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reproductive drugs Flashcards

1
Q

Leuprolide mechanism of action / function

A

GnRH analog:

  • agonist when used in continuous in puslatile fashion
  • antagonists properties when used in continious fashion –> downregulates GnRH receptor
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2
Q

Leuprolide - clinical use

A
  1. uterine fibroids (leiomyoma)
  2. endometriosis
  3. precosious puberty
  4. prostate cancer
  5. infertility
  6. adenomyosis
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3
Q

estrogens - drugs

A
  1. Ethinyl estradiol
  2. Diethylstilbestrol (DES)
  3. mestranol
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4
Q

estrogens drugs - mechanism of action

A

bind estrogen receptor

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5
Q

estrogen drugs - clinical use

A
  1. hypogonadism or ovarian failure
  2. menstrual abnormalities
  3. hormone replacement therapy in postmenopausal women
  4. in men with androgen-depended prostate cancer
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6
Q

estrogens drugs - adverse effects

A
  1. high risk of endometrial cancer
  2. bleeding in postmenopausal women
  3. clear cell adenocarcinoma in females exposed to DES in uterus
  4. high risk for thrombi
  5. contraindications in ES+ breast cancer and in DVT history
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7
Q

estrogens drugs - contraindications in

A

ES+ breast cancer and in DVT history

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8
Q

Aromatase inhibitors - drugs

A
  1. Anastrozole
  2. Letrozole
  3. exemestane
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9
Q

Aromatase inhibitors - mechanism

A

inhibit peripheral conversion of androgens to estrogen

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10
Q

Aromatase inhibitors - clinical use

A

ER+ breast cancer in postmenopausal women

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11
Q

SERM?

A

selective estrogen receptor modulators

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12
Q

SERM - drugs

A
  1. Clomiphene
  2. Tamoxifen
  3. Raloxifen
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13
Q

Clomiphene - mechanism of action

A

antagonist at estrogen receptor in hypothalamus –> prevent normal feedback inhibition and increases release of LH and FSH –> stimulates ovaluation

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14
Q

Clomiphene - used to treat

A

infertility due to anovulation (eg. PCOS)

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15
Q

Clomiphene - adverse effects

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

Tamoxifen - mechanism of action

A
  • antagonist at estrogen receptor at breast

- agonist at bone, uterus

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17
Q

tamoxifen - adverse effects

A

high risk of thromboembolic events and enometrial cancer, hot flashes

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18
Q

tamoxifen - used to

A

treat and prevent recurrence of ER/PR + breast cancer

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19
Q

Raloxifene - mechanism of action

A
  • antagonist at breast, uterus

- agonist at bone

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20
Q

Raloxifen - adverse effects

A

high risk of thromboembolic events but not increased risk of endometrial cancer risk (vs tamoxifen)
hot flashes

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21
Q

Raloxifen - used to

A

used primarily to tread osteoporosis

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22
Q

hormone replacement therapy - used to

A

relief or prevention of menopausal symptoms (eg. hot flashes, vagina atrophy), osteoporosis

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23
Q

hormone replacement therapy - adverse effects

A
  1. unopposed estrogen replacement therapy increases the risk of endometrial cancer, so progesterone is added
  2. possible increased cardiovascular risk
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24
Q

hormone replacement therapy - 1. unopposed estrogen replacement therapy increases the risk of endometrial cancer, so

A

progesterone is added

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25
Q

Progestins - drugs

A

Levonogestrel, medroxyprogesterone, etonogestrel, norethindrone, megestrol and many others when combined with estrogen

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26
Q

Progest drugs - mechanism

A

bind progesterone receptors, decrease growth and increase vascularization of endometrium, thicken cervical mucus

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27
Q

Progest drugs - clinical use

A
  1. contraception (forms include pill, intrauterine deivece, implant, depot injection)
  2. Progestin challenge: presence of withdrawal bleeding excludes anatomc defects (Asherman syndrome) and chronic anovulation without estrogen
  3. endometrial cancer
  4. adnormal uterine bleeding
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28
Q

Asherman syndrome?

A

is the formation of scar tissue in the uterine cavity. The problem most often develops after uterine surgery.

