Thursday 9 April 2020
Arrhythmia of the heart | arrhythmia symptoms
April 09, 2020
Arrhythmia definition
Arrhythmia of the heart
Arrhythmia symptoms
Arrhythmia medication
Arrhythmia of the heart
Arrhythmia symptoms
Arrhythmia medication
😊 Hello dear visitors...
Your welcome,
You are learning Pharmacology at onlycology.
ARRHYTHMIA
Arrhythmia is disturbances in cardiac rhythm (i.e abnormality in site of origin of impulse, its rate, regularity or conduction).
Types of arrhythmia
1) Tachyarrhythmia :- Arrhythmia with increased heart rate
2) Brady arrhythmia :- Arrhythmia with decreased heart rate
Drugs used to restore normal rhythm are known as anti-arrhythmic drugs.
CLASSIFICATION
I (A) e.g :-quinidine , procanamide , disopyramide ,
I (B) e.g :- lidocaine , phenytoin , tocainide
I (C) e.g :- encainide , flecainide , propafenone
II beta-blockers- e.g :- propanolol , metaprolol , esmolol
III potassium-blockers e.g :- amiodarone , bretylium , sotalol
IV calcium channel blockers e.g :- verapamil , nifedepine , amlodepine
Class I anti arrhythmic agents have membrane stabilising properties this agents act on the fast sodium channels and interfere with the process by which the depolarisation occurs.
Class I A have intermediate affinity for sodium channel.
Class I B have least affinity for sodium channel and dissociate rapidly.
Class I C agents have highest affinity for sodium channel and dissociate slowly.
The first line drugs used in treatment of -
TSVT (peroxy/prophylactic supra ventricular tachycardia - adenosine , verapamil
AV block - atropine
Atrial extra systole - quinidine
Atrial flutter or atrial fibrillation - verapamil
Ventricular extra systole or ventricular trachycardia - lidocaine
Wolf - parkinson's white syndrome - amipdarone or flecanide
TSVT (peroxy/prophylactic supra ventricular tachycardia - adenosine , verapamil
AV block - atropine
Atrial extra systole - quinidine
Atrial flutter or atrial fibrillation - verapamil
Ventricular extra systole or ventricular trachycardia - lidocaine
Wolf - parkinson's white syndrome - amipdarone or flecanide
ARRHYTHMIA SYMPTOMS
It includes -
Chest pain
Dizziness
Fainting
Light headedness
Palpitation or slow heart rate
Shortness of breath
Chest pain
Dizziness
Fainting
Light headedness
Palpitation or slow heart rate
Shortness of breath
ARRHYTHMIA MEDICATION/PHARMACOLOGY OF ANTI-ARRHYTHMIC DRUGS
QUINIDINE :- It is an alkaloid obtained from cinchona bark, it has direct cardiac depressant, anticholinergic and alpha adrenergic blocking effects.
PHARMACOLOGICAL ACTION OF QUINIDINE :
HEART : Supresses automaticity
Depresses excitability
Depresses ectopic foci
Decreases contractility
Prolongs effective refractory period
Slows conduction velocity
AV node : Enhances AV conduction and increases ventricular rate by vagolytic action. It depresses AV conduction by direct action.
ECG : Quinidine prolongs QRS complex and QT interval. BP : Fall in blood pressure. SKELETAL MUSCLE : Quinidine reduces skeletal muscle contraction, it also has antimalerial, antipyretic, oxytocic activity.
PHARMACOKINETIC : Absorbed from git, metabolized in liver, high plasma protien binding, about 20% excreted unchanged in urine.
ADVERSE EFFECTS :1. Diarrhoea
2. Thrombocytopenia.
3. Fall in blood pressure.
4. Hepatitis and fever rarely.
5. Large dose causes CINCHONISM.
Oral administration, bioavailability is about 30%. It can be given intravenously for rapid effect. It accumulates in fat, muscle, lungs, liver, skin, etc. and has a long half life (1-2 months). Amiodarone is metabolized in the liver.
ADVERSE EFFECTS 1. Hypotension
2. Peripheral neuropathy.
3. Pulmonary fibrosis
4. Nausea, hepatitis
5. Photosensitivity.
6. Corneal deposits
7. Hypothyroidism, hyperthyroidism.
VERAPAMIL It blocks both activated and inactivated L-type Ca2+ channels - depresses calcium mediated depolarization. Verapamil decreases conduction velocity and increases refractory period of AV node; useful in
PHARMACOLOGICAL ACTION OF QUINIDINE :
HEART : Supresses automaticity
Depresses excitability
Depresses ectopic foci
Decreases contractility
Prolongs effective refractory period
Slows conduction velocity
AV node : Enhances AV conduction and increases ventricular rate by vagolytic action. It depresses AV conduction by direct action.
