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Pharm > Androgens > Flashcards

Androgens Flashcards

1
Q

What cells synthesize testosterone? What is the precursor to this?

A

Cells of Leydig

Cholesterol

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2
Q

What are the two general functions of androgens?

A

Androgenic effects

Metabolic effects

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3
Q

What are the androgenic effects of androgens?

A

Maturation and continued function of male reproduction

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4
Q

What are the metabolic effects of androgens?

A

Regulates formation of Muscle, bone, marrow, liver

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5
Q

Describe the HPA axis in regards to the gonadotropes.

A

GnRH from hypothalamus goes to the pituitary gonadotropes, which release LH and FSH into the blood. These go to the testicular Leydig cells or Sertoli cells.

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6
Q

What are the cells in the pituitary that are stimulated by GnRH? What do they release?

A

Pituitary gonadotropes

LH and FSH

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7
Q

What is the function of LH in the male? Where does this go?

A

Stimulates the cells of leydig to secrete Testosterone

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8
Q

What is the function of FSH in the male? Where does this go?

A

Goes to sertoli cells, to secrete ABP and inhibin

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9
Q

What allows for a higher concentration of LH/FSH in the testicles?

A

Androgen binding protein

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10
Q

What is the enzyme that is present in the testicles that is not present in the adrenal cortex, and allows for the conversion of androstenedione to testosterone?

A

17-beta-HSD

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11
Q

What is the function of 5-alpha-reductase?

A

Converts testosterone into 5-alpha-dihydrotestosterone, a more potent form of testosterone

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12
Q

What is the general way in which GnRH is released from the hypothalamus?

A

Pulsatile fashion

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13
Q

How does LH increase the production of testosterone?

A

increasing the expression of cholesterol desmolase

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14
Q

What is the feedback mechanism for LH?

A

Testosterone inhibits hypothalamus from releasing GnRH

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15
Q

What are the two products of further metabolizing testosterone? What do these do in the HPA axis?

A

DHT
Estradiol

Inhibit pituitary gonadotropes

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16
Q

Draw out the pathway of cholesterol synthesis.

A

Draw.

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17
Q

What is the enzyme Leydig cells express that convert androstenedione to testosterone?

A

17beta-HSD

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18
Q

True or false: testosterone is highly bound to albumin in the blood. What (other) protein is it bound to?

A

True

Sex hormone binding globulin.

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19
Q

What happens to the amount of sex hormone binding globulin as we age? What is the significance of this?

A

Decreases, meaning less testosterone circulating as we age.

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20
Q

What is the MOA of testosterone? DHT?

A

Binds to cytoplasmic receptor, which can then transverse the nucleus, and increase transcription

DHT is the same, but more potent

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21
Q

What is the enzyme that converts testosterone into estradiol?

A

p450s

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22
Q

What enzyme is found in high concentrations in the prostate? What is the significance of this?

A

5-alpha-reductase

Increases DHT there

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23
Q

What is the chemical that can freely diffuse into cells, and can then by converted into testosterone? What is the enzyme that does this?

A

DHEAS

17-beta-HSD

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24
Q

What is the effect of testosterone in the liver in regards to lipids? What is the significance of this?

A

Increase VLDL and LDL
Decrease

This may be why males have an increased rate of artherosclerosis

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25
Q

What is the effect of testosterone on lipid accumulation in adipocytes?

A

Inhibits

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26
Q

What is the effect of testosterone on blood glucose levels? How?

A

Lowers by increasing the expression of glucose transporters on the plasma membrane of adipocytes

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27
Q

What is the effect of testosterone on RBCs?

A

Increases production of erythropoietin

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28
Q

Why is it that very close monitoring is required when using testosterone replacement therapy in growing children?

A

May prematurely close the growth plates

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29
Q

What is the gynecological disorder where testosterone is used?

A

Severe endometriosis

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30
Q

What are the primary causes of hypogonadism? (2)

A
  • Testicular dysfunction (cryptorchidism)

- Klinefelter

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31
Q

What is hypergonadotropic hypogonadism?

A

Primary cause of hypogonadism with increased levels of GnRH, but low levels of testosterone

32
Q

What is hypogonadotropic hypogonadism?

A

Secondary cause of hypogonadism with lowered levels of GnRH, and low testosterone levels

33
Q

What is methyltestosterone? Route of administration? SIde effects?

A

-17-alkylated derivative of testosterone
This prevents first pass effect of the liver
-PO
-Causes hepatocellular CA

34
Q

What is the MOA of testosterone enanthate? Route of administration?

A

Ester of testosterone that is VERY lipophilic.

Causes slow release and slow metabolism.

IM

35
Q

What is the route of exogenous testosterone?

A

Transdermal

36
Q

What is the two hematological/metabolic side effect of testosterone replacement?

A
  • Polycythemia

- Increased FAs, LDL in circulation

37
Q

How does exogenous testosterone cause gonadal atrophy?

A

Causes increased feedback to inhibit FSH/LH production, which lowers endogenous testosterone synthesis

38
Q

What is the main use of antiandrogens in females?

39
Q

What are the four main uses of antiandrogens in makes?

A
  • Precocious puberty
  • BPH
  • Prostate CA
  • Alopecia
40
Q

What is the general MOA of GnRH agonists/antagonists?

A

Increase/inhibit LH production by the pituitary

41
Q

What are the two androgen receptor antagonists?

