11 Flashcards
1
Q
- What is the basis of selective toxicity in anti-infective therapy?
a) Targeting common structures between the pathogen and host cells.
b) Targeting biochemical or structural differences between pathogens and host cells.
c) Using the same drugs for both bacterial and viral infections.
d) Ensuring that drugs affect human cells more than pathogens.
e) Targeting only host cells and ignoring pathogens.
A
B
2
Q
- Which of the following antibiotics inhibits bacterial DNA synthesis by targeting folate metabolism?
a) Penicillin
b) Acyclovir
c) Sulfonamides
d) Macrolides
e) Amphotericin B
A
C
3
Q
- Penicillin belongs to which class of antibiotics that target bacterial cell wall synthesis?
a) Aminoglycosides
b) Beta-lactams
c) Fluoroquinolones
d) Macrolides
e) Sulfonamides
A
B
4
Q
- What is the main mechanism of action of aminoglycosides in bacterial protein synthesis inhibition?
a) Binding to the 50S subunit of the ribosome.
b) Binding to the A-site of the 30S ribosomal subunit, preventing tRNA binding to mRNA.
c) Disrupting bacterial cell wall synthesis.
d) Inhibiting DNA gyrase activity.
e) Inhibiting folate metabolism.
A
B
5
Q
- Which of the following antibiotics targets bacterial DNA coiling and prevents DNA gyrase from resealing nicks in the bacterial DNA?
a) Acyclovir
b) Penicillin
c) Macrolides
d) Fluoroquinolones
e) Azoles
A
D
6
Q
- Acyclovir is an antiviral drug that inhibits the replication of viruses. What is its mechanism of action?
a) Inhibits the phosphorylation of nucleosides by thymidine kinase.
b) Inhibits reverse transcriptase directly through allosteric inhibition.
c) Blocks protease cleavage of viral polyproteins.
d) Inhibits viral protein synthesis by binding to ribosomes.
e) Acts as a nucleoside analogue, getting incorporated into viral RNA but preventing further DNA synthesis.
A
E
7
Q
- Which class of antiviral drugs works by preventing reverse transcriptase from transcribing RNA into DNA?
a) Protease inhibitors
b) Nucleoside analogues
c) Non-nucleoside reverse transcriptase inhibitors
d) Thymidine kinase inhibitors
e) Antifungal drugs
A
C
8
Q
- What is the mechanism of action of protease inhibitors in antiviral therapy?
a) Inhibit the phosphorylation of nucleosides.
b) Block reverse transcription of viral RNA.
c) Prevent the cleavage of polyproteins, resulting in non-functional viral proteins.
d) Bind to the ribosome and inhibit protein synthesis.
e) Inhibit viral DNA replication by interfering with DNA gyrase.
A
C
9
Q
- Which antifungal drug binds to ergosterol in the fungal cell membrane, disrupting its integrity?
a) Echinocandins
b) Azoles
c) Amphotericin B
d) Fluoroquinolones
e) Penicillin
A
C
10
Q
- Azole antifungal drugs inhibit which enzyme, leading to the production of toxic sterols in fungal cell membranes?
a) DNA gyrase
b) Lanosterol 14α-demethylase
c) Thymidine kinase
d) Reverse transcriptase
e) Peptidoglycan synthase
A
B
11
Q
- Echinocandins, an antifungal class, target which component of the fungal cell wall?
a) Ergosterol
b) 1,3-β-glucan synthesis
c) Protein synthesis
d) DNA replication
e) RNA polymerase
A
B
12
Q
- Which of the following is a key feature of selective toxicity when using antifungal drugs?
a) The target is usually a feature shared by both the pathogen and the host cell.
b) Antifungal drugs target specific structures or enzymes that are unique to fungal cells.
c) Fungal cells are treated with the same drugs as bacterial cells.
d) Host cells are directly damaged by antifungal drugs.
e) Antifungal drugs are more toxic to human cells than pathogens.
A
B
13
Q
- Which class of drugs inhibits bacterial protein synthesis by binding to the 50S subunit of the ribosome?
a) Fluoroquinolones
b) Sulfonamides
c) Aminoglycosides
d) Macrolides
e) Beta-lactams
A
D
14
Q
- Which of the following is true about fluoroquinolones?
a) They inhibit bacterial protein synthesis by binding to ribosomes.
b) They interfere with bacterial DNA coiling by targeting DNA gyrase.
c) They target cell wall synthesis by binding to peptidoglycan synthase enzymes.
d) They inhibit folate metabolism by targeting PABA.
e) They directly disrupt viral RNA replication.
A
B
15
Q
- Which of the following is the most common target of beta-lactam antibiotics, like penicillin?
a) Peptidoglycan synthesis
b) DNA gyrase activity
c) Reverse transcriptase function
d) Thymidine kinase activity
e) Protein synthesis
A
A
16
Q
- Which of the following describes the mechanism of action of thymidine kinase inhibitors such as acyclovir?
a) Inhibit viral RNA replication by blocking reverse transcription.
b) Inhibit DNA replication by acting as nucleoside analogues and competing for incorporation into viral DNA.
c) Block protein synthesis by binding to viral ribosomes.
d) Prevent cleavage of viral polyproteins.
e) Inhibit fungal cell membrane synthesis by binding to ergosterol.
A
B
17
Q
- Why is antifungal therapy considered more difficult than antibacterial therapy?
a) Fungal cells are more structurally similar to human cells than bacterial cells.
b) There are more antifungal agents than antibacterial agents.
c) Fungal infections are usually easier to treat than bacterial infections.
d) Fungal cells are acellular, making them more challenging to target.
e) Fungal cells do not have cell membranes, unlike bacterial cells.
A
A
18
Q
- Which of the following antibiotics is most likely to cause bacterial lysis by disrupting cell wall integrity?
a) Sulfonamides
b) Fluoroquinolones
c) Beta-lactams (e.g., penicillin)
d) Aminoglycosides
e) Macrolides
A
C
19
Q
A
