Cardio Pharm Flashcards
Direct acting arteriole dilator (increases cGMP). Decreases TPR (afterload).
Hydralazine mechanism of action?
Sever hypertension, CHF. First line HTN tx in pregnancy (with methyldopa).
Hydralazine uses?
Drug-induced SLE in slow acetylators, reflex tachycardia, headache, angina.
Hydralazine side effects?
Inhibits L-type voltage gated calcium channels. Vasodilator (arteiroles). Low heart affinity.
Nifedipine, amlodipine mechanism of action?
Prinzmetal’s angina, Raynaud’s phenomenon, Berry aneurysms, hypertension.
Nifedipine, amlodipine uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation. Reflex tachycardia, gingival hyperplasia.
Nifedipine, amlodipine side effects?
Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
Verapamil mechanism of action?
Hypertension, angina, arrhythmias (SVT).
Verapamil uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, heavy constipation. Gingival hyperplasia.«_space;Increases toxicity of digoxin by displacing from tissue-binding sites.»
Verapamil side effects?
Inhibits L-type voltage gated calcium channels. Decreases contractility, AV conduction velocity. Low artery affinity. Class IV antiarrhythmics (increase ERP, PR interval).
Diltiazem mechanism of action?
Hypertension, angina, arrhythmias (SVT).
Diltiazem uses?
Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation.
Diltiazem side effects?
Vasodilation and venodilation (increases cGMP via direct release of nitrous oxide).
Nitroprusside mechanism of action?
Malignant hypertension.
Nitroprusside uses?
Limit treatment to 24-36 hours. Cyanide toxicity (altered mental status, lactic acidosis). Treat toxicity with nitrites, hydroxocobalamin, and sodium thiosulfate (sulfur).
Nitroprusside side effects?
D1 receptor agonist; relaxes renal vascular smooth muscle. Artery vasodilator.
Fenoldopam mechanism of action?
Malignant hypertension. Increases renal perfusion.
Fenoldopam uses?
Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
Diazoxide mechanism of action?
Malignant hypertension. Insulinomas.
Diazoxide uses?
Hyperglycemia (reduces insulin release).
Diazoxide side effects?
Direct acting arteriole vasoldiator. ATP dependent K+ channel opener; hyperpolarizes and relaxes vascular smooth muscle.
Minoxidil mechanism of action?
Sever hypertension (IV), baldness (topical).
Minoxidil uses?
{{Hypertrichosis, pericardial effusion}}, reflex tachycardia, angina, salt retention. {{Hyperglycemia (reduces insulin release).}}
Minoxidil side effects?
Venodilation (increases cGMP, inducing dephosphorylation of myosin light chain). Has largest effect on large veins. Production of NO requires cystine on glutathione (GSH).
Nitroglycerin, isorbide dinitrate mechanism of action?
Effort angina, pulmonary edema.
Nitroglycerin, isorbide dinitrate uses?
Reflex tachycardia, orthostatic hypotension, HEADACHE*. Rapid tolerance (tachyphylaxis due to depletion of GSH). Cardiotoxicity when used with sildenafil (massive drop in TPR causes reflex tachycardia and possible MI).
Nitroglycerin, isorbide dinitrate side effects?
Inhibits HMG-CoA reductase (decrease mevalonate/cholesterol production). Improves survival by inhibiting inflammation.
Lovastatin (-statin) mechanism of action?
Decreases VLDL (TGs), LDL (cholesterol). Increases HDL. Primarily used to lower CHOLESTEROL.
Lovastatin (-statin) uses?
Hepatotoxicity, myositis, rhabdomyolysis (especially with gemfibrozil).
Lovastatin (-statin) side effects?
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.
Niacin mechanism of action?
Increases HDL, lowers LDL (cholesterol). Greatly lowers VLDL (triglycerides). Primarily used to lower TRIGLYCERIDES.
Niacin uses?
