| 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+ |
