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Pharmacology > Antifungal Agents > Flashcards

Antifungal Agents Flashcards

1
Q

MOA of Azoles

A

inhibit cytochrome P 450
impaired synthesis of ergosterol
impaired fungal cell membrane formation

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2
Q

MOA of polyenes

A

bind to ergosterol in fungal cell membrane and disrupt membrane integrity

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3
Q

MOA of Flucytosine

A
  • is an anti-metabolite

- inhibits RNA and DNA synthesis

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4
Q

MOA of Echinocandins

A

inhibit synthesis of B(1,3)-D-glucan (cell wall component)

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5
Q

MOA of Griseofulvin

A

anti-mitotic

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6
Q

MOA of Terbinafine

A
  • inhibit squaline epoxidase

- blocks ergosterol synthesis

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7
Q

what are the pharmacokinetics of Triazoles

A
  • metabolized slowly

- less effect on human sterol synthesis

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8
Q

what are the Triaoles drugs

A
  • Itraconazole
  • Voriconazile
  • Fluconazole
  • Posaconazole
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9
Q

what are the Imidazoles

A
  • Clotrimazole
  • Miconazole
  • Ketoconazole
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10
Q

MOA of Azoles

A
  • inhibit cytochrome P 450
  • impaired synthesis of ergosterol
  • impaired fungal cell membrane formation
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11
Q

the selective activity of Azoles is due to what

A

-differences in membrane sterols:
Mammalian: Cholesterol
Fungal: Ergosterol

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12
Q

What are the adverse effects of Ketoconazole

A
  • anorexia, nausea, vomiting, pruritus, rash, dizziness, photophobia
  • reduced plasma testosterone –> gynecomastia, decreased libido and erectile dysfunction in males, menstrual irregularities in females
  • inhibition of adrenal steroidogenesis, decreased cortisol, hepatic toxicity and necrosis
  • teratogenecity
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13
Q

what are the drug interaction of Ketoconazole

A
  • strong inhibitor of CYP3A4 and other enzymes
  • increased serum concentrations of many other drugs
  • Absorption reduced by drugs that decrease gastric acidity (antacids, PPIs, H2-receptor blockers)
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14
Q

Fluconazole is active against what

A

-most Candida species
-Coccidioides and Cryptococcus spp
Histoplasma capsulatum (at higher doses)

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15
Q

Fluconazole is not active against what

A

C. krusei
Many strains of C. glabrata
Most molds

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16
Q

what are the pharmacokinetics of Fluconazole

A
  • lowest affinity for mammalian P450 enzymes

- good water solubility and CSF penetration

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17
Q

what are the adverse effects of Fluconazole

A
  • headache, GI distress, facial edema, rash, pruritus
  • Stevens-Johnson syndrome, anaphylaxis, hepatic toxicity , leukopenia, hypokalemia, QT prolongation, torsades de pointes reported
  • Teratogenic
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18
Q

Fluconazole drug interactions

A
  • strong inhibitor of CYP2C9 and 2C19
  • moderate inhibitor of CYP3A4
  • may increase serum concentrations of drugs metabolized by enzymes especially those metabolized by CYP2C9 and CYP2C19 or CYP3A4 may increase risk of QT prolongation and torsades de pointes
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19
Q

what is the spectrum of activity of Itraconazole

A

broader than fluconazile

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20
Q

Itraconazole is active against what

A 
Cryptococcus neoformans
Aspergillus spp.
Coccidioides spp.
H. capsulatum
Sporothrix spp.
Dermatophytes
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21
Q

Itraconzole is not active against what

A

Scedosporium spp
Scopulariopsis spp.
Flusarium spp
Zygomycetes

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22
Q

what are the adverse effects of Itraconazole

A

-GI distress- nausea, vomiting, rash
-Stevens-Johnson syndrome, hepatic toxicity, edema, hypokalemia, hypertension, negative inotropic effects, congestive heart failure
Peripheral neuropathy, visual disturbances, hearing loss
Teratogenic

