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Anti tuberculosis drugs

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Anti tuberculosis drugs

  1. 1.  Chronic granulomatous disease caused by Mycobacterium tuberculosis.  Tuberculosis typically attacks the lungs, but can also affect other parts of the body.  It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air.
  2. 2.  Sites of extra-pulmonary tuberculosis
  3. 3. FirstlineSecondline  Isoniazid  Rifampicin  Pyrazinamide  Ethambutol  Streptomycin  Ethionamide  Thiacetazone  Para Aminosalicylic acid (PAS)  Amikacin  Capreomycin  Cycloserine  Ciprofloxacin  Kanamycin  Rifabutin  Rifapentine
  4. 4. tuberculocidaltuberculostatic  Isoniazid  Streptomycin  Capromycin  Ciprofloxacin  Rifampicin  Pyrazinamide  Kanamycin  Ethambutol  Thiacetazone  PAS  Ethionamide  Cycloserine
  5. 5.  Most effective and cheapest primary anti tubercular drug.  Effective in both acidic and alkaline medium  Tuberculocidal for rapidly multiplying bacilli  Tuberculostatic for resting bacilli
  6. 6. Mycolic acids synthesizes Isoniazid inhibits this synthesis
  7. 7.  Peripheral neuritis  Hepatitis  Psychosis  Seizures  Anorexia  GIT discomfort  Fever  Allergic reactions Less common
  8. 8.  Semisynthetic derivative of rifamycin , am anitibiotic obtained from streptomyces mediterranei.  Highly effective tuberculocidal  Acts on both intra and extracellular organisms.  It is called a sterilizing agent.
  9. 9.  Rifampicin binds to beta subunit of DNA dependant RNA polymerase and inhibits RNA synthesis in bacteria.  It cannot bind to human RNA polymerase, thus selectively destroying the bacteria.
  10. 10.  Hepatotoxicity  GIT disturbances  Flu-like syndrome  CNS symptoms – drowsiness, ataxia, confusion, peripheral neuropathy etc  Hypersensitivity reactions  Staining of secretions
  11. 11. TB & atypical mycobacterial infections Leprosy Prophylaxis in H. influenza Resistant staph infections Brucellosis Pneumococcal meningitis To eradicate carrier state
  12. 12.  Analog of nicotinamide  Tuberculocidal  Requires acidic pH for its activity  Mechanism of action not clearly known.  HEPATOTOXICITY is the Most common adverse effect May inhibit synthesis of mycolic acids
  13. 13.  Tuberculocidal  Acts only against extracellular organisms  Has to be given IM  When used alone resistance develops.  Least preferred first line drug.
  14. 14.  Tuberculostatic  Also effective against atypical mycobacteria.  Well absorbed on oral administration  Dose should be reduced in renal failure  Optic neuritis is an important adverse effect which needs withdrawal of the drug.  It decreases the renal excretion of uric acid and enhances plasma urate levels.
  15. 15.  INH: potent bactericidal  Rifampicin: potent bactericidal  Pyrazinamide: weak bactericidal  Ethambutol: bacteriostatic  Streptomycin: bactericidal Synergistic effect NEVER USE A SINGLE DRUG FOR CHEMOTHERAPY IN TUBERCULOSIS, A COMBINATION OF 2 OR MORE IS ALWAYS BETTER
  16. 16.  Less effective  More toxic  Used only if organism is resistant to first line drugs  Ethionamide , PAS, cycloserine : bacteriostatic  Amikacin, capromycin, fluoroquinolones are used in Multi Drug Resistant TB
  17. 17. Phase I •1-3 months •Rapidly kills bacilli •Symptomatic relief Phase II •4-6 months •Eliminates remaining bacilli •Prevents relapse
  18. 18. 1. INH+S+T daily for 2 months 2. INH+T daily for 10 months INH – isoniazid S – Streptomycin T - Thiacetazone
  19. 19. 1. INH+R+Z+E/S daily or thrice a week for 2 months followed by: 2. INH+R daily or thrice a week for 4 months 3. INH+R+Z trice a week for 2 months followed by 4. INH+R daily for 7 months.

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