Tuberculosis
Tuberculosis symptoms
Tuberculosis causes
Tuberculosis treatment
Tuberculosis tests
Tuberculosis medication
CLASSIFICATION
Tuberculosis symptoms
Tuberculosis causes
Tuberculosis treatment
Tuberculosis tests
Tuberculosis medication
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TUBERCULOSIS
Tuberculosis is a chronic infectious disease caused by M. tuberculosis. Up to 1940, there were no effective chemotherapeutic agents for the treatment of tuberculosis.
In 1947, streptomycin was the first drug developed for the treatment of tuberculosis.
Mycobacterial infections require prolonged treatment because of some peculiarities of both the organism and the lesions. Since TB is chronic infection, it consist of excessive fibrous tissue with central necrosis.
So vascularity of lesion is poor, hence the penetration of drug into the lesion is decreased.
Tuberculosis is a chronic infectious disease caused by M. tuberculosis. Up to 1940, there were no effective chemotherapeutic agents for the treatment of tuberculosis.
In 1947, streptomycin was the first drug developed for the treatment of tuberculosis.
Mycobacterial infections require prolonged treatment because of some peculiarities of both the organism and the lesions. Since TB is chronic infection, it consist of excessive fibrous tissue with central necrosis.
So vascularity of lesion is poor, hence the penetration of drug into the lesion is decreased.
CLASSIFICATION
1. First line (standard drugs)
Isoniazid, Rifampicin, Pyrazinamide, Ethambutol, Streptomycin.
2. Second line (reserve drugs)
Para-aminosalicylic acid, Thiacetazone, Cycloserine, Ethionamide, Kanamycin, Capreomycin, Amikacin.
Newer agents are :-
Ciprofloxacin, Moxifloxacin, Gatifloxacin, Clarithromycin, Azithromycin, Rifabutin, Refapentine.
TUBERCULOSIS SYMPTOMS
Cough
Chest pain
Back pain
Fever
Weight loss
Hemoptysis
Weakness
Night sweats
TUBERCULOSIS TREATMENT
The therapy of tuberculosis has undergone remarkable change. The conventional 12 to 18 months treatment has been replaced by more effective and less toxic 6 month treatment which also yields higher completion rates.
The goals of antitubercular chemotherapy are :Kill dividing bacillii : drugs with early bactericidal action rapidly reduce bacillary load in the patient and achieve quick sputum negativity so that the patient is non contagious to the community : transmission of TB is interrupted. this also affords quick symptom relief.
Kill persisting bacilii : To effect cure and prevent relapse. This depends on the sterilizing capacity of drug.
Prevent emergence of resistance : So that the bacilli remain susceptible to the drugs.
Tuberculosis medications/Antitubercular drugs are explained below, continue reading...
GENERAL PRINCIPLES OF ANTITUBERCULAR CHEMOTHERAPY ARE :
Use of any single drug in tuberculosis results in the emergence of resistant organisms and relapse in almost 3/4th patients. A combination of two or more drugs must be used.
During protracted treatment, these bacilli multiply and become dominant in 3-4 months. Because insensitivity to one drug is independent of that to another, i.e. incidence of H resistance among bacilli resistant to R will be 10-6 and vice versa; only few bacilli will be resistant to both; these can be handled by host defence.
Isoniazid and R are the most efficacious drugs; their combination is definitely synergistic - duration of therapy is shortened form > 12 months to 9 months. Addition of Z for the initial 2 months further reduces duration of treatment to 6 months.
A single daily dose of all first line antitubercular drugs is preferred. The 'directly observed treatment short course, (DOTS) was recommended by the WHO in 1995.
Response is fast in the first few weeks as the fast dividing bacilli are eliminated rapidly. Symptomatic relief is evident within 2-4 weeks.
SHORT COURSE CHEMOTHERAPY
These are regimens of 6-9 months duration which have ben found very efficacious. The dose of first line Antitubecular drug has been standardized on the basis of body weight and is applicable on both adults and children. table
All regimens have an initial intensive phase, lasting for 2-3 months aimed to rapidly kill the TB bacilli, bring about sputum conversion and afford symptomatic relief. This is followed by continuation phase lasting for 4-6 months during which the remaining bacilli are eliminated so that relapse does not occur.
