Sunday, March 6, 2011
Adenosine
It is one of the naturally occurring nucleoside.
Action:
It causes a reduction in conduction velocity. It causes an increased refractory period and reduces automaticity in the AV node.
Pharmacokinetics:
Its duration of action is short. Its half life is approximately 10 seconds.
Therapeutic uses:
Acute supraventricular tachycardia (IV administration)
Adverse effects:
Flushing, chest pain, dyspnea, hypotension
Action:
It causes a reduction in conduction velocity. It causes an increased refractory period and reduces automaticity in the AV node.
Pharmacokinetics:
Its duration of action is short. Its half life is approximately 10 seconds.
Therapeutic uses:
Acute supraventricular tachycardia (IV administration)
Adverse effects:
Flushing, chest pain, dyspnea, hypotension
Digoxin
Action:
It causes a decrease in refractory period in atrial and ventricular cells of heart muscles. It causes an increase in effective refractory period and decreasing conduction velocity in AV node.
Therapeutic uses:
Atrial fibrillation and flutter (while controlling ventricular response rate).
Adverse effects:
It may cause ventricular beats originating from abnormal place. These beats may cause ventricular tachycardia and fibrillation. (treated with lidocaine or phenytoin)
It causes a decrease in refractory period in atrial and ventricular cells of heart muscles. It causes an increase in effective refractory period and decreasing conduction velocity in AV node.
Therapeutic uses:
Atrial fibrillation and flutter (while controlling ventricular response rate).
Adverse effects:
It may cause ventricular beats originating from abnormal place. These beats may cause ventricular tachycardia and fibrillation. (treated with lidocaine or phenytoin)
Verapamil and Diltiazem
Verapamil has major affect on heart muscles than on vascular smooth muscles. has major affect on heart muscles than on vascular smooth muscles.
Nifedipine has major affect on vascular smooth muscles than on heart. So, used to treat hypertension.
Diltiazem has medium affect.
Actions:
Calcium enters the cells through two channels:
1. Voltage sensitive channels
2. Receptor operated channels
The entry of calcium is controlled by the binding of agonists like catecholamines to the receptors.
Calcium entry blockers have pronounced effect on voltage sensitive channels leading to the slow influx of calcium resulting in contraction of cardiac muscles.
Verapamil and diltiazem gets bind to open, depolarized channels only, thus blocking the repolarization till the drug is dissociated from the channel.
They are therefore helpful only when there is rapid heart beat. (Normally, the calcium channels takes time for the repolarization until then the bound drug gets detached from the channel).
By reducing the inward flow, verapamil and diltiazem:
1. Decreases the conduction and
2. Increases the effective refractory period in AV node.
Therapeutic uses:
1. Atrial and ventricular arrhythmias
2. Reentrant supraventricular tachycardia
3. Decreases the ventricular rate in atrial flutter and fibrillation
4. Hypertension
5. Angina
Pharmacokinetics:
They are absorbed orally. Verapamil is extensively metabolized in the liver.
Adverse effects:
1. Negative inotropism
2. Reduces blood pressure (due to peripheral vasodilation. This effect is helpful in hypertension.)
Nifedipine has major affect on vascular smooth muscles than on heart. So, used to treat hypertension.
Diltiazem has medium affect.
Calcium enters the cells through two channels:
1. Voltage sensitive channels
2. Receptor operated channels
The entry of calcium is controlled by the binding of agonists like catecholamines to the receptors.
Calcium entry blockers have pronounced effect on voltage sensitive channels leading to the slow influx of calcium resulting in contraction of cardiac muscles.
Verapamil and diltiazem gets bind to open, depolarized channels only, thus blocking the repolarization till the drug is dissociated from the channel.
They are therefore helpful only when there is rapid heart beat. (Normally, the calcium channels takes time for the repolarization until then the bound drug gets detached from the channel).
By reducing the inward flow, verapamil and diltiazem:
1. Decreases the conduction and
2. Increases the effective refractory period in AV node.
Therapeutic uses:
1. Atrial and ventricular arrhythmias
2. Reentrant supraventricular tachycardia
3. Decreases the ventricular rate in atrial flutter and fibrillation
4. Hypertension
5. Angina
Pharmacokinetics:
They are absorbed orally. Verapamil is extensively metabolized in the liver.
Adverse effects:
1. Negative inotropism
2. Reduces blood pressure (due to peripheral vasodilation. This effect is helpful in hypertension.)
Class IV Antiarrhythmic Drugs
These are calcium entry blockers. Its major effect is seen in vascular smooth muscle and the heart.
Action:
It reduces the influx of calcium leading to reduced rate of Phase 4 (spontaneous depolarization).
It also causes a reduction of conduction in those tissues which are dependent on calcium flow i.e. AV node.
Action:
It reduces the influx of calcium leading to reduced rate of Phase 4 (spontaneous depolarization).
It also causes a reduction of conduction in those tissues which are dependent on calcium flow i.e. AV node.
Dofetilide
Pharmacokinetics:
Its half life is about 10 hours. It is excreted in urine.
Therapeutic uses:
1. First line agent in sustained atrial fibrillation. Alongwith, amiodarone and β-blocking agents it is mostly used for atrial fibrillation.
2. In coronary disease of artery when left ventricular function is disturbed.
Its half life is about 10 hours. It is excreted in urine.
Therapeutic uses:
1. First line agent in sustained atrial fibrillation. Alongwith, amiodarone and β-blocking agents it is mostly used for atrial fibrillation.
2. In coronary disease of artery when left ventricular function is disturbed.
Sotalol
It also has a potent non-selective β-blocking agent.
As indicative of β-blocking agents, it also has the ability of decreasing mortality from acute myocardial infarction.
Actions:
It causes the inhibition of potassium outflow (also referred to as delayed rectifier). This inhibition increases both
1. Repolarization and
2. Action potential duration
And have the ability of prolonging the effective refractory period.
It has the ability of suppressing the ectopic beats and decreases myocardial oxygen demand. In the case of myocardial ischemia, it has prominent anti-fibrillatory affect.
Therapeutic uses:
1. Myocardial Ischemia
2. Sustained ventricular tachycardia
Adverse effects:
Prolonging the QT interval leading to torsade de pointes syndrome.
As indicative of β-blocking agents, it also has the ability of decreasing mortality from acute myocardial infarction.
Actions:
It causes the inhibition of potassium outflow (also referred to as delayed rectifier). This inhibition increases both
1. Repolarization and
2. Action potential duration
And have the ability of prolonging the effective refractory period.
It has the ability of suppressing the ectopic beats and decreases myocardial oxygen demand. In the case of myocardial ischemia, it has prominent anti-fibrillatory affect.
Therapeutic uses:
1. Myocardial Ischemia
2. Sustained ventricular tachycardia
Adverse effects:
Prolonging the QT interval leading to torsade de pointes syndrome.
Class III Antiarrhythmic Drugs
These are potassium channel blockers.
Actions:
They reduce the outward flow of potassium during repolarization phase of cardiac cells.
They have the ability of increasing the duration of action potential without changing Phase 0 of depolarization or the resting membrane potential.
They also have the ability of prolonging the effective refractory period.
Class III antiarrhythmic agents have the potential of induction of arrhythmias.
Actions:
They reduce the outward flow of potassium during repolarization phase of cardiac cells.
They have the ability of increasing the duration of action potential without changing Phase 0 of depolarization or the resting membrane potential.
They also have the ability of prolonging the effective refractory period.
Class III antiarrhythmic agents have the potential of induction of arrhythmias.
Esmolol
It is one of the very short acting β-blocker.
Therapeutic uses:
It is used intravenously in acute arrhythmias that occur in surgical and emergency situations.
