Showing posts with label Classification. Show all posts
Showing posts with label Classification. Show all posts
Monday, 30 March 2020
Tuberculosis treatment | tuberculosis symptoms
March 30, 2020
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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Your welcome,
You are learning Pharmacology at onlycology.
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 The conventional 12 to 18 months treatment has been replaced by more effective and less toxic 6 month treatment which also yields higher completion rates.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
Tuesday, 12 March 2019
Anti anxiety | anti anxiety medications
March 12, 2019
Anti anxiety
Anti anxiety drugs
Classification of antianxiety drugs
Adverse effects
Anti anxiety medications
Anti anxiety treatment
Anti anxiety drugs
Classification of antianxiety drugs
Adverse effects
Anti anxiety medications
Anti anxiety treatment
You will learn in this article above mentioned topics.
😊 Hello dear visitors...
Your welcome,
You are learning Pharmacology at onlycology.
ANTI ANXIETY
Anxiety : It is an emotional state, unpleasant in nature, associated with uneasiness, discomfort and concern or fear about some defined or undefined future threat.
Some degree of anxiety is a part of normal life.
Treatment is needed when it is disproportionate to the situation and excessive.
Anti anxiety drugs
These are an ill-defined group of drugs, these are mostly mild CNS depressants which are aimed to control the symptoms of anxiety.
Drug produce a restful state of mind without interfering with normal mental or physical functions.
The anxiolytic-sedative drugs differ markedly from antipsychotics and more closely resemble sedative-hypnotics.
CLASSIFICATION
1. Benzodiazepines : Diazepam, Chlorodiazepoxide, Oxazepam, Lorazepam, Alprazolam.
2. Azapirones : Buspirone, Gepirone, Ispapirone.
3. Sedative antihistaminic : Hydroxyzine.
4. beta blocker : Propranolol.
ANTI ANXIETY MEDICATIONS
The most commonly used drugs are :
Benzodiazepines - Diazepam, Chlorodiazepoxide, Oxazepam, Lorazepam, Alprazolam.
Some drugs if Benzodiazepines have a slow and prolonged action, relieve anxiety at low doses without producing global CNS depression.
They have a selective taming effect on aggressive animals and suppress induced aggression.
They also suppress the performance impairing effect of punishment.
They are more selective for limbic system and have proven clinically better in both quality and quantity of improvement in anxiety and stress related symptoms.
They act primarily by facilitating inhibitory GABAergic transmission, but other additional mechanisms of action have been suggested.
Higher doses induce sleep and impair performance.
1. Chlordiazepoxide :
It was the first BZD to be used clinically.
Oral absorption is slow.
Produces smooth long lasting effect.
Preferred in chronic anxiety states.
Its t1/2 is 5-12 hours but active metabolites are produced which extend the duration of action. It has poor anticonvulsant action.
2. Diazepam :
Quickly absorbed.
Produces a brief initial phase of strong action followed by prolonged milder effect due to a two phase plasma concentration decay curve (distributive phase t1/2 1 hr, elimination phase t1/2 20-30 hours).
Preferred in acute panic states and anxiety associated with organic disease.
3. Oxazepam :
Slowly absorbed.
Penetration in brain is also slow.
Plasma t1/2 is about 10 hrs.
Duration of action is relatively shorter.
Preferred in the elderly and in those with liver disease.
Mainly used in short lasting anxiety states.
4. Lorazepam :
Has slow oral absorption.
Its rate of entry in brain is slower.
t1/2 (10-20 hrs).
Preferred for shortlived anxiety states, tension syndromes etc.
5. Alprazolam :
Particularly useful in anxiety associated with depression.
Good response has been obtained in panic disorders with severe anxiety and autonomic symptoms.
t1/2 is about 12 hrs.
Cause less drowsiness.
6. Buspirone :
It is the first azapirone, a new class of antianxiety drugs, distinctly different from BZDs.
Relieves mild to moderate generalized anxiety, but is ineffective in severe cases, in those showing panic reaction and in OCD.
Buspirone is rapidly absorbed.
Undergoes extensive first pass metabolism.
Bioavailability <5% .
Excretion occurs both in urine and faeces.
t1/2 is 2 - 3.5 hrs.
Adverse effects of Benzodiazepines
Sedation
Lightheadedness
Psychomotor
Cognitive impairment
Vertigo
Confusional state
Increased appetite
Weight gain
Alterations in sexual function
Rashes
Adverse effects of Buspirone
Dizziness
Nausea
Headache
Light headedness
Excitement
Rise in BP
ANTI ANXIETY TREATMENT
If anxiety symptoms are frequent and persist in a severe form, they are a cause of distress and markedly impair performance.
It should be treated with drugs only when excessive and disabling in its own right.
Drug should be used in the smallest possible dose. The dose has to be found out for each patient by titration with symptoms of anxiety.
The drug should be withdrawn as soon as it is no longer required. But when large dose have been used for longer periods, withdrawal should be gradual.
