Term
| what is the mechanism of action of adenosine |
|
Definition
| increase in diastolic intracellular potassium of the AV node that causes marked hyperpolarization and conduction block and it reduces intracellular calcium |
|
|
Term
| what is the clinical application of adenosine |
|
Definition
|
|
Term
| what is the toxicities associated with adenosine |
|
Definition
| flushing, broncospasm, chest pain, and headache |
|
|
Term
| what class drug is amidarone |
|
Definition
|
|
Term
| what is the mechanism of action of amiodarone |
|
Definition
| strong intracellular potassium block that produces marked prolongation of action potential and refractory period. |
|
|
Term
| how does amiodarone show class I activity |
|
Definition
| by slowing the conduction velocity |
|
|
Term
| how does amiodarone show class II and IV activity |
|
Definition
| it confers additional antiarrhythmic activity |
|
|
Term
| what are the clinical applications of amiodarone |
|
Definition
| refractory arrhythmias, used in off label in may arrythmias |
|
|
Term
| what toxicities are associated with amiodarone |
|
Definition
| thyroid abnormalities, deposits in skin and cornea, pulmonary fibrosis, optic neuritis, torsades are rare |
|
|
Term
| what is the mechanism of action of metoprolol |
|
Definition
| it blocks beta one receptors; slow pacemaker activity |
|
|
Term
| what is the mechanism of action of sotalol |
|
Definition
| blocks intracellular potassium and beta adernoceptor blocker |
|
|
Term
| what are the clinical applications of sotalol |
|
Definition
| ventricular arrhythmias and atrial fibrillation |
|
|
Term
| how does sotalol blockage of beta adrenoceptors affect the heart |
|
Definition
| it decreases heart rate and AV conduction |
|
|
Term
| what toxicities are associated with sotalol |
|
Definition
| dose related torsades de pointes, cardiac depression |
|
|
Term
| what class does sotalol belong to |
|
Definition
|
|
Term
| what class of drugs does diltiazem belong to |
|
Definition
|
|
Term
| what is the clinical application of dilitiazem |
|
Definition
| rate control in atrial fibrillation |
|
|
Term
| what is the mechanism of action of verapamil |
|
Definition
state and use dependent intracellular calcium block which slows conduction of the AV node and pacemaker activity.
PR interval is prolonged |
|
|
Term
| what are the clinical applications of verapamil |
|
Definition
| AV nodal arrhythmias, especially prophylaxis, supraventricular tachycardias |
|
|
Term
| what are the toxicities associated with verapamil |
|
Definition
| cardiac depression, constipation, hypotension, AV block, dizziness, flushing |
|
|
Term
| what effect does verapamil have with beta blockers |
|
Definition
| additive AV block which causes the prolonged PR interval on EKG |
|
|
Term
| how does verapamil interacts with digoxin |
|
Definition
| it displaces digoxin from the tissue binding sites |
|
|
Term
| what class of drugs does quinidine belong to |
|
Definition
|
|
Term
| what is the toxicity associated with quinidine |
|
Definition
| cinchonism (tinnitus, headache, gastointestinal disturbances), cardiac depression and thrombocytopenia |
|
|
Term
| how does quinidine interact with digoxin |
|
Definition
| it reduces the clearance and may increase serum concentration of glycoside signficantly |
|
|
Term
| what receptors does quinidine block |
|
Definition
| muscarinic receptor and alpha receptor |
|
|
Term
| how does muscarinic blockage by quinidine effects the heart |
|
Definition
| it increases the heart rate |
|
|
Term
| how does alpha blockage by quinidine effect the heart |
|
Definition
| it could possible cause reflex tachycardia |
|
|
Term
| what are the clinical applications of quinidine |
|
Definition
| used in many arrythmias, atrial fibrillation, intial digitalization |
|
|
Term
| how does intial digitalization effect the heart |
|
Definition
|
|
Term
| how does quinidine effect EKG |
|
Definition
| causes a prolongation of QRS and QT interval |
|
|
Term
| how does hyperkalemia effect quinidine |
|
Definition
|
|
Term
| what class of drugs does procainamide |
|
Definition
|
|
Term
| what is the mechanism of action of procainamide |
|
Definition
| use ands state dependent block of intracellular sodium channels; some block of potassium channels. slowed conduction velocity and pacemaker activity; prolonged action potential during and refractory period |
|
|
Term
| what are the clinical applications of procainamide |
|
Definition
| atrial and ventricular arrhythmias, especially after myocardial infarction |
|
|
Term
| what are the toxicities associated with procainamide |
|
Definition
| increased arrhythmias, hypotension, lupus-like syndrome |
