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Endocrine > Androgens & Anabolic Steroids > Flashcards

Androgens & Anabolic Steroids Flashcards

1
Q

Where are steroids hormones primarily secreted from?

A
  1. Testes

- Lesser amounts from adrenals (10% males)

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2
Q

Where is Testosterone generated in females and how much?

A
  1. Ovaries generate about half the circulating T
  2. Adrenals contribute to other half
    - Initially as Androstenedione and DHEA
  3. T levels in females are less than 10% of males
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3
Q

What is the principal androgen?

A
  1. Testosterone

8 mg/day, 0.5 ug/dL (males)

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4
Q

What is DHEA?

A
  1. Dehydroepiandrosterone
  2. Most abundant testosterone intermediate
  3. Much weaker androgenic properties
  4. Produced in Adrenals
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5
Q

What is Androstenedione?

A
  1. Last intermediate in T synthesis
  2. 2-3 mg/day from adrenals and testes/ovaries, 0.15 ug/dL.
  3. Levels vary greatly in females w/ menstrual cycle
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6
Q

What are the therapeutic uses of Androgens?

A
  1. Male Hypogonadism (T def.)
    - Prepubertal/postpubertal
  2. Male Senescence/Impotence
    - May increase bone mass, libido, cause prostatic hypertrophy
  3. Wasting states (AIDS) Anabolic needed
  4. Female Hypopituitarism/hypogonadism
    - Androgens are necessary fro long-bone growth, some secondary sex charac.
  5. Endometriosis
    - Suppression of ovarian hormones (Danocrine)
  6. Male anti-fertility? (still impotent)
  7. Enhancement of female libido?
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7
Q

What are the therapeutic uses of Anti-Androgens?

A
  1. Prostate Cancer
  2. Benign Prostatic Hypertrophy (BPH)
    - Reverse impaired urinary flow
  3. Female hirsutism
  4. Male pattern baldness (Propecia)
  5. Precocious Puberty
  6. Chemical Castration?
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8
Q

Why are Anti-Androgens used for Prostate Cancer?

A
  1. Prostatic cancer cells are initially androgen dependent.
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9
Q

What structures secrete testosterone?

A
  1. Leydig cells of testes

2. Corpus Luteum of ovary.

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10
Q

What is the rate limiting step in the synthesis of Testosterone?

A
  1. Conversion of Cholesterol to Pregnenolone by side chain cleavage.
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11
Q

What regulates Testosterone secretion?

A
  1. LH from pituitary

2. Binds a cell surface receptor to Increase cAMP.

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12
Q

What CYP converts Pregnenolone to DHEA?

A
  1. CYP17 (Steroid 17a-hydroxylase)

- Removes side chain leaving KETONE group

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13
Q

What is caused by a deficiency in CYP17?

A
  1. CAH and Female phenotypy, w/ inability to reach sexual maturity.
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14
Q

How is DHEA converted to Androstenedione and then to Testosterone?

A
  1. 3B-hydroxysteroid dehydrogenase

2. 17B-hydroxysteroid dehydrogenase (testes, ovaries)

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15
Q

What is special about 17 beta-hydroxysteroid dehydrogenase?

A

It is unique to the sex steroid synthesis pathway.

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16
Q

What is LH release in response to?

A
  1. Gonadotropin Releasing Hormone (GnRH)
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17
Q

How is GnRH secreted?

A
  1. By the Hypothalamus into the hypothalamohypophyseal portal system. (blood)
  2. Released in Pulsatile pattern
  • 120 min frequency in males, 60-90 min frequency in females.
  • LH (and FSH) release follows this pattern
  • Constant GnRH levels inhibit LH release.
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18
Q

What type of variation do Testosterone levels exhibit?

A
  1. Diurnal and Pulsatile Variation.

- Levels are greatest in early morning and lowest in evening.

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19
Q

How does Testosterone inhibit LH and FSH release from pituitary?

