Antibiotic Mechanisms of Action — Classification

Antibiotics are classified by how they kill or inhibit bacteria. The major mechanisms map to cellular targets. Cell wall synthesis inhibitors (penicillins, cephalosporins, carbapenems, vancomycin) are bactericidal. Penicillins, cephalosporins, and carbapenems inhibit transpeptidase (penicillin-binding proteins), blocking peptidoglycan cross-linking; vancomycin binds D-Ala-D-Ala on peptidoglycan precursors, preventing both transglycosylation and transpeptidation. Protein synthesis inhibitors target the ribosome: 30S inhibitors (aminoglycosides, tetracyclines) and 50S inhibitors (macrolides, clindamycin, linezolid). Aminoglycosides are bactericidal; most other protein synthesis inhibitors are bacteriostatic. DNA synthesis inhibitors include fluoroquinolones (block DNA gyrase/topoisomerase IV, bactericidal) and metronidazole (damages DNA in anaerobes). Folic acid synthesis inhibitors (sulfonamides, trimethoprim) block sequential steps in folate production — trimethoprim-sulfamethoxazole exploits this dual blockade. Spectrum matters: narrow-spectrum drugs target specific organisms (e.g., vancomycin for gram-positive); broad-spectrum drugs (carbapenems, fluoroquinolones) cover wider ranges but increase superinfection risk, including C. difficile. The bactericidal versus bacteriostatic distinction matters most in immunocompromised clients, where static drugs may not suffice. Key class-linked adverse effects: aminoglycosides → ototoxicity/nephrotoxicity; fluoroquinolones → tendon rupture, QT prolongation; vancomycin → red man syndrome (infusion rate-related); sulfonamides → photosensitivity, Stevens-Johnson syndrome. Nursing priority: obtain culture and sensitivity specimens BEFORE administering the first antibiotic dose.