Cardiovascular Pharmacology from First Aid 2013
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| Drug categories for treating essential hypertension? | Diuretics, ACE-I's, ARB's, Ca-channel blockers
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| Drug categories for treating CHF? | K-sparing diuretics, ACE-I's, ARB's, beta-blockers (use cautiously if decompensated)
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| Anti-hypertensive that is protective against diabetic nephropathy? | ACE inhibitors
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| Calcium channel blockers: MOA, Use, Tox | Nifedipine, verapamil, diltiazem, amlodipine
MOA: reduce muscular contractility
Use: HTN, angina, Prinzmetal's, Raynaud's, arrhythmias (Not Nifedipine)
Tox: A/V block, peripheral edema, flushing, dizziness, constipation
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| Which calcium channel blocker should not be used with arrhythmias? | Nifedipine ("Not Nif")
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| Which calcium channel blockers should be used preferentially for vascular smooth muscle? | Amlodipine or Nifedipine
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| Which calcium channel blocker should be used preferentially to reduce contractility of the heart? | Verapamil ("Verapamil =Whic Ventricle")
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| Which calcium channel blockers should be used for arrhythmias? Which type of arrhythmia? | Verapamil, diltiazem
MOA: decrease conduction velocity and increase PR-interval
Use for SVT.
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| Hydralazine: MOA, Use, Tox | Increase cGMP -> smooth muscle relaxation
Vasodilates ARTERIES > VEINS, so reduces afterload.
Use: severe HTN
Tox: reflex tachycardia (co-administer beta-blockers), fluid retention, nausea, headache, angina, Lupus-like syndrome.
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| What should be given with hydralazine and why? | Beta-blockers, to prevent reflex tachycardia.
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| What should be given in the case of malignant hypertension? | Nitroprusside
Fenoldopam
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| Nitroprusside: MOA, Use, Tox | Short acting release of NO -> cGMP
Use: Malignant HTN
Tox: releases CN-
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| Fenoldopam: MOA, Use, SFX | D1 receptor agonist (Gs)
Coronary, renal, peripheral, and splanchnic vasodilation.
Use: decrease BP
SFX: increase natriuresis
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| Nitrates: MOA, Use, Tox | NO -> cGMP in VEINS > ARTERIES, decreases preload.
Use: angina, pulmonary HTN
Tox: reflex tachycardia, hypotension, flushing, headache, "Monday Disease"
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| "Monday Disease" | Tolerance to nitrates is built up by industrial exposure during the work week. This tolerance is lost on Monday, causing tachycardia, dizziness, and headache.
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| In anti-angina therapy, what should be co-administered with nitrates? Why? | Beta blockers, to prevent reflex tachycardia.
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| Cardiac glycosides: MOA, Use | Digoxin, digialis: block Na/K pump -> inhibit Na/Ca-ATPase -> inc. intracellular Ca -> positive inotropy. Also stimulates vagus nerve -> dec. HR.
Use: CHF (increase contractility), atrial fibrillation (decrease conduction)
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| What are the side effects/toxicity of digoxin and digitalis? Its remedy? | Cholinergic effects: GI, nausea, blurry vision
Increased PR, decreased QT, AV block
Hyperkalemia
Rx: normalize K, give lidocaine, anti-digoxin Ig, Mg2+
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| List five classes of lipid-lowering agents. | Stains, niacin (B3), bile acid resins, cholesterol absorption blockers, and Fibrates
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| Statins: MOA, Tox | HMG-CoA reductase inhibitors, "-statin"
Decrease LDL, Trig; increase HDL
Tox: hepatotoxicity and rhabdomyolysis
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| Niacin (B3, as a lipid-lowering agent): MOA, Tox | Inhibit lipolysis in adipose tissue, reduce hepatic VLDL secretion.
Decrease LDL and Trig; increase HDL
Tox: flushed face, hyperglycemia, hyperuricemia (gout)
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| Bile acid resins: MOA, Tox | Prevent intestinal reabsorption of bile acids.