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23
Q

Itraconazole is contraindicated in what patients

A

patients with history of heart failure/ventricular dysfunction

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24
Q

drug interactions of Itraconazole

A
  • strong inhibitor of CYP3A4
  • increased serum levels of other drugs metabolized by this system
  • absorption reduced by drugs that decrease gastric acidity (antacids, PPIs, H2 receptor blockers)
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25
Q

spectrum activity of Voriconazole

A

similar to itraconazole

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26
Q

Voriconazole is active against

A

-most species of Candida
-Blastomyces dermatitidis
-Cryptococcus neoformans
-Paracoccidioides brasiliensis
Scedosproium spp
-Aspergillus spp
-Coccidioides spp.
-H. capsulatum
-Dermatophytes
-Fusarium spp

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27
Q

Voriconazole is not active against

A

Zygomycetes spp

Sporothrix

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28
Q

Is Voriconazole or Amphotericin more effective for invasive aspergillosis

A

Voriconazole

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29
Q

what are the pharmacokinetics of Voriconazole

A

-serum concentrations vary - may required monitoring

30
Q

what are the adverse effects of Voriconazole

A

Transient visual disturbances- blurred vision, photophobia, altered color or image perception
Rash, Stevens-Johnson syndrome, hepatic toxicity, confusion, hallucinations
Anaphylaxis
Teratogenic

31
Q

drug interactions of Voriconazole

A

Metabolized by and inhibits, CYP2C19, CYP2C9, and CYP3A4 → serum levels may be influenced by drugs that affect these enzymes and serum levels of other drugs metabolized by these enzymes may be increased

32
Q

what is the spectrum of activity of Posaconazole

A
  • similar to Itraconazole

- activity is twice that of itraconzole

33
Q

Posaconazole has increased activity against

A

Absidia spp

34
Q

how is Posaconazole administered

A

oral, taken with meals

35
Q

what are the adverse effects of Posaconazole

A

Headache, GI distress, rash
Hepatic toxicity, QT prolongation
Arrythmias, anaphylaxis, angioedema (rare)
Teratogenic

36
Q

Prosaconazole drug interactions

A

Metabolized by UDP glucuronidation
Substrate of P-glycoprotein (permeability glycoprotein)
Strong inhibitor of CYP3A4 → increased serum levels of other drugs metabolized by this system
Used with caution with other drugs known to prolong the QT interval; contraindicated with such drugs that are metabolized by CYP3A4

37
Q

Absorption of Posaconazole is reduced by

A

drugs that decrease gastric acidity (antacids, PPIs, H2-receptor blockers)

38
Q

what is the solubility of Polyenes: Amohotericin B

A
  • insole in water

- solubility increased by formation of complex with deoxycholate (bile salt)

39
Q

what are the Lipid Amphotericin B products

A

Ampho B lipid complex - Ribbon- like sheets
Ampho B cholesteryl complex - disk-shaped colloidal dispersion
Liposomal amphotericin B - Unilamellar vesicle

40
Q

MOA of ampotericin B

A

binds to ergosterol in fungal cell membrane, disrupts membrane integrity

41
Q

selectivity of Amphotericin B is based on

A

-differences in membrane sterols:
Mammalian: Cholesterol
Fungal: Ergosterol

42
Q

Spectrum of Amphotericin B

A

broad-spectrum fungicidal

*initial therapeutic agent, treatment continued with less toxic antigunal

43
Q

Amphotericin B is the DOC for

A

life-threatening, fungal infections

-Aspergillus, cryptococcus, histoplasmosis, invasive candidiasis, blastomycosis, mucor, neuropenic fever

44
Q

what are the pharmacokinetics of Amphotericin B

A 
No oral bioavailability
Metabolism not understood-
Hepatic or renal impairment does not affect levels
Extensive tissue binding → 
	Long T1/2 (~15 days)\
	Concentrates in liver & spleen
45
Q

what are the adverse effects of Amphotericin B deoxycholate

A
  • infusion rxns; related to cytokine release; premdedicate with acetaminophen, diphenhydramine, hydrocortisone, and meperidine
  • nephrotoxicity: dose-limited toxicity; sodium loading with normal saline may provide protection
  • hypokalemia, hypomagnesemia common due to a mild renal tubular acidosis
  • anemia, weight loss, thrombocytopenia, mild leukopenia
46
Q

what are the adverse effects of Amphotericin B lipid formuations

A

Infusion reactions least severe with liposomal amphotericin B
Nephrotoxicity less common and less severe than with amphotericin B deoxycholate
Hepatotoxicity (rare)

