Fungal Flashcards

1
Q

Which fungi are opportunistic?

A

Aspergillus and Candida Albicans

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2
Q

Which fungi cause systemic disease?

A

Coccidiodies
Histoplasmosis
Blastomycosis
Cryptococcus

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3
Q

What is the target of anti-fungals?

A

cell wall

ergosterol (a sterol unique to fungi)

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4
Q

What is MOA of Amphotericin B?

A

binds ergosterol and forms leaky pores in fungal membrane?

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5
Q

What is clinical application for Amphotericin B? What form is used for systemic infection?

A
IV form
Opportunistic: 
Aspergillus, 
Candidemia :
Systemic:
Coccidiodies
Histoplasmosis 
Blastomycosis 
Cryptococcus
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6
Q

What are ADE of amphotericin?

A

Nephrotoxicity

Infusion site rxn’s : fever, muscle spasms, chills, hypotension

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7
Q

What is MOA of flucytosine? What form is it given in?

A

interferes with RNA and DNA synthesis in fungi

Oral form given

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8
Q

What are the clinical applications of flucytosine?

A

Treats cryptococcus and chromoblastomycosis inflections

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9
Q

What are ADE of flucytosine?

A

Renal excretions

Myelosuppression

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10
Q

What is MOA for Azoles?

A

inhibit the P450 enzyme system in fungi to stop production of ergosterol

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11
Q

What is the disadvantage to using azoles?

A

If used long term can develop resistance

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12
Q

Which azole is used to treat aspergillosis?

A

Voriconazole

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13
Q

Which azole can cause visual disturbances and is a class D pregnancy?

A

Voriconazole

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14
Q

Which azoles are used to treat blastomycosis?

A

itraconazole and fluconazole

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15
Q

Which azole is used to treat mucormycosis?

A

posaconazole

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16
Q

How is dermatophytosis treated? mycosis?

A

topical or oral azoles

oral/parenteral azoles

17
Q

T/F Most azoles undergo hepatic metabolism?

A

True

18
Q

Which azole is eliminated in urine unchanged?

A

Fluconazole

19
Q

What are ADE of azoles?

A

GI upset and rash

20
Q

Why is ketaconazole rarely used?

A

inhibits hepatic and adrenal P450 dependent enzymes

21
Q

what are the 4 ways of azole resistance

A
  1. mutation or upregulation of P450 enzymes-decreases binding of azoles
  2. increased efflux proteins pump that push the drug out the cell
  3. alteration to anti fungal drug proteins
  4. alteration to membrane sterols
  5. reduced permeability
22
Q

What is MOA of echinocandins?

A

Caspofungin: prototype

work at the cell wall to stop production of B 1-3 glucan to causes apoptosis (disrupts cell wall synthesis)

23
Q

What is the clinical application of echinocandins? What form is it given in?

A

Candida, Aspergillus, replaces amphotericin during febrile neutropenia
IV only

24
Q

What is mode of elimination for echinocandins?

A

GI elimination, you adjust the dose if liver issues but not necessary for renal

25
Q

What are ADE of echinocandins?

A

facial swelling, itchiness, histamine release

26
Q

What is MOA of terbinafine?

A

stops epoxidation of squalene

27
Q

What is the clinical application of terbinafine?

A

mucocutaneous fungal infections

?accumulates in keratin

28
Q

What is pharmacokinetics of terbinafine?

A

oral, long duration of action

can last weeks

29
Q

What are ADE of terbinafine? (2)

A

GI upset, headache