A

2 Mechanisms

  1. Inhibition of GnRH release
  2. Down-regulation of GnRH receptors in pituitary.
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20
Q

How is Testosterone converted to dihydrotestosterone (DHT)?

A

By 5alpha-reductase.

gets rid of double bond in T

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21
Q

What is DHT and what does it do?

A
  1. Dihydrotestosterone

2. Binds the androgen receptor w/ 10 fold higher affinity and is believed to be the active form of Testosterone.

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22
Q

What is 5alpha-reductase type2?

A
  1. T –> DHT

2. found in external genitalia & T responsive tissues in men and women.

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23
Q

What happens in the absence of 5alpha-reductase?

A
  1. Results in female phenotype
  2. At puberty the sex organs in these pseudofemales may develop (appear) w/ surge in T.
  3. Deficient individuals will have normal to elevated T levels.
  4. Tissues that lack the reductase have minimal and primarily an ANABOLIC response to T (muscle)
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24
Q

What is 5alpha-reductase Type 1?

A
  1. Found in the Liver and some in Braine areas.
  2. NOT involved in Sexual Development
  3. 100-fold LOWER affinity for T.
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25
Q

What is Testosterone and DHT metabolized to and where?

A
  1. Androsterone, Etiocholanolone, androstandedione, and Androstanediol.
  2. Liver
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26
Q

How are metabolites of T excreted?

A

ALL metabolites are inactive and excreted in urine.

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27
Q

What is necessary for spermatogenesis?

A
  1. Testosterone
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28
Q

What cells secrete Androgen-Binding Protein (ABP)?

A

Sertoli Cells

-Retains Testosterone in seminiferous tubules.

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29
Q

What is the level of Testosterone in Testes compared to Serum?

A
  1. Level in testes 100x > serum.
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30
Q

What is circulating Testosterone bound to?

A
  1. Sex Hormone-Binding Globulin (SHBG)

2. Albumin.

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31
Q

Which is the higher affinity carrier, Albumin or SHBG?

A
  1. SHBG is the high affinity carrier.
  2. 98% of circulating T protein bound and unavailable for biological action.
  • 40% to SHBG
  • 60% to Albumin
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32
Q

What is the reputed male pheromone?

A
  1. Androstandienone
  2. Has a strong odor of sweat to most
  3. Lacks androgenic or anabolic effects
  4. Reported to positively affect mood of women, increase “caring feelings”
    - Commonly used in male fragrances
    - Selectively activates the vomeronasal organ in women
  5. Not everyone can smell AND to some it smells like vanillin to some it smells like sweat/unpleasant.
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33
Q

What happened in the carefully controlled test of AND?

A

repeated sniffing of androstadienone maintained elevated levels of salivary Cortisol.
AND maintained better mood, higher sexual arousal, and physiological arousal.

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34
Q

Why do fetal testes secrete Testosterone?

A
  1. To stimulate development of internal and external male genitalia.
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35
Q

What drives T secretion in fetal testes?

A
  1. Human Chorionic Gonadotropin (hCG) early and fetal LH late.
  2. Deficiency or Insensitivity results in ambiguous or female genitalia.
  3. T levels fall to near zero after birth.
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36
Q

During puberty what happens to levels of Testosterone?

A

Rise to:

  1. 500-700 ng/dL (males)
  2. 30-50 ng/dl (females)
  3. Lack of androgens in either sex results in incomplete sexual maturation.
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37
Q

At what age do Testosterone levels gradually fall?

A

After age 30 in BOTH sexes.

  1. Not significant until after age 70, as metabolic clearance of T also decreases.
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38
Q

What happens to SHBG levels as age increases?

A
  1. Levels gradually INCREASE with age, contributing to lower FREE T levels.
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39
Q

What is the level of Free Testosterone in elderly men compared to young adults?

A

Elderly men have levels 40% of young adult.

