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Novolin-R, Humulin-R Fast and short acting, used in emergencies (ketoacidosis), or for general SC maintenance ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Humalog faster acting than regular insulin but same duration, used in emergencies (ketoacidosis), or for general SC maintenance ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Novolog faster acting than regular insulin but same duration, used in emergencies (ketoacidosis), or for general SC maintenance ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Humulin-H, Novolin-H Intermediate acting Not suitable for emergencies because of solubility. Often doses in the morning and evening to provide 24 basal insulin level ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Lantus Long acting slow onset, not used in IV because of solubiltiy. Once daily injection provides 24 hour basal insulin level ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Levemir Long acting slow onset, not used in IV because of solubiltiy. Once daily injection provides 24 hour basal insulin level ADR: Severe Hypoglycemia, Immunologic reactions, Weight gain |
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Diabeta, Micronase Sulfonylurea MOA: stimulate the release of endogenous insulin, largely independent of blood glucose level. Uses: Type 2 ADR: hypoglycemia, weight gain, sulfonamide like drug allergy Interactions: Insulin, alcohol, sulfonamides, aspirin, chloramphenicol |
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Glucotrol Sulfonylurea MOA: stimulate the release of endogenous insulin, largely independent of blood glucose level. Uses: Type 2 ADR: hypoglycemia, weight gain, sulfonamide like drug allergy Interactions: Insulin, alcohol, sulfonamides, aspirin, chloramphenicol |
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Prandin Meglitinid Stimulates endogenous insulin release, in a more blood-glucose concentration dependent fashion than sulfonylureas ADR: Hypoglycemia, Weight gain |
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Starlix Prandin Meglitinid Stimulates endogenous insulin release, in a more blood-glucose concentration dependent fashion than sulfonylureas ADR: Hypoglycemia, Weight gain |
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Glucophage, Fortamet, Riomet Insulin sensitizing biguanide- antihyperglycemic agent Uses: Type 2 MOA: Improves sensitivity of peripheral tissues to insulin action, Decreases hepatic glucose output, decreases glucose absorption from intestine (primary mechanism), may also lower blood pressure and serum lipids. Elimination: Kidneys very quickly ADR: GI effects, lactic acidosis Interactions: increased blood levels of metformin with digoxin, morphine, quinidine, triamterene, and radio-contrast dye |
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Avandia Thiazolidinediones- antihyperglycemic agent Use: Type 2 MOA: Increased synthesis of new glucose transport molecules in insulin resistant tissues, thus correcting insulin resistance Elimination: Hepatic, feces/bile ADR: Vascular fluid retention and edema, Weight gain, not as good at decreasing risk for MI |
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Actos Thiazolidinediones- antihyperglycemic agent Use: Type 2 MOA: Increased synthesis of new glucose transport molecules in insulin resistant tissues, thus correcting insulin resistance Elimination: Hepatic, feces/bile ADR: Vascular fluid retention and edema, Weight gain |
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Precose alpha-glucosidase inhibitor MOA: inhibits enzyme responsible for complex carbohydrate digestion, smoothes out post prandial of glucose peaks Uses: Type 1 and 2 adjunctive therapy Elimination: Renal ADR: GI disturbances Precautions: diseases in which absorption is impaired |
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Byetta GLP-1 agonist MOA: enhances glucose-dependent insulin, inhibits glucagon secretion, slows gastric emptying, increases satiety Uses: monotherapy or adjunct for type 2 Elimination: renal ADR: hypoglycemia when combined with sulfonylureas, GI effects Interactions: decreased absorption by oral medications, anitbiotics and OCs taken 1 hour before byetta. |
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Januvia DPP-IV inhibitor MOA: prolongs effects of incretins that would be metabolized. incretins then increase glucose-dependent insulin release, decrease glucagon secretion Uses: monotherapy and adjunct of Type 2 ADR: hypoglycemia when combined with sulfonylureas |
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Symlin Amylin analog MOA: slows gastric emptying, inhibits glucagon secretion, increases satiety Uses: adjunct therapy type 1 and 2 Elimination: Renal ADR: Hypoglycemia; more risk when combined with insulin especially type 1, GI effects Interactions: decreased absorption of oral medications |
