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38 Cards in this Set
- Front
- Back
Spironolactone (Aldactone®)
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Indication – hypertension, edema
Mechanism – blocks aldosterone action at distal tubule Dose – 25-100 mg daily Onset/Duration – 1-2 d / 2-3 d Adverse effects – hyperkalemia, endocrine effects (gynecomastia, menstrual irregularities); interactions with other diuretics, ACE-inhibitors, potassium supplements - blocks aldosterone effects |
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Lisinopril (Prinivil®, Zestril®)
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Indication – hypertension, HF, MI, nephropathy
Mechanism – reduces angiotensin II, elevates bradykinin (affects RAAS system) CV Effect – vasodilation, ↓ AL, PL, Na reabsorption Dose – 5-10 mg daily (max 40 daily) Onset – the only ACE-I that is not a prodrug Elimination – renal excretion Adverse effects – hypotension, hyperkalemia, cough, angioedema, dysgeusia, rash; contraindicated in pregnancy, bilateral renal artery stenosis; interactions with diuretics or other antihypertensives, potassium supplements |
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Losartan (Cozaar®)
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Indication – hypertension, HF, nephropathy
Mechanism – blocks type-1 angiotensin II receptor Dose – 25-50 mg daily (max 100 mg/d) Elimination – renal excretion Adverse effects – hypotension, (hyperkalemia), angioedema, dysgeusia, rash; contraindicated in pregnancy, bilateral renal artery stenosis; interactions with diuretics or other antihypertensives, potassium supplements |
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Carvedilol (Coreg®)
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Indication – HF, hypertension
Mechanism – β (and α1) adrenergic blockade CV Effect – ↓ HR, contractility, AV conduction Dose – 3.125 mg bid (slow titration to 25 mg bid) Indication – HF, hypertension Onset – 1-3 months to full benefit Elimination – extensive hepatic metab, renal excretion Adverse effects – fluid retention, bradycardia, dizziness, worsening HF - starts at low dose, takes a while for effect - need to be uvolemic/stable to start, so not a drug you'd start right away |
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Digoxin (Lanoxin®)
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- doesn't do anything for HF mortality
Indication – Atrial fibrillation, HF Mechanism – inhibits Na-K ATP-ase causes ↑ Ca which inc. ht. contractility Dose – 0.125-0.25 mg daily (tabs, caps, elixir) - small therapeutic window Onset – 1-3 months to full benefit; 1/2 lifr of 24 hrs so 4-5 days for therapeutic and stable level Elimination – renal excretion Adverse effects – dysrhythmias, ANV, fatigue, visual disturbances; interactions diuretics (excess K can compete w/drug so important to measure level), β-blockers, Ca-channel blockers, verapamil, quinidine, cholestyramine (can bind to dig. in GI tract and keep it from being absorbed) |
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Angina
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a clinical manifestation of CAD (chest pain, discomfort, heaviness,
pressure, radiation, shortness of breath, fatigue, …); commonly due to atherosclerotic disease, associated with multiple risk factors (non-modifiable, modifiable) |
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progression of artherosclerosis and angina
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- stable angina
- unstable angina - non ST elevation MI - STEMI - sudden death |
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types of angina:
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Stable Angina – during physical or emotional strain; relieved by rest or
nitroglycerin Unstable Angina – while at rest (nocturnal) or of long duration; relieved by nitroglycerin |
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angina treatment
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Non-pharmacologic (smoking cessation, physical activity, healthy diet)
• Pharmacologic (nitrates, β-blockers, calcium channel blockers, (short acting agent prn/nigroglycerine for all patients and long acting agent for all patients to prevent recurrence/beta, Ca and long acting nitrates) antiplatelet agents, anticoagulants, ACE inhibitors) |
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Nitroglycerin