Treatment of TB is categorized by :
1. Site of disease its severity.
2. Sputum smear - positivity/negativity : positive cases are infectious and have higher mortality.
3. History of previous treatment : risk of drug resistance is more in irregularly treated patient.
Initial treatment with 4 drugs reduces risk of selecting resistant bacilli as well as covers patients with primary resistance. When few bacilli are left only 2 drugs are in continuation phase are enough to effect cure.
Regimens containing only 3 drugs in initial phase and 2 in the continuation phase are of proven efficacy. Accordingly, previously treated/failure/default/ relapse cases are treated with a longer intensive phase-5 drugs for 2 months and 4 drugs for 1 month followed by 3 drugs in the continuation phase of 5 months duration instead of usual 4 months.
TUBERCULOSIS TESTS
1. Heaf test
2. Mantoux test
3. Tine test
Heaf test : Heaf test is a diagnostic test used to confirm whether or not children had been exposed to tuberculosis infection. Heaf test is also known as sterneedle test.
Heaf gun is used to inject testing serum samples under the skin at once by dipping the needle point in tuberculin purified protien derivative and pricked into the skin.5 skin dose is injected which is equals to 0.5 ml.
Mantoux test : 1 skin dose which is equals to 0.1 ml is injected by intracutaneously or intradermaly, it shows reaction as inflammation, necrosis at the site of injection, if reaction happens means person is immune. if no reaction means person does not have antibody to fight against tuberculli organism.
Tine test : Each needle contains 5 skin dose, it should be sterilised by ethylene oxide sterilisation process.
TUBERCULOSIS MEDICATION
Some of the drug given in classification is discussed here :
ISONIAZID
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Tuberculosis treatment | tuberculosis symptoms,, please comment i will be very happy.
Thanks
Isoniazid, Rifampicin, Pyrazinamide, Ethambutol, Streptomycin.
2. Second line (reserve drugs)
Para-aminosalicylic acid, Thiacetazone, Cycloserine, Ethionamide, Kanamycin, Capreomycin, Amikacin.
Newer agents are :-
Ciprofloxacin, Moxifloxacin, Gatifloxacin, Clarithromycin, Azithromycin, Rifabutin, Refapentine.
TUBERCULOSIS SYMPTOMS
Cough
Chest pain
Back pain
Fever
Weight loss
Hemoptysis
Weakness
Night sweats
TUBERCULOSIS TREATMENT
The therapy of tuberculosis has undergone remarkable change. The conventional 12 to 18 months treatment has been replaced by more effective and less toxic 6 month treatment which also yields higher completion rates.
The goals of antitubercular chemotherapy are :Kill dividing bacillii : drugs with early bactericidal action rapidly reduce bacillary load in the patient and achieve quick sputum negativity so that the patient is non contagious to the community : transmission of TB is interrupted. this also affords quick symptom relief.
Kill persisting bacilii : To effect cure and prevent relapse. This depends on the sterilizing capacity of drug.
Prevent emergence of resistance : So that the bacilli remain susceptible to the drugs.
Tuberculosis medications/Antitubercular drugs are explained below, continue reading...
GENERAL PRINCIPLES OF ANTITUBERCULAR CHEMOTHERAPY ARE :
Use of any single drug in tuberculosis results in the emergence of resistant organisms and relapse in almost 3/4th patients. A combination of two or more drugs must be used.
During protracted treatment, these bacilli multiply and become dominant in 3-4 months. Because insensitivity to one drug is independent of that to another, i.e. incidence of H resistance among bacilli resistant to R will be 10-6 and vice versa; only few bacilli will be resistant to both; these can be handled by host defence.
Isoniazid and R are the most efficacious drugs; their combination is definitely synergistic - duration of therapy is shortened form > 12 months to 9 months. Addition of Z for the initial 2 months further reduces duration of treatment to 6 months.
A single daily dose of all first line antitubercular drugs is preferred. The 'directly observed treatment short course, (DOTS) was recommended by the WHO in 1995.