The usual practice is to give 1/2 to 2/3 of the daily dose at bed time to ensure good nightly rest; the remaining is divided in 2-3 doses given at day time.
Buspirone is a nonsedating alternative to BZDs for less severe forms of generalized anxiety.
The tricyclic and SSRI anti depressants are now being increasingly used in many forms of severe anxiety.
They produce a delayed but often gratifying response and can be combined with BZDs. The SSRIs are now drugs of choice for social anxiety in which BZDs though effective, carry abuse potential on long term use.
Patient with hypertension, peptic ulcer, ulcerative colitis, irritable bowel, gastroesophageal reflux, thyrotoxicosis, angina pectoris, are often given low dose of BZD in addition to specific therapy, though anxiety may not be prominent manifestation.
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It should be treated with drugs only when excessive and disabling in its own right.
Drug should be used in the smallest possible dose. The dose has to be found out for each patient by titration with symptoms of anxiety.
The drug should be withdrawn as soon as it is no longer required. But when large dose have been used for longer periods, withdrawal should be gradual.
The usual practice is to give 1/2 to 2/3 of the daily dose at bed time to ensure good nightly rest; the remaining is divided in 2-3 doses given at day time.
Buspirone is a nonsedating alternative to BZDs for less severe forms of generalized anxiety.
The tricyclic and SSRI anti depressants are now being increasingly used in many forms of severe anxiety.
They produce a delayed but often gratifying response and can be combined with BZDs. The SSRIs are now drugs of choice for social anxiety in which BZDs though effective, carry abuse potential on long term use.
Patient with hypertension, peptic ulcer, ulcerative colitis, irritable bowel, gastroesophageal reflux, thyrotoxicosis, angina pectoris, are often given low dose of BZD in addition to specific therapy, though anxiety may not be prominent manifestation.
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Wednesday, 6 March 2019
Epilepsy treatment | Epilepsy medication | Overview
March 06, 2019
• Epilepsy overview
• Epilepsy types
• Classification of drugs
• Epilepsy treatment
• Epilepsy medication
• Top 10 antiepileptic drug
Adverse effect
Hypertrophy and Hyperplasia.
Hypersensitivity reactions.
Hirsutism.
Hyperglycaemia.
Megaloblastic anaemia.
Osteomalacia.
Hypocalacaemia.
Foetal Hydantoin syndrome.
Sedation, drowsiness, ataxia, vertigo, blurred vision, nausea, vomiting, mental confusion.
Pharmacokinetics
Rapidly and completely absorbed from GIT.
Highly bound to plasma protiens.
Metabolized in liver.
Excreted in urine.
Adverse effect
Common - Nausea, vomiting, anorexia, abdominal discomfort.
CNS - Sedation, ataxia, tremor.
Rashes, alopecia, curling of hair.
Rare but serious complication is fulminant hepatitis.
Teratogenicity
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• Epilepsy types
• Classification of drugs
• Epilepsy treatment
• Epilepsy medication
• Top 10 antiepileptic drug
EPILEPSY OVERVIEW
Epilepsy is a Greek word that means convulsions.
Epilepsy is a disorder of brain function characterized by paroxymal cerebral dysrhythmia, manifesting as brief episodes ( seizures) of loss or without characteristic body movements (convulsions), sensory or psychiatric phenomena.
EPILEPSY TYPES
GENERALIZED SEIZURES
1. Generalized tonic-clonic seizures (GTCS, grand mal epilepsy) : It is characterised by the following sequence of symptoms: Aura-epileptic cry-loss of consciousness-fall to the ground-tonic phase-clonic phase-period of relaxation-post-epileptic automatism with confusional states.
2. Absence seizures (petit mal epilepsy) : It is characterised by sudden onset of starting, unresponsiveness with momentary loss of consciousness.
3. Myoclonic seizures : It consist of single or multiple sudden, brief, shock-like contractions.
PARTIAL SEIZURES
1. Simple partial seizures (SPS) : The manifestations depend on the region of the cortex involved. There may be convulsions or light flashes without loss of consciousness.
2. Complex partial seizures (CPS) : It is characterised by aura-amnesia-abnirmal behaviour and automatism.
CLASSIFICATION
1. Barbiturate : Phenobarbitone
2. Deoxybarbiturate : Primidone
3. Hydantoin : Phenytoin
4. Iminostilbene : Carbamazepine
5. Succinimide : Ethosuximide
6. Aliphatic Carboxylic acid : Valproic acid
7. Benzodiazepines : Clonazepam, Diazepam
8. Phenyltriazine : Lamotrigine
9. Cyclic GABA analogue : Gabapentin
10. Newer drugs : Vigabatrin, Topiramate, Levetiracetam
7. Benzodiazepines : Clonazepam, Diazepam
8. Phenyltriazine : Lamotrigine
9. Cyclic GABA analogue : Gabapentin
10. Newer drugs : Vigabatrin, Topiramate, Levetiracetam
EPILEPSY TREATMENT
Antiepileptic drugs suppress seizures but do not cure the disorder; the disease may fadeout though after years of successful control.
