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Pharm - Cardio

Cardiovascular Pharmacology from First Aid 2013

QuestionAnswer
Drug categories for treating essential hypertension? Diuretics, ACE-I's, ARB's, Ca-channel blockers
Drug categories for treating CHF? K-sparing diuretics, ACE-I's, ARB's, beta-blockers (use cautiously if decompensated)
Anti-hypertensive that is protective against diabetic nephropathy? ACE inhibitors
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
Which calcium channel blocker should not be used with arrhythmias? Nifedipine ("Not Nif")
Which calcium channel blockers should be used preferentially for vascular smooth muscle? Amlodipine or Nifedipine
Which calcium channel blocker should be used preferentially to reduce contractility of the heart? Verapamil ("Verapamil =Whic Ventricle")
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.
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.
What should be given with hydralazine and why? Beta-blockers, to prevent reflex tachycardia.
What should be given in the case of malignant hypertension? Nitroprusside Fenoldopam
Nitroprusside: MOA, Use, Tox Short acting release of NO -> cGMP Use: Malignant HTN Tox: releases CN-
Fenoldopam: MOA, Use, SFX D1 receptor agonist (Gs) Coronary, renal, peripheral, and splanchnic vasodilation. Use: decrease BP SFX: increase natriuresis
Nitrates: MOA, Use, Tox NO -> cGMP in VEINS > ARTERIES, decreases preload. Use: angina, pulmonary HTN Tox: reflex tachycardia, hypotension, flushing, headache, "Monday Disease"
"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.
In anti-angina therapy, what should be co-administered with nitrates? Why? Beta blockers, to prevent reflex tachycardia.
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)
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+
List five classes of lipid-lowering agents. Stains, niacin (B3), bile acid resins, cholesterol absorption blockers, and Fibrates
Statins: MOA, Tox HMG-CoA reductase inhibitors, "-statin" Decrease LDL, Trig; increase HDL Tox: hepatotoxicity and rhabdomyolysis
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)
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
Cholesterol absorption blockers: Use, Tox Ezetimibe: acts on brush border. Decrease LDL. Tox: diarrhea
Fibrates: MOA, Tox Upregulates LPL -> increase triglyceride clearance. Contain "-fibr-", e.g. gemfibrozil. Tox: Myositis, hepatotoxicity, cholesterol gallstones
What is the mnemonic for anti-arrhythmics? SoBePoCa: "Some Block Potassium Channels" Class I, II, III, IV
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.
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
Toxic side effect of Quinidine? Headache and tinnitus
Toxic side effects of Procainamide? SLE-like syndrome
Toxic side effects of Disopyramide? Heart failure
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
What class of anti-arrhythmics should be used after an acute MI? Class IB: Lidocaine
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.
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
Toxic side effect of Metoprolol? Dyslipidemia, give glucagon to correct
Toxic side effect of Propanolol? Prinzmetal's vasospasm
How do Class III anti-arrhythmics work? Potassium-channel blockers: increase AP duration, ERP, and QT interval (-> Torsades) Use when other anti-arrhythmics fail
Class III anti-arrhythmics: Names "AIDS": Amiodarone Ibutilide Dofetilide Sotalol
Toxic side effects of amiodarone? Pulmonary fibrosis, hepatotoxicity, hypothyroidism. Check all function tests.
Toxic side effect of ibutilide, sotalol? Torsades
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
Which Calcium channel blockers should be used for arrhythmias? Verapamil ("ventricle") and diltiazem NEVER Nifedipine
What can be administered to quickly diagnose (and abolish) SVT? Adenosine
How does adenosine work? Hyperpolarize cells by opening K-channels. Works very rapidly and painfully.
What can block the effects of adenosine? Theophylline and caffeine
What can be effective in treating Torsades (also given for digoxin toxicity)? Mg2+
Created by: wmwebb89
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