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Asif Nawas
4th year student,TMC-5
 Mycobacterial tuberculosis is a serious health hazard
in all over the world now-a-days. Its caused by some
organism following,
 Mycobacterium tuberculosis
 M. bovis
 M. intercellulari
 Atypical mycobacterium
 According to the efficacy
◦ 1st line drugs
 Isoniazid(INH)
 Rifampicin(RMP)
 Ethambutol(EMP)
 Pyrazinamide(PZA)
 Streptomycin(But now-a-days its maximum strains
are
resistant).
2nd line drugs:
-Aminogycosides,
(Amikacin,Kanamycin)
-Polypeptides,
(Capreomycin)
-Fluroquinolones
(Ciprofloxacin,
Levofloxacin, Moxifloxacin)
-Para-aminosalicylic acid
-Cycloserine.
 Should be bactericidal.
 should have greatest level of therapeutic
efficacy.
 Acceptable degree to toxicity.
 No rapid development of resistant.
 1.Pulmonary tuberculosis
 2.Extra-pulmonary tuberculosis:
 Pleural tuberculosis
 Bone And joint tuberculosis
 Intestinal tuberculosis
 Genitourinary tuberculosis.
Category Initial Phase Continuous phase
Pulmonary
tuberculosis and extra
pulmonary
tuberculosis
2 months 4 months
Lymphadenitis
Pleural
Intestinal,
Genitourinary
tuberculosis
2 months 4months
Bones and joints
tuberculosis.
2 months 18 months
(7-10 months) for TB
meningitis
 Compound therapy is used in the treatment
of tuberculosis.The main objectives of
compund therapy are-
 1. To avoid better emergence of resistant
develops rapidly.
 To reduce toxicity of drugs.
 Rifampicin+ Isoniazid=Rimactazid
 Hypersensitivity:
 INH
 Rifampicin
 Ethambutol.
 Hepatotoxicity:
 INH
 Rifampicin
 Pyrazinamide
 Thiacetazone
 Optic neuritis:
 Ethambutol
 INH
 Arthralgia:
 Pyrazinamide
 Ethambutol.
 Ototoxicity: Streptomycin
 GIT upset: Pyrazinamide
◦ patients requiring retreatment should initially receive at
least 5 drugs including rifampicin, Isoniazid,
ethambutol, Pyrazinamide (at least 2 drugs )
◦ Pregnant woman is treated with rifampicin isoniazid and
ethambutol.
◦ In case of MDR(multi-drug resistant TB), pyrazinamide
is the effect for pregnant woman.
◦ Most children are treated with isoniazid and rifampicin
but not ethambutol. Because it causes difficulty in visual
acuity and color perception.
◦ Pregnant woman has high risk of isoniazid –induced
hepatotoxicity. So ALT must be monitored during
treatment.
1.Isoniazid
-100%
2.Rifampicin
-10-20%
3.Ethambutol
-25-50%
4.Pyrazinamide
-100%
5.Cycloserine
-80-100%
 The useful corticosteroid is
 Prednisolone, or dexamethasone
 In Case of TB meningitis- Dexamethasone(8-12mg/d)
 In case of TB pericarditis-Prednisolone(60mg/d)
 Broad spectrum ANTIBIOTIC
 Bactericidal activity(kills semi dormant
bacilli)
 Kills both extracellular and intracellular
mycobacterium.
 Rifampicin also effective against gram-
positive and gram negative cocci.
 Rifampin
 Rifabutin
 Rifapentine.
 It inhibits DNA dependent RNA polymerase.
 So it inhibits bacterial RNA synthesis
Rifampicin
Binds with the beta-subunit
of bacterial DNA dependent
RNA polymerase
It does not bind with
human cell. So it inhibits
bacterial RNA synthesis.
 oral or parenteral route
 Well absorbed in the GIT
 2-4 hours of administration
 Distributed in most body fluid and
tissues.CSF ,pleural cavity, abscess cavities.
 Metabolized in the liver and excreted
through bile feces and urine.
 It causes orange red in color of the urine,
tears, sputum that harmless,
 Tuberculosis
 Leprosy
 Chemoprophylaxis of meningococcal
Meningitis.
 Streptococcal endocarditis
 Osteomyelitis
 Prophylaxis of children H. Influenza.
