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BIOM*40909 > Antifungal & Antiviral > Flashcards

Antifungal & Antiviral Flashcards

1
Q

Fungal infections are AKA:

A

Mycosis

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2
Q

Primary targets for antifungal therapy:

A

Enzymes and other molecules involved in fungal DNA synthesis, mitosis, plasma membrane synthesis, and cell wall synthesis

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3
Q

What makes the plasma membrane of fungi unique?

A

Contains ergosterol instead of cholesterol

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4
Q

Target of many antifungal agents:

A

Ergosterol in fungal plasma membrane

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5
Q

Five main antifungal drug classes:

A

Polyenes, azoles, pyrimidines, echinocandins, and allylamines

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6
Q

Amphoterin B, nystatin, natamycin are all examples of:

A

Polyenes

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7
Q

Itraconazole, and voriconazole are examples of:

A

Azoles

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8
Q

Flucytosine is an example of:

A

Pyrimidines

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9
Q

Capsofungin is an example of:

A

Echinocandins

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10
Q

Cellular target of polyenes:

A

Targets ergosterol directly, disrupts fungal membrane stability

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11
Q

Azoles and allylamines inhibit ____ by _____

A

Ergosterol synthesis, targeting the ER

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12
Q

Cellular targets of pyrimidines

A

Interfere with nucleic acid and protein synthesis (DNA synthesis)

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13
Q

Echinocandins disrupt_____

A

The cell wall

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14
Q

The binding of amphotericin B to ergosterol produces:

A

Channels/pores that alter fungal membrane permeability and allow for leakage of essential cellular contents, ultimately leading to cell death

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15
Q

How does amphotericin B lead to toxicity in humans?

A

Can also bind to cholesterol

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16
Q

When is amphotericin B prescribed?

A

In patients w life-threatening systemic mycoses, especially those that are immunocompromised

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17
Q

Against what is amphotericin B ineffective?

A

Dermatophytes (such as ringworm)

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18
Q

What is the most toxic antimicrobial drug in clinical use?

A

Amphotericin B

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19
Q

Main adverse effect of amphotericin B:

A

Dose-dependent nephrotoxicity
- Changes in urine found before increased levels of urea and nitrogen found in the blood

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20
Q

Why must IV dosing of amphotericin B be slowly infused over 4-6 hours?

A

May cause thrombosis

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21
Q

Common side effects of amphotericin B?

A

Fever, nausea, vomiting, phlebitis (inflammation of veins)

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22
Q

How to lessen nephrotoxicity after amphotericin B administration?

A

Administering fluids containing NaCl prior to treatment

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23
Q

Lipid formulations of amphotericin B:

A

Abelcet, Amphotec, AmBisome

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24
Q

Why are lipid formulations of amphotericin B preferred?

A
  • Much less toxic
  • Can be infused at higher dosages over a 1-2hr period, making them more effective
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25
Q

Pharmacokinetics of amphotericin B:

A

Drug is distributed everywhere in the extracellular space but in the CNS

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26
Q

Pharmacokinetics of Abelcet:

A

Concentrates in lungs and reticuloendothelial system

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27
Q

Half-life of Abelcet:

A

Over 100 hours, continues to be excreted for weeks after discontinuation of therapy

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28
Q

Types of azoles:

A

Imidazoles and triazoles

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29
Q

Mechanism of imidazoles:

A

Inhibit mammalial sterol synthesis

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30
Q

For systemic use, what branch of azoles is more effective and less toxic?

A

Triazoles

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31
Q

How do triazoles work?

A

Inhibit fungal P450 enzymes that are involved in ergosterol formation

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32
Q

Where do triazoles distribute?

A

Throughout the body except for CNS

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33
Q

Where do triazoles concentrate, and how long is their half-life?

A

Skin, two days

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34
Q

Why do triazoles have fewer adverse effects than imidazoles?

A

Triazoles interfere with host hepatic enzymes far less than imidazoles

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35
Q

Itraconazole administration:

A

Orally

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36
Q

What makes fluconazole different from other azoles?

A

Distributes to the CNS

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37
Q

Oral bioavailability of fluconazole and its half-life:

A

100% and can also be administered intravenously. Half life is 20-40 hours so oral doses are acceptable

38
Q

Fluconazole is as effective as amphoterin B for _____

A

Cryptococcal meningitis, also effective against dermatophytes

39
Q

Voriconazole is a derivative of ____

A

Fluconazole

40
Q

Which triazole has the broadest spectrum of activity?

A

Voriconazole

41
Q

Posaconazole is a derivative of ___

A

Itraconazole

42
Q

Cellular activity of flucytosine:

A
  • Metabolizes to 5-FU via a transmembrane cytosine permease which is incorporated into messenger RNA and inhibits protein synthesis.
  • Further metabolizes 5-FU to 5-dUMP which inhibits thymidylate synthase and thereby blocks the conversion of dUMP to dTMP.
  • DNA synthesis is inhibited in the absence of dTMP
43
Q

What is flucytosine mainly used to treat?

A

Fungal cryptococcal meningitis in combination w other drugs

44
Q

MOA of echinocandins:

A

Inhibit beta-(1,3)-D-glucan synthase, which is an enzyme necessary for cell wall synthesis in fungi

45
Q

Echinocandins have fungistatic activity against which species of fungi?