Therapeutic uses:
It is used intravenously in acute arrhythmias that occur in surgical and emergency situations.
Metoprolol
It is selective β1 blocker.
Therapeutic uses:
1. Hypertension
2. Angina pectoris (increase endurance to exercise)
Safe in patients with diabetes or peripheral vascular disease. It decreases the risk of bronchospasm.
Therapeutic uses:
1. Hypertension
2. Angina pectoris (increase endurance to exercise)
Safe in patients with diabetes or peripheral vascular disease. It decreases the risk of bronchospasm.
Bretylium
Mechanism of action:
1. It is an adrenergic neuronal blocking agent. It is collected in adrenergic nerve terminals, where it stimulates norepinephrine release firstly but then causes inhibition of the release of norepinephrine in response to neuronal stimulation.
2. It also has direct electrophysiologic effects on heart.
Actions:
1. Promoted duration of ventricular action potential and effective refractory period is more pronounced in ischemic cells.
2. It also causes an increase of action potential duration and effective refractory period of atrial muscle and AV node.
3. Some positive inotropic effect is also observed from initial release of norepinephrine.
Therapeutic uses:
It is used for those life threatening ventricular arrhythmias which are unresponsive to other therapy.
Adverse effects:
Orthostatic hypotension (adrenergic neuron blocking mechanism), Nausea, vomiting
1. It is an adrenergic neuronal blocking agent. It is collected in adrenergic nerve terminals, where it stimulates norepinephrine release firstly but then causes inhibition of the release of norepinephrine in response to neuronal stimulation.
2. It also has direct electrophysiologic effects on heart.
Actions:
1. Promoted duration of ventricular action potential and effective refractory period is more pronounced in ischemic cells.
2. It also causes an increase of action potential duration and effective refractory period of atrial muscle and AV node.
3. Some positive inotropic effect is also observed from initial release of norepinephrine.
Therapeutic uses:
It is used for those life threatening ventricular arrhythmias which are unresponsive to other therapy.
Adverse effects:
Orthostatic hypotension (adrenergic neuron blocking mechanism), Nausea, vomiting
Propranolol
It is helpful in myocardial ischemia. It decreases mortality rate by reducing ventricular arrhythmia.
Mechanism of action:
It acts on both β1 and β2 adrenoceptors i.e. cause their blockage.
Actions:
It has both negative inotropic and chronotropic effect resulting in the decrease of cardiac output.
It also decreases SA and AV nodal activity.
It shows promising effects in angina by decreasing cardiac output, work load on the heart and oxygen consumption of the heart muscles at rest and in physical activity.
In the first instance, it produces anti-hypertensive effects by reduced cardiac output associated with bradycardia. And its long term use inhibits renin secretion, which results in reduced peripheral resistance leading to anti-hypertensive effects.
Due to β2-blockade, it causes an elevated airway resistance.
It causes an increased sodium retention.
Antiarrhythmic action:
Its effects are due to β-adrenoceptor blockade but also due to a direct membrane effect. It
1. Suppresses SA nodal firing
2. Reduces automaticity in purkinje fibers
3. A substantial promotion in effective refractory period of AV node
Therapeutic uses:
1. Chronic form of angina pectoris
2. prophylaxis of myocardial infarction and migraine
3. Hypertension
4. Hyperthyroidism
Antiarrhythmic uses:
It is used for:
1. Atrial flutter or fibrillation
2. Sudden outburst of supraventricular tachycardia
3. Ventricular arrhythmias due to:
a. increased adrenergic activation
b. Toxicity caused by digitalis
Adverse effects:
Sedation, depression, cardiac failure, nausea, vomiting, bronchconstriction, diarrhea, rashes, fever, impaired metabolism (Due to reduced glycogenolysis and glucagon secretion caused by β-blockade)
Mechanism of action:
It acts on both β1 and β2 adrenoceptors i.e. cause their blockage.
Actions:
It has both negative inotropic and chronotropic effect resulting in the decrease of cardiac output.
It also decreases SA and AV nodal activity.
It shows promising effects in angina by decreasing cardiac output, work load on the heart and oxygen consumption of the heart muscles at rest and in physical activity.
In the first instance, it produces anti-hypertensive effects by reduced cardiac output associated with bradycardia. And its long term use inhibits renin secretion, which results in reduced peripheral resistance leading to anti-hypertensive effects.
Due to β2-blockade, it causes an elevated airway resistance.
It causes an increased sodium retention.
Antiarrhythmic action:
Its effects are due to β-adrenoceptor blockade but also due to a direct membrane effect. It
1. Suppresses SA nodal firing
2. Reduces automaticity in purkinje fibers
3. A substantial promotion in effective refractory period of AV node
Therapeutic uses:
1. Chronic form of angina pectoris
2. prophylaxis of myocardial infarction and migraine
3. Hypertension
4. Hyperthyroidism
Antiarrhythmic uses:
It is used for:
1. Atrial flutter or fibrillation
2. Sudden outburst of supraventricular tachycardia
3. Ventricular arrhythmias due to:
a. increased adrenergic activation
b. Toxicity caused by digitalis
Adverse effects:
Sedation, depression, cardiac failure, nausea, vomiting, bronchconstriction, diarrhea, rashes, fever, impaired metabolism (Due to reduced glycogenolysis and glucagon secretion caused by β-blockade)
Class II Antiarrhythmic Drugs
Class II drugs are β-adrenergic receptor antagonists.
Action:
These agents have the ability of decreasing Phase 4 depolarization thus suppresses the automaticity, causing a prolonged AV conduction and decreased cardiac rate and contractility.
Therapeutic uses:
Class II drugs are used in the treatment of tachycardia due to promoted activity of sympathetic system.
They are also useful in the treatment of atrial flutter and fibrillation.
They are used in AV nodal re-entrant tachycardia.
Action:
These agents have the ability of decreasing Phase 4 depolarization thus suppresses the automaticity, causing a prolonged AV conduction and decreased cardiac rate and contractility.
Therapeutic uses:
Class II drugs are used in the treatment of tachycardia due to promoted activity of sympathetic system.
They are also useful in the treatment of atrial flutter and fibrillation.
They are used in AV nodal re-entrant tachycardia.
Propafenone
Same as that of flecainide. It has the ability of allowing conduction in all the tissues of heart.
Flecainide
It binds to sodium channels and slowly detaches from sodium channels.
Mechanism of action:
It is a sodium channel blocker. It suppresses phase 0 of action potential in purkinje fibers and fibers of the muscles of the heart.
Actions:
It does not affect greatly the action potential.
1. In this case, automaticity of the ectopic pacemaker is decreased by the promoted threshold potential (not by a reduction in the slope of phase 4 depolarization).
2. It causes a decreased conduction and excitability and promoted refractory period (pronounced in the depolarized tissue).
Pharmacokinetics:
It is absorbed orally and it has a half life of about 16-20 hours.
Therapeutic uses:
1. It is used in premature ventricular contractions, refractory ventricular tachycardia and supraventricular tachycardia.
2. It is used for the inhibition of sudden outburst of atrial fibrillation or flutter.
Adverse effects:
It may cause dizziness, blurred vision, anorexia, nausea, vomiting, impotence and in some cases may worsen preexisting arrhythmias.
Mechanism of action:
It is a sodium channel blocker. It suppresses phase 0 of action potential in purkinje fibers and fibers of the muscles of the heart.
Actions:
It does not affect greatly the action potential.
1. In this case, automaticity of the ectopic pacemaker is decreased by the promoted threshold potential (not by a reduction in the slope of phase 4 depolarization).
2. It causes a decreased conduction and excitability and promoted refractory period (pronounced in the depolarized tissue).
