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Pharmacology (3) > CH6 | Antifungals > Flashcards

CH6 | Antifungals Flashcards

1
Q

What are infectious diseases caused by fungi called?

A

Mycoses.

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2
Q

What are the main types of mycotic infections?

A
  • Cutaneous.
  • Subcutaneous.
  • Systemic.
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3
Q

What type of cells do fungi have?

A

Eukaryotic cells with a rigid cell wall made of chitin.

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4
Q

What is the main component of the cell membrane in fungi?

A

Ergosterol.

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5
Q

What is the target of antifungal drugs?

A

Ergosterol.

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6
Q

Why are antifungal drugs selective?

A

Because antibiotics are ineffective against fungi.

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7
Q

What factors have contributed to the increased incidence of mycoses?

A

Cancer chemotherapy, HIV, and organ transplantation leading to immune suppression.

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8
Q

What type of drug is Amphotericin B?

A

An amphoteric polyene macrolide.

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9
Q

What is the source of Amphotericin B?

A

It is naturally occurring and produced by Streptomyces nodosus.

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10
Q

What is the drug of choice for several life-threatening mycoses?

A

Amphotericin B.

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11
Q

How is Amphotericin B administered for systemic infections?

A

It is water insoluble, so it is administered as a colloidal suspension of amphotericin B and sodium deoxycholate or liposomes via slow IV infusion.

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12
Q

What is the formulation of Amphotericin B for local GI tract treatment?

A

Oral amphotericin B.

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13
Q

What is the mechanism of action (MOA) of Amphotericin B?

A

It is fungicidal and binds to ergosterol, forming pores that disrupt membrane function, leading to leakage and cell death.

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14
Q

What is the antifungal spectrum of Amphotericin B?

A

It has a wide antifungal spectrum including Candida albicans, Histoplasma capsulatum, Cryptococcus neoformans, Coccidioides immitis, Blastomyces dermatitidis, and many strains of Aspergillus.

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15
Q

What is the resistance mechanism associated with Amphotericin B?

A

Changes in ergosterol content and structure.

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16
Q

How is Amphotericin B administered?

A

As a colloidal suspension of amphotericin B and sodium deoxycholate or liposomes, parenterally via slow IV infusion.

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17
Q

What is the solubility characteristic of Amphotericin B?

A

It is water insoluble.

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18
Q

How extensively is Amphotericin B bound in the body?

A

It is extensively bound to plasma proteins.

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19
Q

What is the distribution characteristic of Amphotericin B?

A

It has high distribution, but little of the drug is found in CSF, vitreous humor, peritoneal fluid, and synovial fluid.

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20
Q

How is Amphotericin B excreted from the body?

A

It is excreted in the urine over a long period of time.

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21
Q

What are the adverse effects of Amphotericin B?

A

Fever, chills, kidney failure, hypotension, anemia, thrombophlebitis.

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22
Q

What are the infusion-related toxicities associated with Amphotericin B?

A

Fever, chills, muscle spasm, headache, hypotension, vomiting.

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23
Q

How can infusion-related toxicities of Amphotericin B be managed?

A

By decreasing the infusion rate or daily dose, and premedication with corticosteroids and antipyretics.

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24
Q

What is the most significant cumulative toxicity of Amphotericin B?

A

Renal damage.

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25
Q

What are the effects of cumulative toxicity on the kidneys when using Amphotericin B?

A

Decreased glomerular filtration rate and decreased renal tubular function.

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26
Q

What happens to creatinine clearance with Amphotericin B use?

A

It decreases.

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27
Q

What electrolytes are wasted due to Amphotericin B?

A

Potassium (K) and Magnesium (Mg).

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28
Q

What type of acidosis can occur with Amphotericin B?

A

Renal tubular acidosis.

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29
Q

Is the renal damage caused by Amphotericin B reversible?

A

Yes, but there can be residual damage at high doses (>4g cumulative dose; prolonged).

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30
Q

What is azotemia and how is it related to Amphotericin B?

A

Azotemia is a condition that may occur with Amphotericin B use, potentially requiring dialysis.

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31
Q

What can help decrease the severity of azotemia caused by Amphotericin B?

A

Hydration.

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32
Q

How can the risk of nephrotoxicity be minimized when using Amphotericin B?

A

By infusing normal saline prior to administration.

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33
Q

What type of antifungal drug is Flucytosine?

A

It is an antimetabolite antifungal.

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34
Q

What is the chemical classification of Flucytosine?

A

Synthetic pyrimidine.

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35
Q

With which antifungal agent is Flucytosine commonly combined for a synergistic effect and being overall safer?

A

Amphotericin B.

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36
Q

What is the mechanism of action (MOA) of Flucytosine?

A

Fungistatic with selective toxicity; disrupts nucleic acid and protein synthesis.

