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38 Cards in this Set

  • Front
  • Back
Spironolactone (Aldactone®)
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
Lisinopril (Prinivil®, Zestril®)
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
Losartan (Cozaar®)
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
Carvedilol (Coreg®)
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
Digoxin (Lanoxin®)
- 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)
Angina
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)
progression of artherosclerosis and angina
- stable angina
- unstable angina
- non ST elevation MI
- STEMI
- sudden death
types of angina:
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
angina treatment
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)
Nitroglycerin
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
Metoprolol (Lopressor®, Toprol XL®)
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
Verapamil (Calan®, Isoptin®, Verelan®)
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
Aspirin
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
ACS
Actute coronary syndrome
- unstable angina
- MIs - with ST elevation and non-ST elevation MI
ACS treatment
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
Nitroglycerin
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
Metoprolol (Lopressor®)
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
Drugs for heart failure
- furosemide
- spironolactone
- lisinopril
- losartan
- carvediol
- digoxin
Interfering with Hemostasis
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
Drugs for stable angina
- nitroglycerin
- metoprolol
- verapamil
- asprin
ACS drugs
- acute coronary syndrome drugs

- nitroglycerin
- metoprolol
- asprin
- clopidogrel
- heparin
- enoxaparin
- warfarin
- alteplase
Drugs that interfere with Hemostasis
- asprin
- clopidogrel
- heparin
- enoxaparin
- warfarin
- alteplase
Asprin - the hemostasis use
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
Clopidogrel (Plavix®, others)
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?)
Heparin (i.e., UFH)
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
note on clotting
you want activated factor 10 and activated thrombin
- thrombin changes fibrinogen to fibrin to form a clot
LMWH
Low molecular weight heparin
Enoxaparin (Lovenox®)
(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
Warfarin (Coumadin®)
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)
Alteplase (Activase®)
- 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
hyperlipidemia


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
antilipidemic meds - general
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”)
What are the antilipidemic meds?
- Ezetimibe
- Cholesevelam
- Niacin
- Gemfibrozil
- Pravastatin
Ezetimibe (Zetia®)
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
Colesevelam (Welchol®)
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)
Niacin
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)
Gemfibrozil (Lopid®) - a fibrin???
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
Pravastatin (Pravachol®)
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