Pharmacokinetics:
It is absorbed orally and it has a half life of about 16-20 hours.
Therapeutic uses:
1. It is used in premature ventricular contractions, refractory ventricular tachycardia and supraventricular tachycardia.
2. It is used for the inhibition of sudden outburst of atrial fibrillation or flutter.
Adverse effects:
It may cause dizziness, blurred vision, anorexia, nausea, vomiting, impotence and in some cases may worsen preexisting arrhythmias.
Mexiletine and tocainide
Phenytoin
Antiarrhythmic action
Its effects are almost same to that of lidocaine
1. It depresses unprovoked automaticity in atrial and ventricular tissues although it does no affect on intraventricular conduction.
2. It causes a promoted conduction through impaired purkinje fibers.
3. It is especially useful for ventricular arrhythmias related to digitalis toxicity or myocardial ischemia.
Its effects are almost same to that of lidocaine
1. It depresses unprovoked automaticity in atrial and ventricular tissues although it does no affect on intraventricular conduction.
2. It causes a promoted conduction through impaired purkinje fibers.
3. It is especially useful for ventricular arrhythmias related to digitalis toxicity or myocardial ischemia.
Lidocaine
It is a local anesthetic containing amide in structure.
Mechanism of action:
They act fast on sodium channels and also get detached from sodium channels rapidly. It shortens Phase 3 repolarization and blocks sodium channels and has the ability of shortening the duration of action potential.
Actions:
Due to short duration of action potential it prolongs diastole. On the other hand, it decreases the effective refractory period of purkinje fibers.
Therapeutic uses:
It is used for ventricular arrhythmias during open heart surgery, digitalis toxicity and myocardial ischemia.
It is used as local anesthesia.
Pharmacokinetics:
It undergoes first pass metabolism by the liver, so that is why it is given intravenously. In the liver, the drug is dealkalyted and approximately the entire drug is excreted by the liver.
Adverse effects:
It may cause paresthesias, hypotension, tremor, drowsiness, convulsions and respiratory arrest.
Administration and Dosage:
It is given IV with a loading dose of 150-200 mg in 15 minutes succeeded by maintenance dose of 2-4 mg/min.
Mechanism of action:
They act fast on sodium channels and also get detached from sodium channels rapidly. It shortens Phase 3 repolarization and blocks sodium channels and has the ability of shortening the duration of action potential.
Actions:
Due to short duration of action potential it prolongs diastole. On the other hand, it decreases the effective refractory period of purkinje fibers.
Therapeutic uses:
It is used for ventricular arrhythmias during open heart surgery, digitalis toxicity and myocardial ischemia.
It is used as local anesthesia.
Pharmacokinetics:
It undergoes first pass metabolism by the liver, so that is why it is given intravenously. In the liver, the drug is dealkalyted and approximately the entire drug is excreted by the liver.
Adverse effects:
It may cause paresthesias, hypotension, tremor, drowsiness, convulsions and respiratory arrest.
Administration and Dosage:
It is given IV with a loading dose of 150-200 mg in 15 minutes succeeded by maintenance dose of 2-4 mg/min.
Amiodarone
Amiodarone contains iodine and is structurally related to thyroxine. It shows the affects of all classes i.e. class I, II, III and IV.
Mechanism of action:
Amiodarone blocks the sodium channels in inactivated state. It also blocks the calcium channels but to a less extent. It also noncompetitively inhibits α- and β- adrenoceptors.
Actions:
Its dominant action is the increase in duration of action potential. It also causes an increase in effective refractory period in the atrial and ventricular muscles.
It causes an increase in PR, QRS and QT intervals.
It causes a decrease in sinus rate and AV conduction as well as systemic and coronary vasodilation.
Pharmacokinetics:
It is not well absorbed orally. It has a prolonged half life of about 20-100 days and distributes mostly into adipose tissues. Its full effects are seen after 6 weeks of start of treatment.
Therapeutic uses:
It is used in
1. Angina
2. Premature ventricular contractions
3. Ventricular tachyarrhythmia
4. Refractory supraventricular arrhythmias
5. Arrhythmias in patients with wolf Parkinson white syndrome
Adverse effects:
It may cause gastrointestinal intolerance (nausea, vomiting, and constipation), headache, dizziness, paresthesias, pulmonary fibrosis and blue skin discoloration (due to the increased concentration of iodine in the skin).
Mechanism of action:
Amiodarone blocks the sodium channels in inactivated state. It also blocks the calcium channels but to a less extent. It also noncompetitively inhibits α- and β- adrenoceptors.
Actions:
Its dominant action is the increase in duration of action potential. It also causes an increase in effective refractory period in the atrial and ventricular muscles.
It causes an increase in PR, QRS and QT intervals.
It causes a decrease in sinus rate and AV conduction as well as systemic and coronary vasodilation.
Pharmacokinetics:
It is not well absorbed orally. It has a prolonged half life of about 20-100 days and distributes mostly into adipose tissues. Its full effects are seen after 6 weeks of start of treatment.
Therapeutic uses:
It is used in
1. Angina
2. Premature ventricular contractions
3. Ventricular tachyarrhythmia
4. Refractory supraventricular arrhythmias
5. Arrhythmias in patients with wolf Parkinson white syndrome
Adverse effects:
It may cause gastrointestinal intolerance (nausea, vomiting, and constipation), headache, dizziness, paresthesias, pulmonary fibrosis and blue skin discoloration (due to the increased concentration of iodine in the skin).
Saturday, March 5, 2011
Disopyramide
Mechanism of action:
Similar to quinidine
Actions:
It also possesses properties of class III agents.
It has same actions as that of quinidine but it is more pronounced in causing anti-muscarinic actions. It causes peripheral vasoconstriction and produces negative inotropic effects.
It causes a prominent decline in myocardial contraction in patients whose left ventricular function has already been impaired.
Therapeutic uses:
Ventricular arrhythmias
Pharmacokinetics:
It is taken orally and about 50 percent of the drug is excreted without any change through the kidneys. It has been found that about 30 percent of the drug is metabolized in the liver into mono-N-dealkylated metabolite.
Adverse effects:
It causes anticholinergic effects such as constipation, dry mouth, retention of the urine and blurred vision. It may also cause hypotension.
Contraindications:
It is contraindicated for patients with
1. 2nd or 3rd degree AV block
2. cardiogenic shock
3. severe uncompensated cardiac failure
Dosage:
It is given 300-800 mg daily in divided doses.
Similar to quinidine
Actions:
It also possesses properties of class III agents.
It has same actions as that of quinidine but it is more pronounced in causing anti-muscarinic actions. It causes peripheral vasoconstriction and produces negative inotropic effects.
It causes a prominent decline in myocardial contraction in patients whose left ventricular function has already been impaired.
Therapeutic uses:
Ventricular arrhythmias
Pharmacokinetics:
It is taken orally and about 50 percent of the drug is excreted without any change through the kidneys. It has been found that about 30 percent of the drug is metabolized in the liver into mono-N-dealkylated metabolite.
It causes anticholinergic effects such as constipation, dry mouth, retention of the urine and blurred vision. It may also cause hypotension.
It is contraindicated for patients with
1. 2nd or 3rd degree AV block
2. cardiogenic shock
3. severe uncompensated cardiac failure
Dosage:
It is given 300-800 mg daily in divided doses.
Procainamide
It is a derivative of procaine which is a local anesthetic.
Mechanism of action:
Same as that of quinidine
Actions:
Cardiac effects:
Almost similar to quinidine.
It decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
However unlike quinidine it has less effecient antimuscarinic action.
Due to its ganglionic receptor blocking properties, it results in more pronounced negative inotropic effects than quinidine.
It instigates serious CCF in patients with already ventricular dysfunction.
Other effects:
It reduces peripheral vascular resistance and may cause hypotension due to its ganglionic blocking properties.
Procainamide is well-absorbed orally.
Its half life is 2 – 3 hours. Some of the procainamide is metabolized in the liver into N-acetylprocainamide (NAPA). NAPA has the same properties as that of class III agents as it prolongs the duration of action potential.
It is used in atrial and ventricular arrhythmias and ventricular arrhythmias which comes with acute myocardial infarction.
Adverse effects:
It may cause mental confusion, anorexia, nausea, urinary retention and hepatitis. After prolonged use, it may cause reversible form of lupus erythematosus like syndrome in 20-30 percent of patients. Its toxic dose may cause asystole or instigation of ventricular arrhythmias.
Its effects on CNS include depression, hallucination and psychosis.
Contraindications:
It is contraindicated in patients with AV block or systemic lupus erythematosus.
Dosage:
It is given up to 50 mg/kg daily in divided doses every 3 to 6 hours.
Mechanism of action:
Same as that of quinidine
Actions:
Cardiac effects:
Almost similar to quinidine.
It decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
However unlike quinidine it has less effecient antimuscarinic action.
Due to its ganglionic receptor blocking properties, it results in more pronounced negative inotropic effects than quinidine.
It instigates serious CCF in patients with already ventricular dysfunction.
Other effects:
It reduces peripheral vascular resistance and may cause hypotension due to its ganglionic blocking properties.
Pharmacokinetics:
Procainamide is well-absorbed orally.
Its half life is 2 – 3 hours. Some of the procainamide is metabolized in the liver into N-acetylprocainamide (NAPA). NAPA has the same properties as that of class III agents as it prolongs the duration of action potential.
Therapeutic uses:
It is used in atrial and ventricular arrhythmias and ventricular arrhythmias which comes with acute myocardial infarction.
Adverse effects:
It may cause mental confusion, anorexia, nausea, urinary retention and hepatitis. After prolonged use, it may cause reversible form of lupus erythematosus like syndrome in 20-30 percent of patients. Its toxic dose may cause asystole or instigation of ventricular arrhythmias.
Its effects on CNS include depression, hallucination and psychosis.
Contraindications:
It is contraindicated in patients with AV block or systemic lupus erythematosus.
Dosage:
It is given up to 50 mg/kg daily in divided doses every 3 to 6 hours.
Pharmaceutical Management
The careful management and skillful administration of the business of pharmaceuticals is referred to as Pharmaceutical Management.
Quinidine
It is one of the alkaloids of cinchona also known as beta-quinine (it is an a C-9 epimer of quinine). Quinidine is also referred to as conquinine. It is the most primitive form of class IA drug.
Mechanism of action:
Its most important effect is on Phase 0 of the action potential causing a decrease in rapid depolarization by blocking the sodium channels.
It affects Phase 4 also when there is slow depolarization by slow opening of sodium channels.
Actions:
It causes the inhibition of ventricular arrhythmias, reentry arrhythmia and arrhythmias originating from other than normal place.
Quinidine decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
It increases duration of action potential which along with promoted effective refractory period decreases maximum reentry frequency.
Quinidine has α-adrenoceptor blocking properties which causes vasodilation and a reflex increase in SA nodal rate.
Other effects:
It has
1. antimalarial,
2. antipyretic and
3. oxytocic properties, so that increasing the contractions of the muscles of the womb during childbirth.
Pharmacokinetics:
Quinidine sulfate is well absorbed orally. It is metabolized in the liver by cytochrome p450 enzyme and excreted through the kidneys.
Therapeutic uses:
It is used for
1. Atrial, AV junctional and ventricular tachyarrhythmias
2. Premature atrial and ventricular contractions
3. It has the ability of maintaining sinus rhythm after sudden outburst of atrial fibrillations and flutter
4. Interatrial and atrioventricular nodal reentrant arrhythmias
5. Wolf Parkinson white tachycardia
Adverse effects:
Cinchonism (characterized by headache, tinnitus, photophobia, confusion), Anorexia, Gastrointestinal intolerance (Nausea), Rashes, Hepatitis
It may cause worsening of arrhythmia. It may block SA or AV nodes.
Mechanism of action:
Its most important effect is on Phase 0 of the action potential causing a decrease in rapid depolarization by blocking the sodium channels.
It affects Phase 4 also when there is slow depolarization by slow opening of sodium channels.
Actions:
It causes the inhibition of ventricular arrhythmias, reentry arrhythmia and arrhythmias originating from other than normal place.
Cardiac effects:
High concentration of Quinidine directly affects the cardiac cells whereas low concentrations of Quinidine causes indirect (anti-cholinergic) effects on the heart.Quinidine decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
Quinidine has α-adrenoceptor blocking properties which causes vasodilation and a reflex increase in SA nodal rate.
It has
1. antimalarial,
2. antipyretic and
3. oxytocic properties, so that increasing the contractions of the muscles of the womb during childbirth.
Pharmacokinetics:
Quinidine sulfate is well absorbed orally. It is metabolized in the liver by cytochrome p450 enzyme and excreted through the kidneys.
Therapeutic uses:
It is used for
1. Atrial, AV junctional and ventricular tachyarrhythmias
2. Premature atrial and ventricular contractions
3. It has the ability of maintaining sinus rhythm after sudden outburst of atrial fibrillations and flutter
4. Interatrial and atrioventricular nodal reentrant arrhythmias
5. Wolf Parkinson white tachycardia
Adverse effects:
Cinchonism (characterized by headache, tinnitus, photophobia, confusion), Anorexia, Gastrointestinal intolerance (Nausea), Rashes, Hepatitis
It may cause worsening of arrhythmia. It may block SA or AV nodes.
Classification of the anti-arrhythmic drugs
Detailed Classification of Anti-arrhythmic drugs
Class I (Na+ Channel blockers):Class IA drugs (Fast Channel Blockers):
Quinidine, Procainamide, Disopyramide, Imipramine, Amiodarone, Moricizine, Diphenylhydantoin, Ajmaline, Dronedarone, KB130015
Class IB drugs:
Lidocaine, Tocainide, Mexiletine, Phenytoin
Class IC drugs:
Flecainide, Encainide, Indecainide, Lorcainide, Propafenone
Class II Drugs (β-blockers):
Propranolol, Esmolol, Atenolol, Timolol, Metoprolol, Bisoprolol
Class III Drugs (K-Channel blockers):
Amiodarone, Sotalol, Bretylium, Dofetilide, Ibutilide, N-acetylprocainamide, Almokalant, Nibentan, Nifekalant, Azimilide, AVE0118, Ronalozine
Class IV drugs (Ca-Channel blockers or Slow Channel Blockers):
(V) Verapamil, Diltiazem, Bepridil, Nifedipine
Class V drugs:
Digitalis, Adenosine, Digoxin
Miscellaneous Drugs:
Magnesium, Potassium, BIIB-513, Cariporide, H345/52, SSR149744C, Tecadenoson, Tedisamil, ZP123
Further Reading:
Current Trends in Pharmacology by Ray, A.and Gulati, K. 2007, International Publishing house private Ltd.
Fundamental Approaches to the management of Cardiac Arrhythmias by Sung, R. J. and Lauer, M. R. 2000, Kluwer Academic Publishers.
Physiology and Pharmacology of the Heart by Brown, H.; Kozlowski, R. and Davey, P. 1997, Willey Blackwell.
Anti-arrhythmic drugs
Arrhythmia:
The rhythmic activity of the heart is disturbed by any of the following phenomena:
Delayed after depolarization:
It is due to abnormally high level of calcium ions inside the cell.
Re-entry:
It is represented by the entry of the same impulse on a part of heart muscle that it has recently activated.
Here some of the parts of the muscles of the heart get abnormally depolarized. At this, conduction depends on slow calcium current.
For example Wolff-Parkinson White syndrome and AV reentry.
Abnormal pacemaker activity:
Under normal conditions, SA node is most prominent in Phase 4 depolarization and has higher rate of firing.
When there is generation of impulses from other than the SA node resulting in the competitive stimulation of the heart muscles. This causes arrhythmia.
This is promoted by sympathetic stimulation.
Heart block:
This results from the impairment of AV node or ventricular conduction.
Potential:
It is the work done (W) on a unit positive charge (+q) for its movement from a reference point, which is located somewhere outside of the field to a specific point in the field, against electric field (direction).
It is represented by “V” and its formula is
V = W/q
Potential difference:
It is the difference in potential energy between two points (suppose A and B) within an electric field.
It is represented by “ΔV” and its formula is
VA – VB = ΔV = W/q
Membrane potential:
Potential difference across the membranes is referred to as membrane potential. It is therefore a difference of potential (V) inside a nerve, cell membrane or some other tissue (which have the ability of excitation) and space or fluid outside the membrane or nerve cell.
It is negative in normal conditions i.e. resting potential and changes to positive value when excited or generating an impulse i.e. action potential.
Resting potential:
1. Potential difference is negative i.e. V = -75 to -70 milliVolts.
2. Inner side or surface is more negative than the outer side i.e. sodium ions (positive ions) are more on the outer side or surface and chloride ions (negative ions) are more inside. (minute amount of potassium ions (positive ions) are also there inside).
3. When the inner side is more negative than the outer; the cell membrane, neuron or the tissues at this place are referred to as polarized.
When, some condition or any disturbance, cause to make the inner side more negative than the normal state; at this place it is referred to as hyperpolarized.
Action potential:
1. Potential difference is positive i.e. V = +55 milliVolts
2. It is a temporary change in membrane potential due to a stimulus or excitation.
When some condition or any disturbance cause to make the inner side less negative than the normal state; at this place it is referred to as depolarized.
The action potential is declined by closing sodium channels and opening potassium channels, which helps to maintain approximately same amount of positive charge.
Phases of action potential:
Cells of cardiac muscles have somewhat long duration of action potential. So, it is divided into 5 phases:
Phase 0:
This is characterized by fast depolarisation.
On excitation, voltage gated sodium channels start opening resulting in the inward movement of sodium ions so that the inner side starts to become less negative.
Threshold potential:
At a certain point, potential difference reaches at -60 mV. This is referred to as threshold potential.
At this point, the sodium channels completely open resulting in the influx of a large amount of sodium ions. This depolarization cause the neighboring sodium channels to be activated resulting in the movement of impulse along with action potential.
After the inactivation of the sodium channels there is no flow of sodium ions.
Phase 1:
This is characterized by partial repolarisation.
Here the sodium channels are inactivated and potassium channels get activated resulting in the outward movement of potassium ions (positive ions). This outward movement of positive ions results and the concentration of positive ions inside the fiber or membrane remain same.
Phase 2:
This is characterized by the plateau phase.
Here calcium channels get opened resulting in the inward movement of calcium ions. So that the balance remains and not more positive ions get concentrated outside by the outward flow of positive ions.
Phase 3:
This is characterized by repolarisation.
At this stage calcium channels get inactivated. Potassium channels remain open resulting in the outward flow of potassium ions leading to membrane repolarisation. Here at this point there is an increase of sodium ions inside the membrane and decrease of potassium ions outside.
Phase 4:
This is characterized by the potential pacemaker in whom there is slow depolarisation.
At this stage, the sodium channels start opening again for another threshold potential. Depolarization again started for another action potential.
The rhythmic activity of the heart is disturbed by any of the following phenomena:
Delayed after depolarization:
It is due to abnormally high level of calcium ions inside the cell.
Re-entry:
It is represented by the entry of the same impulse on a part of heart muscle that it has recently activated.
Here some of the parts of the muscles of the heart get abnormally depolarized. At this, conduction depends on slow calcium current.
For example Wolff-Parkinson White syndrome and AV reentry.
Abnormal pacemaker activity:
Under normal conditions, SA node is most prominent in Phase 4 depolarization and has higher rate of firing.
When there is generation of impulses from other than the SA node resulting in the competitive stimulation of the heart muscles. This causes arrhythmia.
This is promoted by sympathetic stimulation.
Heart block:
This results from the impairment of AV node or ventricular conduction.
Potential:
It is the work done (W) on a unit positive charge (+q) for its movement from a reference point, which is located somewhere outside of the field to a specific point in the field, against electric field (direction).
It is represented by “V” and its formula is
V = W/q
Potential difference:
It is the difference in potential energy between two points (suppose A and B) within an electric field.
It is represented by “ΔV” and its formula is
VA – VB = ΔV = W/q
Membrane potential:
Potential difference across the membranes is referred to as membrane potential. It is therefore a difference of potential (V) inside a nerve, cell membrane or some other tissue (which have the ability of excitation) and space or fluid outside the membrane or nerve cell.
It is negative in normal conditions i.e. resting potential and changes to positive value when excited or generating an impulse i.e. action potential.
Resting potential:
1. Potential difference is negative i.e. V = -75 to -70 milliVolts.
2. Inner side or surface is more negative than the outer side i.e. sodium ions (positive ions) are more on the outer side or surface and chloride ions (negative ions) are more inside. (minute amount of potassium ions (positive ions) are also there inside).
3. When the inner side is more negative than the outer; the cell membrane, neuron or the tissues at this place are referred to as polarized.
When, some condition or any disturbance, cause to make the inner side more negative than the normal state; at this place it is referred to as hyperpolarized.
Action potential:
1. Potential difference is positive i.e. V = +55 milliVolts
2. It is a temporary change in membrane potential due to a stimulus or excitation.
When some condition or any disturbance cause to make the inner side less negative than the normal state; at this place it is referred to as depolarized.
The action potential is declined by closing sodium channels and opening potassium channels, which helps to maintain approximately same amount of positive charge.
Phases of action potential:
Cells of cardiac muscles have somewhat long duration of action potential. So, it is divided into 5 phases:
Phase 0:
This is characterized by fast depolarisation.
On excitation, voltage gated sodium channels start opening resulting in the inward movement of sodium ions so that the inner side starts to become less negative.
Threshold potential:
At a certain point, potential difference reaches at -60 mV. This is referred to as threshold potential.
At this point, the sodium channels completely open resulting in the influx of a large amount of sodium ions. This depolarization cause the neighboring sodium channels to be activated resulting in the movement of impulse along with action potential.
After the inactivation of the sodium channels there is no flow of sodium ions.
Phase 1:
This is characterized by partial repolarisation.
Here the sodium channels are inactivated and potassium channels get activated resulting in the outward movement of potassium ions (positive ions). This outward movement of positive ions results and the concentration of positive ions inside the fiber or membrane remain same.
Phase 2:
This is characterized by the plateau phase.
Here calcium channels get opened resulting in the inward movement of calcium ions. So that the balance remains and not more positive ions get concentrated outside by the outward flow of positive ions.
Phase 3:
This is characterized by repolarisation.
At this stage calcium channels get inactivated. Potassium channels remain open resulting in the outward flow of potassium ions leading to membrane repolarisation. Here at this point there is an increase of sodium ions inside the membrane and decrease of potassium ions outside.
Phase 4:
This is characterized by the potential pacemaker in whom there is slow depolarisation.
At this stage, the sodium channels start opening again for another threshold potential. Depolarization again started for another action potential.
Quinolone
Introduction:
It is an anti-bacterial drug and is derived from hydroxylated quinolines.
Mechanism of Action:
It causes the replication of DNA of bacteria.
It is an anti-bacterial drug and is derived from hydroxylated quinolines.
Mechanism of Action:
It causes the replication of DNA of bacteria.
Area postrema
Area postrema: A small elevated area in the fourth ventricle in the brain involving the chemoreceptor trigger zone.
Arachidonic Acid
Arachidonic Acid: It is a 20-carbon fatty acid, usually essential in nutrients, and is the primary precursor of prostaglandins and related compounds. It is present as a component of the phospholipids of cell membranes. Enzyme Phospholipase A2 causes the release of free Arachidonic acid.
Aplastic anemia
Aplastic anemia: Aplastic means inability to produce new cells. Referring to this hemolytic anemia is a serious type of anemia caused by the inability of bone marrow cells to produce red blood cells. It is also referred to as pancytopenia.
Antithrombin III
Antithrombin III: it is an α-globulin protease inhibitor causing the inhibition of serine proteases and factor IIa and factor Xa.
Antigen
Antigen: A kind of substance that increases the production of antibodies. They are also called as immunogen. A protein molecule present on the surface of the cell, bacterium or some virus involved in activating the synthesis of an antibody.
Antibody
Antibody: It is a particular type of protein (immunoglobulin molecule) synthesized by B-cell involved in primary immune responses to a disease. These are produced in reaction to the presence of antigens such as bacterium or virus.
Ankylosing spondilitis
Ankylosing spondilitis: This is the arthritis of the spine in which there is fusion of the spine.
Transferosome
Transferosome is a proprietary drug delivery technology of the German company IDEA AG.
Transferosome means "Carrying body". It is a type of artifical vesicle and is considered to be suitable for carrying drug to required target.
Transferosome means "Carrying body". It is a type of artifical vesicle and is considered to be suitable for carrying drug to required target.
Friday, March 4, 2011
The lagrangian method
Lagrangian method is one of the optimization methods and is an extened form of Classic method of simplifying the formulae and methods. This method helps in finding the maxima i.e. greatest possible amount, and minima i.e. minimum possible degree, of a function depending on the constraints.
Following steps are usually followed in the langragian method:
1. Objective function is determined:
Objective function is a function in optimization theory. This function is to be maximized or minimized i.e. to be optimized. Here function is a quantity depending on another quantity and it can be changed by changing the values of the other quantity.
We can express objective funcion with expression like "Z(X')"
Where X' is the decision variable representing variable for which we can make decisions or which can be changed i.e. X' = (X1, X2,...Xn)
2. Constraints are determined
Constraints are the factors that causes limitations to the freedom of something. Problems related to pharmaceutical product and process desgin are considered as constrained optimization problems.
3. Inequality constraints are converted into equality constraints
4. From the lagrange function, assign
a. One lagrange multiplier i.e. lambda for each constraint
b. One slack variable i.e q for each inequaltiy constraint
5. The lagrange function for each variable, is differentiated partially, and setting the derivative equal to zero.
6. The set of simultaneous equations are solved
7. Resulting values are substituted into the objective functions
Provision for this method is the completion of the experiment before the optimization so that the mathematical models can be generated. Moreover, in lagrangian method several responses or dependent variables can be handled but work can be done on only two independent variables.
Following steps are usually followed in the langragian method:
1. Objective function is determined:
Objective function is a function in optimization theory. This function is to be maximized or minimized i.e. to be optimized. Here function is a quantity depending on another quantity and it can be changed by changing the values of the other quantity.
We can express objective funcion with expression like "Z(X')"
Where X' is the decision variable representing variable for which we can make decisions or which can be changed i.e. X' = (X1, X2,...Xn)
2. Constraints are determined
Constraints are the factors that causes limitations to the freedom of something. Problems related to pharmaceutical product and process desgin are considered as constrained optimization problems.
3. Inequality constraints are converted into equality constraints
4. From the lagrange function, assign
a. One lagrange multiplier i.e. lambda for each constraint
b. One slack variable i.e q for each inequaltiy constraint
5. The lagrange function for each variable, is differentiated partially, and setting the derivative equal to zero.
6. The set of simultaneous equations are solved
7. Resulting values are substituted into the objective functions
Provision for this method is the completion of the experiment before the optimization so that the mathematical models can be generated. Moreover, in lagrangian method several responses or dependent variables can be handled but work can be done on only two independent variables.
Indian Journal of Cancer
The Indian journal of cancer is a peer reviewed journal published on behalf of Indian society of oncology and indian cancer society giving free access to articles on its website http://www.indianjcancer.com.it/ was established in 1963.
Following are the topics included in the Indian Journal of Cancer:
1. Oncology
2. Oncopathology
3. Radiation Oncology
4. Surgical Oncology
Its Pubmed articles are also present in the link below:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=Indian+Journal+of+Cancer[jo]
The Address of its editorial office is as follows:
Following are the topics included in the Indian Journal of Cancer:
1. Oncology
2. Oncopathology
3. Radiation Oncology
4. Surgical Oncology
Its Pubmed articles are also present in the link below:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=Indian+Journal+of+Cancer[jo]
The Address of its editorial office is as follows:
INDIAN CANCER SOCIETY
Lady Ratan Tata Medical and Research Centre
M. Karve Road, Cooperage, Bombay 400021, India.
Phone: 91-22-2202 9941/2202 9942,
Fax: 91-22-2287 2745
Thursday, March 3, 2011
Indian Journal of Pharmaceutical Sciences
"Indian Journal of Pharmaceutical Sciences" is one of the peer reviewed medical journals having free full text articles on its website, http://www.ijpsonline.com/. This journal is an official publication of science from Indian Pharmaceutical Association. Initially, this publication came on quarterly basis but now this journal is bimonthly and works since 1939.
Following are the subjects covered by Injian Journal of Pharmaceutical Sciences:
1. Pharmaceutics including Biopharmaceutics, Pharmacy practice, hospital and clinical pharmacy
2. Pharmacology
3. Pharmacognosy
4. Pharmaceutical Analysis
Following link gives the results of Indian Journal of Pharmaceutical Sciences in Pubmed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=Indian+Journal+of+Pharmaceutical+Sciences[jo]
Address of the editorial office of "Indian Journal of Pharmaceutical Sciences" is as follows:
Following are the subjects covered by Injian Journal of Pharmaceutical Sciences:
1. Pharmaceutics including Biopharmaceutics, Pharmacy practice, hospital and clinical pharmacy
2. Pharmacology
3. Pharmacognosy
4. Pharmaceutical Analysis
Following link gives the results of Indian Journal of Pharmaceutical Sciences in Pubmed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=Indian+Journal+of+Pharmaceutical+Sciences[jo]
Address of the editorial office of "Indian Journal of Pharmaceutical Sciences" is as follows:
The Editor,
Indian Journal of Pharmaceutical Sciences,
Kalina, Santacruz East,
Kalina, Santacruz East,
Mumbai-400 098.
Email: ijps2002(at)rediffmail(dot)com
Fifth Professional, Second Semester, Pharmaceutical Management
PHARMACEUTICS-XXI (Pharmaceutical Management and; Marketing-II)
(Theory)
Cr. Hr. 03
1. MARKETING MANAGEMENT:
Marketing channels, Promotion and Advertising and Salesmanship.
2. SALES MANAGEMENT:
Personnel, Buying, Receiving, Pricing, Sales promotion and Customer Services.
3. PHARMACY LAYOUT DESIGN:
Objectives of Layout Design, Types of Community Pharmacies (Pharmaceutical Centre, Prescription-oriented Pharmacies, Traditional Pharmacies and The Super Drug Store), Consumer goods and purchases, Classes of Layout designs, Principles and characteristics of Layout Design and Traffic Flow analysis.
Recommended Books
1. M Ahmad & N I Bukhari, Pharmaceutical Management and Marketing, Tariq Academy, Faisalabad-Pakistan (2002).
2. Patrick Tharp & Pedro J Lecca, Pharmacy Management for students and practitioners, The C V Mosby Company, St Louis, Toronto, London (1979).
3. Harry A Smith, Principles & Methods of Pharmacy Management, Lea & Febiger, Philadelphia, 1986.
(Theory)
Cr. Hr. 03
1. MARKETING MANAGEMENT:
Marketing channels, Promotion and Advertising and Salesmanship.
2. SALES MANAGEMENT:
Personnel, Buying, Receiving, Pricing, Sales promotion and Customer Services.
3. PHARMACY LAYOUT DESIGN:
Objectives of Layout Design, Types of Community Pharmacies (Pharmaceutical Centre, Prescription-oriented Pharmacies, Traditional Pharmacies and The Super Drug Store), Consumer goods and purchases, Classes of Layout designs, Principles and characteristics of Layout Design and Traffic Flow analysis.
Recommended Books
1. M Ahmad & N I Bukhari, Pharmaceutical Management and Marketing, Tariq Academy, Faisalabad-Pakistan (2002).
2. Patrick Tharp & Pedro J Lecca, Pharmacy Management for students and practitioners, The C V Mosby Company, St Louis, Toronto, London (1979).
3. Harry A Smith, Principles & Methods of Pharmacy Management, Lea & Febiger, Philadelphia, 1986.
Fifth Professional, Second Semester, Pharmaceutics
PHARMACEUTICS-XX (Forensic Pharmacy-II)
(Theory)
Cr. Hr. 01
1. THE PHARMACY ACT, 1967.
2. THE DANGEROUS DRUGS ACT, 1930.
3. THE FACTORY LAW 1934.
4. SHOPS AND ESTABLISHMENT ORDINANCE, 1969 WITH
RULES.
5. THE POISONS ACT, 1919.
6. CONTROL OF NARCOTICS SUBSTANCES ACT, 1997.
Recommended Books
1. R Z Hussain, The Manual of Drug Laws in Pakistan, Irfan Law Book House, Lahore-Pakistan (2003).
2. The Pharmacy Act, 1967
3. The Poisons Act, 1919
4. The Dangerous Drugs Act, 1930
5. The Factory Law, 1934
6. Shop and Establishment Ordinance, 1969
7. Control of Narcotics Substances Act, 1997.
(Theory)
Cr. Hr. 01
1. THE PHARMACY ACT, 1967.
2. THE DANGEROUS DRUGS ACT, 1930.
3. THE FACTORY LAW 1934.
4. SHOPS AND ESTABLISHMENT ORDINANCE, 1969 WITH
RULES.
5. THE POISONS ACT, 1919.
6. CONTROL OF NARCOTICS SUBSTANCES ACT, 1997.
Recommended Books
1. R Z Hussain, The Manual of Drug Laws in Pakistan, Irfan Law Book House, Lahore-Pakistan (2003).
2. The Pharmacy Act, 1967
3. The Poisons Act, 1919
4. The Dangerous Drugs Act, 1930
5. The Factory Law, 1934
6. Shop and Establishment Ordinance, 1969
7. Control of Narcotics Substances Act, 1997.
Fifth Professional, Second Semester, Pharmaceutical Technology
PHARMACEUTICS-XIX (Pharmaceutical Technology-II)
(Theory)
Cr. Hr. 03
1. MODIFIED DRUG RELEASE DOSAGE FORM:
The concept of sustained release, First order release approximation, Multiple dosing, Implementation of designing, Approaches based upon dosage form modification, Product evaluation and testing, Matrices tablets, Control release technology, Microencapsulation, Method of particle coating and Instrumentation in granule manufacturing.
2. PHARMACEUTICAL BIOTECHNOLOGY:
Biotechnological aspects in the product development, Fundamentals of Genetic Engineering and its Application in Medicine, Principle, Synthesis and Application of Monoclonal, Antibodies, Introduction to Gene therapy, Immobilized Enzymes and their application in Medicine, General Principle and Methods of Microbial Assay.
PHARMACEUTICS-XIX (Pharmaceutical Technology-II)
(Laboratory)
Cr. Hr. 01
NOTE:- Practicals of the subject shall be designed from time to time on the basis of the above mentioned theoretical topics and availability of the facilities, e.g. Microbial assay, Particle size analysis using various methods, Stability studies of Pharmaceuticals, Coating of particles and To prepare, examine and control specifications of packaging materials.
Recommended Books
1. Anya M Hellery, Drug delivery and targeting, Taylor & Francis, London, 2001.
2. Joseph R Robinson Controlled drug delivery, Marcel & Dakker Inc, New York, 2nd Ed., 1987.
3. T V Ramabhadran, Pharmaceutical design and development, Ellis Horwood, New York, 1994.
4. M E Aulton, Pharmaceutics: Science of Dosage Forms Design, ELBS/Churchill Livingstone, London, 1998.
5. Banker, Modern pharmaceutics, Marchell Dakker Inc, New York, 1990.
6. John A Bontempo, Development of biopharmaceutical parenteral dosage forms, Marchell Dakker Inc, New York, 1997.
7. N K Jain, Controlled and Novel drug delivery, CBS Publishers and Distributers, New Dehi, 1997.
8. Ansel, Pharmaceutical Dosage Form in Drug Delivery System, Lee and Febiger, London, 1990.
9. Attaurahman and M I Chaudry, Bioassay techniques for drug development, CRC Press, LLC, USA, 2001.
10. Pramod K Gupta, Inject able drug development, CRC Press, LLC, USA, 1999.
11. H John Smith, Introduction to the principals of drug design and action, CRC Press, LLC, USA, 1998.
12. Rong Liu, Water Insoluble Drug Formulations, CRC Press, LLC, USA, 2000.
13. Peter Blaisdell, Twenty First Century Pharmaceutical Development. CRC Press, LLC, USA, 2000.
14. Lachman L, Theory and Practice of Industrial Pharmacy, Lee & Febiger, Philadelphia, 3rd Ed., 1986.
(Theory)
Cr. Hr. 03
1. MODIFIED DRUG RELEASE DOSAGE FORM:
The concept of sustained release, First order release approximation, Multiple dosing, Implementation of designing, Approaches based upon dosage form modification, Product evaluation and testing, Matrices tablets, Control release technology, Microencapsulation, Method of particle coating and Instrumentation in granule manufacturing.
2. PHARMACEUTICAL BIOTECHNOLOGY:
Biotechnological aspects in the product development, Fundamentals of Genetic Engineering and its Application in Medicine, Principle, Synthesis and Application of Monoclonal, Antibodies, Introduction to Gene therapy, Immobilized Enzymes and their application in Medicine, General Principle and Methods of Microbial Assay.
PHARMACEUTICS-XIX (Pharmaceutical Technology-II)
(Laboratory)
Cr. Hr. 01
NOTE:- Practicals of the subject shall be designed from time to time on the basis of the above mentioned theoretical topics and availability of the facilities, e.g. Microbial assay, Particle size analysis using various methods, Stability studies of Pharmaceuticals, Coating of particles and To prepare, examine and control specifications of packaging materials.