ECG : Quinidine prolongs QRS complex and QT interval. BP : Fall in blood pressure. SKELETAL MUSCLE : Quinidine reduces skeletal muscle contraction, it also has antimalerial, antipyretic, oxytocic activity.
PHARMACOKINETIC : Absorbed from git, metabolized in liver, high plasma protien binding, about 20% excreted unchanged in urine.
ADVERSE EFFECTS :1. Diarrhoea
2. Thrombocytopenia.
3. Fall in blood pressure.
4. Hepatitis and fever rarely.
5. Large dose causes CINCHONISM.
PROCAINAMIDE
Procainamide also have similar effect to those of quinidine but it has no anticholinergic and alpha adrenergic blocking effects.
PHARMACOKINETIC : Procainamide is well absorbed after oral administration. It can also be given by i.v. and i.m. routes. Metabolized in liver by acetylation. The major metabolite is n-acetyl procainamide. that has K+ channel blocking activity. NAPA is excreted in urine.
ADVERSE EFFECTS1. Hypotension and Heart block are main adverse effects.
2. Nausea, vomiting.
3. Confusion, depression, hallucination.
4. Long term therapy often produces lupus like syndrome with arthralgia and arthritis.
AMIODARONE
It is an iodine containing compound and structurally related to thyroid hormone, it has a broad spectrum of antiarrhythmic activity.
Procainamide also have similar effect to those of quinidine but it has no anticholinergic and alpha adrenergic blocking effects.
PHARMACOKINETIC : Procainamide is well absorbed after oral administration. It can also be given by i.v. and i.m. routes. Metabolized in liver by acetylation. The major metabolite is n-acetyl procainamide. that has K+ channel blocking activity. NAPA is excreted in urine.
ADVERSE EFFECTS1. Hypotension and Heart block are main adverse effects.
2. Nausea, vomiting.
3. Confusion, depression, hallucination.
4. Long term therapy often produces lupus like syndrome with arthralgia and arthritis.
AMIODARONE
It is an iodine containing compound and structurally related to thyroid hormone, it has a broad spectrum of antiarrhythmic activity.
- Amiodarone blocks potassium channels>>>increases duration of action potential>>>prolongs refractory period and suppresses abnormal automaticity.
- Blocks sodium channels in the inactivated state>>>decreases conduction mainly in the partially depolarized tissue.
- Blockade of sodium and potassium channels prolongs refractory period in the cardiac.
- It also has weak beta-adrenergic blocking and calcium channel blocking actions. It decreases heart rate and AV conduction.
Oral administration, bioavailability is about 30%. It can be given intravenously for rapid effect. It accumulates in fat, muscle, lungs, liver, skin, etc. and has a long half life (1-2 months). Amiodarone is metabolized in the liver.
ADVERSE EFFECTS 1. Hypotension
2. Peripheral neuropathy.
3. Pulmonary fibrosis
4. Nausea, hepatitis
5. Photosensitivity.
6. Corneal deposits
7. Hypothyroidism, hyperthyroidism.
VERAPAMIL It blocks both activated and inactivated L-type Ca2+ channels - depresses calcium mediated depolarization. Verapamil decreases conduction velocity and increases refractory period of AV node; useful in
- terminating reentry involving AV node.
- reducing ventricular rate in atrial flutter and fibrillation.
PHARMACOKINETICS:
Well absorbed through GI tract, highly bound to plasma protiens, metabolized in liver and excreted in urine.
ADVERSE EFFECTS
1. Constipation
2. Sinus bradycardia
3. Oedema
4. A-V block and headache rarely
Well absorbed through GI tract, highly bound to plasma protiens, metabolized in liver and excreted in urine.
ADVERSE EFFECTS
1. Constipation
2. Sinus bradycardia
3. Oedema
4. A-V block and headache rarely
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Arrhythmia of the heart | arrhythmia symptoms,, please comment i will be very happy.
Thanks
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
😊 Hello dear visitors...
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.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Anti anxiety | anti anxiety medications,, please comment i will be very happy.
Thanks
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.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Anti anxiety | anti anxiety medications,, please comment i will be very happy.