Response is fast in the first few weeks as the fast dividing bacilli are eliminated rapidly. Symptomatic relief is evident within 2-4 weeks.
SHORT COURSE CHEMOTHERAPY
These are regimens of 6-9 months duration which have ben found very efficacious. The dose of first line Antitubecular drug has been standardized on the basis of body weight and is applicable on both adults and children. table
All regimens have an initial intensive phase, lasting for 2-3 months aimed to rapidly kill the TB bacilli, bring about sputum conversion and afford symptomatic relief. This is followed by continuation phase lasting for 4-6 months during which the remaining bacilli are eliminated so that relapse does not occur.
Treatment of TB is categorized by :
1. Site of disease its severity.
2. Sputum smear - positivity/negativity : positive cases are infectious and have higher mortality.
3. History of previous treatment : risk of drug resistance is more in irregularly treated patient.
Initial treatment with 4 drugs reduces risk of selecting resistant bacilli as well as covers patients with primary resistance. When few bacilli are left only 2 drugs are in continuation phase are enough to effect cure.
Regimens containing only 3 drugs in initial phase and 2 in the continuation phase are of proven efficacy. Accordingly, previously treated/failure/default/ relapse cases are treated with a longer intensive phase-5 drugs for 2 months and 4 drugs for 1 month followed by 3 drugs in the continuation phase of 5 months duration instead of usual 4 months.
TUBERCULOSIS TESTS
1. Heaf test
2. Mantoux test
3. Tine test
Heaf test : Heaf test is a diagnostic test used to confirm whether or not children had been exposed to tuberculosis infection. Heaf test is also known as sterneedle test.
Heaf gun is used to inject testing serum samples under the skin at once by dipping the needle point in tuberculin purified protien derivative and pricked into the skin.5 skin dose is injected which is equals to 0.5 ml.
Mantoux test : 1 skin dose which is equals to 0.1 ml is injected by intracutaneously or intradermaly, it shows reaction as inflammation, necrosis at the site of injection, if reaction happens means person is immune. if no reaction means person does not have antibody to fight against tuberculli organism.
Tine test : Each needle contains 5 skin dose, it should be sterilised by ethylene oxide sterilisation process.
TUBERCULOSIS MEDICATION
Some of the drug given in classification is discussed here :
ISONIAZID
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Tuberculosis treatment | tuberculosis symptoms,, please comment i will be very happy.
Thanks
Chest pain
Back pain
Fever
Weight loss
Hemoptysis
Weakness
Night sweats
TUBERCULOSIS TREATMENT
The therapy of tuberculosis has undergone remarkable change. The conventional 12 to 18 months treatment has been replaced by more effective and less toxic 6 month treatment which also yields higher completion rates.
The goals of antitubercular chemotherapy are :Kill dividing bacillii : drugs with early bactericidal action rapidly reduce bacillary load in the patient and achieve quick sputum negativity so that the patient is non contagious to the community : transmission of TB is interrupted. this also affords quick symptom relief.
Kill persisting bacilii : To effect cure and prevent relapse. This depends on the sterilizing capacity of drug.
Prevent emergence of resistance : So that the bacilli remain susceptible to the drugs.
Tuberculosis medications/Antitubercular drugs are explained below, continue reading...
The goals of antitubercular chemotherapy are :Kill dividing bacillii : drugs with early bactericidal action rapidly reduce bacillary load in the patient and achieve quick sputum negativity so that the patient is non contagious to the community : transmission of TB is interrupted. this also affords quick symptom relief.
Kill persisting bacilii : To effect cure and prevent relapse. This depends on the sterilizing capacity of drug.
Prevent emergence of resistance : So that the bacilli remain susceptible to the drugs.
Tuberculosis medications/Antitubercular drugs are explained below, continue reading...
GENERAL PRINCIPLES OF ANTITUBERCULAR CHEMOTHERAPY ARE :
Use of any single drug in tuberculosis results in the emergence of resistant organisms and relapse in almost 3/4th patients. A combination of two or more drugs must be used.