 Cholestatic Jaundice
 Hepatitis(Drug induced)
 Rash. Fever, Flu-like syndrome
 Nausea ,vomiting, Cramp, epigastric disress.
 diarrhoea.
 Chronic liver disease
 Old age
 Alcoholism
 Vasculitis.
 Rifampicin+ warfarin= effectiveness
 Rifampicin +OCP= effectiveness of oral pill
 Rifampicin+ steroid= metabolized by liver
enzyme
 Rifampicin+ phenytoin= effectiveness of
phenytoin.
 INH is the principle chemotherapeutic agent
for tuberculosis.
 Bactericidal activity
 Able to penetrate into phagocytic cell
 Active against gram positive and gram
negative organism.
Isoniazid is activated by mycobacterial catalase
peroxidase
Form a covalent complex with an acyl carrier
protein and beta-ketoacyl carrier protein.
Block the synthesis of mycolic acid leading to
bactericidal action.
 Oral route of transmission
 INH is well absorbed in the GIT
 Plasma concentration is at least 1-2 hours
 Distributed in the body cavity specially
CSF(20-100)%
 Hepatic metabolism by acetylation
 Renal excretion.
◦ Treatment of tuberculosis
◦ Prophylaxis of tuberculosis
 Those young children whose tuberculin test
negative.
 HLV-infected and AIDS infected patients.
 Those who are in close contact may have
increased risk of contamination,
 INH-induced hepatotoxicity.
 Peripheral neuropathy.
 SLE
 Numbness and tingling of the feet.
 optic neuritis, arthralgia.
 Insomnia, restlessness, convulsion.
 Hemolytic anemia in G6PD
 Ethambutol is a synthetic ,water soluble,
Heat stable compound.
 Well absorbed from GIT.
 Can cross the blood brain barrier.
 Accumulated in renal failure.
Ethambutol
inhibits
mycobacterial
arabinosyl
transferases.
Polymerization
reaction of
arabinoglycan is
inhibited
Defect in
mycobacterial
cell wall
synthesis.
 Retro bulbar neuritis
 Retinal damage.
 pyrazinamide is the first line drug used with
INH & rifampicin.
 It acts as a sterilizing agents of some
intercellular organism.
 Well absorbed in the GIT
 No cross resistance with other anti –TB drug.
Pyrazinamide is up
taken by macrophage
Mycobacterial
pyrazinamidase
activate it
Exert activity against
the organism &
produce “sterilizing”
effect
 Hepatotoxicity.
 Nausea
 Vomiting.
 Hyperuricaemia
 Gouty Arthritis.

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Anti tubercular drug

  • 1. Asif Nawas 4th year student,TMC-5
  • 2.  Mycobacterial tuberculosis is a serious health hazard in all over the world now-a-days. Its caused by some organism following,  Mycobacterium tuberculosis  M. bovis  M. intercellulari  Atypical mycobacterium
  • 3.  According to the efficacy ◦ 1st line drugs  Isoniazid(INH)  Rifampicin(RMP)  Ethambutol(EMP)  Pyrazinamide(PZA)  Streptomycin(But now-a-days its maximum strains are resistant).
  • 5.  Should be bactericidal.  should have greatest level of therapeutic efficacy.  Acceptable degree to toxicity.  No rapid development of resistant.
  • 6.  1.Pulmonary tuberculosis  2.Extra-pulmonary tuberculosis:  Pleural tuberculosis  Bone And joint tuberculosis  Intestinal tuberculosis  Genitourinary tuberculosis.
  • 7. Category Initial Phase Continuous phase Pulmonary tuberculosis and extra pulmonary tuberculosis 2 months 4 months Lymphadenitis Pleural Intestinal, Genitourinary tuberculosis 2 months 4months Bones and joints tuberculosis. 2 months 18 months (7-10 months) for TB meningitis
  • 8.  Compound therapy is used in the treatment of tuberculosis.The main objectives of compund therapy are-  1. To avoid better emergence of resistant develops rapidly.  To reduce toxicity of drugs.  Rifampicin+ Isoniazid=Rimactazid
  • 9.  Hypersensitivity:  INH  Rifampicin  Ethambutol.