Thanks
Monday 11 March 2019
Pharmacology Quiz
March 11, 2019
Question 01) Explanation :
Penicillin inhibits cell wall synthesis in susceptible bacteria, inhibits transpeptidase 》 prevents peptidoglycan synthesis 》 cell wall deficient forms 》 autolysis 》 cell death 》 Bactericidal effect.
Neostigmine is a quaternary ammonium compound, directly stimulates the Nm receptors at NMJ. Thus it improves muscle power in patients with Myasthenia gravis.
Pyridostigmine features are same as Neostigmine. Pyridostigmine is preferred over Neostigmine in Myasthenia gravis because it has longer duration of action.
Question 03) Explanation :
Reserpine is chief chemical constituent of Rauwolfia, and its structure contains beta carboline ring, and it is also used as adrenergic blocker.
Question 06) Explanation :
Pyrazinamide is converted to pyrazinoic acid by mycobacterial pyrazinamidase and distrupts cell membrane metabolism and transport function.Chloramphenicol binds with 50s ribosome and prevents peptide bond formation between the newly attached amino acid and peptide chain.
Omeprazole : supresses gastric acid secretion : Gastro esophageal reflux, Peptic ulcer.
Question 08 Explanation :Atropine is an antimuscarinic
Dexamethasone is used to treat allergic disorders, skin conditions, ulcerative colitis, arthritis, lupus, psoriasis, or breathing disorders.Deferoxamine is used in iron poisioning.
Saturday 9 March 2019
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
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Epilepsy treatment | Epilepsy medication | Overview,,please comment i will be very happy.
• 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
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Epilepsy treatment | Epilepsy medication | Overview,,please comment i will be very happy.
Saturday 16 February 2019
Penicillin and penicillin allergy
February 16, 2019
- Penicillin
- Mechanism of action
- Mechanism of bacterial resistance
- Spectrum of activity
- Pharmacokinetics
- Precaution
- Therapeutic uses
- Limitations / drawbacks of PenicillinG
- Penicillin allergy/ adverse effects
- Semisynthetic penicillins
You will learn in this article above mentioned topics.
😊 Hello dear visitors...
Your welcome,
You are learning Pharmacology at onlycology.
PENICILLIN
Penicillin was the first antibiotic to be used clinically in 1941. It is a miracle that the least toxic drug of its kind was the first to be discovered.
It was originally obtained from the fungus Penicillium notatum, but the present source is a high yielding mutant of Penicillium chrysogenum.
The penicillin nucleus consists of fused thiazolidine and beta-lactum rings to which side chains are attached through an amide linkage.
Penicillin G is highly water soluble, it is stable in the dry state but solution deteriorates rapidly at room temperature.
MECHANISM OF ACTION
Beta-lactum antibiotics produce bactericidal effect by inhibiting cell wall synthesis in susceptible bacteria.
Bacterial cell wall is composed of peptidoglycan, which is highly cross linked structure that makes the cell wall rigid and also gives it stability.
There are three stages involved in the biosynthesis of peptidoglycan.
The third stage is inhibited by beta-lactum antibiotics. The mode of action of Penicillin is given below as flowchart.👇
MECHANISM OF BACTERIAL RESISTANCE
Bacteria develop resistance to beta-lactums mainly through the release of beta-lactumases, which hydrolyse the beta-lactum ring and inactivate them.
The other mechanism of resistance to beta-lactums are due to :
i) altered penicillin binding protein (PBPs)
ii) decreased penetration of the drug to its site of action.
SPECTRUM OF ACTIVITY
1. Bactericidal effect on Gram +ve cocci - Streptococci, Pneumococci. etc.
2. Bactericidal effect on Gram -ve Gonococci - Neisseria gonorrhea, Neisseria meningitis.
3. Bactericidal effect on Bacilli - Bacillus anthracis, etc.
4. Bactericidal effect on Trypanoma palladium.
PHARMACOKINETICS
Most of the orally administered penicillin G is destroyed by gastric acid.
Absorption of sod.PnG from i.m. site is rapid and complete. It is distributed mainly extracellulary; reaches most body fluids but penetration is serous cavities and CSF is poor.
About 60% is plasma protien bound.
It is little metabolized because of rapid excretion.
The plasma t 1/2 of PnG in healthy adult is 30 min.
Tubular secretion of PnG can be blocked by probenecid-higher and longer lasting plasma concentration are achieved.
Probenecid has also been shown to decrease the volume of distribution of Penicillins.
