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Derm Pharm 2020 > 2 - Antiandrogens and Androgen Inhibitors > Flashcards

2 - Antiandrogens and Androgen Inhibitors Flashcards

1
Q

Androgens influence cutaneous structures such as hair follicles and sebaceous glands

A

True

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2
Q

Free testosterone and dihydrotestosterone are biologically active androgens that affect the pilosebaceous unit

A

True

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3
Q

Dihydrotestosterone is the target tissue active androgen

A

True

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4
Q

Testosterone and dihydrotestosterone have a central role in the pathogenesis of androgenetic alopecia, acne vulgaris and hirsutism

A

True

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5
Q

Antiandrogen refers to agents that block the androgen receptor I.e. Spironolactone, flutamide and cyproterone acetate

A

True

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6
Q

Spironolactone is an antiandrogen (blocks the androgen receptor)

A

True

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7
Q

Flutamide is an antiandrogen (blocks the androgen receptor)

A

True

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8
Q

Androgen inhibitors block androgen synthesis

A

True

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9
Q

Finasteride and Dutasteride are androgen inhibitors that specifically inhibit 5-alpha reductase

A

True (less conversion of free testosterone to dihydrotestosterone)

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10
Q

Leuprolide is a gonadotropin-releasing hormone agonist that initially increases LH and FSH production by the pituitary before sustained feedback inhibition of the secretion of these 2 gonadotropins

A

True

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11
Q

Progesterone and medroxyprogesterone act as both antiandrogens (block androgen receptor) and androgen inhibitors (inhibit dihydrotestosterone formation via 5-alpha reductase inhibition)

A

True

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12
Q

Finasteride (type II 5-alpha reductase inhibitor) is FDA approved for men with androgenetic alopecia

A

True (in contrast, the more potent Dutasteride is FDA approved for benign prostatic hypertrophy but not for androgenetic alopecia due to blockade of both isoenzymes I and II of 5-alpha reductase)

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13
Q

Testosterone can be formed in cutaneous sites, from the androgen precursor androstenedione derived from the adrenal cortex

A

True (this occurs when large amounts of androstenedione are secreted by adrenal tumours or in congenital adrenal hyperplasia)

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14
Q

The ovary and adrenal cortex are the primary sources of testosterone and other androgens in women

A

True

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15
Q

Androstenedione and dehydroepiandrosterone (DHEA) are produced by the ovary and adrenal gland

A

True

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16
Q

Androstenedione and dehydroepiandrosterone (DHEA) produced by the ovary and adrenal gland can be converted to more potent androgens I.e. Testosterone or to Oestrogens in peripheral organs including skin

A

True

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17
Q

The average daily rate of testosterone production in women is approx 0.25mg with half of this derived from metabolic conversion of androstenedione to testosterone at extra glandular sites including skin

A

True

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18
Q

PCOS is caused by increased quantities of androgens secreted by the ovary resulting in alopecia, acne and hirsutism

A

True

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19
Q

The 2 isoenzyme forms of 5-alpha reductase are type I and type II

A

True

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20
Q

Testosterone has minimal biological activity at the pilosebaceous unit and prostate until it is converted to dihydrotestosterone by 5-alpha reductase

A

True

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21
Q

Both testosterone and dihydrotestosterone bind to intracellular androgen receptor

A

True

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22
Q

Both type I and type II forms of 5-alpha reductase are located in the pilosebaceous unit

A

True

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23
Q

Type II isoenzyme form of 5-alpha reductase is also found in the prostate gland, epididymis and seminal vesicles (genital skin)

A

True

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24
Q

Type I isoenzyme form of 5-alpha reductase is found in non-genital skin

A

True (also includes scalp and face)

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25
Q

The hair follicles and sebaceous glands ducts on top of the scalp from frontal to vertex scalp host the Type II isoenzyme of 5-alpha reductase

A

True

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26
Q

The type II isoenzyme of 5-alpha reductase is absent from the occipital scalp

A

True

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27
Q

Spironolactone is an aldosterone antagonist which also blocks the androgen receptor

A

True

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28
Q

Spironolactone has no effect on 5-alpha reductase

A

True

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29
Q

Spironolactone is a steroid molecule which resembles mineralocorticoids

A

True (aldosterone antagonist with anti-mineralocorticoid activity)

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30
Q

Spironolactone may be converted to other active metabolites via progesterone 17-hydroxylase with the net result of decreased testosterone and dihydrotestosterone production

A

True

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31
Q

Spironolactone is 98% protein bound

A

True

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32
Q

Canrenone is the primary metabolite of Spironolactone contributing to the diuretic and antiandrogen activities of Spironolactone

A

True

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33
Q

The liver rapidly metabolised Spironolactone to its primary and active aldosterone antagonist metabolite, Canrenone