Recommended Books
1. Anya M Hellery, Drug delivery and targeting, Taylor & Francis, London, 2001.
2. Joseph R Robinson Controlled drug delivery, Marcel & Dakker Inc, New York, 2nd Ed., 1987.
3. T V Ramabhadran, Pharmaceutical design and development, Ellis Horwood, New York, 1994.
4. M E Aulton, Pharmaceutics: Science of Dosage Forms Design, ELBS/Churchill Livingstone, London, 1998.
5. Banker, Modern pharmaceutics, Marchell Dakker Inc, New York, 1990.
6. John A Bontempo, Development of biopharmaceutical parenteral dosage forms, Marchell Dakker Inc, New York, 1997.
7. N K Jain, Controlled and Novel drug delivery, CBS Publishers and Distributers, New Dehi, 1997.
8. Ansel, Pharmaceutical Dosage Form in Drug Delivery System, Lee and Febiger, London, 1990.
9. Attaurahman and M I Chaudry, Bioassay techniques for drug development, CRC Press, LLC, USA, 2001.
10. Pramod K Gupta, Inject able drug development, CRC Press, LLC, USA, 1999.
11. H John Smith, Introduction to the principals of drug design and action, CRC Press, LLC, USA, 1998.
12. Rong Liu, Water Insoluble Drug Formulations, CRC Press, LLC, USA, 2000.
13. Peter Blaisdell, Twenty First Century Pharmaceutical Development. CRC Press, LLC, USA, 2000.
14. Lachman L, Theory and Practice of Industrial Pharmacy, Lee & Febiger, Philadelphia, 3rd Ed., 1986.
Fifth Professional, Second Semester, Pharmaceutics
PHARMACEUTICS-XVIII (Clinical Pharmacy-IV)
(Theory)
Cr. Hr. 03
1. PHARMACEUTICAL CARE, ITS SCOPE, MANAGEMENT AND APPLICATION OF CARE PLAN.
2. ROLE OF CLINICAL PHARMACIST IN COMMUNITY PHARMACY.
3. CLINICAL THERAPEUTICS:
(a) General Strategy: Terminology of Disease. Management and Treatment. Drug Selection.
(b) Basic introduction of some clinical situations, their clinical features, etiology, pathophysiology and treatment of causes:
Common Cold, Pharyngitis and Tonsilitis, Pneumonia, Tuberculosis, Diarrhea, Malaria, Meningitis, Tetanus, Typhoid Fever, Measles, Rabies, AIDS, Congestive cardiac failure,
Conjunctivitis, Anaemia, Gout, Asthma, Ulcer, Diabetes mellitus, Hypertension, Hapatitis, Dermatology (Scabies, Fungal diseases).
4. CLINICAL TOXICOLOGY:
(a) General information. Role of pharmacist in treatment of poisoning and general management of poisoning & overdosage. Role and Status of Poison Control Centre.
(b) Antidotes and their mechanism of action
5. SAVE INTRAVENOUS THERAPY & HAZARDS OF INTRAVENOUS THERAPY.
6. NON-COMPLIANCE:
Definition, introduction and importance, Extent of non-compliance, Methods of assessment, Reasons for non-compliance, Strategies for improving compliance and Designing of compliance trials.
PHARMACEUTICS-XVIII (Clinical Pharmacy-IV)
(Laboratory)
Cr. Hr. 01
Clerkship in the Clinical setting. A project related to Clinical Pharmacy Practices will be completed by the students and will be evaluated by the external examiner.
Recommended Books
1. Roger Walker, Clinical Pharmacy & Therapeutics, Churchill Levingstone, London,
2. Guard Paul, A Behavioral Approach to Pharmacy Practice, Black Well, USA,
3. Herfindal Gourley, Clinical Pharmacy & Therapeutics,
4. A J Winfield, Pharmaceutical Practice, Churchill Levingstone, London,
5. Kavin Taylor, Pharmacy Practice, Taylor & Francis, New York, 1998.
6. Deborah Rosenbaun, Clinical Research Coordinator Hand Book,
7. Simon Cook, Clinical Studies Management, a Practical Guide to Success,
8. Joseph T Dipiro, Encyclopaedia of Clinical Pharmacy. Marcel Dekker Publishing,
9. Joseph T Dipiro, Encyclopaedia of Pharmacy. Marcel Dekker Publishing, 2002.
10. Mellainie J Rantucci, Pharmacist Talking with Patients, 1997.
11. Smith GDG and Aronson J K, Oxford Text Book of Clinical Pharmacology and Drug Therapy, Oxford University Press, UK, 1990.
12. Hansten P and Horn J, Drug interactions. Lee & Febiger, Philadelphia, USA, 1989.
(Theory)
Cr. Hr. 03
1. PHARMACEUTICAL CARE, ITS SCOPE, MANAGEMENT AND APPLICATION OF CARE PLAN.
2. ROLE OF CLINICAL PHARMACIST IN COMMUNITY PHARMACY.
3. CLINICAL THERAPEUTICS:
(a) General Strategy: Terminology of Disease. Management and Treatment. Drug Selection.
(b) Basic introduction of some clinical situations, their clinical features, etiology, pathophysiology and treatment of causes:
Common Cold, Pharyngitis and Tonsilitis, Pneumonia, Tuberculosis, Diarrhea, Malaria, Meningitis, Tetanus, Typhoid Fever, Measles, Rabies, AIDS, Congestive cardiac failure,
Conjunctivitis, Anaemia, Gout, Asthma, Ulcer, Diabetes mellitus, Hypertension, Hapatitis, Dermatology (Scabies, Fungal diseases).
4. CLINICAL TOXICOLOGY:
(a) General information. Role of pharmacist in treatment of poisoning and general management of poisoning & overdosage. Role and Status of Poison Control Centre.
(b) Antidotes and their mechanism of action
5. SAVE INTRAVENOUS THERAPY & HAZARDS OF INTRAVENOUS THERAPY.
6. NON-COMPLIANCE:
Definition, introduction and importance, Extent of non-compliance, Methods of assessment, Reasons for non-compliance, Strategies for improving compliance and Designing of compliance trials.
PHARMACEUTICS-XVIII (Clinical Pharmacy-IV)
(Laboratory)
Cr. Hr. 01
Clerkship in the Clinical setting. A project related to Clinical Pharmacy Practices will be completed by the students and will be evaluated by the external examiner.
Recommended Books
1. Roger Walker, Clinical Pharmacy & Therapeutics, Churchill Levingstone, London,
2. Guard Paul, A Behavioral Approach to Pharmacy Practice, Black Well, USA,
3. Herfindal Gourley, Clinical Pharmacy & Therapeutics,
4. A J Winfield, Pharmaceutical Practice, Churchill Levingstone, London,
5. Kavin Taylor, Pharmacy Practice, Taylor & Francis, New York, 1998.
6. Deborah Rosenbaun, Clinical Research Coordinator Hand Book,
7. Simon Cook, Clinical Studies Management, a Practical Guide to Success,
8. Joseph T Dipiro, Encyclopaedia of Clinical Pharmacy. Marcel Dekker Publishing,
9. Joseph T Dipiro, Encyclopaedia of Pharmacy. Marcel Dekker Publishing, 2002.
10. Mellainie J Rantucci, Pharmacist Talking with Patients, 1997.
11. Smith GDG and Aronson J K, Oxford Text Book of Clinical Pharmacology and Drug Therapy, Oxford University Press, UK, 1990.
12. Hansten P and Horn J, Drug interactions. Lee & Febiger, Philadelphia, USA, 1989.
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(For detailed study of Pharmaceutical Incompatibility Click here) Multiple Choice Questions (MCQs) from Pharmaceutical Incompatibility in ...