During protracted treatment, these bacilli multiply and become dominant in 3-4 months. Because insensitivity to one drug is independent of that to another, i.e. incidence of H resistance among bacilli resistant to R will be 10-6 and vice versa; only few bacilli will be resistant to both; these can be handled by host defence.
Isoniazid and R are the most efficacious drugs; their combination is definitely synergistic - duration of therapy is shortened form > 12 months to 9 months. Addition of Z for the initial 2 months further reduces duration of treatment to 6 months.
A single daily dose of all first line antitubercular drugs is preferred. The 'directly observed treatment short course, (DOTS) was recommended by the WHO in 1995.
Response is fast in the first few weeks as the fast dividing bacilli are eliminated rapidly. Symptomatic relief is evident within 2-4 weeks.
Isoniazid and R are the most efficacious drugs; their combination is definitely synergistic - duration of therapy is shortened form > 12 months to 9 months. Addition of Z for the initial 2 months further reduces duration of treatment to 6 months.
A single daily dose of all first line antitubercular drugs is preferred. The 'directly observed treatment short course, (DOTS) was recommended by the WHO in 1995.
Response is fast in the first few weeks as the fast dividing bacilli are eliminated rapidly. Symptomatic relief is evident within 2-4 weeks.
SHORT COURSE CHEMOTHERAPY
These are regimens of 6-9 months duration which have ben found very efficacious. The dose of first line Antitubecular drug has been standardized on the basis of body weight and is applicable on both adults and children. table
All regimens have an initial intensive phase, lasting for 2-3 months aimed to rapidly kill the TB bacilli, bring about sputum conversion and afford symptomatic relief. This is followed by continuation phase lasting for 4-6 months during which the remaining bacilli are eliminated so that relapse does not occur.
Treatment of TB is categorized by :
1. Site of disease its severity.
2. Sputum smear - positivity/negativity : positive cases are infectious and have higher mortality.
3. History of previous treatment : risk of drug resistance is more in irregularly treated patient.
Initial treatment with 4 drugs reduces risk of selecting resistant bacilli as well as covers patients with primary resistance. When few bacilli are left only 2 drugs are in continuation phase are enough to effect cure.
Regimens containing only 3 drugs in initial phase and 2 in the continuation phase are of proven efficacy. Accordingly, previously treated/failure/default/ relapse cases are treated with a longer intensive phase-5 drugs for 2 months and 4 drugs for 1 month followed by 3 drugs in the continuation phase of 5 months duration instead of usual 4 months.
TUBERCULOSIS TESTS
1. Heaf test
2. Mantoux test
3. Tine test
Heaf test : Heaf test is a diagnostic test used to confirm whether or not children had been exposed to tuberculosis infection. Heaf test is also known as sterneedle test.
Heaf gun is used to inject testing serum samples under the skin at once by dipping the needle point in tuberculin purified protien derivative and pricked into the skin.5 skin dose is injected which is equals to 0.5 ml.
Mantoux test : 1 skin dose which is equals to 0.1 ml is injected by intracutaneously or intradermaly, it shows reaction as inflammation, necrosis at the site of injection, if reaction happens means person is immune. if no reaction means person does not have antibody to fight against tuberculli organism.
Tine test : Each needle contains 5 skin dose, it should be sterilised by ethylene oxide sterilisation process.
TUBERCULOSIS MEDICATION
Some of the drug given in classification is discussed here :
ISONIAZID
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Tuberculosis treatment | tuberculosis symptoms,, please comment i will be very happy.
Thanks
All regimens have an initial intensive phase, lasting for 2-3 months aimed to rapidly kill the TB bacilli, bring about sputum conversion and afford symptomatic relief. This is followed by continuation phase lasting for 4-6 months during which the remaining bacilli are eliminated so that relapse does not occur.
Treatment of TB is categorized by :
1. Site of disease its severity.
2. Sputum smear - positivity/negativity : positive cases are infectious and have higher mortality.
3. History of previous treatment : risk of drug resistance is more in irregularly treated patient.
Initial treatment with 4 drugs reduces risk of selecting resistant bacilli as well as covers patients with primary resistance. When few bacilli are left only 2 drugs are in continuation phase are enough to effect cure.
