## Mechanism of Action of First-Line Antitubercular Drugs ### Correct Mechanisms | Drug | Mechanism | Classification | |------|-----------|----------------| | **Isoniazid (INH)** | Inhibits InhA (enoyl-ACP reductase) after KatG activation → blocks mycolic acid synthesis | Bactericidal | | **Pyrazinamide (PZA)** | Converted to pyrazinoic acid by pyrazinamidase → disrupts membrane potential and energy metabolism | Bactericidal | | **Ethambutol (EMB)** | Inhibits arabinosyl transferases → prevents arabinogalactan synthesis in cell wall | Bacteriostatic | | **Rifampicin (RIF)** | Inhibits bacterial DNA-dependent RNA polymerase → blocks transcription | **Bactericidal** | ### Key Point: **Rifampicin is bactericidal, NOT bacteriostatic.** This is a critical distinction. Rifampicin is one of the most potent antitubercular agents and is bactericidal against both intracellular and extracellular M. tuberculosis. ### High-Yield: **Bactericidal vs. Bacteriostatic First-Line Drugs:** - **Bactericidal:** Isoniazid, Rifampicin, Pyrazinamide (the "big three") - **Bacteriostatic:** Ethambutol, Streptomycin ### Clinical Pearl: The combination of bactericidal drugs (INH + RIF + PZA) in the intensive phase is what allows for the short 6-month standard regimen. Bacteriostatic drugs alone would require much longer treatment durations. ### Mnemonic: **"RIF is a KILLER"** — Rifampicin is bactericidal and kills rapidly. Do not confuse it with bacteriostatic agents like ethambutol.
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