-Contributes to decrease in Energy, Libido, Muscle Mass, and Strength.

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40
Q

What is shown to happen to Testosterone levels when men become fathers?

A
  1. T levels drop
  2. Biggest drop occurs in most devoted dads.
  3. Single men w/ higher T levels were more likely to find partners and become fathers.
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41
Q

What is the Biochemical definition of Testosterone Deficiency?

A
  1. Less than 300 ng/dL plasma T for men less than 40 yr.
  2. Less than 200 ng/dL for men 40-70 yr and 3 clinical signs
    - Yields an incidence of TD of 6-12%.
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42
Q

In which people is Testosterone Deficiency most common?

A
  1. Obesity
  2. Diabetes (50% incidence in obese diabetic men)
  3. Hypertension
  4. Hyperlipidemias
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43
Q

What does a lower ratio of Testosterone to SHBG predict?

A

Poorer memory and cognitive status in men older than 50 years.

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44
Q

What are lower testosterone levels associated with?

A

Greater incidence of Cardiovascular disease in elderly men (>70yr)
1. > 550 ng/dL were protective in a second study of 2400 men >age 69

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45
Q

What are main signs and symptoms of T deficiency?

A
  1. Reduced Libido
  2. Erectile Dysfunction (ED)
  3. Reduced intensity of orgasm and sensation
  4. Osteoporosis or low BMD
  5. Decreased spontaneous erection
  6. Oligospermia or Azoospermia
  7. Very small or shrinking testes
  8. Hot flushes, sweats
  9. Breast discomfort, gynecomastia
  10. Loss of pubic and axillary hair, reduced shaving.
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46
Q

What are less specific signs and symptoms of T deficiency?

A
  1. Decreased energy, or vitality, increased fatigue
  2. Depressed mood
  3. Reduced muscle mass and strength
  4. Poor concentration and memory
  5. Sleep disturbance, increased sleepiness
  6. Mild anemia
  7. Increased body fat, body mass index
  8. Diminished physical or work performance.
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47
Q

What are the consequences of androgen deficiency in prepubertal males?

A
  1. Lack of sexual maturation: growth of genitals, pubic and axial hair, increase in muscle mass, deepening of voice.
  2. Elongated arm and leg bones, gynecomastia.
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48
Q

What are consequences of androgen deficiency in adult males?

A
  1. Loss of libido, energy, hematocrit, muscle mass and strength, bone density, sexual hair.
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49
Q

What are consequences of androgen deficiency in adult females?

A
  1. Decrease in sexual hair (slow to develop)

2. Loss of energy, libido muscle mass, bone mass?

50
Q

What is the goal of therapy for testosterone deficiency?

A
  1. Obtain normal serum T levels at midpoint of dosing schedule.
51
Q

What should happen with therapy for T deficiency?

A
  1. Libido and energy should increase within several weeks
  2. Hematocrit should return to normal within a month
  3. Muscle mass and strength may take up to 6 mo to return to normal.
  4. Bone density continues to increase over 2 years.
  5. In pubertal males must evaluate growth hormone status.
    - Testosterone causes closure of bone epiphyseal plates.
52
Q

When is treatment for T Deficiency contraindicated?

A

In men w/ breast/prostate cancer or at risk for prostate cancer. (elevated PSA)

53
Q

What are characteristics of Testosterone Esters as treatment for deficiency?

A
  1. T is rapidly inactivated in liver after oral admin.
    - All preparations are designed to avoid or resist hepatic metabolism.
  2. IM injection biweekly maintains serum testosterone levels within normal range (hypogonadal male)
    - Testosterone enanthate or cypionate
  3. Testosterone undecanoate (Andriol) is ORAL
54
Q

Addition of what to what creates highly lipophilic steroids?

A
  1. Addition of Fatty Acid group to 17alpha-OH group of testosterone.
  • Highly lipophilic
  • Ester hydrolyzed in vivo.
55
Q

What are the characteristics of Testosterone Undecanoate?