{{Flushing (tx with aspirin)}}. Hyperglycemia (acanthosis nigricans). {{Hyperuricemia }}(exacerbates gout).
Niacin side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Cholestyramine mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Cholestyramine uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Cholestyramine side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Cholestipol mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Cholestipol uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Cholestipol side effects?
Prevents intestinal reabsorption of bile acids; liver must consume cholesterol to make replenish lost bile.
Colesevelam mechanism of action?
Decreases LDL (cholesterol); mild increase of VLDL and HDL.
Colesevelam uses?
Patients hate it; tastes horrible and causes GI discomfort. Affects absorption of ADEK vitamins and other medications (digoxin, warfarin). Gallstones. Contraindicate with hypertriglyceridemia.
Colesevelam side effects?
Prevent cholesterol reabsorption at small intestine brush border.
Ezetimibe mechanism of action?
Lowers LDL (cholesterol).
Ezetimibe uses?
Hepatotoxicity (elevated AST, ALT).
Ezetimibe side effects?
Induces LPL (via PPAR-alpha) leading to increased TG clearance).
Gemfibrozil mechanism of action?
Hypertryglyceridemia (increases VLDL uptake).
Gemfibrozil uses?
Myositis, hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase), rhabdomyolysis.
Gemfibrozil side effects?
Induces LPL (via PPAR-alpha) leading to increased TG clearance).
Clofibrate, bezafibrate, fenofibrate (-fibrate) mechanism of action?
Hypertryglyceridemia (increases VLDL uptake).
Clofibrate, bezafibrate, fenofibrate (-fibrate) uses?
Hepatotoxicity, gallstones (inhibits 7-alpha hydroxylase). No rhabdomyolysis.
Clofibrate, bezafibrate, fenofibrate (-fibrate) side effects?
Inhibits Na/K-ATPase leading to increase intracellular sodium (hypersensitive neurons) and calcium (increased contractility). Predominately stimulates vagal tone (decrease AV conductivity, decrease HR).
Digoxin mechanism of action?
CHF, atrial fibrillation, SVT.
Digoxin uses?
{{Cholinergic effects (nausea, vomiting, diarrhea, blurry yellow vision)}}. Increases PR interval, decrease QT interval, scooping, {{T-wave inversion}}, ventricular arrhythmia. Causes hyperkalemia. Increased toxicity with hypokalemia, renal failure, and quinidine/verapamil. In overdose first treat the hyperkalemia, then use digoxin-Fab, then magnesium.
Digoxin side effects?
Recombinant B-type natriuertic peptide. {{Vasodilates}} (increases cGMP).
Nesiritide mechanism of action?
Acute decompensated heart failure.
Nesiritide uses?
Hypotension.
Nesiritide side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Quinidine mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Quinidine uses?
Increases QT interval {{(torsades)}}. Cinchonism - {{headache, tinnitus, visual disturbances,}} constipation or diarrhea). Increased heart rate and hypotension (muscarinic, alpha antagonist). Increased toxicity with hyperkalemia. Increases toxicity of digoxin by displacing from tissue-binding sites.
Quinidine side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Procainamide mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Procainamide uses?
{{Thrombocyptopenia, torsades de pointes }}(increased QT), drug induced SLE (hematotoxic). Increased toxicity with hyperkalemia.
Procainamide side effects?
Class Ia antiarrhythmic. Inhibits OPEN voltage gated sodium channels. Inhibits voltaged gated potassium channels (increases QT interval, AP duration, and ERP).
Disopyramide mechanism of action?
Atrial and ventricular arrhythmias, especially SVT and ventricular tachycardia.
Disopyramide uses?
{{Thrombocyptopenia, torsades de pointes}} (increased QT). Increased toxicity with hyperkalemia.
Disopyramide side effects?
Class Ib antiarrhythmic. Inhibits {{INACTIVE}} voltage gated sodium channels {{(targets ISCHEMIC tissue)}}. Activates voltage gated potassium channels (shortens AP, ERP).
Phenytoin mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Phenytoin uses?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Lidocaine mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Lidocaine uses?
CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
Lidocaine side effects?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Mexiletine mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Mexiletine uses?
CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
Mexiletine side effects?
Class Ib antiarrhythmic. Inhibits INACTIVE voltage gated sodium channels (targets ISCHEMIC tissue). Shortens AP, ERP.
Tocainide mechanism of action?
Acute ventricular arrhytmias (post-MI) and digitalis-induced arrhythmias.
Tocainide uses?
CNS stimulation/depression, cardiovascular depression. Increased toxicitiy with hyperkalemia.
Tocainide side effects?
Class Ic antiarrhythmic Inhibits both open and closed voltage gated sodium channels. No effect on AP, ERP.
Flecanide mechanism of action?
Ventricular tachycardia, SVT.
Flecanide uses?
Proarrhythmic; {{contraindicated post MI}}. Significantly prolongs refractory period in AV node. Increased toxicitiy with hyperkalemia.
Flecanide side effects?
Class Ic antiarrhythmic Inhibits both open and closed voltage gated sodium channels. No effect on AP, ERP.
Propafenone mechanism of action?
Ventricular tachycardia, SVT.
Propafenone uses?
Proarrhythmic; contraindicated post MI. Significantly prolongs refractory period in AV node. Increased toxicitiy with hyperkalemia.
Propafenone side effects?
Non-selective beta adrenergic antagonist. Increases PR interval, decreases slope of phase 4 in AV/SA node. Decreases renin release.
Propranolol mechanism of action?
Ventricular tachycardia, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. {{Antihypertensive post MI/angina.}}
Propranolol uses?
Treat overdose with glucagon. {{Impotence, exacerbation of asthma, CNS}}, cardiovascular effects (bradycardia, AV block, CHF), {{CNS effects (depression, sleep alterations}}). May mask signs of hypoglycemia.
Propranolol side effects?
Beta-1 selective adrenergic antagonist. Very short acting. Increases PR interval, decreases slope of phase 4 in AV/SA node.
Esmolol mechanism of action?
Ventricular tachycardia, {{ACUTE SVT}}, slowing ventricular rate during atrial fibrillation and atrial flutter. Antihypertensive post MI/angina.
Esmolol uses?
Treat overdose with glucagon.{{ Impotence, NO AIRWAY, CNS}} cardiovascular effects (bradycardia, AV block, CHF), CNS effects (depression, sleep alterations). May mask signs of hypoglycemia.
Esmolol side effects?
Beta-1 selective adrenergic antagonist. Increases PR interval, decreases slope of phase 4 in SA/AV node. Decreases renin release.
Metoprolol, atenolol, timolol, acebutolol mechanism of action?
Ventricular tachycardia, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. Antihypertensive post MI/angina.
Metoprolol, atenolol, timolol, acebutolol uses?
Treat overdose with glucagon. {{Impotence, NO airway, CNS,}} cardiovascular effects (bradycardia, AV block, CHF), CNS effects (depression, sleep alterations). May mask signs of hypoglycemia. Dyslipidemia (increase LDLs and TGs).
Metoprolol, atenolol, timolol, acebutolol side effects?
Beta-1 adrenergic antagonist. Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
Sotalol mechanism of action?
Torsades de pointes.
Sotalol side effects?
Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
Ibutilide mechanism of action?
Torsades de pointes.
Ibutilide side effects?
Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
Bretylium mechanism of action?
Not associated with torsades de pointes.
Bretylium side effects?
Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
Amiodarone mechanism of action?
Any arrhythmias. Extremely long half life (80 days).
Amiodarone uses?
