Repro Midterm Pharm

Question 1

17-α ethinyl estradiol

Answer 1

Orally active estrogen, ethinyl modification makes E orally active and avoids first pass metabolism

Question 2

Norethindrone

Answer 2

Highly orally active progestin. Progestogen combined with separate ethinyl estradiol for HRT. No longer used. Increased risk of MI, thrombosis, stroke, breast cancer.

Question 3

Tamoxifen

Answer 3

SERM. Main use is to protect from breast cancer. Agonist in bone, endometrium, liver. Risk for endometrial cancer. Antagonist in breast tissue, ∴ protects from breast cancer recurrence. Antagonist in hypothalamus ∴ causes hot flashes.

Question 4

Raloxifene

Answer 4

SERM. Agonist in bone. Antagonist in breast and endometrium. Used mainly to protect from osteoporosis, does not cause endometrial proliferation.

Question 5

Ospemifene

Answer 5

SERM. Only SERM with effect on vaginal epithelium. Reverses vaginal atrophy, relieves dyspareunia. Agonist in bone & endometrial tissue.

Question 6

Clomiphene citrate

Answer 6

SERM. Main use = ovulation stimulator. Estrogen antagonist in hypothalamus and pituitary, ∴ prevents negative feedback of gonadal estrogen, ∴ FSH and LH surge, ∴ ovulation stimulated.

Question 7

Letrozole

Answer 7

Estrogen synthesis inhibitor ∵ aromatase inhibitor. Blocks local production of E. No increased risk of uterine cancer or venous thrombosis. Produces hot flashes.

Question 8

Leuprolide

Answer 8

GnRH receptor agonist. Hormonal equivalent of surgical orchiectomy. Causes flare of FSH/LH release, block with androgen receptor antagonists (eg flutamide). GnRH receptors will desensitize, ∴ no more FSH/LH release, ∴ no more T production.

Question 9

Goserelin

Answer 9

GnRH receptor agonist. Hormonal equivalent of surgical orchiectomy. Causes flare of FSH/LH release, block with androgen receptor antagonists (eg flutamide). GnRH receptors will desensitize, ∴ no more FSH/LH release, ∴ no more T production.

Question 10

Abarelix

Answer 10

GnRH receptor antagonist. Inhibits FSH/LH release without causing flare (as seen in leuprolide/goserelin). No more FSH/LH release ∴ no more T production.

Question 11

Flutamide

Answer 11

Nonsteroidal androgen receptor antagonist. DHT ⊣ androgen receptors. -mide antiandrogens often combined with GnRH agonist to prevent initial T surge from FSH/LH flare. Side effects: diarrhea, gynecomastia, hepatotoxicity.

Question 12

Bicalutamide

Answer 12

Nonsteroidal androgen receptor antagonist. DHT ⊣ androgen receptors. No hepatotoxicity, less diarrhea than flutamide.

Question 13

Enzalutamide

Answer 13

Nonsteroidal androgen receptor antagonist. Highest affinity for androgen receptor of all antiandrogens. Does not promote androgen receptor translocation to the nucleus. Crosses the blood-brain barrier. Abiraterone + enzalutamide combination more effective than either alone.

Question 14

Abiraterone

Answer 14

Abiraterone acetate. Treatment for metastatic, castration-resistant prostate cancer. Inhibits CYP17 ∴ blocks testosterone synthesis in testes and adrenal cortex. Stops all adrenal glucocorticoid synthesis, supplement with prednisone or dexamethasone. Abiraterone + enzalutamide combination more effective than either alone.

Question 15

Fulvestrant

Answer 15

Universal estrogen receptor competitive inhibitor, promotes degradation of estrogen receptors and decreases synthesis of estrogen-dependent genes. Used after tamoxifen therapy is ineffective.

Question 16

Trastuzumab

Answer 16

MAB against HER2 protein, only effective in HER2 + cancers

Question 17

Mertuzumab

Answer 17

MAB against the dimer that holds the two halves of HER2 together

Question 18

Lapatinib

Answer 18

Tyrosine kinase inhibitor, stops the tyrosine kinase that’s activated by HER2 activation.