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1. What is the difference between bacteriostatic and bactericidal drugs?
Bacteriostatic drugs inhibit bacterial growth reversibly, while bactericidal drugs kill bacteria outright.
2. Why is selective toxicity essential for antimicrobial drugs?
Selective toxicity allows drugs to harm microbes without damaging host cells.
3. What is the difference between narrow-spectrum and broad-spectrum antibiotics?
Narrow-spectrum antibiotics target specific bacteria, while broad-spectrum antibiotics target many types.
4. What is a superinfection and how does it occur?
A superinfection is a secondary infection caused by resistant microbes after antibiotic use.
5. Why must dosage be carefully controlled in antimicrobial therapy?
To maximize effectiveness while minimizing toxicity and resistance.
6. How does route of administration affect drug effectiveness?
It determines how quickly and efficiently the drug reaches therapeutic levels.
7. What is a synergistic drug interaction?
When combined drugs work better together than individually.
8. What is an antagonistic drug interaction?
When one drug reduces the effectiveness of another or causes harm.
9. Why is peptidoglycan an ideal drug target?
Because it is essential for bacterial cell walls and absent in humans.
10. How do beta-lactam antibiotics kill bacteria?
They inhibit transpeptidase, preventing peptide cross-linking in peptidoglycan.
11. What structural feature defines beta-lactam antibiotics?
The beta-lactam ring.
12. How does vancomycin differ from penicillins in mechanism?
Vancomycin blocks attachment of tetrapeptide side chains to NAM.
13. Why is bacitracin used only topically?
Because it lacks selective toxicity when used systemically.
14. Why are actively growing bacteria more susceptible to cell-wall inhibitors?
Because they are actively synthesizing peptidoglycan.
15. Why do protein synthesis inhibitors show selective toxicity?
Because bacterial ribosomes differ structurally from eukaryotic ribosomes.
16. How do aminoglycosides disrupt protein synthesis?
They bind the 30S subunit and cause codon-anticodon mismatches.
17. How do tetracyclines inhibit translation?
They block tRNA entry into the A site of the ribosome.
18. What makes all tetracyclines structurally similar?
A four-ring (tetra) structure.
19. How does chloramphenicol inhibit protein synthesis?
It blocks peptide bond formation at the 50S subunit.
20. How do macrolides differ from chloramphenicol?
Macrolides prevent ribosomal translocation rather than peptide bond formation.
21. What makes oxazolidinones unique?
They prevent ribosomal subunits from assembling.
22. How do fluoroquinolones kill bacteria?
They inhibit DNA gyrase and topoisomerase.
23. Why are polymyxins limited in clinical use?
They damage membranes and lack selective toxicity.
24. Why is folic acid synthesis a good bacterial target?
Bacteria must synthesize folic acid, while humans obtain it from diet.
25. How do sulfonamides inhibit bacterial growth?
They compete with PABA for enzyme binding.
26. How does trimethoprim differ from sulfonamides?
It inhibits dihydrofolate reductase.
27. Why is selective toxicity difficult for antifungal drugs?
Because fungi are eukaryotes like humans.
28. What fungal-specific molecules are targeted by antifungals?
Ergosterol and β-glucans.
29. Why are antiviral drugs difficult to develop?
Viruses use host cell machinery.
30. How does acyclovir work?
It causes viral DNA chain termination.
30. How does acyclovir work?
It causes viral DNA chain termination.
31. Why is HIV difficult to treat?
It mutates rapidly and integrates into host DNA.
33. When does antimicrobial resistance occur?
When microbes survive normally lethal drug concentrations.
34. What are the two general ways bacteria acquire resistance?
Spontaneous mutation and horizontal gene transfer.
35. What enzyme confers resistance to penicillins?
Beta-lactamase.
36. How can bacteria prevent drug entry?
By altering membrane receptors or porins.
37. What is an efflux pump?
A protein that actively exports drugs from the cell.
38. How does target modification cause resistance?
Mutations reduce drug binding affinity.
39. What is metabolic pathway bypass?
Using alternative pathways to avoid drug inhibition.
40. How does natural selection drive antibiotic resistance?
Antibiotics create selective pressure favoring resistant bacteria.