The cause of epilepsy should be searched in the patient; if found and treatable, an attempt to remove it should be made.
General principles of symptomatic treatment with antiepileptic drugs are here :
Choice of drug and dose is according to the seizure type and need of the individual patient.
Initiate treatment early, because each seizure episode increases the propensity to further attacks.
Start with a single drug, preferably at low dose---gradually increase dose till full control of seizure or side effects appear.
If full control is not obtained at maximum tolerated dose of one drug, substitute another drug.
Use combinations when all reasonable monotherapy fails.
Therapy should be as simple as possible. A seizure diary should be maintained.
All drug withdrawals should be gradual (except in case of toxocity), abrupt stoppage of therapy without introducing another effective drug can precipitate status epilepticus.
Prolonged therapy is needed - may be life long or at least 3 years after the last seizure.
When women on antiepileptic therapy conceive, antiepileptic drugs should not be stopped. Though most antiseizure drugs have been shown to increase the incidence of birth defects, discontinuation of therapy carries a high risk of status epilepticus.
Fits occuring during pregnancy themselves increase birth defects and may cause mental retardation in the offspring.
Also read :
Congestive heart failure treatment and medication
When women on antiepileptic therapy conceive, antiepileptic drugs should not be stopped. Though most antiseizure drugs have been shown to increase the incidence of birth defects, discontinuation of therapy carries a high risk of status epilepticus.
Fits occuring during pregnancy themselves increase birth defects and may cause mental retardation in the offspring.
Also read :
Congestive heart failure treatment and medication
EPILEPSY MEDICATION
Top 10 antiepileptic drugs used are :
1. Phenobarbitone
2. Primidone
3. Phenytoin
4. Carbamazepine
5. Valproic acid
6. Gabapentin
7. Topiramate
8. Clonazepam
9. Clobazam
10. Ethosuximide
Phenytoin
Mechanism of action
Phenytoin acts by stabilizing the neuronal membrane and prevents the spread of seizure discharges.
The sodium channels exist in three forms: resting, activated and inactivated states.
Phenytoin delays the recovery of Na+ channels from inactivated state, thereby reduces the neuronal excitability.
At high concentrations, phenytoin inhibits Ca2+ influx into the neuron, reduces glutamate levels and increases responses to GABA.
Phenytoin acts by stabilizing the neuronal membrane and prevents the spread of seizure discharges.
The sodium channels exist in three forms: resting, activated and inactivated states.
Phenytoin delays the recovery of Na+ channels from inactivated state, thereby reduces the neuronal excitability.
At high concentrations, phenytoin inhibits Ca2+ influx into the neuron, reduces glutamate levels and increases responses to GABA.
Pharmacokinetics
Absorbed slowly through GIT,
Widely distributed and highly bound to plasma protiens,
Metabolized in liver.
Absorbed slowly through GIT,
Widely distributed and highly bound to plasma protiens,
Metabolized in liver.
Adverse effect
Hypertrophy and Hyperplasia.
Hypersensitivity reactions.
Hirsutism.
Hyperglycaemia.
Megaloblastic anaemia.
Osteomalacia.
Hypocalacaemia.
Foetal Hydantoin syndrome.
Carbamazepine
Mechanism of action
Like phenytoin, Carbamazepine slows the rate of recovery of Na+ channels from inactivation, thereby reduces the neuronal excitability.
Pharmacokinetics
Absorbed slowly from GIT,
Binds to plasma protiens,
Well distributed in the body including the CSF and metabolized in the liver.
Well distributed in the body including the CSF and metabolized in the liver.
Repeated use of drug causes enzyme induction and reduces the effectiveness of drug itself.
Adverse effect
Sedation, drowsiness, ataxia, vertigo, blurred vision, nausea, vomiting, mental confusion.
Rashes
Eosinophilia
Lymphadenopathy
Hepatitis
Bone marrow depression
Aplastic anaemia
Agranulocytosis
Valproic acid
Mechanism of action
Valproate delays the recovery of Na+ channels from inactivation.
It blocks T-type Ca2+ current in thalamic neurons.
Increases the activity of GABA in brain by...
By increasing synthesis of GABA by stimulating GAD (glutamic acid decarboxylase).
By decreasing degradation of GABA by inhibiting GABA-T (GABA transaminase) enzyme.
Pharmacokinetics
Rapidly and completely absorbed from GIT.
Highly bound to plasma protiens.
Metabolized in liver.
Excreted in urine.
Adverse effect
Common - Nausea, vomiting, anorexia, abdominal discomfort.
CNS - Sedation, ataxia, tremor.
Rashes, alopecia, curling of hair.
Rare but serious complication is fulminant hepatitis.