|
|
Term
| how does procainamide affect TPR |
|
Definition
|
|
Term
| what type of drug is carvedilol |
|
Definition
|
|
Term
| how does carvedilol affect mortality |
|
Definition
| it reduces it possible by decrease remodeling |
|
|
Term
| what is the clinical application of carvedilol |
|
Definition
| chronic heart failure: to slow progression, reduced mortality in moderate and severe heart failure |
|
|
Term
| what toxicities is associated with carvedilol |
|
Definition
| cardiac depression, bronchospasm, bradycardia, AV block, acute cardiac decompensation |
|
|
Term
| what is the mechanism of action of propranolol |
|
Definition
| it is an nonselective competitive beta receptor antagonist |
|
|
Term
| what is propanolol effect on cardiac output and renin secretion |
|
Definition
|
|
Term
| what are the clinical applications of propranolol |
|
Definition
| hypertension and ischemic heart disease, prophlaxis for angina |
|
|
Term
| what toxicities are associated with propanolol |
|
Definition
| bradycardia, worsened asthma, fatigue, vivid dream, cold hands, AV block, acute heart failure, sedation |
|
|
Term
| what is the mechanism of action of reserpine |
|
Definition
| blocks vesicular amine transporter in nonadrenergic nerves and depletes transmitter stores |
|
|
Term
| what are the effects of reserpine |
|
Definition
| it reduces all sympathetic effects especially cardiovascular and reduce blood pressure |
|
|
Term
| what are the clinical applications of reserpine |
|
Definition
| hypertension but it is rarely used |
|
|
Term
| what are the toxicities associated with reserpine |
|
Definition
| psychiatric depression, gastrointestinal disturbances |
|
|
Term
| what is the advantage of using losartan over enalapril |
|
Definition
| less incidence of dry cough and angiodemia |
|
|
Term
| what is the mechanism of action of losartan |
|
Definition
| blocks AT1 angiotensin receptor |
|
|
Term
| what are losartan effects |
|
Definition
| reduces angiotensin II levels, reduced vasoconstriction and aldosterone secrection |
|
|
Term
| what are the clinical applications of losartan |
|
Definition
| hypertenstion and heart failure |
|
|
Term
| what toxicities are associated with losartan |
|
Definition
| hyperkalemia, angioneurotic edema |
|
|
Term
| what is the mechanism of action of prazosin |
|
Definition
| selectively blocks alpha one adrenoreceptors |
|
|
Term
| what are the effects of prazosin |
|
Definition
| prevent sympathetic vasoconstriction, reduce prostatic smooth muscle tone |
|
|
Term
| what are the clinical applications of prazosin |
|
Definition
| hypertension, benign prostate hyperplasia |
|
|
Term
| what toxicity is associated with prazosin |
|
Definition
|
|
Term
| what is the mechanism of action of enalapril |
|
Definition
| reduces levels of angiotensin II by effectively inhibiting ACE |
|
|
Term
| what are the clinical applications of enalapril |
|
Definition
| hypertension and congestive heart failure |
|
|
Term
| what are the toxicities associated with enalapril |
|
Definition
| renal impairment, cough, angiodema, hyperkalemia, teratogenic |
|
|
Term
| what is the mechanism of action of hydralazine |
|
Definition
| causes nitric oxide release |
|
|
Term
| what are the effects of hydralazine |
|
Definition
| vasodilation, reduce vascular resistance, arterioles more sensitive than veins, reflex tachycardia, reduces blood pressure and afterload, increase cardiac output |
|
|
Term
| what are the clinical applications of hydralazine |
|
Definition
|
|
Term
| what toxicities are associated with hydralazine |
|
Definition
| angina, tachycardia, lupus like syndrome, fluid retention |
|
|
Term
| when given alone this antihypertensive drug produces reflex tachycardia and renin release |
|
Definition
| direct acting vasodilators |
|
|
Term
| what is the mechanism of action of digoxin |
|
Definition
| Na/K-ATPase inhibition results in reduced Calcium expulsion and increased Calcium stored in the sarcoplasmic reticulum |
|
|
Term
| what effects does digoxin have on the heart |
|
Definition
| increases cardiac contractility, cardiac parasympathetic effect- slowed sinus heart rate, slowed AV conduction |
|
|
Term
| what are the clinical applications of digoxin |
|
Definition
| chronic sympathetic heart failure, rapid ventricular rate in atrial fibrillation, |
|
|
Term
| what toxicities are associated with digoxin |
|
Definition
| nausea, vomiting, diarrhea, cardiac arrhythmias |
|
|
Term
| what is the DOC for ventricular tachycardias in the ER |
|
Definition
|
|
Term
| what is the mechanism of action of carvediol |
|
Definition
| competitively blocks beta one receptors |
|
|
Term