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37
Q

Why does Flucytosine have selective toxicity?

A

It has no effect on human cells due to the lack of necessary enzymes.

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38
Q

What is the antifungal spectrum of Flucytosine?

A

Restricted (narrow).

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39
Q

With which drugs is Flucytosine commonly combined for treatment?

A

Amphotericin B and itraconazole.

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40
Q

What conditions is Flucytosine used to treat when combined with Amphotericin B?

A

Systemic mycoses and meningitis caused by C. neoformans and C. albicans.

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41
Q

What is the reason Flucytosine is not used alone?

A

High susceptibility to resistance.

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42
Q

What is a key mechanism of resistance to Flucytosine?

A

Altered metabolism of 5-FC.

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43
Q

What type of infections are treated with Flucytosine?

A

Subcutaneous and systemic mycotic infections.

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44
Q

What type of drug is Itraconazole?

A

A triazole antifungal.

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45
Q

What condition is treated with Itraconazole in combination with Flucytosine?

A

Chromoblastomycosis.

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46
Q

How is Flucytosine absorbed?

A

It is well-absorbed orally.

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47
Q

Where does Flucytosine distribute in the body?

A

Throughout body water and penetrates into the cerebrospinal fluid (CSF).

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48
Q

What is detectable in patients due to the metabolism of Flucytosine by intestinal bacteria?

A

5-fluorouracil (5-FU).

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49
Q

How is Flucytosine excreted from the body?

A

In the urine via glomerular filtration (parent drug + metabolites).

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50
Q

What are some adverse effects of Flucytosine?

A

Bone marrow toxicity, nausea, vomiting, diarrhea, severe enterocolitis, and reversible hepatic dysfunction.

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51
Q

What blood disorders can result from Flucytosine’s adverse effects?

A

Anemia, leukopenia, and thrombocytopenia.

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52
Q

What liver-related issue can arise from Flucytosine treatment?

A

Elevation of serum transaminases indicating reversible hepatic dysfunction.

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53
Q

What are the two main classes of azole antifungals?

A

Imidazoles and triazoles.

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54
Q

What is the mechanism of action (MOA) of azole antifungals?

A

They have similar MOA and spectra of activity.

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55
Q

How do imidazoles differ from triazoles?

A

They differ in pharmacokinetic (PK) properties and therapeutic use.

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56
Q

What is the primary application of imidazoles?

A

Applied topically for cutaneous infections.

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57
Q

What is the primary use of triazoles?

A

Administered systemically for the treatment or prophylaxis of cutaneous and systemic mycoses.

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58
Q

Name some examples of triazole antifungals.

A

Fluconazole, itraconazole, posaconazole, voriconazole, isavuconazole.

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59
Q

What is the mechanism of action (MOA) of azole antifungals?

A

They are fungistatic and reduce ergosterol synthesis.

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60
Q

How do azole antifungals disrupt fungal cell growth?

A

By inhibiting 14 α-demethylase, blocking the demethylation of lanosterol to ergosterol, disrupting fungal membrane function and structure.

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61
Q

What is one mechanism of resistance to azole antifungals?

A

Mutations in the 14 α-demethylase gene and efflux pumps.

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62
Q

Which hepatic isoenzyme do all azoles inhibit?

A

CYP450 3A4.

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63
Q

What can occur when concomitant medications are substrates for CYP450 3A4?

A

High concentrations and toxicity due to drug-drug interactions.

64
Q

Which azoles are metabolized by CYP450 3A4?

A

Itraconazole and voriconazole.

65
Q

What type of interactions occur with CYP450 inhibitors and inducers?

A

Drug-drug interactions with azoles like itraconazole and voriconazole.

66
Q

Why do imidazoles have a higher incidence of drug interactions and adverse effects compared to triazoles?

A

Imidazoles exhibit a lesser degree of selectivity.

67
Q

What is a major contraindication for azole antifungals?

A

They are teratogenic and should be avoided in pregnancy unless the benefit outweighs the risk to the fetus.

68
Q

What is the first triazole antifungal?

A

Fluconazole.

69
Q

How does fluconazole compare to other triazoles in terms of activity?

A

Fluconazole is the least active of all triazoles.

70
Q

What is the spectrum of fluconazole?

A

Yeast and some dimorphic fungi.

71
Q

What conditions does fluconazole have no role in treating?

A

Aspergillosis or zygomycosis.

72
Q

Which organisms is fluconazole active against?

A

Cryptococcus neoformans, Candida albicans, and Candida parapsilosis.

73
Q

What is Fluconazole used for prophylactically?

A

Against invasive fungal infections in recipients of bone marrow transplants.

74
Q

What is the drug of choice for Cryptococcus neoformans after induction therapy with amphotericin B and flucytosine?

A

Fluconazole.

75
Q

For which infections is Fluconazole used?