Teratogenicity
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Friday, 8 February 2019
Antibiotics
February 08, 2019
• Antibiotics
• Classification
• Antibiotics selection
• Problems arise with use of Antibiotics
• Why Combination of Antibiotics
• Top 10 Antibiotics
You will know here something interesting about Antibiotics in this article.
Hii dear visitors 😊
Your welcome, you are learning Pharmacology at onlycology.
Hello dear visitors
😊 I hope you've got help, if you have any suggestion or any question regarding this article"Antibiotics,, please comment i will be very happy.
Thanks
Also read : Congestive heart failure
ACE inhibitors
Antihypertensive drugs and classification
• Classification
• Antibiotics selection
• Problems arise with use of Antibiotics
• Why Combination of Antibiotics
• Top 10 Antibiotics
You will know here something interesting about Antibiotics in this article.
Hii dear visitors 😊
Your welcome, you are learning Pharmacology at onlycology.
ANTIBIOTICS
Antibiotics are chemical substances of natural / semisynthetic / synthetic origin, capable of being selectively toxic to pathogen and safe to the parasite, in relatively lower concentrations either by destroying or affecting it's growth/ multiplication.
CLASSIFICATION
Can be classified based on :
A. Chemical structure
1. Sulfonamides and related drugs : Sulfadiazine, Paraaminosalicyclic acid.
2. Diaminopyrimidine : Trimethoprim, pyrimethamine.
3. Quinolones : Norfloxacin, Ciprofloxacin.
4. beta-lactum antibiotics : Penicillin, Cephalosporin, Monobactums, Carbapenems.
5. Tetracyclines : Doxycycline, Oxytetracycline.
6. Nitribenzene derivative :Chloramphenicol.
7. Aminoglycosides : Streptomycin, Gentamycin, Neomycin.
8. Macrolide antibiotics : Erythromycin, Azithromycin.
9. Nitroimidazoles : Metronidazole.
10. Azole derivative : Miconazole, Clotrimazole, Ketoconazole.
11. Nicotinic acid :Pyrazinamide, Ethionamide.
12. Others : Rifampin, Clindamycin, Cycloserine, Viomycin, Thiacetazone.
B. Mechanism of action
1. Inhibit cell wall synthesis : Penicillin, Cephalosporin, Cycloserine, Vanomysin.
2. Cause leakage from cell membrane :Polymixin, Colistin, Amphitericin B, Nystatin, Hamycin.
3. Inhibit protein synthesis : Tetracyclines, Chloramphenicol, Erythromycin, Clindamycin.
4. Cause misreading of m-RNA code and affect permeability : Streptomycin, Gentamycin.
5. Inhibit DNA gyrase : Ciprofloxacin.
6. Interfere with DNA function : Rifampin, Metronidazole.
7. Interfere with DNA synthesis : Idoxuridine, Zidovudine.
8. Interfere with intermediary metabolism : Sulfonamides, Sulfones, Trimethoprim, Pyrimethamine, Ethambutol.
C. Spectrum of activity
1. Narrow spectrum : Penicillin G, Streptomycin, Erythromycin.
2. Broad spectrum : Tetracyclines, Chloramphenicol.
D. Type of action
1. Primarily bacteriostatic : Sulfonamides, Tetracyclines, Erythromycin, Chloramphenicol, Ethambutol.
2. Primarily bactericidal : Penicillin, aminoglycosides, Cephalosporin, vanomycin, Rifampin, Ciprofloxacin, Cotrimoxazole.
E. Antibiotics obtained from
1. Fungi : Penicillin, Cephalosporin, Griseofulvin.
2. Bacteria : Polymyxin B, Colistin, Bacitracin, Tyrothricin, Aztreonam.
3. Actinomycetes : Aminoglycosides, Tetracyclines, Chloramphenicol, Macrolides, Polyenes.
Read important classifications :
Classification of drug used in CHF Congestive heart failure
Read important classifications :
Classification of drug used in CHF Congestive heart failure
1. Identification of infecting organism :
- It is important for selecting an appropriate antibiotics.
- Rapidly identified before treatment from body fluids.
2. Empirical therapy :
- An appropriate antimicrobial agent is used after receiving lab reports of identity and susceptibility except in case of acute illness.
3. Determination of Antimicrobial susceptibility :
This helps to determine the appropriate antimicrobial therapy.
4. Effect of site of infection :
- It is important for an antibiotic to reach appropriate site of action and in appropriate concentration in order to produce effective bactericidal or bacteriostatic effect - i.e. Eradicate the pathogen from site of infection.
- BBB offers challenge.
5. Patient factors :
Following needs to be considered before selecting Antibiotics :
- Host defense / how good is immune response of patient.
- Renal dysfunction.
- Hepatic dysfunction.
- Poor perfusion - i.e. blood supply to site of infection.
- Age.
- Pregnancy.
- Lactation.
6. Drug factors :
When any one of the number of drugs could be used to treat infection - then choice is based on specific properties of drug.
- Spectrum of activity.
- Type of effect required.
- Sensitivity of pathogen.