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Indication – angina
Mechanism – vasodilation (veins) via nitric oxide (and dilation of coronary arteries) Dose – 0.3-0.6 mg SL prn ISDN(Isosorbide dinitrate) 5 mg tid, ISMN 20 mg bid (30-60 mg daily if ER); (when on it long term can develop tolerance, so we use nitrite free intervals to prevent this.) Transdermal patch 0.2-0.8 mg/h Onset/Duration – < 5 min / up to 30 min Elimination – rapid hepatic inactivation Adverse effects – headache, orthostatic hypotension, reflex tachycardia; interaction with antihypertensives and phosphodiesterase inhibitors |
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Metoprolol (Lopressor®, Toprol XL®)
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Indication – hypertension, angina, MI, HF
Mechanism – β1 adrenergic blockade CV Effect – ↓ HR, contractility, AV conduction Dose – 25-200 mg bid (IR); 50-100 mg per day (ER) Elimination – extensive hepatic metab, renal excretion Adverse effects – bradycardia, decreased cardiac output, heart block; caution in heart block and HF; interactions with antihypertensives |
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Verapamil (Calan®, Isoptin®, Verelan®)
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Indication – angina, hypertension, dysrhythmias
Mechanism – blocks Ca channels in vascular smooth muscle, myocardium, and SA/AV nodes Dose – 80 mg tid (240 mg once daily if SR) Onset/Duration – within 30 min / ~5 h Elimination – extensive 1st pass metabolism, hepatic Adverse effects – constipation, peripheral edema, dizziness, headache, flushing, AV block; caution cardiac conduction disturbances, heart block; interactions with digoxin, β-blockers - used for ongoing stable angina |
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Aspirin
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Indication – 1°and 2° prevention of CVD
Mechanism – inhibits COX, ↓ platelet aggregation Dose – 80-160 mg daily Duration – for life of platelet (~7-10 d) Elimination – hepatic, then renal Adverse effects – GI distress, tinnitus, altered hemostasis, renal dysfunction; avoid if allergic |
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ACS
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Actute coronary syndrome
- unstable angina - MIs - with ST elevation and non-ST elevation MI |
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ACS treatment
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Anti-ischemic agents
o Nitrates, β-blockers, Ca channel blockers, others, and thrombolytics • Anti-platelet agents o Aspirin, clopidogrel, abciximab, eptifibatide • Anticoagulant agents o Unfractionated heparin (UFH), low-molecular weight heparins (LMWH), warfarin - often given IV, to deliver rapidly, b/c it's an acute problem |
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Nitroglycerin
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Indication – angina (unstable)
Mechanism – vasodilation (veins) via nitric oxide Dose – 0.3-0.6 mg SL q5min x 3 ; 5-10 µg/min IV infusion Onset/Duration – < 5 min / up to 30 min Elimination – rapid hepatic inactivation Adverse effects – headache, orthostatic hypotension, reflex tachycardia; interaction with antihypertensives and phosphodiesterase inhibitors - can bind to plastics in IV bag, so hung in glass container instead of plastic bag |
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Metoprolol (Lopressor®)
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Indication – hypertension, angina, MI, HF - used in IV form for acute situations
Mechanism – β1 adrenergic blockade CV Effect – ↓ HR, contractility, AV conduction Dose – 5 mg IV q5min x 3; 25-50 mg q6h Elimination – extensive hepatic metab, renal excretion Adverse effects – bradycardia, decreased cardiac output, heart block; caution in heart block and HF; interactions with antihypertensives |
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Drugs for heart failure
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- furosemide
- spironolactone - lisinopril - losartan - carvediol - digoxin |
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Interfering with Hemostasis
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Antiplatelet agents (aspirin, clopidogrel, prasugrel, abciximab) –
decrease platelet aggregation Direct factor Xa inhibitors (rivaroxoban) – inhibits factor Xa Direct thrombin inhibitors (lepirudin) – inhibits thrombin Anticoagulant agents (heparins, warfarin) – inhibit the clotting cascade Thrombolytic agents (alteplase) – increase clot dissolution |
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Drugs for stable angina
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- nitroglycerin
- metoprolol - verapamil - asprin |
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ACS drugs
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- acute coronary syndrome drugs
- nitroglycerin - metoprolol - asprin - clopidogrel - heparin - enoxaparin - warfarin - alteplase |
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Drugs that interfere with Hemostasis
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- asprin
- clopidogrel - heparin - enoxaparin - warfarin - alteplase |
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Asprin - the hemostasis use
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Indication – 1°and 2° prevention of CVD
Mechanism – inhibits COX, ↓ platelet aggregation Dose – 325 mg initially, then 80-160 mg daily - high initial then really low Duration – for life of platelet (~7-10 d) Elimination – hepatic, then renal Adverse effects – GI distress, tinnitus, altered hemostasis, renal dysfunction; avoid if allergic |
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Clopidogrel (Plavix®, others)
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Indication – 2° prevention of CVD (MI and stroke)
Mechanism – ADP antagonist, ↓ platelet aggregation Dose – (300 mg initially) 75 mg daily; high initial dose, then low; it is a prodrug so must be metabolized to have its effect Onset/Peak – in 2 h / 3-7 d Elimination – extensive 1st pass metabolism (CYP3A4, -2C19, …) - (some people don't have a good active cyp2C19, so this drug won't work well, it will stay in the prodrug form) Adverse effects – dyspepsia, abdominal pain, diarrhea, rash (no neutropenia); interaction with antiplatelet and anticoagulants, (PPIs?) |
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Heparin (i.e., UFH)
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Indication – treatment or prevention of thrombosis
Mechanism – ↑ activity of antithrombin (inactivating factors Xa and IIa) Dose – Treatment LD (loading dose): 80 units/kg IV;MD (maintanance dose): 18 units/kg/h IV (aPTT 1.5- 2xcontrol); look at PTT - want it 40-50 seconds long Prevention 5000 units SC q8-12h Onset/Duration – within min (IV) / lasts several hours Elimination – hepatic metab, renal excretion (t½ ~1.5h) Adverse effects – bleeding, heparin-induced thrombocytopenia (HIT); caution in patients with bleeding risk; interaction antiplatelet agents - a very polar molecule and very large, so can't give po - give it parenterally or IV or SQ - blocks action of factor 10 and thrombin |
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note on clotting
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you want activated factor 10 and activated thrombin
- thrombin changes fibrinogen to fibrin to form a clot |
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LMWH
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Low molecular weight heparin
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Enoxaparin (Lovenox®)
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(an example of a LMWH)
Indication – treatment or prevention of thrombosis - only blocks 10a, not 2a, so less likely to cause bleeding Mechanism – ↑ antithrombin activity (inactivates Xa) Dose – (varies with indication) 1 mg/kg SC q12h Onset/Duration – lasts several hours following SC injection Elimination – slower hepatic metabolism (t½ ~6-10 h) Adverse effects – bleeding, heparin-induced thrombocytopenia (HIT); caution in patients with bleeding risk, or spinal/epidural catheter; interaction antiplatelet agents |
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Warfarin (Coumadin®)
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Indication – prevention of venous thrombosis
Mechanism – prevents regeneration of active vitamin K Dose – (quite variable) 2-10 mg daily à goal INR 2-3 (normal is about 1) Onset/Peak – ~12 h / ~3-4 d highly protein-bound (98% to albumin) Elimination – hepatic metabolism, renal/biliary excretion Adverse effects – bleeding; interaction antiplat, anticoag, enzyme inhibitors, enzyme inducers, vitamin K - used for clot prevention... not usually for ACS - to activate prothrombin or factor 10a, you need vit K as a coenzyme; when it does this, vit K turns into inactive form; warfarin blocks the change of inactive K back into active K - effectiveness is based on genetics - category X drugs (teratogen) |
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Alteplase (Activase®)
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- used to be called TPA - tissue plasminogen activator
Indication – acute MI, pulm embolism, ischemic stroke Mechanism – selective activation of fibrin-bound plasminogen Dose – LD: 15 mg IV; MD1: 0.75 mg/kg (50 mg max) IV over 30 min; MD2: 0.5 mg/kg (35 mg max) IV over 60 Adverse effects – bleeding; contraindicated if hemorrhagic stroke or other cerebrovascular event, intracranial neoplasm, internal bleeding; caution HTN (b/c htn in brain could lead to bleeding there etc), CVA, recent trauma or internal bleeding, PUD, pregnancy; interactions with antiplatelet and anticoagulant agents |
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hyperlipidemia
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Hyperlipidemia increases the risk of CVD o Cholesterol synthesis > intake o Trans fats > saturated fats > cholesterol o Pharmacologic management may do more than reduce cholesterol levels |
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antilipidemic meds - general
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Cholesterol absorption blockers (e.g., ezetimibe)
Bile acid resins (e.g., cholestyramine) - bind to fat and keep it from being absorbed Niacin - at larger levels is a B vitamin Omega-3 fatty acids Fibric acid derivatives (e.g., gemfibrozil) HMG-CoA reductase inhibitors (e.g., “statins”) |
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What are the antilipidemic meds?
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- Ezetimibe
- Cholesevelam - Niacin - Gemfibrozil - Pravastatin |
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Ezetimibe (Zetia®)
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Indication – elevated cholesterol
Mechanism – ↓ intestinal cholesterol absorption Dose – 10 mg daily Elimination – biliary/intestinal Adverse effects – rare myopathy, rhabdomyolysis, hepatitis, pancreatitis, thrombocytopenia; interaction statins, cyclosporine - high burden of adverse effects w/o clear benefiit |
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Colesevelam (Welchol®)
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Indication – elevated LDL-cholesterol
Mechanism – complexes with bile acids, preventing reabsorption, indirectly increasing LDL receptors Dose – 1.9 g twice daily (3 625 mg tablets) Onset/Peak – within 1 week / within 1 month Elimination – GI tract (not absorbed) Adverse effects – constipation, bloating, indigestion, hypertriglyceridemia; interaction binds to thiazides, digoxin, warfarin, and some antibiotics - binds to them reducing the other drugs' absorption (note: all adverse effects are GI) |
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Niacin
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Indication – elevated triglycerides, mixed hyperlipidemia
Mechanism – ↓ VLDL production Dose – 1-2 g tid (start low, titrate slow) Onset/Peak – within 1 week (TG) / 1 month (LDL-C) Adverse effects – facial flushing - a LOT (why we don't start the drug quickly), itching, NVD, hyperglycemia, hepatotoxicity (Sustained Release formulations) |
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Gemfibrozil (Lopid®) - a fibrin???
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Indication – elevated triglycerides
Mechanism – ↓ VLDL via PPAR activation Dose – 600 mg bid (30 min before meal) Onset – ~3-4 weeks Adverse effects – nausea, abdominal pain, diarrhea, rash, gallstones, hepatotoxicity, myopathy; interaction statins (b/c they also cause myopathy), warfarin (b/c highly protein bound to albumin, so competition for that space) - used when triglyc. are really high, to get them under control |
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Pravastatin (Pravachol®)
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Indication – 1° and 2° CHD prevention in at risk patients
Mechanism – ↓ cholesterol synthesis, ↑ LDL receptors Dose – 10-20 mg daily (40 mg max) Onset/Peak – 2 weeks / 4-6 weeks Elimination – limited hepatic metabolism (unlike all the other statins which work by cytochrome P metabolism); excretion in bile (some urinary excretion) Adverse effects – GI complaints, headache, rash, hepatotoxicity, myopathy; caution pregnancy category X; interaction fibrates |