A

True

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34
Q

Food increases the absorption of Spironolactone

A

True

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35
Q

Metabolites of Spironolactone (active metabolite canrenone, and inactive canrenoate which is converted from canrenone by hydrolysis) are excreted in urine and bile

A

True

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36
Q

The unmetabolised Spironolactone does not appear in the urine

A

True (only the metabolised metabolites of spironolactone Canrenone and Canrenoate appear in the urine)

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37
Q

Spironolactone has been used to treat hirsutism, acne and androgenetic alopecia

A

True

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38
Q

Flutamide is more effective than Spironolactone in improving hirsutism

A

True

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39
Q

Spironolactone is more effective than Finasteride in improving hirsutism

A

True

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40
Q

Spironolactone may commonly cause menorrhagia and other menstrual dysfunction which usually last during the first 2-3 months of therapy

A

True

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41
Q

Finasteride specifically inhibits the type II isoenzyme of 5-alpha reductase

A

True

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42
Q

Dutasteride inhibits both type I and type II isoenzymes of 5-alpha reductase

A

True

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43
Q

Hyperkalaemia is a potentially serious common adverse effect of Spironolactone, particularly if given to patients with severe renal insufficiency

A

True

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44
Q

Spironolactone may cause gynaecomastia

A

True

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45
Q

Spironolactone may cause mild GI symptoms

46
Q

Agranulocytosis is a rare adverse effect associated with Spironolactone, particularly in those with hepatic or renal impairment

47
Q

Spironolactone is contraindicated in women with a genetic predisposition to breast cancer

A

True (not be given to these women even though causal role is lacking)

48
Q

Spironolactone may cross the placental barrier

A

True (risk of feminisation of a male fetus)

49
Q

Spironolactone should not be given concurrently with other agents that increase the risk of hyperkalaemia

50
Q

Spironolactone should not be given concurrently with ACE-inhibitors (increases the risk of hyperkalaemia)

51
Q

Spironolactone should not be given concurrently with Aliskerin, a direct renin inhibitor (increases the risk of hyperkalaemia)

52
Q

Spironolactone should not be given concurrently with an Angiotensin receptor blocker (increases the risk of hyperkalaemia)

53
Q

Patients on Spironolactone should be cautioned against excessive dietary intake of potassium rich foods

A

True (risk of hyperkalaemia)

54
Q

Drosperinone is a synthetic progestin used in OCP and a Spironolactone analogue with anti-mineralocorticoid (diuretic) activity and anti-androgenic activity

55
Q

Drosperinone may cause hyperkalaemia

A

True (is a Spironolactone analogue)

56
Q

Drosperinone is contraindicated in patients with hepatic dysfunction, renal dysfunction and adrenal insufficiency

57
Q

Besides the progesterone receptor, Progestins may also interact with other steroid hormone receptors I.e. Androgen receptor, estrogen receptor, mineralocorticoid receptor and glucocorticoid receptor

58
Q

Older progestins are derived from progesterone or 17-hydroxyprogesterone I.e. Medroxyprogesterone which are structurally similar to testosterone

59
Q

Due to the structural similarity of androgen and Progesterone/other progestins, these can bind to the androgen receptor and act as a substrate for 5-alpha reductase to be converted to 5-alpha-pregnane-3, 20-dione (similar to dihydrotestosterone)

60
Q

Cyproterone acetate is a progestin with antiandrogen properties

61
Q

Cyproterone acetate competes with dihydrotestosterone for the androgen receptor binding site

62
Q

Cyproterone acetate may also inhibit testosterone production

63
Q

Cimetidine, an H2 antihistamine also has antiandrogen effects through binding with the androgen receptor

64
Q

Finasteride is well absorbed

65
Q

Finasteride is metabolised in the liver and excreted in urine and faeces

66
Q

Finasteride is excreted in the urine and faeces

67
Q

After finasteride administration, serum dihydrotestosterone decreases by 65% in 24 hours

68
Q

Finasteride has no adverse consequences in female partners of men receiving finasteride who are exposed to the drug by sexual contact

A

True (no adverse effects despite minute quantities of finasteride is detectable in semen)

69
Q

Minute quantities of finasteride is detectable in semen

70
Q

The lack of scalp hair improvement in older men taking finasteride for prostatic hypertrophy is most likely due to the innate reduced response of scalp pilosebaceous units to finasteride in older men

71
Q

Finasteride is not efficacious in female pattern alopecia

72
Q

Finasteride (androgen inhibitor of 5-alpha reductase type II isoenzyme) and dutasteride (dual type I and type II 5-alpha reductase inhibitor) was associated with loss of libido, erectile and ejaculatory dysfunction in older men

A

True (though only decreased volume of ejaculate is likely to be causally related to finasteride due to dihydrotestosterone’s central role in the pilosebaceous unit and prostate)

73
Q

Finasteride and dutasteride may cause gynaecomastia

74
Q

Finasteride may cause a 20-30% decrease in PSA in men 18-41 years old

A

True (finasteride reduces the size of the prostate gland and hence is also indicated in benign prostatic hypertrophy)