A

Candidemia and coccidiomycosis.

76
Q

Is Fluconazole active against mucocutaneous candidiasis?

A

Yes, it is active against vulvovaginal candidiasis.

77
Q

What are the routes of administration for Fluconazole?

A

Oral and intravenous (IV).

78
Q

How is Fluconazole excreted from the body?

A

It is excreted in the urine.

79
Q

What are some common adverse effects of Fluconazole?

A

Nausea, vomiting, headache, and skin rashes.

80
Q

What is the broader spectrum antifungal compared to fluconazole?

A

Itraconazole.

81
Q

What is the drug of choice for treating blastomycosis?

A

Itraconazole.

82
Q

What conditions is itraconazole used to treat?

A

Blastomycosis, sporotrichosis, paracoccidioidomycosis, and histoplasmosis.

83
Q

How should itraconazole capsules and tablets be taken?

A

With food and an acidic beverage.

84
Q

How should itraconazole solution be taken?

A

On an empty stomach.

85
Q

What is the distribution characteristic of itraconazole in the body?

A

It has high distribution in the body.

86
Q

Where is itraconazole metabolized?

A

In the liver.

87
Q

What happens to itraconazole after metabolism?

A

It is excreted as drug and inactive metabolites in urine and feces.

88
Q

What are some adverse effects of itraconazole?

A

Nausea, vomiting, rash, hypokalemia, hypertension, edema, headache.

89
Q

Why should itraconazole be avoided in patients with heart failure?

A

Because it has a negative inotropic effect.

90
Q

What is Voriconazole used for?

A

It is the drug of choice for invasive aspergillosis and is used for invasive candidiasis and infections caused by Scedosporium and Fusarium species.

91
Q

What forms is Voriconazole available in?

A

Oral and intravenous (IV).

92
Q

What type of drug interactions does Voriconazole have?

A

It metabolizes and inhibits various CYP450 isoenzymes.

93
Q

What is a significant side effect of high doses of Voriconazole?

A

Visual and auditory hallucinations, and hepatotoxicity.

94
Q

What is the spectrum of activity of Voriconazole?

A

It has a broad spectrum of activity.

95
Q

What are Echinocandins?

A

The newest class of antifungal agents.

96
Q

What is the mechanism of action of Echinocandins?

A

Inhibiting the synthesis of β(1,3)-D-glucan, leading to cell lysis and death.

97
Q

What is the formulation for Echinocandins?

A

They are administered intravenously (IV).

98
Q

Which Echinocandins require a loading dose?

A

Caspofungin and anidulafungin.

99
Q

What type of activity do Echinocandins have against Aspergillus and Candida species?

A

Potent activity, including against those resistant to azoles.

100
Q

What are the structural components of Echinocandins?

A

Large cyclic peptides linked to a long-chain fatty acid, so they’re given IV.

101
Q

What is the effect of Echinocandins on the fungal cell wall?

A

They act on the cell wall, leading to cell death.

102
Q

What are the three main Echinocandins used for antifungal treatment?

A

Caspofungin, micafungin, and anidulafungin.

103
Q

What are the common adverse effects of Echinocandins?

A

Fever, rash, nausea, and phlebitis at the infusion site.

104
Q

How should Echinocandins be administered to prevent adverse reactions?

A

Via a slow IV infusion to prevent histamine-like reactions (flushing).

105
Q

What is the first-line treatment option for patients with invasive candidiasis?

A

Caspofungin.

106
Q

What is the second-line treatment option for invasive aspergillosis?

A

Caspofungin in patients who have failed or cannot tolerate amphotericin B or an azole.

107
Q

How is Caspofungin metabolized?

A

Via CYP450 enzymes, which can lead to drug-drug interactions.

108
Q

Which Echinocandins are first-line options for the treatment of invasive candidiasis?

A

Micafungin and anidulafungin.

109
Q

What condition do micafungin and anidulafungin treat?

A

Invasive candidiasis, including candidemia.

110
Q

Do micafungin and anidulafungin interact with CYP450 enzymes?

A

No, they are not substrates for CYP450 enzymes.

111
Q

What is a significant advantage of Echinocandins regarding drug interactions?

A

They have no drug-drug interactions.

112
Q

What type of fungi primarily cause cutaneous infections?

A

Mold-like fungi known as dermatophytes.

113
Q

What is the term for infections caused by dermatophytes?

A

Dermatophytosis.

114
Q

What are some examples of dermatophytosis?

A

Tinea pedis, tinea corporis (ringworm), tinea capitis, tinea cruris, tinea versicolor, and onychomycoses.

115
Q

Which fungi are the majority causes of dermatophytosis?

A

Trichophyton, Microsporum, and Epidermophyton.

116
Q

What class of antifungal drugs includes terbinafine, naftifine, and butenafine?

