Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BIOM*40909 > Antifungal & Antiviral > Flashcards

Antifungal & Antiviral Flashcards

(91 cards)

Start Studying
1
Q

Fungal infections are AKA:

A

Mycosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What makes the plasma membrane of fungi unique?

A

Contains ergosterol instead of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Target of many antifungal agents:

A

Ergosterol in fungal plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Five main antifungal drug classes:

A

Polyenes, azoles, pyrimidines, echinocandins, and allylamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Amphoterin B, nystatin, natamycin are all examples of:

A

Polyenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Itraconazole, and voriconazole are examples of:

A

Azoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Flucytosine is an example of:

A

Pyrimidines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Capsofungin is an example of:

A

Echinocandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cellular target of polyenes:

A

Targets ergosterol directly, disrupts fungal membrane stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Azoles and allylamines inhibit ____ by _____

A

Ergosterol synthesis, targeting the ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cellular targets of pyrimidines

A

Interfere with nucleic acid and protein synthesis (DNA synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Echinocandins disrupt_____

A

The cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does amphotericin B lead to toxicity in humans?

A

Can also bind to cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When is amphotericin B prescribed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Against what is amphotericin B ineffective?

A

Dermatophytes (such as ringworm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the most toxic antimicrobial drug in clinical use?

A

Amphotericin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

May cause thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Common side effects of amphotericin B?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How to lessen nephrotoxicity after amphotericin B administration?

A

Administering fluids containing NaCl prior to treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Lipid formulations of amphotericin B:

A

Abelcet, Amphotec, AmBisome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Pharmacokinetics of amphotericin B:
Drug is distributed everywhere in the extracellular space but in the CNS
26
Pharmacokinetics of Abelcet:
Concentrates in lungs and reticuloendothelial system
27
Half-life of Abelcet:
Over 100 hours, continues to be excreted for weeks after discontinuation of therapy
28
Types of azoles:
Imidazoles and triazoles
29
Mechanism of imidazoles:
Inhibit mammalial sterol synthesis
30
For systemic use, what branch of azoles is more effective and less toxic?
Triazoles
31
How do triazoles work?
Inhibit fungal P450 enzymes that are involved in ergosterol formation
32
Where do triazoles distribute?
Throughout the body except for CNS
33
Where do triazoles concentrate, and how long is their half-life?
Skin, two days
34
Why do triazoles have fewer adverse effects than imidazoles?
Triazoles interfere with host hepatic enzymes far less than imidazoles
35
Itraconazole administration:
Orally
36
What makes fluconazole different from other azoles?
Distributes to the CNS
37
Oral bioavailability of fluconazole and its half-life:
100% and can also be administered intravenously. Half life is 20-40 hours so oral doses are acceptable
38
Fluconazole is as effective as amphoterin B for _____
Cryptococcal meningitis, also effective against dermatophytes
39
Voriconazole is a derivative of ____
Fluconazole
40
Which triazole has the broadest spectrum of activity?
Voriconazole
41
Posaconazole is a derivative of ___
Itraconazole
42
Cellular activity of flucytosine:
- 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
What is flucytosine mainly used to treat?
Fungal cryptococcal meningitis in combination w other drugs
44
MOA of echinocandins:
Inhibit beta-(1,3)-D-glucan synthase, which is an enzyme necessary for cell wall synthesis in fungi
45
Echinocandins have fungistatic activity against which species of fungi?
Aspergillus species
46
Echinocandins have fungicidal activity against which species of fungi?
Candida species
47
The only echinocandin approved for use in pediatric patients:
Caspofungin
48
Terbinafine distributes to:
Skin, nails, fat, and milk (caution in breastfeeding patients)
49
Why does terbinafine work against dermatophytes?
Inhibits ergosterol synthesis
50
Terbinafine half-life:
Two weeks
51
How long does terbinafine therapy last?
Three months
52
Main adverse effects of terbinafine?
Upset GI, headache, rash
53
Virus definition:
Sub-microscopic infectious agent that cannot grow or reproduce outside of a host cell
54
Virus structure:
- Contains RNA/DNA - A coat (capsid) - Some have a lipid-rich envelope
55
Why is it hard to distinguish between host and virus DNA for drug development?
Viruses replicate by co-opting the host cell's metabolic machinery
56
How many groups of viruses?
7
57
First step of life cycle of viruses:
Virus attaches to host cell - Attachment is mediated by proteins on viral surface that binds to a host membrane component
58
Second step of life cycle of viruses:
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
Third step of life cycle of viruses:
Genome (DNA/RNA) replication
60
Fourth step of life cycle of viruses:
Late protein synthesis
61
Fifth step of life cycle of viruses:
Assembly - Viral proteins that are synthesized assemble with viral genomes within the host cell
62
Final step of the life cycle of viruses:
Release from the cell either by cell lysis or by budding through the cell membrane
63
64
Innate vs. adaptive responses:
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
Innate immunity involves:
Macrophages, dendritic cells, neutrophils, eosinophils
66
Adaptive immunity involves:
Cytotoxic T cells, helper T cells, B cells
67
Treatment of influenza mechanism (two ways):
Targets the virus by either inhibiting viral uncoating or blocking viral release
68
MOA of Oseltamivir:
Blocks viral release from the host cell - Inhibits neuraminidase
69
Where does Oseltamivir affect?
Liver and GI
70
Adverse effects of Oseltamivir?
Nausea, GI discomfort
71
What does amantadine treat?
Influenza
72
MOA of amantadine:
Inhibits viral uncoating
73
Where does amantadine affect?
Throughout the body, including CNS
74
Adverse effects of amantadine:
GI disturbances, CNS disturbances, renal damage
75
What is acyclovir?
Guanosine analogue use to treat herpes
76
MOA of acyclovir:
Phosphorylated acyclovir is produced only in HSV-infected cells, which interferes with viral DNA synthesis Results in DNA chain termination
77
What is HIV:
Human immunodeficiency virus - Causes AIDS (diseases resulting from HIV infection) - Retrovirus that infects CD4 and T cells
78
How is HIV DNA integrated into the host cell genome?
Through uncoating of HIV virus, allowing the genome to be copied (DNA rep)
79
First line treatment of HIV:
Combination of 3 antiviral agents- HAART (highly active antiretroviral therapy)
80
HAART combination usually includes:
Two NRTIs in combination with NNRT or PI
81
Maraviroc MOA:
Inhibits viral entry (HIV)
82
Raltegravir MOA:
Enzyme integrase (HIV)
83
What does Zidovudine treat and its MOA:
Treats HIV - Thymidine analogue - phosphorylated by mammalian kinase
84
Adverse effects of Zidovudine:
Anemia, neutropenia and hepatotoxicity
85
How frequent is AZT monotherapy?
1/3
86
Adverse effects of nevirapine:
Rash, psychiatric effects, hepatotoxicity
87
MOA of nevirapine
inhibits reverse transcriptase
88
MOA of ritonavir:
Inhibits HIV aspartyl protease which cleaves viral polyprotein into specific proteins.
89
Ritonavir adverse effects:
Nausea, diarrhea, vomiting, numbness, elevated liver enzymes, high blood glucose and lipids
90
What is the only drug approved for COVID treatment?
Remdesivir
91
Remdesivir MOA:
Binds to viral RNA polymerase, inhibiting viral replication through premature termination of RNA transcription

BIOM*40909 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions