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52 Cards in this Set
- Front
- Back
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Drugs for essential hypertension
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diuretics, ACE inhibitors, angiotensin II, ARB, calcium channel blockers
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Drugs for CHF
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diuretics, ACE inhibitor/ARB, B blockers (only in compensated CHF), K+ sparing diuretics
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Drugs for DM
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ACE inhibitor/ARBs, Calcium channel blockers, diuretics, b-blockers, a-blockers
ACE inhibitors are protective against diabetic nephropathy |
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Hydralazine MOA, use, toxicity
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MOA - increases cGMP - relaxes smooth muscles - (alters Ca2+ metabolism), vasodilates arterioles > veins- reduces afterload
use: severe hypertension, CHF, first line therapy for hypertension in pregnancy, with methyldopa. Often coadministered with B-blockers to prevent reflex tachycardia toxicity: compensatory tachycardia (don't use in angina/CAD), fluid retention, nausea, headache, angina. Lupus like syndrome!!!! |
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What is the first line therapy for hypertension in women that are pregnant?
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hydralazine - often with methyldopa (to prevent reflex tachycardia)
'HI to the baby" can cause lupus like syndrome!!!! |
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Minoxidil MOA, use, toxicity
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MOA: K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle (makes cell more negative)
use: severe HTN toxicity: hypertrichosis (rogain), pericardial effusion, reflex tachycardia, angina, salt retention *for minimum amount of hair* |
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Calcium channel blockers - how do they work and where do the different ones work?
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Nifedipine, verapamil, diltiazem
block voltage dependent L-type calcium channels of cardiac and smooth muscle and reduce muscle contractility vascular smooth muscle: nifedipine>diltiazem>verapamil Heart: Verapamil (verapamil for ventricles) >diltiazem>nifedipine |
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use and toxicity for calcium channel blockers
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use: HTN, angina, arrhythmias (not nifedipine), Prinzmetal's angina, raynauds
toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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Nitroglycerin, isosorbide dinitrate MOA, use and toxicity
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MOA - vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation. dilate veins>arteries
*decreases preload use: angina, pulmonary edema, aphrodisiac and erection enhancer! toxicity: reflex tachycardia, hypotension, flushing, headache, "monday disease" in industrial exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness and headache on reexposure (nitro is explosive and often used in plants that make amunition - workers get tolerance during the work week then go through withdrawl over the weekend - symptoms go away after reexposure on monday)? |
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How do you treat malignant hypertension?
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1) Nitroprusside - short acting, increase cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)
2) Fenoldopam - dopamine D1 receptor agonist - relaxes renal vascular smooth muscle 3) Diazoxide - K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release) |
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What is the goal of antianginal therapy?
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to reduce the myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2; end diastolic volume, blood pressure, heart rate, contractility, ejection time
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What do nitrates do for antianginal therapy?
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decreases preload
- decreased end diastolic volume - decrease blood pressure - increase contractility (reflex) - increased heart rate (reflex) - decrease ejection time - decreased MVO2 |
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What do B-blockers do for antianginal therapy?
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affect afterload
- increase end diastolic volume - decrease bp - decrease contractility - decrease heart rate - increase ejection time - decrease MVO2 |
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What do nitrates + beta blockers do for antianginal therapy?
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- no effect or little decrease in end diastolic volume
- decrease blood pressure - little to no effect on contractility - decrease heart rate - little to no effect on ejection time - significantly decrease MVO2 |
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What is Nifedipine similar to? What is verapamil similar to?
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nifedipine similar to nitrates
verapamil similar to beta blockers |
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What beta blockers are contraindicated in angina?
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pindolol and acebutolol - because they are partial b- agonists!
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HMG-CoA reductase inhibitors drugs, effect, MOA, SE
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lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
MOA: inhibit cholesterol precursor, mevalonate - in the liver (inhibit cholesterol synthesis) effects: decrease a lot LDL, increase HDL, decrease triglycerides SE: hepatotoxicity (increased LFT's), rhabdomyolysis |
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Niacin, effect, MOA, SE
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MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
effect: decreased LDL, increase HDL, decrease triglycerides SE: red, flushed face - decrease by giving aspirin or with long term use hyperglycemia (acanthosis nigricans) hyperuricemia (exacerbates gout) |
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Bile acid resins drugs, MOA, effects, SE
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cholestyramine, colestipol, colesevelam
MOA: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more effect: decrease LDL, slightly increase HDL and triglycerides SE: patients hate it - tastes bad and causes GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gall stones |
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What lipid-lowering drug slightly increases triglycerides?
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bile acid resins - cholestyramine, colestipol, colesevelam
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Cholesterol absorption blockers drugs, MOA, effect, SE
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ezetimibe
MOA: prevents cholesterol reabsorption at small intestine brush border effect: decreased LDL only! SE: rare increase in LFT's |
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Fibrates drugs, moa, effect, SE
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gemfibrozil, clofibrate, benzafibrate, fenofibrate
MOA: upregulate LPL - increased triglyceride clearance effect: mainly decreases triglycerides, little decrease in LDL and little increase in HDL SE: myositis, hepatotoxicity (increased LFT's), cholesterol gallstones |
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What components are involved with excitation-contraction coupling?
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1) Na/K+ ATPase
2) Na+/Ca2+ exchanger 3) Voltage gated (L-type) calcium channel 4) Calcium pump in wall of sarcoplasmic reticulum 5) ryanodine receptors and calcium release channels in SR 6) site of calcium interaction with troponin-tropomyosin system |
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B1 receptors are what type?