Begin with "chol-", e.g. cholestyramine.
Decrease LDL; increase Trig and HDL
Tox: nasty taste, GI upset, decreased absorption of ADEK, cholesterol gallstones
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| Cholesterol absorption blockers: Use, Tox | Ezetimibe: acts on brush border.
Decrease LDL.
Tox: diarrhea
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| Fibrates: MOA, Tox | Upregulates LPL -> increase triglyceride clearance.
Contain "-fibr-", e.g. gemfibrozil.
Tox: Myositis, hepatotoxicity, cholesterol gallstones
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| What is the mnemonic for anti-arrhythmics? | SoBePoCa: "Some Block Potassium Channels"
Class I, II, III, IV
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| How do Class I anti-arrhythmics work? | Slow or block Na+ conduction, decreasing the slope of Phase 0, and increasing the threshold for firing.
Hyperkalemia increases the toxicity of all Class I anti-arrhythmics.
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| Class IA anti-arrhythmics: Names, Use, Tox | Quinidine, Procainamide, Disopyramide
"The Queen Proclaims Diso's Pyramid"
Use: Increase AP, ERP, and QT in both atria and ventricles.
Tox: Torsades (QT), other drug specific SFX
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| Toxic side effect of Quinidine? | Headache and tinnitus
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| Toxic side effects of Procainamide? | SLE-like syndrome
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| Toxic side effects of Disopyramide? | Heart failure
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| Class IB anti-arrhythmics: Names, Use, Tox | Lidocaine, Mexiletene, Tocainide
"I'd Buy Lido's Mexican Tacos"
Use: Decrease AP duration in ischemic, ventricular Purkinje cells. Use post-MI or post-digitalis-induced toxicity.
Tox: local anesthetic, CNS/CV depression
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| What class of anti-arrhythmics should be used after an acute MI? | Class IB: Lidocaine
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| Class 1C anti-arrhythmics: Names, Use, Tox | Flecainide, propafenone
Use: Last resort Vtach and SVT
No effect on ERP.
Tox: IC is Contraindicated in structural heart damage and post-MI. It can become pro-arrhythmic in these cases.
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| How do Class II anti-arrhythmics work? | Beta blockers: decrease SA and AV nodal activity, lengthening PR. End in "-olol".
Use: VTach, SVT, slowing down ventricles during Afib or Aflutter
Tox: Impotence, asthma, bradycardia, sedation, masking of hypoglycemia
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| Toxic side effect of Metoprolol? | Dyslipidemia, give glucagon to correct
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| Toxic side effect of Propanolol? | Prinzmetal's vasospasm
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| How do Class III anti-arrhythmics work? | Potassium-channel blockers: increase AP duration, ERP, and QT interval (-> Torsades)
Use when other anti-arrhythmics fail
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| Class III anti-arrhythmics: Names | "AIDS":
Amiodarone
Ibutilide
Dofetilide
Sotalol
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| Toxic side effects of amiodarone? | Pulmonary fibrosis, hepatotoxicity, hypothyroidism. Check all function tests.
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| Toxic side effect of ibutilide, sotalol? | Torsades
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| How do Class IV anti-arrhythmics work? What is their toxicity? | Calcium-channel blockers: decrease conduction velocity, inreasing ERP and PR interval.
Used in preventing nodal arrhythmias, e.g. SVT.
Tox: AV block, cardiac depression
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| Which Calcium channel blockers should be used for arrhythmias? | Verapamil ("ventricle") and diltiazem
NEVER Nifedipine
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| What can be administered to quickly diagnose (and abolish) SVT? | Adenosine
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| How does adenosine work? | Hyperpolarize cells by opening K-channels.
Works very rapidly and painfully.
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| What can block the effects of adenosine? | Theophylline and caffeine
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| What can be effective in treating Torsades (also given for digoxin toxicity)? | Mg2+
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