75
Q

Finasteride may cause a 50% decrease in PSA in men aged 50 years old

A

True (the PSA needs to be doubled in all males aged 41 and above without benign prostatic hypertrophy if the PSA is ordered while taking finasteride to reflect the true PSA level)

76
Q

Decreased libido, erectile dysfunction, or decreased volume of ejaculate have been reported in <4% of younger patients on finasteride

A

True (though only decreased volume of ejaculate is likely to be causally related to finasteride due to dihydrotestosterone’s central role in the pilosebaceous unit and prostate)

77
Q

Finasteride should be used with caution in men at high risk for depression

A

True (increased rates of depression noted after 2 months)

78
Q

Finasteride is associated with a 26% risk reduction in prostate cancer, but a greater number of high grade Gleason score tumours

A

True (similar with dutasteride)

79
Q

Finasteride may result in external genitalia abnormalities in male fetuses of pregnant women who take finasteride or handle crush or broken tablets

A

True (pregnancy category X)

80
Q

The antiretroviral agent Nevirapine may reduce finasteride levels and hence efficacy

81
Q

Finasteride is extensively metabolised in the liver primarily by the CYP3A4 subfamily

A

True (but no important interactions result given the drug’s wide therapeutic index)

82
Q

A baseline PSA is appropriate for men 50 years and older before receiving finasteride

83
Q

Blood donation is contraindicated for those taking finasteride and dutasteride for at least 6 months after the last dose of medication to prevent blood donation to a pregnant female transfusion recipient as this may cause external genitalia abnormalities in male fetuses

84
Q

It is contraindicated for dutasteride to be handled by women of childbearing potential

A

True (for the same reasons as finasteride)

85
Q

Dutasteride has a very long half life of approximately 5 weeks

86
Q

Serum concentrations of dutasteride remain detectable for up to 4-6 months after discontinuation of treatment

87
Q

Dutasteride is metabolised by CYP3A4 in the liver and care should be taken in patients on chronic CYP3A4 inhibitors

A

True (Dutasteride has long half life in contrast to Finasteride)

88
Q

HIV protease inhibitors (ritonavir, nelfinavir) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

89
Q

Hep C virus protease inhibitors (telaprevir, boceprevir) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

90
Q

Azole antifungals (ketoconazole, itraconazole) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

91
Q

SSRI antidepressants (fluvoxamine) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

92
Q

Macrolide antibiotics (erythromycin, clarithromycin) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

93
Q

Fluoroquinolones (ciprofloxacin) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

94
Q

Calcium channel blockers (verapamil, diltiazem) are CYP3A4 enzyme inhibitors that may increase the serum levels of dutasteride

95
Q

Anti tuberculous agents (rifampicin, isoniazid) are CYP3A4 enzyme inducers that may decrease the serum levels of dutasteride

96
Q

Cimetidine (H2 antihistamine) is a CYP3A4 enzyme inhibitor that may increase the serum levels of dutasteride

97
Q

Ketoconazole may be used in the treatment of hirsutism (androgen inhibitor)

98
Q

The mini pill contains progestin only

99
Q

The combined OCP contains both an estrogen and progestin

100
Q

The estrogen in all the combined OCP is ethinyl oestradiol

101
Q

Synthetic progestin for the combined OCP are derived from 19-nortestosterone and can have androgenic, estrogenic and antiandrogenic properties

102
Q

The more androgenic progestins I.e. Norgestrel, levonorgestrel, norethindrone may induce acne, androgenetic alopecia and hirsutism

103
Q

The less androgenic progestins in the combined OCP I.e. Norgestimate, desogestrel, etonogestrel may be useful in women with acne and hirsutism

A

True (OCP is first line therapy in premenopausal women since other antiandrogens have a significant risk of teratogenecity)

104
Q

The adverse effects of oestrogen include nausea, increased breast size and tenderness, weight gain, headaches, thromboemboli, mood swings, and vaginal bleeding

105
Q

Lower dosages of oestrogen in the combined OCP result in increased rates of breakthrough bleeding

106
Q

Higher dosages of oestrogen in the combined OCP result in increased risk of thromboemboli

107
Q

Rifampin and griseofulvin alter hormone levels and are biologically plausible causes of OC failure

108
Q

Women aged 65 years and older taking oestrogen for at least 4 years have an increased risk of dementia

109
Q

Women taking Oestrogens for at least 5 years had significant increases in myocardial infarction, stroke, breast cancer, PE and VTE

110
Q

Cyproterone and Drosperinone (antiandrogen progestin) confer a 2 fold risk for VTE than levonorgestrel (progestin with androgenicity)

A

True (the risk decreases with longer duration of use and with lower doses of oestrogen)

Derm Pharm 2020 (47 decks)

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