A

Andriol

  1. Oral
  2. Absorbed into lymphatic circulation and avoids hepatic metabolism.
  3. Is not marketed in US.
56
Q

What are characteristics of Transdermal Testosterone?

A
  1. Delivery provides stable, physiologic levels of testosterone.
  2. Avoids hepatic metabolism
  3. Must be applied daily
  4. Available as patches (Androderm), gels (AndroGel, Fortesta), A buccal tablet (Striant), and and underarm spray (Axiron).
  5. Gel formulation provides most stable blood levels
  6. Striant is placed on inner cheek or gum BID (similar to gel)
57
Q

What is Androderm?

A

Transdermal Testosterone Patch

58
Q

What is AndroGel or Fortesta?

A

Transdermal Testosterone Gel

-Most stable blood levels

59
Q

What is Striant?

A

Buccal Tablet

  • BID
  • Inner Cheek
  • Similar to gel
60
Q

What is Axiron?

A

Underarm T spray.

61
Q

What is the dosing protocol for Transdermal Testosterone?

A
  1. Should be titrated to serum T levels at 2 hr, 14d, and 35 d post initiation.
  2. Wash hands after application, avoid contact w/ dried gel.
  3. Can worsen BPH, polycythemia (monitor hematocrit)
  4. Can lower blood glucose, worsening diabetes.
62
Q

What are AE of Androgen Therapy?

A
  1. Acne (oily skin), Gynecomastia, aggressive sexual behavior/enhanced libido.
  2. T for “low T” raises risk of stroke, MI, and Death.
  3. Prostate hypertrophy (BPH)/Cancer
  4. Masculinization in women.
63
Q

What are the risks of Stroke, MI, and Death with T therapy?

A
  1. 2X risk in men over age 65 (cohort study)

2. 2-3X risk in men

64
Q

What is characteristic of masculinization in women?

A
  1. Hirsutism, male-pattern baldness, menstrual irregularities, deepening of voice, genital enlargement.
  2. Contraindicated in pregnant or potentially pregnant women, or those breast-feeding.
  3. Women and children should avoid contact with application sites on men.
65
Q

Why is Androgen therapy used for Male Senescence?

A
  1. Testosterone will increase bone density and muscle mass in elderly males.
  2. May improve energy levels, libido.
66
Q

Why is Androgen therapy used for Catabolic/Wasting states?

A
  1. Most effective w/ AIDS patients experiencing muscle loss.
  2. Hypogonadism often accompanies AIDS.
67
Q

Why could Androgen therapy be used in Metabolic syndrome in males?

A
  1. IV injection q3mo in hypogonadal patients decreased:

- Weight, Waist circumference, BP, cholesterol levels, plasma glucose (one study of 147 men)

68
Q

Why is Androgen therapy used for Hereditary Angioedema?

A

(Dermal Inflammation and edema)

  1. Autoimmune disease involving C1 esterase inhibitor
    - Leads to excessive bradykinin production (vasodilator peptide)
  2. Treated w/ Danozol (danocrine), Stanozolol (winstrol)
    - Stimulate hepatic synthesis of esterase inhibitor
    - 17a-alkylated androgens can have significant hepatic toxicity.
  3. Newer Tx for endometriosis and hypopituitarism have replaced 17a-alkylated androgens for these indications.
69
Q

How do Androgens suppress LH release for male contraception?

A
  1. Loss of LH suppresses testosterone synthesis in Leydig cells, leading to loss of spermatogenesis
  2. Only effective in 50% of patients
  3. 19-Nortestosterone is an androgen that cannot form DHT.
    - Suppresses LH and, to a lesser extent FSH.
70
Q

How are GnRH receptor antagonists used to suppress FSH as well as LH?

A
  1. Require daily SQ injections
  2. Expensive and inconvenient
  3. Require testosterone supplementation
71
Q

How are Progestins + Testosterone used as male contraception?