A

Flutamide

Bicalutamide

42
Q

What is the MOA, use, and side effects of: Flutamide?

A

Competitive antagonist of the androgen receptor

Treat prostate CA

Causes mild gynecomastia, and is mildly hepatotoxic

43
Q

What is the MOA, use, and side effects of: Bicalutamide?

A

Competitive antagonist of the androgen receptor

Treat prostate CA

Causes mild gynecomastia, and is mildly hepatotoxic

44
Q

Why aren’t androgen receptor antagonists used alone? What are the usually used with?

A

Will cause an increase in LH and FSH production.

Usually given in conjunction with GnRH analogs

45
Q

What is the MOA, use, and side effects of: Enzalutamide? (3 MOAs)

A
  • Competitively inhibits androgen receptors
  • Inhibits the translocation of the nuclear androgen receptor
  • Blocks coactivator recruitment
46
Q

What is the MOA of Leuprolide? Use?

A

GnRH agonists

Treats prostate CA

47
Q

What is the MOA of Goserelin? Use?

A

GnRH agonists

Treats prostate CA

48
Q

How do GnRH agonists decrease testosterone production?

A

Constant presence lower the affinity of receptors (although there is an initial increase in LH)

49
Q

How does the affinity of GnRH agonists compare to physiological GnRH?

A

Increased binding affinity and decreased proteolysis

50
Q

What are the side effects of GnRH agonists? (4)

A

Sexual dysfunction
Osteopenia
Anemia
Fatigue

51
Q

Why are androgen antagonists coadministered with GnRH agonists?

A

Prevent the initial surge in testosterone that can lead to prostate CA growth

52
Q

What is the MOA and use for Degarelix? What is the benefit of this drug over others in its clas?

A

GnRH receptor antagonist with a faster onset than others, and does NOT cause a testosterone surge

53
Q

What is the MOA of Abiraterone? Use? Side effects?

A

Blocks 17-alpha-hydroxylase

Treats metastatic prostate CA

Adrenal insufficiency and hepatotoxic

54
Q

How does Abiraterone cause hypokalemia and fluid retention?

A

Inhibiting 17-alpha- hydroxylase production also shunts cholesterol down cortisol production pathway

55
Q

What is the MOA of Finasteride? Use? Side effects?

A

Inhibit 5-alpha-reductase, reducing DHT in the prostate

BPH treatment

Impotence and gynecomastia

56
Q

What is the MOA of Dutasteride? Use? Side effects?

A

Inhibit 5-alpha-reductase, reducing DHT in the prostate

BPH treatment

Impotence and gynecomastia

57
Q

What is the causative agent in male pattern baldness?

A

DHT-there is increased levels of 5-alpha- reductase in baldies

58
Q

How do high levels of DHT cause baldness?

A

Induce apoptosis of dermal papilla cells

59
Q

What is the drug of choice for treating male pattern baldness?

A

Finasteride (propecia)

60
Q

Why aren’t 5 alpha reductase inhibitors used in the treatment of prostate CA? (2 reasons)

A

Worsens high grade CAs

Lowers PSA levels

61
Q

What are the 3 neurogenic causes of ED?

A

Neuropathy
Stroke
Spinal cord injury

62
Q

What are the 2 hormonal causes of ED?

A

Hypogonadism

Hyperprolactinemia

63
Q

What are the 3 vasculogenic causes of ED?

A

Arthrosclerosis
DM
HTN

64
Q

What are the drugs that can cause ED? (3)

A

EtOH
Antihypertensives
Antidepressants

65
Q

What is the MOA of an erection?

A

Increased NO production, causing increase in cGMP.

This causes relaxation of smooth muscles in the corpus cavernosum

66
Q

What is the MOA of Sildenafil? Use? Side effects?

A

Inhibits phosphodiesterase-5 (PDE-5), increasing cGMP levels.

Treats ED

MI (maybe)

67
Q

What is the MOA of Vardenafil? Use? Side effects?

A

Inhibits phosphodiesterase-5 (PDE-5), increasing cGMP levels

Treats ED

MI (maybe)

68
Q

What is the MOA of Tadalafil? Use? Side effects?

A

Inhibits phosphodiesterase-5 (PDE-5), increasing cGMP levels

Treats ED

MI (maybe)

69
Q

Which of the PDE5 inhibitors has the longest half-life?

A

Tadalafil (18 hours)

70
Q

How are PDE-5 drugs metabolized? What is the significance of this?

A

Liver p450s, meaning anything that inhibits these will increase duration of action of PDE5s

71
Q

What is the major drug interaction with PDE5 inhibitors?

A

Nitrates can cause an unsafe drop in blood pressure

72
Q

What is the role of the inhibin protein that sertoli cells secrete?

A

Inhibits pituitary gonadotropes from secreting LH and FSH

73
Q

What is the feedback mechanism for the gonadotropes on the hypothalamus (1)? Pituitary (4)?

A

Hypothalamus is inhibited by testosterone

Pituitary is inhibited by testosterone, DHT/E2, and Inhibin

74
Q

What is the hormone that is responsible for the closure of the epiphyseal growth plates? What is the significance of this in regards to exogenous androgens?

A

Estradiol

Need to limit use in children

75
Q

What are the two 5-alpha-reductase inhibitors?

A

Finasteride

Dutasteride

Pharm (73 decks)

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