- Relative toxicity.
- Pharmacokinetics profile.
- Route of drug administration.
- Evidence of clinical efficacy.
PROBLEMS THAT ARISE WITH USE OF ANTIBIOTICS/ ADVERSE EFFECT
1. Toxicity :
a) local :- oral use - experienced at the site of administration - gastric irritation, pain.
Parentral use - abscess formation at the site of i.m injection, thromophelibitis.
b) systemic :- All antibiotics produce dose related and predictable organ toxocities.
- Some have high therapeutic index.
- Some have low therapeutic index.
Aminoglycosides : 8th cranial nerve, kidney toxicity.
Tetracyclines : liver and kidney damage.
Chloramphenicol : bone marrow depression.
Polymyxin : neurological and renal toxicity.
Amphotericin : kidney, bone marrow toxicity.
2. Hypersensitivity reaction / allergic reaction :
- All antibiotics are capable of causing hypersensitivity reactions.
- These are unpredictable and unrelated to dose.
- Anaphylactic shock can be produced.
- Penicillin allergy.
- A fungal infection especially after prolonged use of broad spectrum antibiotics.
- Difficult to treat due to alterations in the bormal microbial flora of gut, URT.
- Loss of sensitivity of pathogen to therapeutic effect of an antibiotics - to which it was previously sensitive.
- Developed by microorganisms when consistently exposed to sub therapeutic concentration of particular antibiotics.
- Some pathogens are naturally resistant to some antibiotics.
RESISTANCE DEVELOPMENT
1. Mutation : when insertion of one or more nucleotides within the genome. The mutated organism replicate with features that can be resist the action of an antibiotic.
2. Via R factors :
- Modification of target sites.
- Decreased accumulation of Antibiotic.
- By developing an inactivating enzyme which effectively destroys drug.
☆ You must have seen antibiotics given in combination, do you know why ? If not, continue, you will get to know.
WHY COMBINATION OF ANTIBIOTICS ?
1. To achieve synergism / additive effect :
- Synergistic effect sensitizes the organism to the action of the other member of pair.
- Rapid lethal action - than that of individual member separately.
- Prolonged post antibiotic effect. ( Aminoglycosides).
- Two bacteriostatic agents are often additive, sometimes synergistic, i.e. combination of tetracyclines, Chloramphenicol, Erythromycin etc.
- Two bactericidal drugs are frequently additivd if organism is sensitive ti both.
- Combination of a bactericidal with bacteriostatic drug may be synergistic or antagonistic depending on the organism.
2. To reduce severity or incidence of adverse effects :
- Possible only when combination is synergistic so that dose can be reduced.
- Especially when the antibiotics are if narrow therapeutic index - which when used alone in effective doses produce unacceptable toxicity.
- Streptomycin + Penicillin G for SABE.
3. To prevent emergence of resistance :
- This principle of using two or more AMAs together is valid primarily for chronic infections neeeding prolonged therapy; has been widely employed in tuberculosis, leprosy.
- Sulfonamides given with Streptomycin has been found to prevent emergence of resistant H. influenzae.
4. To broaden the spectrum of Antimicrobial action :
This is needed in :
- Treatment of mixed infection.
- Initial treatment of severe infection.
- Topically : generally AMAs which poorly absorbed from the local site, needs to given in combination.
TOP 10 ANTIBIOTICS
1. Ciprofloxacin
2. Ofloxacin
3. Amoxicillin
4. Streptomycin
5. Gentamycin
6. Neomycin
7. Erythromycin
8. Clindamycin
9. Norfloxacin
10. Levofloxacin
Ciprofloxacin : It is the most potent first generation Fluoroquinolone active against a broad range of bacteria.
- Ciprofloxacin is rapidly absorbed orally, but food delays absorption, and first pass metabolism occurs.
- High tissue penetrability.
- Excreted in urine.
- Adverse effects are - nausea, vomiting, anorexia, dizziness, headache, insomnia, rashes, swelling of lips. Side effects occur only in 10% patients.
Ofloxacin : It is more potent than Ciprofloxacin for gram positive organisms.
- Also inhibits M. Tuberculosis; can be used in place of ciprofloxacin.
- It is lipid soluble, bioavailability is high.
Amoxicillin :
- Oral absorption is good; food does not interfere.
- Higher and more sustained blood levels are produced.
Streptomycin : Oldest aminoglycoside antibiotic obtained from Streptomyces griseus.
- Active primarily against aerobic gram negative bacilli.
- Highly ionized, neither absorbed nor destroyed in g.i.t.
- Not metabolized - excreted unchanged in urine.
- Causes nephrotoxocity, hypertension, eosinophilia, rarely Anaphylaxis.
Gentamycin : obtained from Micromonospora purpurea in 1964 has become most commonly used antibiotic for acute infection.
Neomycin : obtained from S. fradiae, it is a wide spectrum aminoglycoside, active against most gram negative bacilli and some gram positive cocci.
