Anabolic Steroids Pharm

Front 1

what is the role of DHT?

Back 1

testosterone is a prohormone for DHT

Front 2

effects of DHT

Back 2

?

Front 3

what are general effects of structure on function of testoterones?

Back 3

?

Front 4

what is primary testicula failure and how is it treated?

Back 4

?

Front 5

what is secondary testicular failure and how is treated?

Back 5

?

Front 6

lab testing for testostone, FSH, LH etc

Back 6

?

Front 7

controversy of steroids in athletes

Back 7

?

Front 8

male menopause treatment and controversy?

Back 8

?

Front 9

side effects of testosterones

Back 9

?

Front 10

treatement for over production of androgen

Back 10

?

Front 11

effect of long acting GnRH analogs/

Back 11

?

Front 12

ketoconazole

Back 12

?

Front 13

finasteride

Back 13

5alpha recutase inhibitor
effective in benign prostate hyperplasia

other stuff?

Front 14

male contraceptives

Back 14

?

Front 15

1. Describe the sources of anabolic/androgenic hormones.

Back 15

a. In males the androgens are synthesized in the testes and adrenal cortex.
b. In females the androgens are synthesized in the ovaries and adrenal cortex.

Front 16

How are anabolic steroids synthesized?

Back 16

c. For synthesis of androgens from cholesterol, functioning 17-hydroxylase and 3-hydroxysteroid dehydrogenase are needed (also cholesterol desmolase and 17,20-desmolase). Adrostenedione is synthesized in the adrenal cortex (zona reticularis) and converted to testosterone in the testis.

Front 17

what regulates secreation of androgens?

Back 17

d. Gonadotropin releasing hormone is secreted by the hypothalamus and causes release of leutenizing hormone and follicle stimulating hormone from the pituitary. LH and FSH work on the testis to stimulate testosterone production and spermatogenesis. Testosterone gives negative feedback to the hypothalamus and pituitary to suppress GnRH and LH/FSH secretion, respectively.

Front 18

2. Define the roles of LH and FSH on gonadal function. Define the importance of androgens for sexual differentiation and puberty.

Back 18

a. Prior to puberty testosterone levels are low. At puberty, LH secretion increases and stimulates testosterone production in the testes (Leydig cells produce testosterone). Testosterone is required for spermatogenesis.
b. Follicle stimulating hormone binds to Sertoli cell receptors in the testes and stimulates spermatogenesis. Once this occurs, spermatogenesis can be maintained by adequate levels of testosterone.
c. In addition to the increase in testosterone that occurs at puberty, there are surges of testosterone during certain periods of gestation and infancy. The first surges of testosterone are important for development of primary sex characteristics (reproductive organs). The second surge during puberty induces the development of secondary sex characteristics (masculinization).

Front 19

androgens have what two effects?

Back 19

a. Androgens have anabolic and androgenic effects. The androgen effects include the production of masculine characteristics. The anabolic effects include overall body growth, including increased protein synthesis and decreased protein breakdown.

Front 20

what is relation of testosterone to DHT?

Back 20

b. In most tissues, testosterone serves as a prohormone. Many tissues contain 5-reductase, which catalyzes the conversion of testosterone to dihydrotestosterone (DHT). The cytosolic androgen receptor exhibits a higher affinity for DHT than testosterone, and the DHT-receptor complex is more readily transported to the nucleus than the T-receptor complex

c. In the hypothalamus and pituitary, testosterone is the active steroid and is responsible for feedback inhibition.

Front 21

what are the causes of primary hypogonadisM

Back 21

b. Primary causes include genetic/chromosomal causes (i.e. Klinefelters syndrome) and direct damage to Leydig cells or seminiferous tubules.

Front 22

what is the level of testerone and gonadotrpin in primary hypodandism?

Back 22

testerone-low
gonadotropin - high

***************

Front 23

what is used to treat primary hypogonadism?

Back 23

enanthate or cypionate

Front 24

what are enanthate and cypionate?

Back 24

long acting testoserone esters

Front 25

c. Secondary testicular failure is due to ?

Back 25

lack of gonadotropins. This again may be a genetic abnormality (i.e. Prader-Willi syndrome) or may be due to hypopituitarism or decreased hypothalamus release of GnRH.

Front 26

in secondary hypogonadism what will testerone and gonadotropin levels be?

Back 26

test-low
gonad-low

*******

Front 27

how is secondary hypogonadism treated?