A

Aspergillus species

46
Q

Echinocandins have fungicidal activity against which species of fungi?

A

Candida species

47
Q

The only echinocandin approved for use in pediatric patients:

A

Caspofungin

48
Q

Terbinafine distributes to:

A

Skin, nails, fat, and milk (caution in breastfeeding patients)

49
Q

Why does terbinafine work against dermatophytes?

A

Inhibits ergosterol synthesis

50
Q

Terbinafine half-life:

A

Two weeks

51
Q

How long does terbinafine therapy last?

A

Three months

52
Q

Main adverse effects of terbinafine?

A

Upset GI, headache, rash

53
Q

Virus definition:

A

Sub-microscopic infectious agent that cannot grow or reproduce outside of a host cell

54
Q

Virus structure:

A
  • Contains RNA/DNA
  • A coat (capsid)
  • Some have a lipid-rich envelope
55
Q

Why is it hard to distinguish between host and virus DNA for drug development?

A

Viruses replicate by co-opting the host cell’s metabolic machinery

56
Q

How many groups of viruses?

A

7

57
Q

First step of life cycle of viruses:

A

Virus attaches to host cell
- Attachment is mediated by proteins on viral surface that binds to a host membrane component

58
Q

Second step of life cycle of viruses:

A

Early protein synthesis
-Virus crosses the host cell membrane
- Uncoats and nucleic acid becomes available for transcription into mRNA
- mRNA undergo translation on cellular ribosomes

59
Q

Third step of life cycle of viruses:

A

Genome (DNA/RNA) replication

60
Q

Fourth step of life cycle of viruses:

A

Late protein synthesis

61
Q

Fifth step of life cycle of viruses:

A

Assembly
- Viral proteins that are synthesized assemble with viral genomes within the host cell

62
Q

Final step of the life cycle of viruses:

A

Release from the cell either by cell lysis or by budding through the cell membrane

63
Q
A
64
Q

Innate vs. adaptive responses:

A

Innate: immediate, non-specific responses to pathogens that activates the adaptive immune response
Adaptive: Neutralizing reactions that are specific to the offending agent, involve pathogen recognition

65
Q

Innate immunity involves:

A

Macrophages, dendritic cells, neutrophils, eosinophils

66
Q

Adaptive immunity involves:

A

Cytotoxic T cells, helper T cells, B cells

67
Q

Treatment of influenza mechanism (two ways):

A

Targets the virus by either inhibiting viral uncoating or blocking viral release

68
Q

MOA of Oseltamivir:

A

Blocks viral release from the host cell
- Inhibits neuraminidase

69
Q

Where does Oseltamivir affect?

A

Liver and GI

70
Q

Adverse effects of Oseltamivir?

A

Nausea, GI discomfort

71
Q

What does amantadine treat?

A

Influenza

72
Q

MOA of amantadine:

A

Inhibits viral uncoating

73
Q

Where does amantadine affect?

A

Throughout the body, including CNS

74
Q

Adverse effects of amantadine:

A

GI disturbances, CNS disturbances, renal damage

75
Q

What is acyclovir?

A

Guanosine analogue use to treat herpes

76
Q

MOA of acyclovir:

A

Phosphorylated acyclovir is produced only in HSV-infected cells, which interferes with viral DNA synthesis
Results in DNA chain termination

77
Q

What is HIV:

A

Human immunodeficiency virus
- Causes AIDS (diseases resulting from HIV infection)
- Retrovirus that infects CD4 and T cells

78
Q

How is HIV DNA integrated into the host cell genome?

A

Through uncoating of HIV virus, allowing the genome to be copied (DNA rep)

79
Q

First line treatment of HIV:

A

Combination of 3 antiviral agents- HAART (highly active antiretroviral therapy)

80
Q

HAART combination usually includes:

A

Two NRTIs in combination with NNRT or PI

81
Q

Maraviroc MOA:

A

Inhibits viral entry (HIV)

82
Q

Raltegravir MOA:

A

Enzyme integrase (HIV)

83
Q

What does Zidovudine treat and its MOA:

A

Treats HIV
- Thymidine analogue
- phosphorylated by mammalian kinase

84
Q

Adverse effects of Zidovudine:

A

Anemia, neutropenia and hepatotoxicity

85
Q

How frequent is AZT monotherapy?

A

1/3

86
Q

Adverse effects of nevirapine:

A

Rash, psychiatric effects, hepatotoxicity

87
Q

MOA of nevirapine

A

inhibits reverse transcriptase

88
Q

MOA of ritonavir:

A

Inhibits HIV aspartyl protease which cleaves viral polyprotein into specific proteins.

89
Q

Ritonavir adverse effects:

A

Nausea, diarrhea, vomiting, numbness, elevated liver enzymes, high blood glucose and lipids

90
Q

What is the only drug approved for COVID treatment?

A

Remdesivir

91
Q

Remdesivir MOA:

A

Binds to viral RNA polymerase, inhibiting viral replication through premature termination of RNA transcription

BIOM*40909 (6 decks)

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