- Highly toxic to internal ear and to kidneys.
- Poorly absorbed from g.i.t.
Clindamycin :
- It inhibits most gram positive cocci.
- Oral absorption is good, it penetrates to most skeletal and soft tissues, but not brain and CSF.
- Largely metabolized in urine and bile.
- Side effects are rashes, abdominal pain, major problem is diarrhoea.
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Also read : Congestive heart failure
ACE inhibitors
Antihypertensive drugs and classification
Monday, 28 January 2019
Congestive heart failure
January 28, 2019
▪ Congestive heart failure introduction
▪ Classification of drugs used
▪ Pharmacology of drug
▪ Treatment of CHF
CONGESTIVE HEART FAILURE
The function of heart is to pump an adequate amount of blood to various tissues. In CHF (Congestive heart failure), there is an inadequate or inefficient contraction of heart leading to reduced cardiac output.
In initial stages of CHF, the compensatory mechanisms try to maintain the proper cardiac output which are :
• increased sympathetic activity.
• increased renin-angiotensin aldosterone activity.
• myocardial hyertrophy and remodelling.
The basic haemodynamic disturbances seen in congestive cardiac failure are :
• increased pulmonary capillary pressure termed as backward failure, which is characterised by dysnoea and orthopnoea.
• decreased cardiac output termed as forward failure, leading to decreased oxygen supply to the peripheral tissue.
CLASSIFICATION
1) Diuretics.
a. Loop diuretics : furosemide, bumetanide, torsemide.
b. Thiazide diuretics : chlorothiazide, hydrochlorothiazide.
c. K+ sparing diuretics : spironolactone, amiloride.
2) Cardiac glycosides : digoxin, digitoxin.
3) Vasodilator :
a. Arteriolar dilators : hydralazine, minoxidil, nicorandil.
b. Venodilators : nitrates.
c. Arteriolar and venodilators : ACE inhibitors, sodium nitroprusside.
4) beta-blockers : metoprolol, bisoprolol, carvedilol.
5) sympathomimetic amines : dopamine, dobutamine.
6) phosphodiesterase inhibitors : amrinone, milrinone.
b. Thiazide diuretics : chlorothiazide, hydrochlorothiazide.
c. K+ sparing diuretics : spironolactone, amiloride.
2) Cardiac glycosides : digoxin, digitoxin.
3) Vasodilator :
a. Arteriolar dilators : hydralazine, minoxidil, nicorandil.
b. Venodilators : nitrates.
c. Arteriolar and venodilators : ACE inhibitors, sodium nitroprusside.
4) beta-blockers : metoprolol, bisoprolol, carvedilol.
5) sympathomimetic amines : dopamine, dobutamine.
6) phosphodiesterase inhibitors : amrinone, milrinone.
TREATMENT OF CONGESTIVE HEART FAILURE
There are two distinct goals of drug therapy in CHF :
a) Relief of congestive/low output symptoms and restoration of cardiac performance :
Drugs used in this are : digoxin, dobutamine, dopamine, amrinone, furosemide, thiazides, ACE inhibitors, hydralazine, nitrates, metoprolol, bisoprolol, carvedilol.
b) Arrest/reversal of disease progression and prolongation of survival :
Drugs used in this are : ACE inhibitors, Beta blockers, spironolactone.
Also read : Tuberculosis treatment, pharmacology of Anti tubercular drugs
Anti anxiety, classification, etc.. Antihypertensive
Also read : Tuberculosis treatment, pharmacology of Anti tubercular drugs
Anti anxiety, classification, etc.. Antihypertensive
CARDIAC GLYCOSIDES
Chemistry :
The glycosides consist of an aglycone (steroid nucleus with an attached lactone ring) with one or more sugar moieties attached to it. They have potent action on the heart, hence referred to as cardiac glycosides.
Mechanism of action of Digitalis :
Na+ K+ -ATPase is a membrane bound enzyme which is called digitalis receptor. It is also called sodium pump.
PHARMACOLOGICAL ACTION
1.Cardiac
2. Extracardiac
Cardiac actions :
Digitalis has direct and indirect actions on heart.
▪ direct action by inhibiting Na+ K+ -ATPase.
▪ indirect action by stimulating vagus.
1. Myocardial contractility :
- digitalis increases the forces of contraction of the myocardium (positive inotropic effect).
- The positive inotropic effect causes complete emptying of ventricles during systole and increases the cardiac output.
- This decreases pulmonary congestion and systemic venous pressure.
- Diastolic size of heart is reduced and hence size of the muscle fibre length also reduced, thereby, decreases the oxygen requirement of myocardium.
- The digitalised heart, now can do more work for the same energy.
2. Heart rate :
- digitalis reduces the heart rate by direct and indirect action, in small doses, it causes decreased heart rate.
3. Electrophysiological action :
- at therapeutic concentration, digoxin decreases automaticity and increases membrane potential by vagal action in atria and AV node.
