Reproductive - Pharmacology Flashcards Preview

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Flashcards in Reproductive - Pharmacology Deck (21):
1

Control of reproductive hormones (589)

2

Leuprolide

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • GnRH analog with agonist properties when used in pulsatile fashion
    • Antagonist properties when used in continuous fashion (downregulates GnRH receptor in pituitary -->Ž decreased FSH/LH).
    • Leuprolide can be used in lieu of GnRH.
  • Clinical use
    • Infertility (pulsatile), prostate cancer (continuous—use with flutamide), uterine fibroids (continuous), precocious puberty (continuous).
  • Toxicity
    • Antiandrogen, nausea, vomiting.

3

Estrogens

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity

  • Examples
    • Ethinyl estradiol, DES, mestranol
  • Mechanism
    • Bind estrogen receptors.
  • Clinical use
    • Hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausal women
    • Use in men with androgen-dependent prostate cancer.
  • Toxicity
    • Increased risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, increased risk of thrombi.
    • Contraindications—ER (+) breast cancer, history of DVTs.

4

Clomiphene

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Selective estrogen receptor modulator—SERM
  • Mechanism
    • Antagonist at estrogen receptors in hypothalamus.
    • Prevents normal feedback inhibition and increases release of LH and FSH from pituitary, which stimulates ovulation
  • Clinical use
    • Used to treat infertility due to anovulation (e.g., PCOS).
  • Toxicity
    • May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances.

5

Tamoxifen

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Selective estrogen receptor modulator—SERM
  • Mechanism
    • Antagonist on breast tissue
    • Agonist at uterus, bone
  • Clinical use
    • Primarily used to treat and prevent recurrence of ER (+) breast cancer.
  • Toxicity
    • Associated with endometrial cancer, thromboembolic events.

6

Raloxifene

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Selective estrogen receptor modulator—SERM
  • Mechanism
    • Agonist on bone
    • Antagonist at uterus
    • Decreases resorption of bone
  • Clinical use
    • Used to treat osteoporosis.
  • Toxicity
    • Increases risk of thromboembolic events

7

Hormone replacement therapy

  • Clinical use
  • Toxicity

  • Clinical use
    • Relief or prevention of menopausal symptoms (e.g., hot flashes, vaginal atrophy)
    • Osteoporosis (increases estrogen, decreases osteoclast activity).
  • Toxicity
    • Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial cancer, so progesterone is added.
    • Possible increased cardiovascular risk.

8

Anastrozole / exemestane

  • Aromatase inhibitors used in postmenopausal women with breast cancer.

9

Progestins

  • Mechanism
  • Clinical use

  • Mechanism
    • Bind progesterone receptors
    • Decreases growth 
    • Increases vascularization of endometrium.
  • Clinical use
    • Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding.

10

Mifepristone (RU-486)

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Competitive inhibitor of progestins at progesterone receptors.
  • Clinical use
    • Termination of pregnancy.
    • Administered with misoprostol (PGE1).
  • Toxicity
    • Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain.

11

Oral contraception (synthetic progestins, estrogen)

  • Mechanism
  • Toxicity

  • Mechanism
    • Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge.
    • No estrogen surge -->Ž no LH surge Ž--> no ovulation.
    • Progestins cause thickening of the cervical mucus, thereby limiting access of sperm to uterus. 
    • Progestins also inhibit endometrial proliferation, thus making endometrium less suitable for the implantation of an embryo.
  • Toxicity
    • Contraindications—smokers > 35 years old (increased risk of cardiovascular events), patients with history of thromboembolism and stroke or history of estrogen-dependent tumor.

12

Terbutaline

  • Mechanism
  • Clinical use

  • Mechanism
    • β2-agonist that relaxes the uterus
  • Clinical use
    • Used to decrease contraction frequency in women during labor.

13

Danazol

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Synthetic androgen that acts as partial agonist at androgen receptors.
  • Clinical use
    • Endometriosis and hereditary angioedema.
  • Toxicity
    • Weight gain, edema, acne, hirsutism, masculinization, decreased HDL levels, hepatotoxicity.

14

Testosterone, methyltestosterone

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Agonist at androgen receptors.
  • Clinical use
    • Treats hypogonadism and promotes development of 2° sex characteristics
    • Stimulation of anabolism to promote recovery after burn or injury.
  • Toxicity
    • Causes masculinization in females
    • Decreased intratesticular testosterone in males by inhibiting release of LH (via negative feedback) -->Ž gonadal atrophy.
    • Premature closure of epiphyseal plates. 
    • Increased LDL, decreased HDL.

15

Antiandrogens:
Mechanism

  • Testosterone --> [5α-reductase] --> DHT (more potent).

16

Finasteride

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Antiandrogen
  • Mechanism
    • A 5α-reductase inhibitor (decreases conversion of testosterone to DHT).
    • Promotes hair growth
  • Clinical use
    • Useful in BPH.
    • Used to treat malepattern baldness.
  • Toxicity
    • To prevent male-pattern hair loss, give a drug that will encourage female breast growth.

17

Flutamide

  • Type of drug
  • Mechanism
  • Clinical use

  • Type of drug
    • Antiandrogen
  • Mechanism
    • A nonsteroidal competitive inhibitor of androgens at the testosterone receptor
  • Clinical use
    • Used in prostate carcinoma.

18

Ketoconazole

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Antiandrogen
  • Mechanism
    • Inhibits steroid synthesis (inhibits 17,20-desmolase).
  • Clinical use
    • Used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
  • Toxicity
    • Gynecomastia and amenorrhea

19

Spironolactone

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Antiandrogen
  • Mechanism
    • Inhibits steroid binding, 17α-hydroxylase, and 17,20-desmolase.
  • Clinical use
    • Used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
  • Toxicity
    • Gynecomastia and amenorrhea

20

Tamsulosin

  • Mechanism
  • Clinical use

  • Mechanism
    • α1-antagonist
    • Selective for α1A,D receptors (found on prostate) vs. vascular α1B receptors.
  • Clinical use
    • Used to treat BPH by inhibiting smooth muscle contraction

21

Sildenafil, vardenafil

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Inhibit phosphodiesterase 5, causing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection.
    • Sildenafil and vardenafil fill the penis.
  • Clinical use
    • Treatment of erectile dysfunction.
  • Toxicity
    • Headache, flushing, dyspepsia, impaired blue-green color vision.
    • Risk of life-threatening hypotension in patients taking nitrates.
    • Hot and sweaty,” but then Headache, Heartburn, Hypotension.

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