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29
Q

Antiprogestins - drugs

A
  1. mifepristone

2. ulipristal

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30
Q

Antiprogestins - mechanism

A

competitive inhibitors of progestins at progesterone receptor

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31
Q

Antiprogestins - clinical use

A
  1. Termination of pregnancy (mifepristone with misoprostol)

2. emergency contraception (ulipristal)

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32
Q

Combined contraception - drugs and forms

A

Progesins and ethinyl estradiol (forms: pill, patch, vaginal ring)

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33
Q

Combined contraception - mechanism of action

A
  1. inhibit LH, FSH –> prevent estrogen surge –> no LH surge –> no evaluaton
  2. progestins cause thickening of cervical mucus –> limiting access of sperm to uterus
  3. progestins inhibit endometrial proliferation –> endometrium less suitable to the implantation of an embryo
34
Q

Combined contraception - contraindications

A
  1. smokers over 35 (cardiovascular risk)
  2. patietns with increased risk for cardiovascular event
  3. migraine (esp with aura)
  4. breast cancer
35
Q

copper intrauterine device - mechanism

A

produce local inflammatory reaction toxic to sperm and ova –> prevent fertilization and implantation
(HORMONE FREE)

36
Q

copper intrauterine device - clinical use

A
  1. long acting reversible contraception

2. Most effeective emergency contraception

37
Q

copper intrauterine device - adverse effect

A
  1. heavier or longer menses
  2. dysmnenorrhea
  3. risk of PID insertion (contraindicated in active pelvic infection)
38
Q

copper intrauterine device - contraindicated in

A

active pelvic infection

39
Q

β2-agonists on uterus - drugs

A
  1. terbutaline

2. ritodrine

40
Q

terbutaline - mechanism of action

A

β2-agonists on uterus –> relax

41
Q

ritodrine - mechanism of action

A

β2-agonists on uterus –> relax

42
Q

β2-agonists on uterus - drugs, action, clinical use

A
  1. terbutaline 2. ritodrine
    β2-agonists on uterus –> relax
    decreases contraction frequency in women during labor
43
Q

Danazol - mechanism of action

A

synthetic androgen that acts as partial agonists at androgen receptor

44
Q

Danazol - clinical use

A
  1. endometriosis

2. herediatary angioedema

45
Q

Danazol - adverse effects

A
  1. weight gain
  2. edema
  3. acne
  4. hirsutism
  5. masculinization
  6. low HDL levels
  7. hepatotoxicity
46
Q

androgen receptor agonists - drugs

A
  1. testosterone

2. methyltestosterone

47
Q

androgen receptor agonists - drugs and clinical use

A
  1. testosterone 2. methyltestosterone
    a. treat hypogonadism
    b. promonte development of 2ry characteristics.
    c. stimulat anabolism to promote recovery after burn or injury
48
Q

androgen receptor agonists - adverse effects

A
  1. masculinization in females
  2. testicular atrophy
  3. premature closure of epihyseal plates
  4. low HDL
  5. high LDL
49
Q

androgen receptor agonists causes testicular atrophy - mechanism

A

low intratesticular testosterone in males by inhibiting release of LH

50
Q

Testosterone –> DHT (enzyme?, more potent?)

A

enzyme: 5α reductase

DHT is more potent

51
Q

antiandrogens - drugs

A
  1. finasteride
  2. flutamide
  3. ketoconazole
  4. sprironoactone
  5. cyproterone
52
Q

finasteride - mechanism of action

A

inhibits 5α reductase (low converstion of Test to DHT)

53
Q

finasteride - clinical use

A
  1. BPH

2. male baldness

54
Q

Flutamide - mechanism of action

A

nonsteroidal competitive inhibitor of androgen receptors

55
Q

flutaminde - clinical use

A

prosate carcinoma

56
Q

Ketoconazole - mechanism of action (as antiandrogen)

A
  1. inhibits steroid synthesis (inhibits 17,20 desmolase)

2. receptor antagonist

57
Q

Ketoconazole - clinical use (as antiandrogen)

A

polycystic ovarian syndrome (to reduce androgen symptoms)

58
Q

spironolactone - mechanism of action (as antiandrogen)

A

inhibits steroid synthesis, 17α hydroxylase and 17,20 desmolase)

59
Q

spironolactone - clinical use (as antiandrogen)