Extra cardiac :
1. Gasrtointestinal tract : digitalis can produce anorexia, nausea, vomiting, and diarrhoea.
2. Kidney : causes diuresis.
3. Central nervous system : in high doses, it can causes central sympathetic stimulation, confusion, blurring of vision, disorientation.
PHARMACOKINETICS
Digoxin is the commonly used glycoside and administered by oral route.
widely distributed in body, concentrated in the heart, liver, kidneys, and skeletal muscle.
crosses the BBB and is mainly excreted in urine.
ADVERSE EFFECT
1. Extra cardiac :
i) GIT : anorexia, nausea, vomiting.
ii) CNS : headache, confusion, restlessness, disorientation, weakness, visual disturbances, altered mood and hallucination.
iii) Skin rashes and gynaecomastia : it can occur occasionally.
2. Cardiac : digitalis can causes any type of arrhythmia. The most common are ventricular premature beats, pulses bigeminy and ventricular tachycardia. Also cause A-V block , atrial tachycardia, atrial fibrillation, atrial flutter, even severe bradycardia.
DIURETICS
Thiazides are used in mild to moderate cardiac failure. They inhibits Na+ -Cl- symport in the cortical diluting sigment.
Loop diuretics inhibits Na+ - K+ -2Cl- cotransport, mainly in the thick ascending limb of the loop of henle.
Loop diuretcs are mainly used in severe cardiac failure, pulmonary oedema and refractory heart failure.
Causes : Hypokalaemia.
ACE INHIBITORS
These are the first line drugs in treatment of chronic heart failure. They inhibit the conversion of angiotensin-I to angiotensin-II.
Beta BLOCKER
Metaprolol, bisoprolol, are useful in mild to moderate heart failure.
Long term therapy with these drugs improves symptoms, reduces hospitalization and decreases mortality in patients with mild to moderate heart failure.
DOPAMINE
At low concentration, dopamine selectively dilates renal, mesenteric and coronary blood vessels by acting on D1 receptors. Thus dopamine increases GFR and urine output.
At moderate concentration, stimulates Beta receptors of heart, increases myocardial contractility and cardiac output.
At high concentration, it causes generalized vasoconstriction. This increases afterload and reduces blood flow to renal, mesenteric and other vital organs. So the beneficial effects seen with low to moderate doses of dopamine are lost at higher concentration.
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Saturday, 19 January 2019
Pharmacology of ACE inhibitors
January 19, 2019
How angiotensin converting enzyme inhibitors works / pharmacology of ACE inhibitors/angiotensin converting enzyme inhibitors.
Angiotensin converting enzyme inhibitors are used as Antihypertensive drugs.
• they inhibit generation of angiotensin II, which is a potent vasoconstrictor.
• they inhibit the degradation of bradykinin, which is potent vasodilator.
• they stimulate the synthesis of vasodilating PGs through bradykinin.
• reduce sympathetic nervous system activity.
▪ACE inhibitors also reduce aldosterone production hence sodium and water rentention.
▪They dilate both arteries as well as veins, hence they reduce afterload and preload.
▪All these actions contribute to their Antihypertensive effect.
▪ ACE inhibitors are usually given orally.
▪ In emergency, enalapril can be given intravenously.
▪ Food reduces absorption of captopril hence it should be given 1 hour before meals.
▪ They poorly cross the BBB.
▪ Metabolized in liver and excreted in urine.
1.Cough
2.Angioedema.
3.Proteinuria.
4.Taste alteration.
5.Teratogenic effect.
6.Severe hypotension may occur 1-2 hour after taking first dose.
7.Neutropenia.
8.Rashes.
9.Itching.
10.Loss of appetite, nausea, vomiting, diarrhoea.
1 Hypertension : use of ACE inhibitors reduces the incidence of heart disease in hypertensive patient. ACE inhibitors are useful in all grades of hypertension.
2 Congestive cardiac failure : ACE inhibitors should be prescribed to all patients with inpaired left ventricular function.
3 Myocardial infarction : ACE inhibitors should be started within 24 hours in patients with MI.
4 Diabetic nephropathy : ACE inhibitors are preferred in diabetic nephropathy as they control both systemic hypertension and intraglomerular pressure.
5 Scleroderma renal crisis : ACE inhibitors produce dramatic improvement in patients with renal crisis and accerelated hypertension.
ANGIOTENSIN CONVERTING ENZYME INHIBITORS
Angiotensin converting enzyme inhibitors are used as Antihypertensive drugs.
• they inhibit generation of angiotensin II, which is a potent vasoconstrictor.
• they inhibit the degradation of bradykinin, which is potent vasodilator.
• they stimulate the synthesis of vasodilating PGs through bradykinin.
• reduce sympathetic nervous system activity.
MECHANISM OF ACTION
▪ACE inhibitors also reduce aldosterone production hence sodium and water rentention.
▪They dilate both arteries as well as veins, hence they reduce afterload and preload.