  • 10.  Hepatotoxicity:  INH  Rifampicin  Pyrazinamide  Thiacetazone
  • 11.  Optic neuritis:  Ethambutol  INH
  • 13.  Ototoxicity: Streptomycin  GIT upset: Pyrazinamide
  • 14. ◦ patients requiring retreatment should initially receive at least 5 drugs including rifampicin, Isoniazid, ethambutol, Pyrazinamide (at least 2 drugs ) ◦ Pregnant woman is treated with rifampicin isoniazid and ethambutol. ◦ In case of MDR(multi-drug resistant TB), pyrazinamide is the effect for pregnant woman. ◦ Most children are treated with isoniazid and rifampicin but not ethambutol. Because it causes difficulty in visual acuity and color perception. ◦ Pregnant woman has high risk of isoniazid –induced hepatotoxicity. So ALT must be monitored during treatment.
  • 16.  The useful corticosteroid is  Prednisolone, or dexamethasone  In Case of TB meningitis- Dexamethasone(8-12mg/d)  In case of TB pericarditis-Prednisolone(60mg/d)
  • 17.  Broad spectrum ANTIBIOTIC  Bactericidal activity(kills semi dormant bacilli)  Kills both extracellular and intracellular mycobacterium.  Rifampicin also effective against gram- positive and gram negative cocci.
  • 19.  It inhibits DNA dependent RNA polymerase.  So it inhibits bacterial RNA synthesis
  • 20. Rifampicin Binds with the beta-subunit of bacterial DNA dependent RNA polymerase It does not bind with human cell. So it inhibits bacterial RNA synthesis.
  • 21.  oral or parenteral route  Well absorbed in the GIT  2-4 hours of administration  Distributed in most body fluid and tissues.CSF ,pleural cavity, abscess cavities.  Metabolized in the liver and excreted through bile feces and urine.
  • 22.  It causes orange red in color of the urine, tears, sputum that harmless,
  • 23.  Tuberculosis  Leprosy  Chemoprophylaxis of meningococcal Meningitis.  Streptococcal endocarditis  Osteomyelitis  Prophylaxis of children H. Influenza.
  • 24.  Cholestatic Jaundice  Hepatitis(Drug induced)  Rash. Fever, Flu-like syndrome  Nausea ,vomiting, Cramp, epigastric disress.  diarrhoea.
  • 25.  Chronic liver disease  Old age  Alcoholism  Vasculitis.
  • 26.  Rifampicin+ warfarin= effectiveness  Rifampicin +OCP= effectiveness of oral pill  Rifampicin+ steroid= metabolized by liver enzyme  Rifampicin+ phenytoin= effectiveness of phenytoin.
  • 27.  INH is the principle chemotherapeutic agent for tuberculosis.  Bactericidal activity  Able to penetrate into phagocytic cell  Active against gram positive and gram negative organism.
  • 28. Isoniazid is activated by mycobacterial catalase peroxidase Form a covalent complex with an acyl carrier protein and beta-ketoacyl carrier protein. Block the synthesis of mycolic acid leading to bactericidal action.
  • 29.  Oral route of transmission  INH is well absorbed in the GIT  Plasma concentration is at least 1-2 hours  Distributed in the body cavity specially CSF(20-100)%  Hepatic metabolism by acetylation  Renal excretion.
  • 30. ◦ Treatment of tuberculosis ◦ Prophylaxis of tuberculosis
  • 31.  Those young children whose tuberculin test negative.  HLV-infected and AIDS infected patients.  Those who are in close contact may have increased risk of contamination,
  • 32.  INH-induced hepatotoxicity.  Peripheral neuropathy.  SLE  Numbness and tingling of the feet.  optic neuritis, arthralgia.  Insomnia, restlessness, convulsion.  Hemolytic anemia in G6PD
  • 33.  Ethambutol is a synthetic ,water soluble, Heat stable compound.  Well absorbed from GIT.  Can cross the blood brain barrier.  Accumulated in renal failure.
  • 35.  Retro bulbar neuritis  Retinal damage.
  • 36.  pyrazinamide is the first line drug used with INH & rifampicin.  It acts as a sterilizing agents of some intercellular organism.  Well absorbed in the GIT  No cross resistance with other anti –TB drug.
  • 37. Pyrazinamide is up taken by macrophage Mycobacterial pyrazinamidase activate it Exert activity against the organism & produce “sterilizing” effect
  • 38.  Hepatotoxicity.  Nausea  Vomiting.  Hyperuricaemia  Gouty Arthritis.