47
Q

what is MOA of Flucytosine

A
  • converted in fungal cytosol to 5-fluoruracil

- 5-fluorouracil inhibits DNA and RNA synthesis

48
Q

Flucytosine seletive activity based on

A
  • cellular uptake by specific enzyme, cytosine pernease

- conversion to 5-fluorouracil by another specific fungal enzyme, cytosine deaminase

49
Q

Flucytosine active against

A

Cryptococcus neoformans
Candida spp
Chromoblastomycosis

50
Q

Flucytosine used in combination with

A

amphotericin B afor cryptococcal meningitis or systemic candidiasis

51
Q

what are the pharmacokinetics of Flucytosine

A

Good oral bioavailability- administered orally
Volume of distribution equals total body water
Penetrates the blood brain barrier
Renal excretion

52
Q

what are the adverse effects of Flucytosine

A

dose-related bone marrow toxicity

53
Q

what are the Echinocandins

A

Caspofungin
Anidulafungin
Micafungin

54
Q

what is the MAO of Echinocandins

A

inhibit synthesis of B(1,3)-D-glucan (fungal cell wall component) –> cell wall becomes permeable

55
Q

Echinocandins selective activity based on

A

absence of cell wall in mammalian cells

56
Q

Echinocandins active against

A

most species of Candida, Aspergiullus spa

57
Q

what are the Pharmacokinetics of Echinocandins

A

No oral bioavailability
T1/2 ~ 10 hours after IV infusion
Extensively bound to albumin
Hepatic metabolism, does not significantly involve cytochrome P450 enzymes
No clinically significant drug interactions
No dose adjustment required in renal dysfunction

58
Q

what are the adverse effects of Echinocandins

A

Generally well tolerated
Occasional rash, fever, nausea, vomiting, headache, hypokalemia and mild hepatic toxicity
Stevens-Johnson syndrome, exfoliative dermatitis, anaphylaxis - rare
Teratogenic

59
Q

hat is Griseofulvin used for

A
  • mucocutaneous infections

- fungal skin, nail, hair infections

60
Q

what is the MAO of Griseofulvin

A

antimitotic-interacts with polymerized microtubules leading to disruption of the mitotic spindle

61
Q

what is the activity of Griseofulvin

A

Fungistatic for various species of the dermatophytes

Microsporum, Epidermophyton, and Trichophyton

62
Q

what are the pharmacokinetics of Griseofulvin

A

Blood levels quite variable
Best absorption when taken with a fatty meal
T1/2 = 24 hours
Keratophilic- binds to keratin, protects skin and nails from further infection

63
Q

what are the adverse effects of Griseofulvin

A

Generally well tolerated- incidence of adverse effects is very low
Headache, nausea, vomiting
Teratogenic

64
Q

Griseofulvin interactions

A

induces hepatic cytochrome P450 isoforms

65
Q

what is Terbinafine used for

A

mucococutaneous infections

66
Q

what is the MAO of Terbinafine

A

inhibit squaline epoxidase
-blocks ergosterol synthesis
-impaired fungal cell membrane synthesis
FUNGICIDAL

67
Q

selective activity of Terbinafine is due to

A

1000 to 10,000 times higher binding affinity for the fungal enzyme

68
Q

what are the pharmacokinetics of Terbinafine

A 
Well absorbed but significant first pass metabolism to inactive metabolites
Highly lipophilic
Accumulates in skin and nails
T1/2 = 200 to 400 hours at steady state
Keratophilic
69
Q

what are the adverse effects of Terbinafine

A

Well tolerated- incidence of adverse effects is very low
Nausea, diarrhea, headache, rash
Hepatotoxicity, neutropenia, Stevens-Johnson syndrome (rare)
Teratogenic

70
Q

Drug Interactions of Terbinafine

A

none

does not affect cytochrome P450 isoforms

Pharmacology (23 decks)

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