Pharm Flashcards
administration of testosterone
IM or transdermal
cannot be administered oral
reason testosterone not oral
metabolized by small intestine and undergoes extensive first pass
low bioavailability
topical gel
acts as 24 h depot
no patch on scrotum
can absorb too much testosterone
caution with MRI and testosterone patch
aluminum can cause burns
adverse reactions in female partner of patch
acne and abnormal hair growth
children coming in contact with gels and topical solutions
virilization can occur
testosterone esters
testosterone cypionate and enanthate
more lipophilic
administration of testosterone esters
IM longer duration (administer every 2-4 weeks)
use of testosterone esters
hypogonadism
metastatic breast cancer in women
17 alpha alkylated testosterone
methyltestosterone, fluoxymesterone
use of 17 alpha testosterone
hypogonadism
metastatic breast cancer in women
contraindications 17 alpha testosterone
male breast cancer
prostate cancer
pregnancy
adverse reactions 17 alpha testosterone
cholestatic hepatitis and jaundice
edema
liver cancer
bleeding (decline in II, V, VII, and X)
adverse reactions all testosterone analogs
salt and water retention leading to HTN
jaundice (greatest risk with 17 alpha)
hepatic carcinomas from high dose or prolonged use
MOA danazol
depreses preovulatory surge in FSH and LH which results in reduction of estrogen and progesterone
anovulation
uses danazol
endometriosis
hereditary angioedema
fibrocytic breast disease
adverse effects danazol
weight gain acne thrombosis mood swings hepatic dysfunction
contraindications danazol
pregnancy
breast feeding
MOA stanazolol
derivative 17alpha
increases C1 inh and C4
use stanazolol
hereditary angioedema
drug contraindicated for hereditary angioedema
ACEi
adverse effects stanazolol
increased bleeding times (decrease II, VII, IX, X) edema acne virilization in women, baldness hepatic toxicity
contraindications stanazolol
pregnancy
male breast cancer or prostate cancer
female breast cancer with hypercalcemia
MOA oxandrolone
derivative of testosterone
high anabolic to androgenic ratio
use oxandrolone
weight gain
side effects oxandrolone
edema, water retention
HTN
irritability, aggression, excitation
contraindications oxandrolone
breast cancer (men or women) prostatic cancer pregnancy
MOA finasteride and dutasteride
reduce DHT
finasteride type 2 competitive inhibitor
dutasteride type 1 and 2 competitive inhibitor
use finasteride and dutasteride
BPH (may take 6 weeks to reduce)
male baldness
MOA tamsulosin and alfuzosin
alpha 1 adrenergic receptor inhibitors
decrease smooth muscle tone in prostate and bladder neck
adverse effects finasteride and dutasteride
gynecomastia
decrease PSA
elevated T but decreased DHT
hepatic dysfunction-finasteride
contraindications finasteride and dutasteride
contraindicated in women and children
should not handle tablets if pregnant
MOA leuprolide
GnRH agonist
continuous GnRH leads to down regulation of LH and FSH and decreased T
use leuprolide
prostatic cancer
endometriosis
adverse effects leuprolide
hot flashes/night sweats
gynecomastia
bone pain, higher risk of osteoporosis
greater risk of thrombosis
MOA flutamide
interferes with binding of DHT and T
use flutamide
prostatic cancer (oral) acne (topical
side effects flutamide
gynecomastia
elevated liver function tests
estrogen synthesis premenopausal
granulosa cells of ovary
estrogen synthesis pregnancy
fetoplacental unit
conversion of androstenedione and testosterone to estrone
hepatic tissue and adpisoe
most potent endogenous estrogen
17B estradiol
starting point of estrogen
cholesterol
excretion of estrogen
conjugated with glucuronide and sulfate conjugates
estrogen in ovary
follicular growth
estrogen in uterus
endometrial growth
estrogen in vagina
cornification of epithelial cells with thickening and stratification of epithelium
estrogen in cervix
lowers viscosity
helps the swimmers
estrogen on external and internal genitalia
development and maintenance
estrogen on bone
osteoblastic
estrogen on cholesterol
hypocholesterolemic effect
estrogen on electrolytes
retention of NaCl and water by kidney
sites of synthesis progesterone
ovary (corpus luteum)
placenta
adrenal cortex
testis
physiological action of progesterone
secretory endometrium
increases viscosity
decline initiates mensturation
hormones in follicular phase
pulsatile GnRH leading to pulsatile FSH and LH
ovary leading to E and P
E inhibits release of FSH and LH from pituitary
hormones midcycle
E positive feedback on pituitary
preovulatory surge of LH and FSH
hormones in luteal phase
E and P from corpus luteum
P controls LH, important for implantation
drop in P leads to menses
if pregnancy occurs, hCG maintains elevated E and P
therapeutic use of E and P
contraception and postmenopausal hormone therapy
therapeutic use of P only
dysmenorrhea
endometriosis
dysfunctional uterine bleeding
monophasic OCP
constant level of estrogen and progesterone
biphasic OCP
2 levels of progesterone and constant estrogen
triphasic OCP
3 levels of progesterone with estradiol
Mircette
2 days placebo
only 5 days of unopposed estrogen-prevents early folliculogenesis during placebo period
fewer estrogen-withdrawal HA
Yaz
4 days of placebo
24 days of EE and diospirenone
used for premenopausal dysphoric disorder
Seasonale
84 days with 7 days of placebo
Seasonique
10 EE instead of placebo
better follicular suppression and less unscheduled bleeding
Lybrel
365 days without placebo or pill free days
Xulane
patch with norelgestromin
3 weeks on, 1 week off
localized rash
NuvaRing
EE and etonogestrel
inserted for 3 weeks, 1 break week
synthetic estrogens
mestranol and EE
mestranol metabolized to EE to be active
less weight gain progesterone component
drospirenone
also less acne
monitor while on drospirenone
monitor K
antimineralocorticoid component
highest androgenic activity progestins
levonorgestrel and norgestrel
leads to acne and hirsutism
timing for effectiveness tricyclics
7 days
timing for effectiveness monophasics
21 days
starting of pack
first or fifth day of menses
timing of pills
same time of day to minimize adverse effects
better therapeutic success
general adverse OCP effects
nausea, headache, breast tenderness, weight gain, bleeding, migraines, depression, lethargy
metabolic adverse OCP effects
decreased HDL, worsens abnormal glucose tolerance, increased gall stones
cardiovascular adverse OCP effects
increased coag factors II, VII, VIII, IX, X
greater platelet aggregation
higher incidence of thrmbophlebitis and thromboembolism
higher incidence of HTN and MI
higher incidence thrombotic strokes
contraindications OCP
pregnancy
thrombophlebitis or thromboembolic disease
breast or estrogen dependnet carcinoma
cerebrovascular or CAD
liver disease
cholestatic jaundice during pregnancy or with OC
estrogen associated benign or malignant hepatic tumors
diabetes with vascular disease
cigarette smoker (>15/day) over 35
non-contraceptive benefits OCP
cycle regulation decreased flow increased bone mineral density decreased dysmenorrhea decreased peri-menopausal symptoms decreased acne decreased hirsutism decreased endometrial cancer decreased epithelial ovarian cancer decreased fibroids, fewer ovarian cysts lower ectopic pregnancy
PID patient with past ectopic pregnancy put them on
OCP
side effects due to excess estrogen
nausea, bloating HA cyclic weight gain irritability chloasma, hyperpigmentation hypermenorrhea hypertension breast fullness leg cramps, edema
side effects due to too little estrogen
spotting and bleeding early hypomenorrhea nervousness vasomotor symptoms atrophic vaginitis
side effects due to progestin excess
depression, fatigue
breast regression
hirsutism
libido change