Regimens containing only 3 drugs in initial phase and 2 in the continuation phase are of proven efficacy. Accordingly, previously treated/failure/default/ relapse cases are treated with a longer intensive phase-5 drugs for 2 months and 4 drugs for 1 month followed by 3 drugs in the continuation phase of 5 months duration instead of usual 4 months.
TUBERCULOSIS TESTS
1. Heaf test
2. Mantoux test
3. Tine test
Heaf test : Heaf test is a diagnostic test used to confirm whether or not children had been exposed to tuberculosis infection. Heaf test is also known as sterneedle test.
Heaf gun is used to inject testing serum samples under the skin at once by dipping the needle point in tuberculin purified protien derivative and pricked into the skin.5 skin dose is injected which is equals to 0.5 ml.
Mantoux test : 1 skin dose which is equals to 0.1 ml is injected by intracutaneously or intradermaly, it shows reaction as inflammation, necrosis at the site of injection, if reaction happens means person is immune. if no reaction means person does not have antibody to fight against tuberculli organism.
Tine test : Each needle contains 5 skin dose, it should be sterilised by ethylene oxide sterilisation process.
TUBERCULOSIS MEDICATION
Some of the drug given in classification is discussed here :
ISONIAZID
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
2. Mantoux test
3. Tine test
Heaf test : Heaf test is a diagnostic test used to confirm whether or not children had been exposed to tuberculosis infection. Heaf test is also known as sterneedle test.
Heaf gun is used to inject testing serum samples under the skin at once by dipping the needle point in tuberculin purified protien derivative and pricked into the skin.5 skin dose is injected which is equals to 0.5 ml.
Mantoux test : 1 skin dose which is equals to 0.1 ml is injected by intracutaneously or intradermaly, it shows reaction as inflammation, necrosis at the site of injection, if reaction happens means person is immune. if no reaction means person does not have antibody to fight against tuberculli organism.
Tine test : Each needle contains 5 skin dose, it should be sterilised by ethylene oxide sterilisation process.
TUBERCULOSIS MEDICATION
Some of the drug given in classification is discussed here :
ISONIAZID
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
Mechanism of action : Isoniazid converted to isonicotinic acid by inhibiting the membrane bound KatG enzyme (catalase peroxidase) which inhibits the mycolic acid synthesis.
Pharmacokinetic : INH is absorbed from the gut, distributed throuout the body, reaches skin, body fluids like asiatic acid, CSF, saliva. IT is metabolised by acetylation and metabolite are excreted in urine, rate of acetylation of INH is under genetic control resulting in either rapid or slow acetylatos.
Adverse effect : Peripheral neuritis, hepatitis, skin rshes, ethralgia, gi disturbance, optic neuritis, jaundice.
RIFAMPICIN
Mechanism of action : Rifampicin inhibits bacterial DNA depentednt RNA polymerase and there by supresses chain initiation in RNA synthesis.
Pharmacokinetic : Given by oral route, Rpaidly absorbed from git, but presence of food reduces absorption. Distrubeted widely throuout the body and gets metabolised in liver, excreted in bile, urine.
Adverese effect : Hepatitis, Flu like syndrome, gi didturbance, skin rashes, itiching, flushing.
PYRAZINAMIDE
Mechanism of action : It is synthetic analogue of nitoniamide, it is active against intracellular bacilli in acidic ph. It has tuberculididal activity like INH.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Averse effect : Hepatotoxicity, Hyperurecemia, Gout, vomitting, anorexia.
ETHAMBUTOL
Mechanism of action : it inhibits arabenosyl transferse that are involved in micobacterial cell wall synthesis.
Pharmacokinetic : Absorbed orally, distrubed throuout the body, specially CSF. Metabolised in liver and excreted in urine.
Adverse effect : optic neuritis, vision defects.
PARA-AMINO-SALISYLIC ACID
Mechanism of action : it inhibits folate synthetase enzyme and formation of tetra hydro folic acid.
Pharmacokinetic : distributed throuout body, poor penetration to bbb, metabolised in liver by acetylation, and excreted in urine.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Tuberculosis treatment | tuberculosis symptoms,, please comment i will be very happy.
Thanks
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