A
  1. Most promising approach
  2. Progestins stop release of FSH and LH
  3. Both can be administered inexpensively and reliably in a patch.
72
Q

What were study results when T was used for Ageing men?

A
  1. Gel or placebo for 3 years, 308 men, >60 yo, low-low normal T.
  2. No change in carotid artery atherosclerosis
  3. No improvement in 4 out of 5 measures of sexual function.
    - Men were not hypogonadal.
73
Q

What is the principal source of DHEA?

A

Adrenal Cortex in men and Women.

  • DHEA/DHEAS most abundant steroid in circulation.
  • Levels are high prior to birth, rise again at puberty, and peak at ~30 yrs of age.
74
Q

What is the role of DHEA?

A
  1. No Known physiological role
  2. Converted to Testosterone/estrogen in peripheral tissues (skin, breast, liver)
  3. 30-50% of androgen synthesis in men, and 50-100% of estrogen synthesis in women, is from DHEA.
75
Q

Why has decline of DHEA after age 30 been suggested to contribute to ageing effects?

A
  1. Not related to cortisol production
  2. DHEA is marketed as an anti-ageing supplement
    - Clinical studies indicate no benefit
    - Does not prevent cognitive decline.
  3. Low DHEA levels have been associated w/ increased rates of death in men but not women, and increased disease frequency.
76
Q

What is DHEA supplementation of value to?

A

Appears to be good for Adrenal Insufficiency.

  • Improved well-being, less fatigue
  • Improved libido in women.
77
Q

What is possible use of Testosterone in women?

A
  1. loss of libido in post menopausal is common complaint.
  2. 9-14% of post-menopausal women have hypoactive sexual desire disorder (HSDD)
  3. Falling T levels with age have been though to contribute to loss of libido.
    - NO diagnostic threshold for “low T” in women.
78
Q

What are characteristics of the 2008 Aphrodite study?

A
  1. Demonstrated that 300ug of T/ day boosts sexual satisfaction in women not taking estrogen.
  2. Approximately a doubling of “satisfaction”
  3. Was not due to conversion to estradiol
  4. Took 6-8weeks to be evident
  5. Approximately 60% of women respond.
  6. Most common adverse effect was excessive hair growth (facial), followed by acne and voice deepening.
79
Q

What does the 2010 Study suggest?

A

T is not deficient in women w/ HSDD

  1. Serum T levels werent different between patients and controls.
  2. Metabolites were no lower than controls (NO T def)
  3. Serum DHEAS and androstenedione were lower. (tissue specific synthesis of T was def.)
  4. Trial may have been too small
  5. DHEA may be acting through non-androgenic pathways to stimulate desire. (GABA and NMDA)
80
Q

What are clinical contraindications to testosterone therapy?

A
  1. Pregnancy and lactation
  2. Current use of anti-androgen therapy
  3. Troublesome acne or hirsutism
  4. Hormone dependent malignancy current or past.
  5. Sex hormone binding globulin level below the lower limit of normal.
  6. Free testosterone level in the mid-normal range for young women and above.
81
Q

What is Flibanserin?

A

newly approved drug for premenopausal HSDD.

  1. Serotonin 1A agonist/ 2A antagonist
  2. Mechanism of improving sexual desire is not known.
  3. Initially developed to treat depression.
82
Q

What happened in clinical trials of Flibanserin?

A
  1. Increased number of satisfying sexual events by 0.5-1 per month and Lowers distress.
  2. Increased the number of patients reporting improvement by 10%.
    - Does not enhance sexual performance.
83
Q

What is the AE of Flibanserin?

A
  1. Can cause severe hypotension and syncope
  2. increased w/ alcohol and by cyp3A4 inhibitors.
  3. Contraindicated with liver disease.
  4. dizziness, somnolence, insomnia, fatigue, nasuea, dry mouth.
84
Q

How is Flibanserin dosed?