{{Doesn’t increase risk of torsades de pointes.}} {{Pulmonary fibrosis}}, hepatotoxicity, {{hypothyroidism/hyperthyroidism, corneal deposits, blue/gray skin deposits}} resulting in photodermatitis, neurological effects, constipation, bradycardia/heart block/CHF.
Amiodarone side effects?
Blocks voltage-gated potassium channels. Increases AP, ERP. Increases QT interval.
Dofetilide mechanism of action?
Torsades de pointes.
Dofetilide side effects?
Increaes potassium efflux, hyperpolarizing the cell. Causes G(i)-coupled decrease in cAMP. Decreases SA/AV nodal activity.
Adenosine mechanism of action?
Drug of choice for paroxysmal SVT.
Adenosine uses?
Flushing, hypotension, chest pain, bronchospasm/dyspnea. Effects blocked by theophylline/caffeine.
Adenosine side effects?
Decreases neuron excitability.
Magnesium mechanism of action?
Digoxin toxicity, torsades de pointes.
Magnesium uses?
Inhibits ACE, reducing levels of A-II and preventing inactivation of bradykinin (vasodilation). Increased renin release.
Captopril (-pril) mechanism of action?
Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
Captopril (-pril) uses?
{{Cough, angioedema,}} proteinuria, {{taste changes,}} hypotension, rash, increased renin, hyperkalemia. {{Contraindicate with pregnancy (fetal renal damage)}} and bilateral renal stenosis (causes decrease in GFR by preventing constriction of efferent arterioles leading to increased creatinine).
Captopril (-pril) side effects?
Angiotensin II receptor type 1 antagonist.
Losartan (-sartan) mechanism of action?
Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
Losartan (-sartan) uses?
{{NO COUGH OR ANGIOEDEMA}}. Proteinuria, {{taste changes, hypotension, rash, increased renin, hyperkalemia***}}. {{Contraindicate with pregnancy}} (fetal renal damage) and bilateral renal stenosis (causes decrease in GFR by preventing constriction of efferent arterioles leading to increased creatinine).
Losartan (-sartan) side effects?
Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
Furosemide, torsemide mechanism of action?
Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.
Furosemide, torsemide uses?
{{Ototoxicity, hypokalemic metabolic alkalosis}}, dehydration,{{ sulfa allergy}}, interstitial nephritis, {{hyperuricemia (gout)}}, hypocalcemia/hypomagnesemia.
Furosemide, torsemide side effects?
Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
Ethacrynic acid mechanism of action?
Diuresis in patients allergic to sulfa drugs.
Ethacrynic acid uses?
{{NO SULFA ALLERGY, can be used with gout.}} Otoxoticity (more toxic than furosemide), hypokalemic metabolic alkalosis, dehydration, nephritis, hypocalcemia/hypomagnesemia.
Ethacrynic acid side effects?
{{Inhibits NaCl reabsorption in the early distal tubule. Opens ATP-dependent K+ channel}} (beta islet cells, arterioles).
Hydrochlorothiazide, indapamide, metolazone mechanism of action?
Hypertension, CHF, idiopathic hypercalcinuria (nephrolithiasis), nephrogenic diabetes insipidus. DON’T USE IN PATIENTS WITH DIABETES MELLITUS TYPE 2.
Hydrochlorothiazide, indapamide, metolazone uses?
{{HYPOkalemic metabolic alkalosis, HYPOnatremia,}} {{HYPERglycemia (inhibits insulin release), HYPERlipidemia (LDL, cholesterol), HYPERuricemia, and HYPERcalcemia. Sulfa allergy.}}
Hydrochlorothiazide, indapamide, metolazone side effects?
Aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
Spironlactone mechanism of action?
Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling. Anti-androgen (for acne, hirsutism).
Spironlactone uses?
{{Hyperkalemic metabolic acidosis. Gynectomastia (anti-androgen effects).}}
Spironlactone side effects?
Selective aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
Eplerenone mechanism of action?
Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling.
Eplerenone uses?
