Nicotinic acid is useful in treating dyslipidemia. Nicotinic acid is a vitamin B3 with a lipid lowering mode of action. Nicotinic acid will act as an additional / adjunct therapy to dyslipidemia or as replacement due to contraindicated to statin.
Nicotinic acid may increase the high density lipoprotein. There will reduction in the release of very low density lipoprotein from the hepatocytes and decrease in the synthesis of the plasma triglycerides. There will also be a low level of low density lipoprotein. Nicotinic acid is given orally while nicotinic acid is excreted through urine.
Nicotinic acid may present with flushing. It is wise to consider ibuprofen to reduce the incidence of flushing before administrating nicotinic acid. Nicotinic acid may lead to gout, rashes, and pruritus as well as gastrointestinal discomfort. Glucose tolerance and impairment of the liver function are common in cases of high intake of nicotinic acid. Other rare side effects may include peripheral edema, dyspnea and palpitation.
Gemfibrozil is useful in treating patient with low high density lipoprotein, mixed cases of dyslipidemia ( increase in both plasma triglycerides and increase in cholesterol) and prevention of atheroma.
Gemfibrozil is a lipid lowering fibrates which increase the low density lipoprotein - cholesterol uptake by the low density lipoprotein - cholesterol receptors. Gemfibrozil will increase the transcription of the gene encoding for the apoprotein apoA1 and apoprotein apoA5 as well as for the lipoprotein lipase. Generally gemfibrozil may lead to slight increase in the high density lipoprotein, moderate decrease in low density lipoprotein with marked decreased in plasma very low density lipoprotein.
Gemfibrozil is given orally and gemfibrozil will be excreted via the kidney by metabolizing to glucuronide conjugates. Gemfibrozil should be avoided to be used with statin as it may lead to severe myositis. The common side effect may include gallstones formation, rashes and gastrointestinal discomfort.
Ezetimibe is a useful cholesterol lowering drug. Ezetimibe is given orally. The half life of ezetimibe is around 22- 23 hours. Ezetimibe will be excreted in the forms of feces. Colestryamine will decrease the plasma concentration of ezetimibe while fibrates will increase the concentration of ezetimibe.
Ezetimibe is useful in treating hypercholesterolemia by decreasing the plasma concentration of LDL and inhibit the absorption of the cholesterol from the intestine. Ezetimibe will activated in the liver. Ezetimibe will inhibits and blocks a sterol carrier protein which present in the brush border of the enterocytes. This will lead to the reduction of the amount of cholesterol transfer through the liver via chylomicrons. These cholesterols may include biliary cholesterol and dietary cholesterol. As a consequences, there will be reduction in the cholesterol level in the liver and increase in the LDL hepatic absorption. There will also be an increase in the clearance of the LDL - cholesterol from the plasma.
Ezetimibe will achieved its maximum concentration 2 hours after ingestion where it undergoes enterohepatic cycling.The common side effects of ezetimibe may include myalgia, gastrointestinal discomfort ( constipation, diarrhea, bloating), rashes and headache.
Colestyramine will be given orally with no systemic absorption. Colestyramine will be used in treating patient with hypercholesterolemia. Colestyramine will reduce the absorption of the cholesterol from the gastrointestinal tract. Colestyramine will act as bile acid binding resin. Colestyramine which is a positively charged drugs will bind to bile acid which is negatively charged particles which lead to an inhibition of bile acid absorption.
The hepatic stores of cholesterol will be reduced due to reduction in the pools of bile acid in the liver. As a result there will be an increase in the synthesis of LDL receptors which lead to an increase in uptake of the LDL / low density lipoprotein into hepatic cells.
The common side effects of colestyramine may include diarrhea, constipation or bloating which are the common gastrointestinal discomfort.
Flecainide is a class Ic anti arrhythmic agent. Flecainide is useful in treating patient with severe ventricular arrhythmias who is unresponsive to other forms of treatment. Flecainide is also used as preventive measure against paroxysmal atrial fibrillation.
Flecainide will acts by blocking the opening of the sodium ion channels which will reduce the rates of depolarisation of the phase 0. This will lead to an increase in the refractory period with slowness in the atrioventricular conduction ( AV conduction). Flecainide will react at a slower rates to sodium channel than other class of anti arrhythmic agents.
Flecainide is a well known anti dysrhythmic agent which is excreted unchanged in the urine. Flecainide is administered orally with half life of 20 hours.
The common side effects of flecainide may include ventricular fibrillation which occur post infarction/ increase the risk of fatality and negative inotropic effects as well as ventricular dysrhythmic effects.
Amiodarone is class III anti arrhythmic agent which is useful in treating patient with atrial flutter, ventricular ectopic beat, atrial fibrillation and tachyarrhythmia.
Amiodarone will block the beta adrenoceptors and block sodium ion channel. Amiodarone will also block the potassium ion channel in the cell membrane. Amiodarone will lead to an increase in the duration of the action potential while delaying the repolarization. This will finally lead to an increase in the refractory period. The half life of amiodarone may last for several weeks.
Amiodarone is a long acting drugs which will bind to the tissue extensively. The common side effects of amiodarone may include thyroid disorders, liver damage/ hepatotoxicity, photosensitivity skin rashes, pulmonary fibrosis and torades de pointes.
Lidocaine is also known as class Ib anti arrhythmic agent. Lidocaine is useful in treating patient with digoxin induced arrhythmia and treating and prevention of ventricular fibrillation due to / post infarction. Lidocaine is mostly given intravenously with very high first pass metabolism. Lidocaine may metabolized by cytochrome P450 with half life of 2 hours.
Lidocaine will block the opening of the sodium ion channel and lead to inactivation of the sodium ion channel in the cell membrane. Blockage of the sodium ion channel may lead to reduction the rate of depolarisation of the phase 0 which cause the slow AV conduction and increase in the refractory period. Lidocaine is associated with use dependence. Lidocaine is more likely to react on the depolarised damaged tissue.
The common side effects of lidocaine may include convulsion, drowsiness and tremor.
Disopyramide is class Ia anti arrhythmic agent. Disopyramide is mostly used in treating patient with ventricular dysrhythmia and supraventricular dysrhythmia.
Disopyramide is administered orally or via intravenous solution. Half of disopyramide will be metabolized in the hepatic system while half of disopyramide will remain unchanged and excreted by the kidney.
Disopyramide will block the opening of the Na+ channel and lead to inactivation of the sodium ion channel in the cell membrane. This will cause and increase in the effective refractory period with slow AV conduction due to reduction in the rate of phase 0 depolarisation. There will also slowness in the repolarisation of the action potential. The half life of disopyramide is approximately 5 hours to 10 hours.
Disopyramide may produce side effects such as dry mouth, constipation, blurred vision and urinary retention. Disopyramide may produce side effects associated with negative inotropic action. In certain cases, disopyramide may lead to the development of torsade de pointes.
Magnesium sulfate is an anti arrhythmic agents. Magnesium sulfate is useful in treating patient with torsade de pointes, digoxin toxicity which lead to ventricular dsyarrhythmia and after by pass surgery with hope in preventing patient developing ventricular arrhythmias or supra ventricular tachycardia.
Magnesium sulfate will be given intravenously. Magnesium sulfate will affect the permeability of the membrane for ion transport. This will cause the slowness of the AV node conduction and reduction in cardiac excitability after cardiac surgery mostly due to hypomagnesemia. Magnesium sulfate is also useful as an osmotic purgative.
Magnesium sulfate commonly associated with side effects such as weakness of the muscle.