A

once daily at bedtime, 100mg.

85
Q

Which type of Androgens are thought to have reduced sexual effects?

A

Ones that cannot be converted to DHT.

86
Q

Which androgens have “anabolic” effects?

A

ALL
1. Most noticeable in tissues lacking 5alpha-reductase

  • Bone, skeletal muscle, liver, kidney, heart.
  • Promotes protein synthesis and increased mass.
87
Q

What are the traditional anabolic steroids?

A
  1. 17alpha-alkylated androgens
    - Methyltestosterone (Oretin Methyl), Oxandrolone (Oxandrin)
    - Animal studies show these have greater anabolic activity than androgenic activity.
88
Q

What is the risk with anabolic steroids?

A

Significant Hepatotoxicity has decreased use.

1. Low HDL, High LDL, Cholestasis, hyperbilirubinemia, Peliosis hepatis (blood in liver)

89
Q

What are preferred anabolic steroids derived from?

A
  1. 19-nortestosterone
    - Removal of 19-methyl group decreases androgenic activity and increases estrogenicity.
  • Most popular is Nandrolone
  • widely used by body-builders.
  • Primobolan
90
Q

How is Nandrolone used?

A
  1. All are injectable; 200-400 mg/wk, detectable for up to 1 year in urine.
91
Q

How are Anabolic steroids scheduled?

A

DEA schedule III.

  • Potential for abuse less than the drugs or other substances in schedule I and II.
  • Currently accepted emdical use.
  • Abuse of the drug or other substance may lead to moderate or low physical dependence or high psychological dependence.
92
Q

What is the goal of designer novel anabolic steroids?

A
  1. to avoid detection by sports organizations.
93
Q

What is the first known designer steroid?

A
  1. Tetrahydrogestrinone (THG) (“The clear”)
    - Derived from gestrinone –> used to treat endometriosis.
  2. Contains 17alpha-ethyl group
    - likely to be hepatotoxic.
  3. Binds androgen receptor with affinity equal to DHT.
    - Likely to be androgenic.
94
Q

To avoid detection what are many users choosing?

A

Testosterone and Precursors (androstenedione, DHEA)

DHEA not federally regulated and is considered a supplement.
Androstenedione was recently placed on schedule III

  • Weak androgenic/anabolic effects due to conversion to testosterone and DHT
  • leads to LH suppression and hypogonadism
95
Q

Why are there estrogenic effects while taking anabolic steorids?

A
  1. due to direct conversion to estrone by CYP19 (aromatase)
    - Estrogenic effects may actually dominate in men
    - Lower Km for CYP19 vs 17BHSD (25 vs 1500/nmol/L)
    - Low endogenous estrogen levels in men
96
Q

What is the limit for T levels in women set by the IAAF and IOC?

A
  1. 10 nmol/L is limit in women
    - Falls within normal range for men
    - Higher levels require treatment (surgery or anti-androgens)
97
Q

What percent of women have T above normal range (athletes)?

A

13.7%

and 4.7% within male range

98
Q

What percent of males had T below normal male range?

A
  1. 5%

1. 8% within female range.

99
Q

AE of all anabolic steroids?

A
  1. Suppression of gonadotropin secretion from pituitary (LH and FSH)
  2. Prostate Enlargement
  3. Androgens that can be converted to estradiol will have estrogenic effects.
  4. 17alpha-alkylated steroids have liver, cardiac toxicity
100
Q

What does the AE of suppression of gonadotropin secretion cause?

A

Decreased testicular testosterone levels and decreased spermatogenesis.

  • Infertility, loss of libido, impotence
  • Decrease in testicular size
  • Recovery can take months to years.
101
Q

What does the AE of prostate enalargement cause?

A
  1. Difficulty in urination

2. Promotion of cancer?

102
Q

What does the 17alpha-alkylated steroids cause?

