Pharmacology- Reproductive

Front 1

Finasteride
-Mechanism

Back 1

5Alpha-reductase inhibitor ( decrease conversion of testosterone to dihydrotestosterone)

Front 2

Finasteride
-Clinical use

Back 2

Benign Prostate Hyperplasia (BPH).
Also promotes Hair growth- used to treat male-pattern baldness

Front 3

Flutaminde
-Mechanism

Back 3

Nonsteroidal competitive inhibitor of androgen at the testosterone receptor

Front 4

Flutaminde
-Clinical use

Back 4

Prostate Carcinoma (tumor regression)

Front 5

Ketoconazole
-Mechanism

Back 5

Inhibits Steroid Synthesis

Front 6

Spironolactone
-Mechanism

Back 6

Inhibits steroid binding

Front 7

Ketoconazole
-Side Effects

Back 7

Gynecomastia and Amenorrhea
Similar to Spironolactone

Front 8

Sprinolactone
-Side effects

Back 8

Gynecomastia and Amenorrhea
Similar to Ketoconazole

Front 9

Ketoconazole
-Clinical use

Back 9

PCOS and to prevent hirsutism
similar to Spironolactone

Front 10

Sprinolactone
-Clinical use

Back 10

PCOS and prevent Hirsutism
similar to Ketoconazole

Front 11

Leuprolide
-Mechanism

Back 11

GnRH analog with agonist properties when used in pulsatile fashion and anatagonist property when used in continuous function

Front 12

Leuprolide
-Clinical use

Back 12

Infertility (pulsatile), prostate cancer (continuous use with flutaminde), uterine fibrosis

Front 13

Leuprolide
-Toxicity

Back 13

Antiandrogen, nausea, vomitting

Front 14

Sildenafile, vardenafil
-Mechanism

Back 14

Inhibits cGMP Phosphodiesterase causing increase cGMP, smooth muscle relaxation in the corpus cavernosum, increase blood flow and penile erection

Front 15

Sildenafil, verdenafil
-Clinical use

Back 15

Treatment of erectile dysfunction

Front 16

Sildenafil, verdenafil
-Toxicity

Back 16

Headache, flushing, dyspepsia, impaired blue-green color vision. Risk of life threatening hypotension in patients taking nitrates

Front 17

Mifepristone
-Mechanism

Back 17

Competitive inhibitor of progestins at progesterone receptor

Front 18

Mifepristone
-Clinical use

Back 18

Termination of pregnancy,. administered with misoprostol.

Front 19

Mifepristone
-Toxicity

Back 19

Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain

Front 20

How do oral contraceptive work?

Back 20

Prevent estrogen surge, LH surge does not occur --> Ovulation does not occur

Front 21

Oral contraceptives
-decreases risk of which cancers and what else

Back 21

Endometrial and ovarian cancers and (also decrease pelvic infection and decrease incidence of ectopic pregnancies)

Front 22

Oral contraceptives
-side effects

Back 22

Hypercoaguble, increase triglycerides, weight gain

Front 23

Hormone replacement therapy
-Why is it used

Back 23

Used after menopause to cure symptoms ( hot flashes, vaginal atrophy) and osteoporosis (due to decrease estrogen)

Front 24

Hormone replacement therapy
-Side effects

Back 24

Increases risk of endometrial cancer especially if estrogen thats why progesterone is added

Front 25

Dinoprostone
-Mechanism

Back 25

PGE2 analog

Front 26

DInoprostone
-Clinical Use

Back 26

Cervical dilation and uterine contraction, inducing labor

Front 27

Ritodrine/ terbutaline
-Mechanism

Back 27

Beta-2- Agonist

Front 28

Ritodrine/ terbutaline
-Clinical use

Back 28

Relaxes the uterus, reducing premature uterine contractions

Front 29

Anastrozole/ exemestane
-Mechanism

Back 29

Aromatase inhibitors

Front 30

Anastrozole/ exemestane
-Clinical use

Back 30

used in postmenopausal women with breast cancer. Profound estrogen deprivation so used in estrogen dependent breast cancer

Front 31

Testosterone
Mechanism

Back 31

Agonist at Androgen receptor

Front 32

Testosterone
-Clinical use

Back 32

Treat hypogonadism and promote development of secondary sex characteristics; stimulation of anabolsim to promote recovery after burn or injury; treat ER-positive breast cancers (Exemestane)

Front 33

Testosterone
-Toxicity

Back 33

Causes masculinization in females; reduces intratesticular testosterone in males by inhibiting leydig cells; leads to gonadal atrophy. Premature closure of epiphyseal plates. Increase LDL and decreases HDL

Front 34

Estrogens (ethinyl estradiol, DES, Mestranol)
-Mechanism

Back 34

Bind estrogen receptors

Front 35

Estrogens (ethinyl estradiol, DES, Mestranol)
-Clinical use

Back 35

Hypogonadism or ovarian failure, menstrual abnormalites, HRT in postmenopausal women; use in men with androgen-dependent prostate cancer

Front 36

Estrogens (ethinyl estradiol, DES, Mestranol)
-Toxicity

Back 36

- Increase risk of endomterial cancer,
- bleeding in postmenopausal women
- clear cell adenocarcinoma of vagina in females exposed to DES in utero
- increase risk of thrombi

Front 37

Estrogens (ethinyl estradiol, DES, Mestranol)
-Contraindicated

Back 37

ER + Breast cancers

Front 38

Progestins
-Mechanisn

Back 38

Bind progesterone receptors, reduce growth, and increase vascularization of endometrium

Front 39

Progestins
-Clinical use

Back 39

Used in oral contraceptives and in treatment of endometrial cancer and abnormal uterine bleeding

Front 40

Raloxifene
-Clinical use

Back 40

Estrogen partial agonists (SERM)
Agonist on Bone; reduces resorption of bone, used to treat osteoperosis

Front 41

Tamoxifen
-Clinical use

Back 41

Estrogen partial agonists (SERM)
Antagonist on breast tissue; used to treat and prevent recurrence of ER+ breast cancer

Front 42

Clomiphene
-Mechanism

Back 42

Estrogen partial agonists (SERM) Partial agonist at estrogen receptor in Pituitary glands. Prevents normal feedback inhibition and increases release of LH and FSH from pituitary which stimulates ovulation.

Front 43

Clomiphene
-Clinical use

Back 43

Used to treat infertility and PCOS by blocking estrogen

Front 44

Clomiphene
-Side effects

Back 44

May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances