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27 Cards in this Set

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what hormone do the leydig cells of the testes make?
the androgen testosterone is made in the testes
where is testosterone produced?
leydig cells of the testes, adrenal glands, and small amount in the ovary
what are the physiological effects of androgens?
1)ANABOLIC: increase in overall body growth, muscle mass, and RBC production; 2)ANDROGENIC: growth of the larynx and skeleton, development of facial hair, darkening of skin 3)virilization and spermatogenic
what do androgens stimulate in both sexes?
body hair growth, positive nitrogen balance, bone growhth, muscle development, and erythropoiesis
explain the serum testosterone levels of a male throughout life.
TESTOSTERONE PEAKS: during gestation -fetal male development, at birth, during infancy, then largest peak at puberty; LOW TESTOSTERONE: childhood; testosterone decreases after adulthood as males age
what are the serum differences of testosterone levels of men and women while going through puberty?
men: ~500ng/dl; women: ~30ng/ml
describe the pathway from cholesterol to testosterone synthesis.
cholesterol -> pregnenolone -> progesterone -> 17-Hydroxyprogesterone -> Androstenedione -> testosterone
if testosterone is in the presence of (CYP 19)aromatase, what does it turn into?
if testosterone is in the presence of 5 alpha reductase, what does it turn into? where are the intranuclear receptors for this hormone?
DHT (dihydrotestosterone) binds better to androgen receptor than testosterone; external genitalia and hair follicles
what are the direct effects of testosterone and where are the receptors?
receptors are on the internal genitalia for wolffian development during gestation; on skeletal muscle
LH acts on ________ cells to produce testosterone and FSH acts on __________ cells to produce inhibin (negative feedback on pituitary).
leydig; sertoli
How are the synthetic analogues administered and why?
because of signigican first-pass metabolism, adrogens are best injected or given transdermally.
name some therapeutic uses of androgens.
ANDROGENIC EFFECTS: replacement therapy in male hypogonadism; ANABOLIC EFFECTS: (remember anabolism is to build) treat osteoporosis and severe burns, speed recovery from surgery and to counter the catabolic effects of externally administered adrenal cortical hormones; GROWTH promotion in prepubertal body with pituiatry dwarfism; DANAZOL (mild androgen used to treat endometriosis and fibrocystic dz of the breast - no effect on aromatase; AEs: weight gain, acne, decreased breast size, deepening voice, increase libido and hair growth; occasionally reported that it suppresses adrenal function)
why are androgens abused? name the precursor to testosterone that is commonly found in these products.
athletes and body builders take advantage of androgens anabolic mechanism of building lean body mass, muscle strength, and increase in aggression; DHEA
what are the adverse effects of androgen use in females and males?
females: virilization, hirsuitism, deepened voice, menstrual irregularities, (if pregnant, virilization of the fetus); MALES: excessive doses can cause feminization because continuous stimulation will inhibit feedback and cause conversion of exogenous androgens to estrogens (gynecomastia, small testes, and infertility); HIGH DOSES also cause behavior effects, including hostility and aggression. BOTH SEXES: cholestatic jaundice, elevate liver enzymes, possible hepatocellular carcinoma
list the synthetic androgens.
methyltestosterone, fluoxymesterone, oxandrolone, stanozolol
there are four categories of androgen antagonists, what are they?
1) gonadotropin releasing analogues (leuprolide) given in continuous dose; 2)Receptor Inhibitors (flutamide and bucalutamide and cyproterone); 3) Steroid synthesis inhibitors(ketoconazole and spironolactone); 4) 5alpha reductase inhibitors (finasteride)
name the treatments for hypogonadism.
androgen replacement therapy includes: testosterone enanthate or testosterone cypionate, methyltestosterone, fluoxymesterone, testosterone patch
what meds would you use to treat anabolic protein synthesis?
oxandrolone or stanozolol
what meds would you use to treat BPH (benign prostatic hypertrophy)?
5a reductase inhibitor: finasteride (aka Propecia- used for hairloss)
what meds would you use to treat prostate carcinoma?
GnRH agonist like leuprolide (continuous dose) given with an androgen receptor antagonist (ie. flutamide); the flutamide is given to prevent the initial surge in testosterone production that may cause a flare in tumor growth
what meds would you use to treat hirsutism (hair growth)?
combined oral contraceptive, spironolactone (steroid synthesis inhibitor and a K+ sparing diuretic), flutamide (receptor inhibitor), GnRH agonist (continuous dose)
in regard to flutamide and bicalutamide, how do they work? when are they used? what are the side-effects?
they are nonsteroidal drugs that act as competitive antagonists at teh androgen receptor; used to treat PROSTATE CA (usually in combo with GnRH analogue); S/E: hepatitis and gynecomastia
what tissues rely on DHT and therefore would benefit from a 5a reductase inhibitor?
prostate and hair follicles have receptors for DHT and since 5a reductase is needed to convert testosterone to DHT, this group of drugs would be benefical in treating BPH and hair loss; since it doesn't affect testosterone action, there are less s/e like impotence, infertility, and loss of libido (FINASTERIDE is the drug)
why would combined hormonal contraceptives work in women with hirsutism?
since estrogen causes an increase in the SHBG production from the liver, less testosterone would be present in the blood since it would now bind to the SHBG and decrease the androgen effects
how does the antifungal, ketoconazole prevent steroid synthesis?
ketoconazole reduces the enzyme 17a-reductase; this enzyme is needed to convert many of the steroids into their next steps (ie. from pregnenolone to 17-hydroxypregnenolone); therefore it is used to treat patients with steroid-responsive metastatic tumors
what happens when you expose too much hormone to anything?
the receptors will downregulate - the mechanism behind contiuous GnRH stimulation