. gynecomastia

2. amenorrhea

62
Q

what is tamsulosin?

A

alpha-1 antagonist used to treat BPH

63
Q

mechanism tamsulosin

A

alpha-1 antagonist –> inhibits smooth muscle contraction

selective for alpha-1 receptors on prostate and not on vasculature

64
Q

clinical use tamsulosin

A

BPH

65
Q

mechanism sildenafil

A

inhibits phosphodiesterase 5 –> increase cGMP –> smooth muscle relaxation in corpus cavernosum –> erection

66
Q

mechanism vardenafil

A

inhibits phosphodiesterase 5 –> increase cGMP –> smooth muscle relaxation in corpus cavernosum –> erection

67
Q

clinical use sildenafil

A

erectile dysfunction

68
Q

clinical use vardenafil

A

erectile dysfunction

69
Q

side effects sildenafil

A
  1. headache
  2. flushing
  3. impaired blue-green vision
  4. heartburn (dyspepsia)
  5. risk life-threatening hypotension in pts taking nitrates
70
Q

side effects vardenafil

A
  1. headache
  2. flushing
  3. impaired blue-green vision
  4. heartburn (dyspepsia)
  5. risk life-threatening hypotension in pts taking nitrates
71
Q

can you use sildenafil/vardenafil in patients taking nitrates?

A

NO!! (risk life-threatening hypotension)