A

Squalene epoxidase inhibitors.

117
Q

What is the mechanism of action of squalene epoxidase inhibitors?

A

They inhibit squalene epoxidase, blocking the synthesis of ergosterol.

118
Q

What happens as a result of squalene accumulation in fungal cells?

A

Increased membrane permeability leading to cell death.

119
Q

What class of antifungal drugs does Terbinafine belong to?

A

Squalene epoxidase inhibitors.

120
Q

What is the mechanism of action of Terbinafine?

A

Fungicidal.

121
Q

What is the drug of choice for onychomycosis?

A

Terbinafine (orally).

122
Q

How does Terbinafine compare to itraconazole and griseofulvin in terms of tolerance and effectiveness?

A

Better tolerated, shorter duration of therapy, and more effective.

123
Q

What is the typical duration of therapy with Terbinafine for onychomycosis?

A

3 months (shorter than griseofulvin).

124
Q

What condition requires an oral formulation of Terbinafine?

A

Tinea capitis.

125
Q

What are the topical formulations of Terbinafine available?

A

1% cream, gel, or solution.

126
Q

What is the treatment duration for tinea pedis, tinea corporis, tinea cruris, and tinea versicolor when using Terbinafine topically?

A

1 week.

127
Q

What are the routes of administration for Terbinafine?

A

Oral and topical administration.

128
Q

What is the bioavailability percentage of Terbinafine?

A

40% due to first-pass metabolism.

129
Q

What is the half-life range of Terbinafine?

A

200 to 400 hours.

130
Q

How is oral Terbinafine metabolized and excreted?

A

Metabolized in the liver and excreted in the urine.

131
Q

In which patients should Terbinafine be avoided?

A

Patients with moderate to severe renal impairment or hepatic dysfunction.

132
Q

What is the protein binding characteristic of Terbinafine?

A

Highly protein-bound and deposited in skin, nails, and adipose tissue.

133
Q

Which CYP450 isoenzyme does Terbinafine inhibit?

A

CYP450 2D6 isoenzyme.

134
Q

What type of drug interactions can occur with Terbinafine?

A

Drug-drug interactions due to CYP450 2D6 inhibition.

135
Q

What are some adverse effects of Terbinafine?

A

Diarrhea, dyspepsia, nausea, headache, rash.

136
Q

What visual disturbances have been reported with Terbinafine use?

A

Taste and visual disturbances.

137
Q

What laboratory abnormality can occur with Terbinafine?

A

Elevations in serum hepatic transaminases.

138
Q

What type of action does Griseofulvin exhibit?

A

Fungistatic and keratophilic.

139
Q

How does Griseofulvin affect fungal cells?

A

It causes disruption of the mitotic spindle, inhibiting fungal mitosis.

140
Q

Where is Griseofulvin deposited in the body?

A

In newly forming skin where it binds to keratin.

141
Q

For what condition was Griseofulvin previously used?

A

Onychomycosis, requiring 6 - 12 months of treatment.

142
Q

What current conditions is Griseofulvin still used for?

A

Dermatophytosis of the scalp and hair.

143
Q

How should Griseofulvin be taken for optimal absorption?

A

With high-fat meals.

144
Q

What effect does Griseofulvin have on the liver?

A

It induces hepatic CYP450, leading to drug-drug interactions.

145
Q

In which patients is Griseofulvin contraindicated?

A

In pregnancy and patients with porphyria.

146
Q

What does Nystatin resemble?

A

Amphotericin B.

147
Q

What infections is Nystatin used to treat?

A

Cutaneous and oral Candida infections.

148
Q

How is Nystatin absorbed in the body?

A

Not absorbed from the gastrointestinal tract; systemic toxicity can occur if given parenterally.

149
Q

What is the method of administration for oral Nystatin?

A

Swish and swallow or swish and spit.

150
Q

What condition is treated with oral Nystatin?

A

Oropharyngeal candidiasis (thrush).

151
Q

How is Nystatin administered for vulvovaginal candidiasis?

A

Intravaginally.

152
Q

What is the topical use of Nystatin?

A

To treat cutaneous candidiasis.

153
Q

What class of antifungal drugs includes butoconazole, clotrimazole, econazole, ketoconazole, miconazole, oxiconazole, sertaconazole, sulconazole, terconazole, and tioconazole?

A

Imidazoles.

154
Q

What are some common uses of imidazoles?

A

Tinea corporis, tinea cruris, tinea pedis, oropharyngeal and vulvovaginal candidiasis.

155
Q

What systemic fungal infection treatment has historically used oral ketoconazole?

A

Systemic fungal infections.

156
Q

Why is oral ketoconazole rarely used today?

A

Due to the risk for severe liver injury, adrenal insufficiency, and adverse drug interactions.

Pharmacology (3) (15 decks)

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