Repro Drugs Flashcards
Mechanism of leuprolide
GnRH analog with agonist properties when used in pulsatile fashion
antagonist when used in continuous fashion (downregulates GnRH receptor in pituitary –> decreased FSH/LH)
Pulsatile use of leuprolide
infertility
Continuous use of leuprolide
prostate cancer (following androgen receptor blockade with flutamide)
uterine fibroids
precocious puberty
Toxicity of leuprolide
antiandrogen, nausea, vomiting
Name the estrogens
ethinyl estradiol, DES, mestranol
Mechanism of estrogens
bind estrogen receptors
Use of estrogens in females
hypogonadism or ovarian failure, menstrual abnormalities, hormone replacement therapy in postmenopausal women
Use of estrogens in males
androgen-dependent prostate cancer
Toxicity of estrogens
increase risk of endometrial cancer
bleeding in postmenopausal women
clear cell adenomcarcinoma of the vagina (in women exposed to DES in utero)
increased risk of thrombi
Contraindications to estrogen use
ER+ breast cancer
history of DVTs
Name the selective estrogen receptor modulators
clomiphene, tamoxifen, raloxifene
Mechanism of clomiphene
antagonist at estrogen receptors in the hypothalamus
prevents normal feedback inhibition and increases release of LH and FSH from pituitary to stimulate ovulation
Use of clomiphene
infertility due to anovulation (PCOS)
Toxicity of clomiphene
hot flashes
ovarian enlargement
multiple simultaneous pregnancies
visual disturbances
Mechanism of tamoxifen
antagonist at breast
agonist at bone, uterus
Use of tamoxifen
to treat and prevent recurrence of ER/PR+ breast cancers
Toxicity of tamoxifen
increased risk of thromboembolic events
increased risk of endometrial cancer
Mechanism of raloxifene
antagonist at breast, uterus
agonist at bone
Use of raloxifene
to treat osteoporosis
Toxicity of raloxifene
increased risk of thromboembolic events only
Use of hormone replacement therapy
to relieve or prevent menopause symptoms (hot flashes, vaginal atrophy)
to treat osteoporosis (increase estrogen, decrease osteoclast activity)
Toxicity of hormone replacement therapy
unopposed estrogen replacement therapy –> increased risk of:
- endometrial cancer (so add progesterone)
- cardiovascular risk (possibly)
Mechanism and use of anastrozole/exemestane
aromatase inhibitors used in postmenopausal women with ER+ breast cancer
Mechanism of progestins
bind progesterone receptors and decrease growth and vascularization of the endometrium
Use of progestins
oral contraceptives
treatment of endometrial cancer
abnormal uterine bleeding
Mechanism of mifepristone
competitive inhibitor of progestins at progesterone receptors
Use of mifepristone
termination of pregnancy (administered with misopristol (PGE1)
Toxicity of mifepristone
heavy bleeding GI effects (nausea, vomiting, anorexia) abdominal pain
Mechanism of oral contraception (progestins and estrogen)
estrogen and progestins inhibit LH/FSH and thus prevent the estrogen surge
no estrogen surge prevents an LH surge and thus no ovulation occurs
Mechanism of progestins in OCP
thicken cervical mucus
inhibit endometrial proliferation (less suitable for implantation)
Contraindications for OCP use
smokers >35 years old (increase CVD risk)
patients with history of thromboembolism and stroke
history of estrogen-dependent tumor
Mechanism and use of terbutaline and ritodrine
beta2-agonist that relax uterus
used to decrease contraction frequency in women during labor (prolong labor)
Mechanism of danazol
synthetic androgen that acts as partial agonist at androgen receptors
Use of danazol
endometriosis
hereditary angioedema
Toxicity of danazol
weight gain edema acne hirsutism masculinization decrease HDL levels hepatotoxicity
Mechanism of testosterone, methyltestosterone
agonists at androgen receptors
Use of testosterones
treat hypogonadism
promote development of secondary sex characteristics
stimulate anabolism to recovery after burn or injury
Toxicity of testosterones
masculinization in females
decreased intratesticular testosterone in males by inhibiting release of LH (via negative feedback) –> gonadal atrophy
premature closure of epiphyseal plates
increased LDL and decreased HDL
Antiandrogens
finasteride, flutamide, ketoconazole, sprionolactone
testosterone –> DHT via 5-alpha reductase
Mechanism of finasteride
5alpha-reductase inhibitor (decreases conversion of testosterone to DHT)
Use of finasteride
BPH to decrease size and male pattern baldness
Mechanism of flutamide
nonsteroidal competitive inhibitor at androgen receptors
Use of flutamide
prostate carcinoma
Mechanism of ketoconazole
inhibits steroid synthesis (inhibits 17,20 desmolase)
Mechanims of spironolactone
inhibits steroid binding, 17alpha-hydroxylase, and 17,20 desmolase
Use of ketoconazole and spironolactone
to treat PCOS to reduce androgenic symptoms
Side effects of ketoconazole and sprinonolactone
gynecomastia and amenorrhea
Mechanism and use of tamulosin
alpha1-antagonist used to treat BPH by inhibiting smooth muscle contraction
selective for alpha1A,D receptors (found on prostate) vs. vascular alpha1B receptors
Mechanism of sildenafil, vardenafil, tadalafil
inhibit PDE5 –> increased cGMP and smooth muscle relaxation in corpus cavernosum –> increased blood flow and penile erection
Use of sildenafil, vardenafil, tadalafil
erectile dysfunction
Toxicity of sildenafil, vardenafil, tadalafil
headache, flushing, dyspepsia, cyanopsia (blue-tinted vision)
risk of life-treatening hypotension in patients taking nitrates
Mechanism of minoxidil
direct arteriolar vasodilator
Use of minoxidil
androgenetic alopecia
severe refractory hypertension