| what effects does carvediol have on the heart |
|
Definition
| slows heart rate, reduces blood pressure |
|
|
Term
| what type of drug cause postural hypotension |
|
Definition
|
|
Term
| who does hydralazine interact with nitrates |
|
Definition
|
|
Term
| what is the mechanism of action of nitroprusside |
|
Definition
| release of NO spontaneously, activates guanyly cyclase |
|
|
Term
| what are the effects of nitroprusside |
|
Definition
| marked vasodilation, reduces preload and afterload |
|
|
Term
| what are the clinical applications of nitroprusside |
|
Definition
| acute cardiac decompensation, hypertensive emergencies (malignant hypertension) |
|
|
Term
| how do you adminster nitroprusside |
|
Definition
|
|
Term
| what are the toxicities associated with nitroprusside |
|
Definition
| excessive hypertension, thiocynate and cyanide toxicity |
|
|
Term
| how does nitroprusside interact with other vasodilators |
|
Definition
|
|
Term
| class IA antiarrythmics increase |
|
Definition
| QT interval, effective refractory period, repolarization, action potential duration |
|
|
Term
| what is dobutamine mechanism of action |
|
Definition
| beta one selective agonist, increases cAMP synthesis |
|
|
Term
| what is dobutamine effects |
|
Definition
| increase cardiac contractility, output |
|
|
Term
| what are the clinical applications of dopbutamine |
|
Definition
| acute decompensated heart failure, intermittent therapy in chronic failure reduces symptoms |
|
|
Term
| what toxicities are associated with dobutamine |
|
Definition
|
|
Term
| how does dobutamine interact with other sympathominetics |
|
Definition
|
|
Term
| what is the most effective drug in converting paroxysmal tachycardia into normal sinus rhythm |
|
Definition
|
|
Term
| what is the mechanims of action of dopamine |
|
Definition
| dopamine receptor agonist, higher doses activates beta and alpha adrenoceptor |
|
|
Term
| what are the effects of dopamine |
|
Definition
| increase renal blood flow, higher doses increase cardiac force and blood pressure |
|
|
Term
| what are the clinical applications of dopamine |
|
Definition
| acute decompensated heart failure, shock |
|
|
Term
| what toxicities are associated with dopamine |
|
Definition
|
|
Term
| what is the mechanism of action of inamrinone and milrinone |
|
Definition
| phosphodiesterase type 3 inhibitors, decreases cAMP breakdown |
|
|
Term
| what is diltiazem the equivalent to |
|
Definition
|
|
Term
| what is metoprolol role in heart failure |
|
Definition
|
|
Term
| what effects of inamrinone and milrinone cause |
|
Definition
| vasodilators; low peripheral vascular resistance, also increases cardiac output |
|
|
Term
| what are the clinical applications of inamrinone and milrinone |
|
Definition
| acute decompenstate heart failure, increase mortality in CHF |
|
|
Term
| what toxicities are associated with inamrinone and milrinone |
|
Definition
|
|
Term
| what is the mechanism of action of nesiritide |
|
Definition
| activates BNP receptors, increases GMP |
|
|
Term
| what effects does nesiritide have |
|
Definition
| vasodilation and diuresis |
|
|
Term
| what is the clinical application of nesiritide |
|
Definition
| acute decompensated failure |
|
|
Term
| what toxicities are associated with nesiritide |
|
Definition
| renal damage, hypotension, and it may increase mortality |
|
|
Term
| what are the overall effects of propranolol |
|
Definition
| decrease heart reate, cardiac output, blood pressure, and myocardial oxygen demand |
|
|
Term
| how does propranolol interact with cardiac depressants |
|
Definition
| it give an additive effect |
|
|
Term
| what is the mechanism of action of nifedipine |
|
Definition
| blocks vascular L type calcium channels more than cardiac channels |
|
|
Term
| what are the clinical applications of nifedipine |
|
Definition
| prophylaxis of angina and hypertension |
|
|
Term
| what are the effects of nifedipine |
|
Definition
| reduced vascular resistance, cardiac rate and force, decrease in oxygen damage |
|
|
Term
| which drug has the stronger cardiac effect verapamil or nifedipine |
|
Definition
|
|
Term
| what is the mechanism of action of captopril |
|
Definition
| inhibit angiotensin-converting enzyme |
|
|
Term
| what effect does captopril have |
|
Definition
| reduces angiotensin II levels, reduce vasoconstriction and aldosterone secretion, increase bradykinin |
|
|
Term
| what are the clinical applications of captopril |
|
Definition
| hypertension, heart failure, diabetes |
|
|
Term
| what are the toxicities associated with captopril |
|
Definition
| angiodema, hyperkalemia, renal impairment, and teratogenic |
|
|
Term
