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.
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
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.
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.
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