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MOA: Increase myocardial contraction, decrease heart rate Uses: CHF, digitalis may also help with tachycardia associated with CHF, may also relieve fluid retension in CHF patient by indirect diuresis. ADR: arrhythmias, Ventricular tachycardias and fibrillations, delirium, vision impairment |
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MOA: antigen binding fragments that bind to digoxin and are excreted in the urine Uses: Treatment of life-threating digitalis toxicity, or overdose characterized by severe hyperkalemia |
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MOA: Cardioselective B1 agonist Uses: treatment of severe refractory congestive heart failure ADR: tachycardia, increased oxygen demand on heart, Tolerance |
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MOA: Cardioselective B1 agonist, at certain doses can increase renal blood flow Uses: severe refractory congestive heart failure ADR: tachycardia, increased oxygen demand on heart, Tolerance |
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MOA: Increases cardiac contractility in systole, increases diastole filling Uses: Severe refractory CHF, or after tolerance develops to dopamine and dobutamine. ADR: Ischemic heart disease due to increased myocardial oxygen demand, thrombocytopenia |
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MOA: Increases cardiac contractility in systole, increases diastole filling Uses: Severe refractory CHF, or after tolerance develops to dopamine and dobutamine. ADR: Ischemic heart disease due to increased myocardial oxygen demand |
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MOA: ACE inhibitor Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, non-productive cough, Angioedema, fetal harm. |
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MOA: ACE inhibitor Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, non-productive cough, Angioedema, fetal harm. |
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MOA: ACE inhibitor Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, non-productive cough, Angioedema, fetal harm. |
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MOA: ACE inhibitor Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, non-productive cough, Angioedema, fetal harm. |
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MOA: Angiotensin II receptor-1 blocker Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, Angioedema, fetal harm. Better at preventing cardiac hypertrophy than ACE-I |
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MOA: Angiotensin II receptor-1 blocker Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, Angioedema, fetal harm. Better at preventing cardiac hypertrophy than ACE-I |
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MOA: Angiotensin II receptor-1 blocker Use: CHF, through decreased preload and afterload, thus increasing cardiac output, exercise capacity, and decreasing pulmonary congestion ADR: Hyperkalemia, excessive hypotension, Angioedema, fetal harm. Better at preventing cardiac hypertrophy than ACE-I |
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MOA: Thiazide Diuretic Use: reduction of extracellualr fluid, reduced preload, relieve pulmonary congestion, and reduce peripheral edema. Precautions: Use loop diuretics if GFR is < 30ml/min |
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MOA: Loop diuretics Use: reduction of extracellualr fluid, reduced preload, relieve pulmonary congestion, and reduce peripheral edema. |
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MOA: K-sparing diuretic Use: Given in conjunction with loop or thiazides to maintain K levels in patients with CHF, decreases digitalis toxicity, prevents myocardial stiffness due to high levels of aldosterone |
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MOA: K-sparing diuretic Use: Given in conjunction with loop or thiazides to maintain K levels in patients with CHF, decreases digitalis toxicity, prevents myocardial stiffness due to high levels of aldosterone |
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MOA: Direct Vasodilator Use: Primarily a preload reducer in CHF. Patients that benefit most from vasodilators are severe CHF refractory to other therapies, patients that have just experienced a acute MI who had prexisting chronic CHF |
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MOA: Direct Vasodilator Use: Primarily a preload reducer in CHF. Patients that benefit most from vasodilators are severe CHF refractory to other therapies, patients that have just experienced a acute MI who had prexisting chronic CHF |
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MOA: Direct Vasodilator Use: Primarily a afterload reducer in CHF. Patients that benefit most from vasodilators are severe CHF refractory to other therapies, patients that have just experienced a acute MI who had prexisting chronic CHF |
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MOA: Direct Vasodilator Use: Both a preload and afterload reducer in CHF. Patients that benefit most from vasodilators are severe CHF refractory to other therapies, patients that have just experienced a acute MI who had prexisting chronic CHF |
