Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Pharm - Cardio
Cardiovascular Pharmacology from First Aid 2013
| Question | Answer |
|---|---|
| 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
Popular USMLE sets