Androgen, Anabolic Pharmacology Flashcards

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1
Q

An adult male has a low sperm count. Plasma testosterone is low and LH levels are high. What is the next test you should run? what is dx?

A

FSH levels- if normal = Leydig cell failure

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2
Q

Young athletes who abuse androgens should be made aware of the side effects of these drugs. Which one of the following is, however, not of concern and why?

Increased muscle mass
Anemia due to bone marrow failure
Overly aggressive behavior
Decreased spermatogenesis
Stunted growth
A

Anemia… androgens cause hematopoiesis

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3
Q
A week-old newborn male presents to clinic for a routine checkup.   The parents are concerned because he does not seem to have male genital characteristics. Physical examination reveals female external genitalia seen without a scrotum or descended testicles. What androgen is the patient lacking that is the cause of his condition?

(A) Androstenedione
(B) Androsterone
(C) Dehydroepiandrosterone (DHEA)
(D) Dihydrotestosterone (DHT)
(E) Testosterone
A

DHT

Primary sex chc - testosterone
external genitalia = DHT mediated

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4
Q

A 76-year-old man presents to the clinic for follow-up of his benign prostatic hyperplasia. He has been doing well with his symptoms since starting finasteride. He no longer has as much difficulty starting his stream and feels that he empties his bladder completely. What is the mechanism of action of finasteride?

(A) 5α-Reductase inhibitor
(B) α1-Antagonist
(C) GnRH agonist
(D) GnRH antagonist
(E) Nonsteroidal competitive inhibitor at the testosterone receptor
A

(A) 5α-Reductase inhibitor

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5
Q

A 17-year-old girl has never had a menstrual period. Physical examination shows a normal female body habitus, normal breast development, and normal appearing external genitalia. She has no axillary or pubic hair. The patient refuses to have a pelvic or rectal examination. Which of the following is the most likely explanation for the clinical presentation?

(A) Androgen insensitivity
(B) Congenital adrenal hyperplasia
(C) Ectodermal dysplasia
(D) A psychiatric disorder
(E) A sex chromosome mosaicism
A

Androgen insensitivity

Testosterone is responsible for

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6
Q

In a genetic male, Leydig cells support the development of what structure with what homo?

A

Androgens support Mesonephric ducts

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7
Q

mesonephric ducts (under influence of testosterone) develop into what structures in male? (5)

A

internal structures: “BEEDS”

Bladder trigone, Epididymus, Ejaculatory ducts, Ductus defeerens, Seminla vesicles,

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8
Q

DHT controls expression of what chc in males (2)

A

external genitalia before puberty

prostate

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9
Q

3 sites of Estrogen synthesis in females

A

ovaries, adrenals, peripheral conversion of DHEA

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10
Q

What is the only hormone that completes the loop of androgen synthesis with negative feedback? and how?

A

testosterone–> inhibits GnRH and LH/FSH production

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11
Q

What happens at puberty to increase testosterone produciton

A

LH produciton increases

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12
Q

What initiates spermatogenesis (cell and homo) and what maintains spermatogenesis?

A

FSH actiing on sertoli cell initiates it

maintianed by testosterone

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13
Q

If testis don’t drop what is the deficiency

A

DHT

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14
Q

In what 2 tissues in T not DHT the active steroid

A

hypothalamus and pituitary

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15
Q

DHT controls what aspects of reproductive development (and 3 examples)

A

differentiation of male accessory ducts and external genitalia:
prostate
penis
scrotum

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16
Q

T acts on what male reproductive tissues (4)

A

Seminiferous tubules, seminal vesicles, epididymus, vas deferens

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17
Q

17@ (typeB) or ring substiutions (type C) of T: are they metabolized to T?

A

no

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18
Q

17@ or ring substiutions of T: are they orally active

A

yes

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19
Q

methyltestosterone: orally active? what is the modification of T?

A

17@ (typeB) = orally active

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20
Q

mesterolone: orally active? what is the modification of T?

A

ring substiutions (type C) = orally active

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21
Q

ADEs (2) of 17@ (typeB) or ring substiutions (type C)

A

liver toxicity and cancer

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22
Q

Type A; enanthate or cypionate is what kind of change to T?

A

17B- esterification

23
Q

Type A; enanthate or cypionate/ 17B-esterification: orally active? mtb to T?

A

not orally active

is mtb to T

24
Q

all preparations of T have mixed anabolic and androgenic effects. What effect does the androgenic activity have on a person?

A

The androgenic effects blunt intrinsic testosterone production–> inhibition of spermatogenesis, etc

25
Q

What levels dx hypogonadism?

A

Testosterone levels low but gonadotropin (LH, FSH) levels high

26
Q

What is drugs (2) of choice to tx hypogonadism?

A

enanthate or cypionate = Long-acting testosterone ester

27
Q

lwevels that dx secondary testicular failure

A

Testosterone and gonadotropin levels low

28
Q

What familial condition causes secondary testicular failure

A

Prader-Willi syndrome

29
Q

tx for secondary testicular failure

A

gonadotropins, androgens at tim eof normal puberty

30
Q

Why is FSH level high in seminiferous tubule disease?

A

lack of inhibin produced by sertoli cells–> lack of inhibition of pituitary production of FSH

31
Q

What is low (2) and what is high in leydig cell failure

A

low: sperm count, testosterone
high: LH

32
Q

What effect do androgens have on RBC?

A

stimulate erythropoietin synthesis, recruit stem cells

33
Q

what condition are androgens contraindicated for?

A

aplastic anemia

34
Q

What condition do androgens cause

A

hepatocellular carcinmoa

35
Q

What should be used for aplsatic anemia besides androgens

A

colony stimulating factors

36
Q

What is Hereditary angioneurotic edema

A

Lack of an active inhibitor of the first component of compliment

  • complement cascade always ‘on’
  • blood vessel permeability increases
  • painful submucosal swelling develops
37
Q

What is used to tx Hereditary angioneurotic edema and MOA?

A

Danazol - icreases hepatic synthesis of the active inhibitor of thec omplement pathway

38
Q

Why are androgens not used to tx delayed growth in kids

A

they produce growth but also cause epiphyseal calcification

39
Q

What is needed to counter muscle wasting when using androgens?

A

PROPER NUTRITION

40
Q

How do androgens create muscle mass in athletes

A

increased training limit

41
Q

When is male menopause? why is androgen therapy not recommended?

A

androgen levels drop after 55–

increased risk of cancer

42
Q

Side effects of Androgens (6)

A
  1. virilizing effects in adolescents and females
  2. inhibtis spermatogenesis (dt decreased LH/FSH)
  3. Feminization - converted to estrogen by aaromatase
  4. heptic abnormalitites- hepatits, adenocarcinoma
  5. decreased HDL, ^LDL
  6. psychotic sx
43
Q

5 reasons to suppress androgens

A
  1. male pattern baldness
  2. virilization in women
  3. acne
  4. BPH and carcinoma of prostate
  5. male contraception
44
Q

MOA of leuprolide and Goserelin

A

inhibition of LH/FSH production. they are GnRH analogs which through continuous release suppresses Apit

45
Q

Ketoconazole MOA

A

Blocks steroid synthesis P450s

46
Q

side effect of ketoconazole and why

A

gynecomastia via increase of estrogen:testosterone ratio

47
Q

Finasteride MOA

A

5@ reductase inhbitior (stops DHT production)

48
Q

FInasteride used for?

A

BPH, hirsutism in women

49
Q

Cyproterone acetate and Flutamide MOA

A

block androgen receptors

50
Q

Cyproterone acetate and Flutamide uses (2)

A

Effective for excess androgen production in women

Effective for advanced prostate carcinoma

51
Q

What is the combined therapy for male contraception

A

GnRH suppression + T

52
Q

How does GnRH suppression + T work for male contraception without reducing genital development?

A

• Works bc the levels of testosterone required for spermatogenesis are much higher than those required for secondary sex chcs

53
Q

Gossypol MOA

A

Destroys elements of semiferous epithelium–>Impaired spermatogenisis.
Also directly decreases sperm motility