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Vasodilator + Diuretic MOA: decreases both arterial and venous smooth muscle tone by increased levels of cGMP, inhibits reabsorption of Na Patients that benefit most from vasodilators are severe CHF refractory to other therapies, patients that have just experienced a acute MI who had prexisting chronic CHF |
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MOA: Beta blocker Use: CHF treatment by preventing down regulation of beta adrenergic receptors due to constant high levels of catecholamines, preventing excessive tachycardia and arrhythmais, inhibits overexpression of RAAS |
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MOA: Beta blocker Use: CHF treatment by preventing down regulation of beta adrenergic receptors due to constant high levels of catecholamines, preventing excessive tachycardia and arrhythmais, inhibits overexpression of RAAS |
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MOA: Beta and Alpha blocker
Use: CHF treatment by preventing down regulation of beta adrenergic receptors due to constant high levels of catecholamines, preventing excessive tachycardia and arrhythmais, inhibits overexpression of RAAS |
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MOA: Class IA antiarrhythmic drug, inhibits Na and K channels Uses: Supraventricular and ventricular arrhythmais, reentry arrhythmias, ectopic atrial arrhythmias, maintain normal rhythm after cardioversion ADR: TdP, decreased BP, increases SA rate, Increased digoxin levels, alpha block, atropine like effects |
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MOA: Class IA antiarrhythmic drug, inhibits Na and K channels Uses: Supraventricular and ventricular arrhythmais, reentry arrhythmias, ectopic atrial arrhythmias, maintain normal rhythm after cardioversion ADR: Reversible lupus syndrome, CNS effects, GI, TdP, ventricular arrhythmias, alpha block, and atropine like effects Misc: Larger effect in fast acetylaters, NAPA eliminated via kidney |
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Class IB antiarrhythmic drug, rapidly interacts with Na channels to shorten phase 3 Uses: emergency treatment of ventricular arrhythmias due to ischemia, or abnormal automaticity, or reentry pulses, stops TdP ADR: convulsions, arrhythmias, confusion |
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MOA: Class IC antiarrhythmic drug, slowly interacts with Na channels to decrease slope of phase 0, also increases threshold Uses: abnormal automatcity, several refractory arrhythmias ADR: aggravation of CHF, arrhythmias, life-threatening ventricular tachycardia due to hyperkalemia |
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Class II antiarrhythmic drug MOA: Beta blocker, used to decreasing inward Ca currents thus depressing automaticity and phase 4 depolarization especially in nodes. Decreases conduction velocity in nodes, increases APD USES: arrhythmias caused by increased sympathetic neural activity and/or excess catecholamine presense, adrenergically driven arrhythmic death after MI ADR: bradycardia, inhibtion of RAAS |
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Class II antiarrhythmic drug MOA: Beta blocker, used to decreasing inward Ca currents thus depressing automaticity and phase 4 depolarization especially in nodes. Decreases conduction velocity in nodes, increases APD USES: arrhythmias caused by increased sympathetic neural activity and/or excess catecholamine presense ADR: bradycardia, inhibtion of RAAS MISC: reduced risk of broncospasm, partial agonist activity lowers risk of too much suppression |
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Class II antiarrhythmic drug MOA: Beta blocker, used to decreasing inward Ca currents thus depressing automaticity and phase 4 depolarization especially in nodes. Decreases conduction velocity in nodes, increases APD USES: arrhythmias caused by increased sympathetic neural activity and/or excess catecholamine presense, acute arrhythmias during surgery or emergency ADR: bradycardia, inhibtion of RAAS MISC: Very short acting used IV |
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Class III antiarrhythmic drug also has class I, II, IV activity as well MOA: inhibition of K channels, so prolongs phase 3, also decreases cell to cell coupling USES: severe refractory supraventricular and ventricular tachyarrhythmia, adjunctive therapy with ICD ADR: interstitial pulmonary fibrosis, hyper or hypothyroidism, blue skin discoloration |
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Pure class III antiarrhythmic drug MOA: inhibits K channels so prolongs APD, ERP
USES: Supraventricular arrhythmias such as atrial fibrillation
ADR: Ventricular TdP |