▪All these actions contribute to their Antihypertensive effect.
PHARMACOKINETICS
▪ ACE inhibitors are usually given orally.
▪ In emergency, enalapril can be given intravenously.
▪ Food reduces absorption of captopril hence it should be given 1 hour before meals.
▪ They poorly cross the BBB.
▪ Metabolized in liver and excreted in urine.
ADVERSE EFFECT
1.Cough
2.Angioedema.
3.Proteinuria.
4.Taste alteration.
5.Teratogenic effect.
6.Severe hypotension may occur 1-2 hour after taking first dose.
7.Neutropenia.
8.Rashes.
9.Itching.
10.Loss of appetite, nausea, vomiting, diarrhoea.
USES OF ACE INHIBITORS
1 Hypertension : use of ACE inhibitors reduces the incidence of heart disease in hypertensive patient. ACE inhibitors are useful in all grades of hypertension.
2 Congestive cardiac failure : ACE inhibitors should be prescribed to all patients with inpaired left ventricular function.
3 Myocardial infarction : ACE inhibitors should be started within 24 hours in patients with MI.
4 Diabetic nephropathy : ACE inhibitors are preferred in diabetic nephropathy as they control both systemic hypertension and intraglomerular pressure.
5 Scleroderma renal crisis : ACE inhibitors produce dramatic improvement in patients with renal crisis and accerelated hypertension.
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😊 I hope you've got help, if you have any suggestion or any question regarding this article "Pharmacology of ACE inhibitors,, please comment i will be very happy.
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Antihypertensive drugs | Antihypertensive classification
January 19, 2019
You will know here - what is hypertension, blood pressure and Antihypertensive drugs | Antihypertensive classifications.
HYPERTENSION
Hypertension is the most common cardiovascular condition. A persistent and sustained high blood pressure has damaging effect on heart, brain, kidneys, and eyes.
Hypertension is generally classified :
[1] Primary or essential hypertension :
In more than 95% of cases, there is no specific underlying cause.
[2] Secondary hypertension :
It is seen in about 5% of cases. It can be due to specific disease or drug.
BLOOD PRESSURE
▪ Systolic blood pressure (SBP) : It is the maximum pressure recorded during ventricular systole.
▪ Diastolic blood pressure (DBP) : It is the minimum pressure recorded during ventricular diastole.
▪ Pulse pressure (PP) : SBP-DBP
▪ Mean arterial pressure : DBP + 1/3 PP.
ANTIHYPERTENSIVE DRUGS
CLASSIFICATION :
1》 Angiotensin converting enzyme inhibitors : Captopril, enalapril, lisinopril, ramipril.
2》 Angiotensin-II-receptor antagonist : losartan, valsartan, irbesartan, candesartan.
3》 Calcium channel blocker : amlodipine, nicardipine, nimodipine, felodipine, diltiazem.
4》 Diuretics :
a. Thiazides : hydrochlorothiazide, chlorothiazide.
b. Loop diuretics : bumetanide, furosemide.
c. Potassium sparing diuretics : spironolactone, amiloride.
5》 Sympatholytic drugs :
a. Centrally acting agents: clonidine, methyldopa.
b. Ganglionic blocker: trimethaphan.
c. Neuronal blockers : reserpine.
d. Alpha-adrenergic blocker:
(i) non selective: phenoxybenzamine, phentolamine.
(ii) selective: prazosin, terazosin.
e. Beta-adrenergic blockers:
(i) non selective: propranolol, metoprolol.
(ii) selective: atenolol.
6》 Vasodilator :
a. Arteriolar: hydralazine, diazoxide.
b. Arterial and venodilator: sodium nitroprusside.
Also read : Pharmacology of ACE inhibitors
1》 Angiotensin converting enzyme inhibitors : Captopril, enalapril, lisinopril, ramipril.
2》 Angiotensin-II-receptor antagonist : losartan, valsartan, irbesartan, candesartan.
3》 Calcium channel blocker : amlodipine, nicardipine, nimodipine, felodipine, diltiazem.
4》 Diuretics :
a. Thiazides : hydrochlorothiazide, chlorothiazide.
b. Loop diuretics : bumetanide, furosemide.
c. Potassium sparing diuretics : spironolactone, amiloride.
5》 Sympatholytic drugs :
a. Centrally acting agents: clonidine, methyldopa.
b. Ganglionic blocker: trimethaphan.
c. Neuronal blockers : reserpine.
d. Alpha-adrenergic blocker:
(i) non selective: phenoxybenzamine, phentolamine.
(ii) selective: prazosin, terazosin.
e. Beta-adrenergic blockers:
(i) non selective: propranolol, metoprolol.
(ii) selective: atenolol.
6》 Vasodilator :
a. Arteriolar: hydralazine, diazoxide.
b. Arterial and venodilator: sodium nitroprusside.
Also read : Pharmacology of ACE inhibitors
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Antihypertensive drugs and classification,, please comment i will be very happy.
Thanks
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