A

Increased LDL and Lowered HDL

103
Q

What is the AE in females?

A

Masculinization, hirsutism, male pattern baldness, acne, clitoral enlargement, menstrual irregularities, breast reduction, deepening of voice.

104
Q

What is the AE in prepubertal males and females?

A

1.. Phallic/clitoral enlargement, premature closure of bone epiphyses (stunting of growth)

105
Q

What is the Psychological AE of anabolic steroids?

A
  1. Excessiv aggression (roid rage)?
  2. Irritability
  3. Mood swings/depression
  4. Psychosis.
106
Q

What kinds of drugs associated with GnRH are inhibitors of testosterone secretion?

A

GnRH Analogs and Antagonists.

107
Q

How do Antagonists of the GnRH receptor work?

A
  1. Block release of LH and FSH from pituitary.
  2. Degarelix is a long acting synthetic decapeptide
    - approved for advanced prostate cancer.
    - admin monthly injection
    - equivalent to orchetomy in lowering T levels without an initial spike.
  3. Abarelix
    - Very high potential of serious allergic rxn
108
Q

How do GnRH analogs (agonists) work?

A
  1. Down-regulate GnRH receptor by constant stimulation
    - suppresses LH and FSH release
  2. May initially increase sex steroid levels.
  3. Administered as depot IM injections monthly and quarterly, and daily SQ
  4. Leuprolide
    - synthetic nonapeptide analog of GnRH
    - advanced prostate cancer
  5. Goserelin
    - Decapeptide analog
  6. Naferalin
    - Precocious puberty
    - nasal BID
109
Q

When is GnRH analog therapy most appropriate?

A
  1. For pts w/ advanced prostate cancer who have not undergone orchiectomy, and have metastatic cancer.
    - Risk of heart disease and diabetes is increased slightly.
110
Q

What are the 3 GnRH anologs?

A
  1. Leuprolide
  2. Goserelin
  3. Naferalin
111
Q

How do Androgen receptor antagonists work?

A

AR blocker stimulate LH release and elevate serum T levels.

  • Used in conjunction w/ GnRH analogs/antagonists in non-orchiectomized metastatic prostate cancer patients.
  • Equally effective to orchiectomy in survival rates.
112
Q

When can AR blockers be used alone?

A
  1. in Orchiectomized patients.
    - Block effects of adrenal T
    - Adrenal androgens are not regulated by LH
    - Gynecomastia (9% incidence) most common adverse effect.
113
Q

What is the favored AR blocker?

A

Bicalutamide is favored

  • Lower incidence of hepatotoxicity
  • Once daily oral dosing
114
Q

What two AR blockers are associated with hepatotoxicity?

A
  1. Flutamide and Nilutamide
  2. Toxicity is reversible –> may be due to metabolites
  3. Address liver function before use.
  4. Nilutamide is also associated with pulmonary inflammation.
115
Q

What do 5alpha-reductase inhibitors do?

A
  1. Block conversion of T to DHT

2. Finasteride and Dutasteride

116
Q

what does Finasteride block?

A
  1. Type II 5alpha reductase (sex tissue specific)
117
Q

What does dutasteride block?

A
  1. Type I 5alpha reductase (non genital) and type II
118
Q

What are 5alpha reductase inhibitors used for?

A

Treat BPH

  1. obstructed urinary flow
  2. Reduce serum DHT levels, reduce prostate volume, increase urine flow rate.
  3. 5 mg once daily by mouth.
  4. Impotence is most common complaint (5%)
119
Q

What is Finasteride used to treat besides BPH?

A
  1. Male pattern baldness and female hirsutism
    - 1 mg/day by mouth, 3 months for effects.
    - Not approved for baldness in women, not effective
    - AE effects much lower with 1 mg dose (
120
Q

Who should avoid contact with 5alpha-reductase inhibitors?

A
  1. Pregnant women

- significant risk to male fetus.

Endocrine (9 decks)

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