A

polycystic ovarian syndrome (to reduce androgen symptoms)

60
Q

spironolactone - side effects (as antiandrogen)

A
  1. gynecomastia

2. amenorrhea

61
Q

Ketoconazole - side effects (as antiandrogen)

A
  1. gynecomastia

2. amenorrhea

62
Q

antiandrogens - drugs and mechanism of action

A
  1. finasteride –> inhibits 5α reductase
  2. flutamide –> nonsteroidal competitive inhibitor of androgen receptors
  3. ketoconazole –> inhibits steroid synthesis (inhibits 17,20 desmolase) + receptor inhibitor
  4. sprironoactone –> inhibits steroid synthesis, 17α hydroxylase and 17,20 desmolase)
  5. cyproterone –> receptor inhibitor
63
Q

Minoxidil - mechanism of action

A

direct ARTERIOLAR vasodilator

64
Q

Minoxidil - clinical use

A
  1. androgenic alopecia

2. severe refractory hypertension

65
Q

Tamsulosin - clinical use

A

a1 antagonist –> selective for α1A,D receptors (prostate) vs vascular α1B receptors

66
Q

Tamsulosin - clinical use (and how)

A

BPH (by inhibiting SMC contraction) –> selective for α1A,D receptors (prostate) vs vascular α1B receptors

67
Q

Phosphodiesterase type 5 inhibitors - drugs

A
  1. sildenafil
  2. vardenafil
  3. tadalafil
68
Q

Phosphodiesterase type 5 inhibitors - mechanism of action

A

inhibit PDE-5 –> increased cGMP –> prolonged SMCs relaxation in respose to NO –> increases blood flow in corpus carvenosun of penis, decreases vascular resistance

69
Q

Phosphodiesterase type 5 inhibitors - clinical use

A
  1. erectile dysfunction
  2. pulmonary hypertension
  3. BPH (only tadalafil)
70
Q

Phosphodiesterase type 5 inhibitors - adverse effects

A
  1. headache
  2. flushing
  3. dyspepsia
  4. cyanopia (blue-tineted vision)
  5. Risk of life threatening hypotension in patients taking nitrates
71
Q

Polysystic ovarian (Stein-Leventhal) syndrome - treatment

A
  1. weight loss,
  2. OCP
  3. clomiphene citrate
  4. ketoconazole
  5. spironolactone
72
Q

Adenomyosis - treatment

A
  1. GnRH agonists

2. Hysterectomy

73
Q

endometritis - treatment

A

gentamicin + clindamycin +/- ampicillin

74
Q

endomtriosis - treatment

A
  1. NSAID
  2. OCP
  3. progestins
  4. GnRH agonists
  5. Danazol
  6. Laparoscopic removal
75
Q

drugs that causes gynecomastia

A
  1. spironolactone
  2. Hormones
  3. cimetidine
  4. Ketoconazole
76
Q

Gestational hypertension (pregnancy-induced hypertension) - drugs (short mechanism of action) and management

A
  1. hydralazine (vasodilator by cGMP increasing)
  2. labetolol (alpha-beta blocker)
  3. α-methyldopa (a-2 blocker)
  4. nifedipine (dihydropiridine Ca2+ channel blocker)
  5. deliver at 37-39 weeks
77
Q

Preeclampsia - treatment
Eclampsia - treatment
HELLP syndrome - treatment

A

Preeclampsia: 1. anithypertensive 2. IV magnesium sulfate (to prevent seizures) 3. definitive is delivery of fetus
Eclampsia: 1. IV magnesium sulfate 2. antihypertensives 3. immediate delivery
HELLP: immediate delivery

78
Q

Hydatidiform mole - management

A
  1. dilation and curettage and methotrexate

2. Monitor β-hCG

79
Q

ischemic priapism - management

A

treat immediately with corporal aspiration, intracavernosal phenylephrine, or surgical decompression to prevent ischemia

80
Q

Benign prostatic hyperplasia - treatment (and mechanism)

A
  1. a1 antagonists (terazosin, tamsulosin) –> relaxation of SMC
  2. 5α-reductase inhibitors (eg. finasteride
  3. tadalafil (PDE-5 inhibitor)

Reproductive (20 decks)

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