Back 27

ii. Treatment should include treating the underlying cause of the hypogonadism if possible. Gonadotropins have been used, and adrogens are not added until the time of normal puberty. You want to slowly increase to mimic the normal surge of testosterone

Front 28

i. Symptoms of high androgen levels (exogenous or endogenous) include:

Back 28

1. Virilizing effects in adolescent males and females – acne, hirsuitism, male pattern baldness, coarsening of the voice
2. Inhibition of spermatogenesis
3. Feminizing effects because testosterone is converted to an estrogen by aromatase enzymes in peripheral tissues.
4. Hepatic abnormalities – cholestatic hepatitis, hepatic adenocarcinoma
5. Changes in lipoprotein profiles (decrease HDL, increase LDL)
6. Increase in aggressive behavior (roid rage) can cause psychotic symptoms

Front 29

ii. Some situations in which suppression of androgens would be favorable include

Back 29

1. Male pattern baldness
2. Virilizing syndromes in women (i.e. hirsutism)
3. Acne
4. Hyperplasia and carcinoma of the prostate
5. Male contraception

Front 30

iii. Hypergonadism can be treated by

Back 30

androgen suppression, inhibitors of androgen synthesis, 5-reductase inhibitors, and androgen receptor antagonists.

Front 31

c. The effects of androgens on increasing muscle mass is controversial. ?

Back 31

i. They are effective when used to counter muscle wasting due to various causes, such as muscle wasting due to anti-inflammatory steroid use. They induce a positive nitrogen balance in hypogonadal individuals.
ii. Use by athletes with normal gonadal function has not been proven to reliably increase muscle mass. There is often an increase in muscle mass seen in these individuals, but this may be due to increased aggressiveness leading to a greater training limit, rather than the steroids actually causing more muscle to form.
iii. Increased muscle mass is seen in well-trained athletes who use these, but not in a normal male.
iv. There may be a more beneficial effect in females
v. Double-blind studies have yielded both positive and negative results regarding use of androgens to increase muscle mass.

Front 32

5. Describe the rationale for the clinical uses of anabolic/androgenic hormones in: anemia

Back 32

b. Androgens stimulate RBC development, both directly and indirectly. They stimulate the synthesis of erythropoietin by the kidney (indirectly increasing RBC production) and also directly stimulate elements in the bone marrow causing stem cell differentiation. Because of these effects, androgens are useful in treating various anemias.

Front 33

6. Compare the routes of administration, absorption, and relative duration of action of synthetic androgens and testosterone.

Back 33

a. Testosterone is a poor drug. It exhibits a high first pass effect when given orally. When injected, it is rapidly absorbed and metabolized. It also has mixed anabolic and androgenic effects that cannot be separated out.
b. Synthetic manipulation of testosterone seeks to solve these problems.
i. Type B manipulation: 17 substitution (methyltestosterone)
ii. Type C manipulation: ring alteration (mesterolone)
iii. Type B and Type C manipulation allows drugs to be orally active. These drugs are not metabolized to testosterone proper. They can cause liver toxicity and liver cancer.
iv. Type A manipulation: 17 esterification (enanthate or cypionate)
1. This modification causes absorption of the drugs to be greatly delayed. They are injected weekly or monthly and are metabolized to testosterone proper.
v. Most preparations involve combinations of type AC or type BC changes.

Front 34

what are the type B and C manipulations of testostoner?

Back 34

methyltestosterone-typeB

mesterolone-type C

Front 35

what is use/problems of Type B and C?

Back 35

iii. Type B and Type C manipulation allows drugs to be orally active. These drugs are not metabolized to testosterone proper. They can cause liver toxicity and liver cancer.

Front 36

what are the type A manipulations of testosterone?

Back 36

enanthate or cypionate

Front 37

what is use of type A manipulations

Back 37

1. This modification causes absorption of the drugs to be greatly delayed. They are injected weekly or monthly and are metabolized to testosterone proper.

Front 38

how are most preparations of synthetic androgens done?

Back 38

v. Most preparations involve combinations of type AC or type BC changes.

Front 39

7. Describe the adverse effects of androgens/anabolic steroids when used in males and females

Back 39

a. Side effects of high androgen levels:
i. Virilizing effects: acne, hirsutism, male pattern baldness, coarsening of the voice.
ii. Inhibition of spermatogenesis
iii. Feminizing side effects
iv. Hepatic abnormalities, including hepatocellular carcinoma
v. Changes in lipoprotein profiles (decrease HDL and increase LDL)
vi. Increase in aggressive behavior

Front 40

. Correlate the hepatotoxicity of certain androgens/anabolic steroids with their chemical structure.

Back 40

b. High, prolonged doses of drugs that have a 17 substitution or a ring alteration can cause liver toxicity and hepatocellular carcinoma. (types B and C)

Front 41

what are the drugs used for androgen suppression

Back 41

GnRH long acting- constant GnRH is inhibitory instead of stimulating

ketoconazole-blocks androgens synthesis at super high levels(higher than used in corticosteroid blocking) only mildly effective will lead to adrenal hyperplasia to overcome

finasteride- 5alphareductase inhibitor

cyproterone acetate/flutamide-androgen receptor blockers

androgen receptor blockers/5alphareductase inhibitors are both used in prostate cancer.

Front 42

what is gossypol?

Back 42

destroys seminefarious tubules inhibits speratogenesis also decreases sperm motility

Front 43

levels in semineforous tubule disease?

Back 43

high FSH
normal LH
low T

Front 44

levels in leydig cell failure?

Back 44

normal FSH
High LH
low T