| what is the mechanism of action of clonidine |
|
Definition
| activates alpha two andrenoceptors |
|
|
Term
| what effects do clonidine produce |
|
Definition
| reduce central sympathetic outflow, reduce norepinephrine release from nonadrenergic nerve endings |
|
|
Term
| what are the clinical applications of clonidine |
|
Definition
| hypertension, drug abuse withdrawal |
|
|
Term
| what are the toxicities associated with clonidine |
|
Definition
| sedation, methyldopa hemolytic anemia |
|
|
Term
| what is the mechanism of action of nitroglycerin |
|
Definition
| releases nitric oxide in smooth muscle, which activates guanylyl cyclase and increases cGMP |
|
|
Term
| what effects do nitroglycerin have |
|
Definition
| smooth muscle relaxation, especially in vessels, other smooth muscles is relaxed but not markedly, vasodilation decreases venous return and heart size, may increase coronary flow in some areas and in variant angina |
|
|
Term
| what are the clinical applications of nitroglycerin |
|
Definition
|
|
Term
| when would you use oral nitroglycerin |
|
Definition
| for acute episodes of angina |
|
|
Term
| when do you use the oral and transdermal forms of nitroglycerin |
|
Definition
| prophylaxis treatment of angina |
|
|
Term
| when do you use the IV form of nitroglycerin |
|
Definition
|
|
Term
| what toxicities are associated with nitroglycerin |
|
Definition
| orthostatic hypotension, tachycardia, headaches |
|
|
Term
| how does nitroglycerin interact with sildenafil (PDE-5 inhibitors) |
|
Definition
|
|
Term
| what is the mechanism of action of cholestyramine |
|
Definition
| binds to bile acids in gut, prevents reabsorption, increases cholesterol catabolism, upregulates LDL receptors |
|
|
Term
| what effect does cholestyramine have |
|
Definition
|
|
Term
| what are the clinical applications of cholestyramine |
|
Definition
| elevated LDL, digitalis toxicity, pruritus |
|
|
Term
| what toxicities are associated with cholestyramine |
|
Definition
| constipation, bloating, interfers with absorption of some drugs and vitamins |
|
|
Term
| what is the mechanism of action of gemfibrozil and fenofibrate |
|
Definition
| peroxisome proliferator- activated receptor alpha agonist |
|
|
Term
| what effects does gemfibrozil and fenofibrate have |
|
Definition
| decreases secretion of VLDL, increase lipoprotein lipase activity, increase HDL |
|
|
Term
| what are the clinical applications of gemfibrozil and fenofibrate |
|
Definition
| hyperglyceridemia, low LDL |
|
|
Term
| what are the toxicities of fenofibrate and gemfibrozil |
|
Definition
| myopathy, hepatic dysfunction |
|
|
Term
| what is the mechanism of action of -statin drugs |
|
Definition
| inhibit HMG-CoA reductase |
|
|
Term
| which statin drug is the most effictive out of the three atorvastatin, lovastatin, pravastatin |
|
Definition
|
|
Term
| what effects does statin drugs have |
|
Definition
| reduce cholesterol synthesis and up regulate low density lipoprotein receptors on hepatocytes, modest reduction in triglycerides |
|
|
Term
| what are the clinical applications of statin drugs |
|
Definition
| atherosclerotic vascular disease (primary and secondary prevention) acute coronary syndromes |
|
|
Term
| what are the toxicities of statin drugs |
|
Definition
| myopathy and hepatic dysfunction |
|
|
Term
| what is the mechanism of action of orlistat |
|
Definition
| reduces absorption of fats since triglycerides not split |
|
|
Term
| what toxicities are associated with orlistat |
|
Definition
| flatulence, stertorrhea, fecal incontinence |
|
|
Term
| what are the effects of theophylline |
|
Definition
| bronchodilation, cardiac stimulation, increased skeletal muscle strength |
|
|
Term
| what does demeclocyline inhibits |
|
Definition
| the action of antidiruetic hormone in renal tubule |
|
|
Term
| what does desmopressin acetate increase |
|
Definition
|
|
Term
| what is the mechanism of action of amiloride |
|
Definition
| blocks epithelial sodium channels in collecting tubules |
|
|
Term
| what are the effects of amiloride |
|
Definition
| reduced sodium retention and K wasting, increases lithium clearance |
|
|
Term
| what are the clinical applications of amiloride |
|
Definition
| hypokalemia from other diuretics, reduces lithium induced polyuria |
|
|
Term
| what toxicities are associated with amiloride |
|
Definition
| hyperkalemic metabolic acidosis |
|
|
Term
| what is unique about chlorthalidone |
|
Definition
| it has a long half life due to binding to rbc |
|
|
Term
| which of the two drugs are more potent amiloride or triamterene |
|
Definition
|
|
Term
| which of the two drugs are more toxic amiloride or triamterene |
|
Definition
|
|