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Class III but also has Class II activity MOA: beta blocker and inhibtion of K channles thus prolonging APD, ERP USES: arrhythmias recurrences, adjunctive therapy for ICD patients ADR: bradycardia, inhibtion of RAAS |
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Class IV antiarrhythmic drug MOA: Calcium channel blocker, suppressing automaticity by decreasing slope phase 0 and 4, increase APD, ERP USES: reentrant supraventricular arrhythmias, stopping DAD in both supra and ventricular arrhythmias ADR: decreased Sinus Rate and A-V conduction, worsens WPW in atrial fibrillation |
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Class IV antiarrhythmic drug MOA: Calcium channel blocker, suppressing automaticity by decreasing slope phase 0 and 4, increase APD, ERP USES: reentrant supraventricular arrhythmias, stopping DAD in both supra and ventricular arrhythmias ADR: decreased Sinus Rate and A-V conduction, worsens WPW in atrial fibrillation |
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shortens APD and ERP in ventricular muscle cells, and decreases conduction in A-V and Purkinje fibers USES: atrial fibrillation and flutter ADR: arrhythmias, TdP MISC: use lidocaine to treat digoxin induced ventricular arrhythmias |
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decreases abnormal impulse formation in AV node thru hyperpolarization of membrane, increases ERP USES: acute paroxysmal supraventricular tachycardia ADR: flushing, SOB, chest pain MISC: 15 sec duration of action |
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MOA: Irreversibly inhibits COX 1 which prevents platelet aggregation Uses: prevention of MI, ischemia, arterial thrombosis ADR: GI bleed, operative bleeding, damage to fetus |
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Dipyridamole (antiplatelet) |
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MOA: inhibits platelet aggregation by blocking phophodiesterase which raises cAMP Uses: prevents thrombosis, used with coumadin ADR: hypotensin |
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Clopidrogel (antiplatelet) |
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MOA: irreversibly binds to platelet ADP receptor which prevents aggregation USES: MI, Stroke, Vascular death ADR: Bleeding |
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MOA: inactivates factor Xa and thrombin which inhibits thrombin formation USES: catheters, pregnancy, venous and arterial thromboembolic disease ADR: bleeding, thrombocytopenia, local capillary rupture |
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Enoxaparin (anticoagulant) |
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MOA: inactivates factor Xa and thrombin which inhibits thrombin formation USES: catheters, pregnancy, venous and arterial thromboembolic disease ADR: bleeding, thrombocytopenia, local capillary rupture |
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Protamine Sulfate (anticoagulant) |
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MOA: Binds to heparin and inactivates USES: Heparin overdose ADR: Anaphlylactic RXNs when patients are allergic to fish |
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MOA: Blocks vitamin K, an essential cofactor in the post-translational modification of clotting factors. Thus they are unable to bind to calcium. USES: Prevention clotting arteries, veins, prosthetic heart valves ADR: Hemorrhage, necrotic lesions, teratogenic |
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MOA: inhibits factor VIII, thrombin USES: anticoagulation in patients with heparin-induced thrombocytopenia ADR: Hypersensitivity, possibly teratogenic |
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Streptokinase (Thrombolytic) |
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MOA: activates fibrinolytic enzyme plasmin (indirectly) USES: venous and arterial thromboembolic disease, dissolving existing thrombus on shunts and catheters ADR: Allergic rxn if patient had previous strep infection, intercranial hemorrhage |
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serine protease that generates plasmin (directly) USES: venous and arterial thromboembolic disease, dissolving existing thrombus on shunts and catheters ADR: Bleeding, intercranial hemorrhage |
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MOA: activates fibrin-bound plasmin USES: venous and arterial thromboembolic disease, dissolving existing thrombus on shunts and catheters ADR: Bleeding, intercranial hemorrhage |
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MOA: Competitively inhibits plasmin activation USES: Reversal of Thrombolysis |
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MOA: Blood coagulation factor USES: Hemophilia A |
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MOA: Blood coagulation factor USES: Hemophilia B |
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MOA: Vitamin K, required for coagulation USES: Newborn hemorrhagic disease, coumadin overdose ADR: Anaphylaxis |
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