Also read something more about Antibiotics: 👇
Antibiotics • Classification • Antibiotics selection • Problems arise with use of Antibiotics • Why Combination of Antibiotics • Top 10 Antibiotics
Antibiotics • Classification • Antibiotics selection • Problems arise with use of Antibiotics • Why Combination of Antibiotics • Top 10 Antibiotics
PRECAUTION
- Before giving penicillin, history of previous administration and allergic manifestations, if any, must be noted.
- In patients with history of asthma, allergic rhinitis, hay fever, etc, there is an increased risk of Penicillin allergy, hence penicillin should be avoided in such cases.
- Sensitivity test should be performed by an Intradermal test. Itching, erythema and wheal formation are watched for a negative skin test does not ensure absolute safety.
- Inj. Adrenaline and hydrocortisone should be kept ready before injecting penicillin to treat the anaphylactic reaction.
THERAPEUTIC USES
1. Pneumococcal infections : In pneumonia, meningitis or other serious infections, penicillin G can be used as alternative of Cephalosporin if the organism is sensitive, it should be continued for 7 to 10 days.
2. Streptococcal infection : Pharyngitis, sinusitis, rheumatic fever, otitis media, celulitis, etc. are effectively treated with procaine penicillin G 6 lac units i,m, once daily for 10 days.
3. Meningococcal meningitis : penicillin G is effective by intravenously, it should be given only for confirmed cases.
4. Gonococcal infection : penicillin was the drug of choice for gonococcal infections. Because of the emergence of resistant organisms, penicillin are not preferred at present.
5. Syphilis : penicillin G is the drug of choice for syphilis. Treponema pallidum is very sensitive to penicillin and is killed at very low concentration of drug.
6. Diphtheria : it is acute infection of upper respiratory tract caused by C. diphtheriae. Penicillin G is used for this treatment for 10 days.
7. Clostridial infection : The main treatment is the neutralisation of toxin by using human tetanus immunoglobin. For gas gangrene, Penicillin G is the drug of choice.
LIMITATIONS / DRAWBACKS OF PENICILLIN G
1. Orally not very effective.
2. Short duration of action.
3. Narrow spectrum of antibacterial activity.
4. Destroyed by penicillinase enzyme.
5. Possibility of anaphylaxis.
PENICILLIN ALLERGY / ADVERSE EFFECT
Local irritancy and direct toxicity :
- Pain at i.m injection site, nausea on oral ingestion, and thrombophlebitis, of injected vein are dose related expression of irritancy.
- toxicity to brain can cause mental confusion, muscular twitching, convulsions and coma when very large dose is injected.
- bleeding has also occured due interference with platelets function.
- intrathecal injection of Penicillin G is no longer recommended because it has caused arachnoiditis and degenerative changes in spinal cord.
- accidental i.v. injection of procaine penicillin produces CNS stimulation, hallucination.
Hypersensitivity :
- Rash
- itching
- urticaria
- fever
- wheezing, angioneurotic edema, serum sickness, exfoliative dermatitis are less common.
- anaphylaxis is rare but may be fatal.
- Super infection
- Jarisch-Heixheimer reaction.
SEMISYNTHETIC PENICILLIN
Semisynthetic penicillins are produced by chemically combining specific side chains or by incorporating specific precursors in the mould cultures.
They are :
- Ampicillin
- Amoxicillin
- Dicloxacillin
- Nafcillin
- Cloxacillin
- Bacampicillin
- Piperacillin
- Carbenicillin
Ampicillin
- It is active against all organisms sensitive to PnG.
- Due to spread use resistance may develop.
Amoxicillin
It is a close congener of ampicillin, similar to it in all respects except:- Oral absorption is better.
- Incidence of diarrhoea is less.
Carbenicillin
- The special feature of this penicillin congener is its activity against pseudomonus aeroginisa and indole positive proteus which are not inhibited by PnG.
- Klebsiella and gram positive cocci are unaffected by it.
- It is inactive orally and is excreted rapidly in urine.
- High dose can cause bleeding, dose is - 1 to 5 gram every 4 to 6 hours.
Piperacillin
- This antipseudomonal penicillin is about 8 times more active than carbenicillin.
- It has good activity against klebsiella and is used mainly in neutropenic / immunocompromized patients having serious gram negative infections.
- Elimination t1/2 is 1 hr.
😊 I hope you've got help, if you have any suggestion or any question regarding this article "Penicillin and penicillin allergy,, please comment i will be very happy.
Thanks
Also read :
Antianxiety drugs, classification, medication, etc..
Congestive heart failureACE inhibitors
Antihypertensive drugs and classification
Subscribe to:
Posts (Atom)