{{Hyperkalemic metabolic acidosis. No anti-androgen effects.}}
Eplerenone side effects?
{{Block sodium channels in the cortical collecting tubule}}. Potassium sparing diuretic.
Triamterene mechanism of action?
Reverses hypokalemia, CHF, {{lithium-induced nephrogenic diabetes insipidus.}}
Triamterene uses?
Hyperkalemic metabolic acidosis. No gynecomastia
Triamterene side effects?
{{Block sodium channels in the cortical collecting tubule}}. Potassium sparing diuretic.
Amiloride mechanism of action?
Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.
Amiloride uses?
Hyperkalemic metabolic acidosis.
Amiloride side effects?
Direct renin inhibitor.
Aliskiren mechanism of action?
Hypertension with CHF or diabetic renal disease. Prevents unfavorable heart remodeling as a result of chronic hypertension (increases survival).
Aliskiren uses?
Hyperkalemia. {{No cough or edema. Contraindicate with renal artery stenosis.{{
Aliskiren side effects?
Digoxin toxicity
anti-digoxin Fab fragments uses?
Inhibits platelet aggregation by irreversibly {{blocking ADP receptors}}. Inhibits fibrinogen by binding and {{preventing glycoprotein IIb/IIIa expression.}}
Clopidogrel, parsugrel, ticagrelor mechanism of action?
Acute coronary syndrome; coronary stenting. Decreased incidence or recurrence of thrombotic stroke.
Clopidogrel, parsugrel, ticagrelor uses?
Neutropenia, acute thrombocytopenic purpura.
Clopidogrel, parsugrel, ticagrelor side effects?
Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen by binding and preventing glycoprotein Iib/IIIa expression.
Ticlopidine mechanism of action?
Acute coronary syndrome; coronary stenting. Decreased incidence or recurrence of thrombotic stroke.
Ticlopidine uses?
Neutropenia, acute thrombocytopenic purpura.
Ticlopidine side effects?
{{Phosphodiesterase III inhibito}}r; increases cAMP in platelets thus inhibiting platelet aggregation. Vasodilator.
Cilostazol mechanism of action?
Peripheral artery disease. Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.
Cilostazol uses?
Nausea, headache, facial flushing, hypotension, abdominal pain.
Cilostazol side effects?
Phosphodiesterase III inhibitor; increases cAMP in platelets thus inhibiting platelet aggregation. Vasodilator. Thromboxane synthase inhibitor.
Dipyridamole mechanism of action?
Peripheral artery disease. Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.
Dipyridamole uses?
Nausea, headache, facial flushing, hypotension, abdominal pain.
Dipyridamole side effects?
Monoclonal antibody that binds to the{{ glycoprotein receptor IIb/IIIa }}on activated platelets, preventing aggregation.
Abciximab mechanism of action?
Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
Abciximab uses?
Bleeding, thrombocytopenia.
Abciximab side effects?
{{Glycoprotein receptor IIb/IIIa antagonist}} on activated platelets, preventing aggregation.
Eptifibatide mechanism of action?
Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
Eptifibatide uses?
Bleeding, thrombocytopenia.
Eptifibatide side effects?
Glycoprotein receptor IIb/IIIa antagonist on activated platelets, preventing aggregation.
Tirofiban mechanism of action?
Acute coronary syndrome, percutaneous transulminal coronary angioplasty.
Tirofiban uses?
Bleeding, thrombocytopenia.
Tirofiban side effects?
{{Converts both clot bound and free blood plasminogen to plasmin, which cleaves thrombin and fibrin clots. CLOT BUSTER!!}}Increase PT, PTT, but no effect on platelet count.
Streptokinase, urokinase mechanism of action?
{{Early MI, DVT. NEVER USE IN STROKE.}}
Streptokinase, urokinase uses?
{{Hypersensitivity (immunogenic)}}. Bleeding. {{Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery}}, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid.
Streptokinase, urokinase side effects?