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Gs - activate protein kinase A which phosphoylates L-type Ca2+ channels and phospholamban, which both increase intracellular Ca2+ during contraction
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Cardiac glycoside MOA, use
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Digoxin
75% bioavailbility, 20-40% protein bound, t1/2 = 40 hours, urinary excretion MOA: direct inhibition of Na+/K+ ATPase leads to inhibition of Na+/Ca2+ exchanger (so more Ca2+ inside the cell) - positive inotrophy - stimulates the vagus nerve use: CHF (increased contractility); atrial fibrilation (decreased conductance through AV node and depression of SA node) |
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toxicity for cardiac glycoside and antidote
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cholinergic - nausea, vomiting, diarrhea, blurry yellow vision
ECG - increased PR, decreased QT, scooping, T-wave inversion, arrhythmia, hyperkalemia. worsened by renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na/K ATPase, quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites) antidote: slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+ |
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drug whose toxicity is blurry yellow vision?
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digoxin
inhibits Na+/K+ ATPase, decreased Na+/Ca2+ exchanger - more intracellular Calcium |
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What are class 1 antiarrhythmics?
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Na+ channel blockers - local anesthetics. Slow or block conducuction (especially through depolarized cells). Decreased slope of phase 4 depolarization and increased threshold for firing in abrnoaml pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized, ex. fast tachycardia)
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Class IA antiarrhythmics
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'Queen proclaims discopyramide'
Quinidine, Procainamide, Discopyramide increases action potential duration, increased effective refractory period, increased QT interval. Affect both atrial and ventricular arrythmias, especially reentratna nd ectopic supraventricular and ventricular tachycardia toxicity: quinidine (cinchonism - headache, tinnitus; thrombocytopenia; torsades de pointes due to increasd QT interval) procainamide (reversible SLE like syndrome |
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toxicity of quinidine?
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class IA antiarrhythmic - Na+ channel blocker
cinchonism - headache, tinnitus; thrombocytopenia, torsades de pointes from increased QT interval |
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What drugs are good for reentrant and ectopic supraventricular and ventricular tachycardia?
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Class IA anti-arrthymics
Quinidine, Procainmide, Discopyramide |
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Class IB anti-arrhythmics
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'Lidy's Mexican Tacos'
Lidocaine, Mexiletine, Tocainide Phenytoin can also fall into the IB category. decrease AP duration. preferentially affect ischemic or depolarized purkinje and ventricular tissue. useful in acute ventricular arrhythmias (especially post MI) and in digitalis induced arrhythmias toxicity: local anesthetic, CNS stimulation/depression, cardiovascular depression |
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SE of procainamide?
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SLE like syndrome
it is a Class IA antiarrythmic Na channel blocker |
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What antiarrythmic drugs are good post MI?
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Class IB
Lidocaine, mexiletine, Tocainide |
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Class IC antiarrythmics
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'Flees eat produce'
Flecainide, Encanide, Propafenone. No effect on AP duration. Useful in V-tachs that progress to VF and intractable SVT. Usually use only as last resort in refractory tachyarrhythmias. For patients w/o structural abnormalities toxicity: proarrhythmic, especially post MI (contraindicated). Significantly prolongs refractory period of AV node |
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What anti arrhythmic drug is contraindicated post MI?
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Class IC drugs
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What causes increased toxicity for all Class I antiarrhthmics?
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hyperkalemia
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What are class II antiarrhythmics?
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Beta blockers!
propranolol, esmolol, metoprolol, atenolol, timolol MOA: decrease cAMP, decrease Ca2+ currents. Suppress abnormal pacemakers by decreasing the slope of phase 4. AV node particularly sensitive - increase PR interval. Esmolol very short acting use: V-tach, SVT, slowing ventricular rate during A-fib and A-flutter toxicity: impotence, exaccerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask signs of hypoglycemia. Metoprolol can cause dyslipidemia - treat overdose with glucagon |
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What helps slow the ventricular rate during A-fib or A-flutter?
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Beta blockers - class II antiarrhythmics
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What are class III antiarrhythmics? Drugs and MOA?
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K+ channel blockers
'A BIDS' Amiodarone, Bretylium, Ibutilide, Dofetilide, Sotalol MOA: increase AP duration, increase ERP, used when other antiarrhythmias fail. increase QT interval |
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when do you use class III antiarrhythmics?
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when other ones fail - lots of toxicities
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sotalol toxicity
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class III antiarryhthmic
torsades de pointes, excessive B block |
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Ibutilide toxicity
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class III antiarrythmic
torsades |
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bretylium toxicity
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new arryhthmia, hypotension
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amiodarone toxicity
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pulmonary fibrosis, hepatoxicitity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in phodermtitis, neurologic effectes, constipation, cardiovascular effectes (bradycardia, heart block, CHF)
amiodarone has class I, II, III, and IV effects because it alters the lipid membrane |
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Class IV antiarrhythmics
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Ca2+ channel blockers
Verapamil (most effective on the heart) and diltiazem MOA: primarly affects AV nodal cells. Decrease conduction veolocity, increased ERP, increase PR interval. use in prevention of nodal arryhthmia toxicity: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression) |
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What antiarrythmic primarily affects AV nodal cells?
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type IV - verapamil, diltiazem
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Adenosine as antiarrhythmic
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increases K+ out of cells - hyperpolarizing the cell plus decrease Ca. Drug of choice in diagnosing/abolishing supraventricular tachycardia. Very short acting (15 sec).
toxicity: flushing, hypotension, chest pain. effects blocked by theophylline |
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what drug blocks the effects of adeosine?
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theophylline (drug used for COPD)
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What drug is used for diagnosing/treating suprventricular tachycardia?
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adenosine
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K+ as an antiarrhythmic
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depresses ectopic pacemakers in hypokalemia (digoxin toxicity)
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Mg2+ as an antiarrhythmic
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effective in torsades de pointes and digoxin toxicity
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