Tuberculosis
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Tuberculosis

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prevention & cure of tuberculosis

prevention & cure of tuberculosis

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Tuberculosis Tuberculosis Presentation Transcript

  • TUBERCULOSIS
  • WHAT IS TUBERCULOSIS  infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis. ( gram positive bacteria)  It is a chronic granulomatous disease.  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.
  •  The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss . Infection of other organs causes a wide range of symptoms.
  • Diagnosis  radiology commonly chest X-rays  microbiological culture of body fluids.
  • SIGNS AND SYMPTOMS  most commonly occurs in the lungs (known as pulmonary tuberculosis).Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extra pulmonary TB may coexist with pulmonary TB as well.  fever, chills, night sweats, loss of appetite, weight loss, and fatigue.[9] Significant finger clubbing.
  • Pulmonary  it most commonly involves the lungs (in about 90% of cases).  Symptoms may include chest pain and a prolonged cough     producing sputum. About 25% of people may not have any symptoms (i.e. they remain "asymptomatic"). Occasionally, people may cough up blood in small amounts, and in very rare cases, the infection may erode into thepulmonary artery, resulting in massive bleeding (Rasmussen's aneurysm). Tuberculosis may become a chronic illness and cause extensive scarring in the upper lobes of the lungs. The upper lung lobes are more frequently affected by tuberculosis than the lower ones. The reason for this difference is not entirely clear. It may be due either to better air flow, or to poor lymph drainage within the upper lungs.
  • Extrapulmonary  n 15–20% of active cases, the infection spreads outside the lungs, causing other kinds of TB.  Extrapulmonary TB occurs more commonly in immunosuppressed persons and young children. In those with HIV, this occurs in more than 50% of cases.  Notable extrapulmonary infection sites include the pleura (in tuberculous pleurisy), the central nervous system (in tuberculous meningitis), the lymphatic system (inscrofula of the neck), the genitourinary system (in urogenital tuberculosis), and the bones and joints (in Pott's disease of the spine), among others. When it spreads to the bones, it is also known as "osseous tuberculosis".  a form of osteomyelitis. Sometimes, bursting of a tubercular abscess through skin results in tuberculous ulcer. An ulcer originating from nearby infected lymph nodes is painless.
  •  Transmission: air born disease , When people with active pulmonary TB cough, sneeze, speak, sing, or spit, they expel infectious aerosol droplets 0.5 to 5.0 µm in diameter. A single sneeze can release up to 40,000 droplets.  Pathogenesis:TB infection begins when the mycobacteria reach the pulmonary alveoli,
  •  WHO expert gp has farmed clear cut treatment guidelines     for different categories of TB patient The dose of drug std on the basis of body weight. The regimens have two phase Inititial intensive phase: lasting 2 3 month ,amied to rapidly kill the TB bacilli Continuation phase : lasting for 4-6 months ,estimated bacilli relapse dose not occur
  • Category wise treatment regimens  Category 1: untreated T.B  CATEGORY 2: RELAPSE, INTERRUPTED TREATMENT  CATEGORY3: LESS SEVERE FORMS OF EXTRAPULMONRY T.B  CATEGORY 4: THESE ARE CHRONIC CASE WHO HAVE REMAINED OR HAVE BECOME +VE AFTER COMPLETING FULLY SUPERVISED RETREATMENT REGIMEN.
  • How is TB treated?  Several antibiotics need to be taken over a number of months to prevent resistance developing to the TB drugs. The great majority of TB bacteria are sensitive to the antibiotics used.  1st line drug : have high antitubercular efficacy,low toxicity  2nd line drug: low antitubercular effficacy ,low toxicity       Name of antibiotic used: Cycloserine Ethambutol Ethiona mide Isoniazid Protionamide
  • RECOMMENDED DOSES OF ANTITUBERCULAR DRUGS  DRUG DAILY DOSE  ISONIAZID 300MG  RIFAMPIN 600MG  PYRAZINAMIDE 1500MG  ETHAMBUTOL 1000MG  STREPTOMYCIN 1000MG WEEK DOSE 600MG 600MG 2000MG 1600MG 1000
  •  Pyrazinamide  Rifampicin  Dapsone  Discription of antibiotic used:  Cycloserine: 2nd line drug  Max: 1 gm in day  Interaction:  B12 ,FOLIC ACID DEFIciency, inhibit s phenytoin metabolism & may increase of risk of epileptic seizuers, alcohal increase of convulsions, increase cns toxicity.  ADR: megaloblastic anaemia, convulsions (dose related)  Drowsiness, vertigo, depression.
  •  ETHAMBUTOL:1st line drug  Max dose: 15mg/kg/day  Interaction: synergistic effect wd other antitubercular agent  ADR: reduced renal clearance of urates.  GI disturbence  ETHIONAMIDE: 2nd line drug  Max dose: 1gm/day  Interaction: increase hepatotoxicity wd rifampicin, increase cns toxicity wd cycloserine  ADR: ANOREXIA, excessive salivation, metallic TASTE,
  •  ISONIAZID: 1st line drug  Max dose: 300 mg daily  Interaction: may increase toxicity of carbamazepine      ,ethosuximide, phenytoin, diazepam, triazolam, theophylline, clofazimine,warferine. ADR: peripheral neuritis ,optic neuritis, psychotic reaction Protionamide: 2ND LINE drug Max dose: 1gm daily Interaction: increase neurotoxic effect wd cycloserine, increase hepatotoxicity wd rifampicin ADR: thrombocytopenia, gyanecomastia , stomatitis
  •  Pyzinamide: multi drug regimen  1st LINE DRUG  Max dose: 3gm DAILY  INTERACTION: excretion may be blocked by probencid  ADR : hyperureicaemia  Rifampicin:  1ST line drug  Max dose : 600 mg /day  Interaction: absorption may be decrease when taken wd antacids, opioid, ketokonazole,  ADR: Abnormalities of liver , influenza like symptoms, reddish colors urine.
  • Multi drug therapy & combinations of drugs  ISONIAZID+ETHAMBUTOL  RIFAMPICIN+ISONIAZID  RIFAMPICIN+ ISONIAZID+PYRAZINAMIDE  RIFAMPICIN+ISONIAZID+PYRAZINAMIDE+ETHAMB UTOL  OTHER ANTI T.B AGENT: DAPSONE, CIPROFLOXACIN.
  • MULTIDRUG RESISTANT (MDR) T.B  RESISTANCE TO BOTH ISONIAZID AND RIFAMPIN  MDR TB has a more rapid course ( some die in 4-16 weeks)  1st nd 2nd line drug are given for 12 to 24 months  Regimen of dose depend on associated disease  For isonizid resistance: rifampin ,pyrozinamide,ethambutol given 12 months  For isoniazid +rifampin resistance: pyrazinamide+ethambutol,+streptomycin/kmc/amic/cpro/ ofl/can be used.
  • Prevention  The only currently available vaccine as of 2011 is bacillus Calmette–Guérin (BCG) which, while it is effective against disseminated disease in childhood, confers inconsistent protection against contracting pulmonary TB.  Drug-resistant forms of the bacteria require treatment for longer  than six months. MDR TB is particularly serious, requiring prolonged (up to 24 months) treatment, with the infectious period lasting much longer.
  •  Treatment in pregnant women: isoniazid,ripampin,pyrazinamide to safe for foetus  (2HRZ+4HR) RECOMMMENTED FOR STD 6 MONTHS  SOMETIMES Z CREATE TERATOGENICITY EFFECT