Tissue plasminogen activator (tPA). CLOT BUSTER! Clot specific. Directly or indirectly {{aid conversion of plasminogen to plasmin,}} which cleaves thrombin and fibrin clots. Increase PT, PTT, but no effect on platelet count.
Alteplase mechanism of action?
Early MI, early ischemic stroke.
Alteplase uses?
No hypersensitivity. Bleeding. {{Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. }}Treat toxicity with aminocaproic acid.
Alteplase side effects?
{{aid conversion of plasminogen to plasmin…CLOT BUSTER}}, which cleaves thrombin and fibrin clots. Increase PT, PTT, but no effect on platelet count.
APSAC (anistreplase) mechanism of action?
Early MI, early ischemic stroke.
APSAC (anistreplase) uses?
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid.
APSAC (anistreplase) side effects?
Positively charged molecule that binds negatively charged heparin.
Protamine sulfate mechanism of action?
Rapid antidote to heparin toxicity.
Protamine sulfate uses?
{{Low-molecular-weight heparin. Acts more on factor Xa}}. Better bioavailability, longer half life.
Enoxaparin, fondaparinux mechanism of action?
Not easily reversible. Doesn’t need lab monitoring (doesn’t affect PTT). Less likely to cause HIT.
Enoxaparin, fondaparinux side effects?
Cofactor for the {{activaiton of antithrombin III,}}{{ decreases thrombin (IIa), decreases factor Xa}}. Also IXa and XIIa. Short half life. Works in blood. Rapid onset. Works in vitro.
Heparin mechanism of action?
Immediate anticoagulation for pulmonary embolism, stroke, acute coronary syndrome, MI, DVT. May be used during pregnancy (unlike warfarin). Water soluble (must give IV, short half life).
Heparin uses?
{{Must monitor PTT}}. Bleeding, heparin-induced thrombocytopenia, osteoporosis, drug-drug interactions. Treat overdose with protamine sulfate.
Heparin side effects?
Interferes with vitamin K synthesis (gamma-carboxylation), thus decreases factors II, VII, IX, X, protein C and S. Works on the liver. Slow onset. Only works in vivo.
Warfarin (coumadin) mechanism of action?
Chronnic anticoagulation therpay (DVT, post STEMI). Don’t use in pregnant women. Lipid soluble (give orally, long half life).
Warfarin (coumadin) uses?
{{Must monitor PT/INR.}} Bleeding, {{teratogenic (bone disruption}}), skin/tissue necrosis (with protein C and S deficiency), drug-drug interactions. Treat overdose with fresh frozen plasma (for immediate recovery) or vitamin K (gradual). Increased toxiicity with sulfonamides, sulfonylureas, NSAIDs. Decreased absorption with cholestyramine.
Warfarin (coumadin) side effects?
Direct thrombin inhibitor; hirudin derivative.
Lepirudin, bivalirudin mechanism of action?
Used as an alternative to heparin for anticoagulating in patients with heparin-induced thrombocytopenia. Used in unstable angina prior to percutaneous fibrinolysis.
Lepirudin, bivalirudin uses?
Doesn’t cause HIT.
Lepirudin, bivalirudin side effects?
Epsilon-aminocaproic acid
EACA mechanism of action?
Treats thrombolytic (alteplase) toxicity.
EACA uses?
Direct thrombin inhibitor; (blocks factor IIa). Prevents fibrin formation.
Argatroban, dabigatran mechanism of action?
Doesn’t cause HIT.
Argatroban, dabigatran side effects?
Treats thrombolytic (alteplase) toxicity.
Tranexamic acid uses?
Oral factor Xa inhibitor.
Rivaroxaban mechanism of action?
Phosphodiesterase inhibitor (increases cAMP), thus increasing inotropy and decreasing TPR.
Milrinone, inamrinone mechanism of action?
Congestive heart failure. Override beta-blockers.
Milrinone, inamrinone uses?