Flashcards in Cardio Pharm Deck (91):
What are the L-type calcium channel blockers?
What are the l-type channels?
On cardiac and smooth muscle
What is the toxicity of calcium channel blockers?
What is the MOA of hydralazine?
Increase cGMP causing smooth muscle relaxation --> reduces afterload
What is hydralazine used for?
First line for HTN in pregnancy with methyl dopa (alpha 2 agonist)
Frequently used with beta blockers to prevent reflex tachycardia
What is the toxicity of hydralazine?
What is the MOA of nitroprusside?
Increases cGMP via direct release of NO
What is the draw back to nitroprusside?
What is hydralazine contraindicated in?
CAD and angina because it causes reflex tachycardia increases the need for oxygen of the heart
What is the MOA of fenoldopam?
D1 agonist --> vasodilation of coronary, peripheral, renal, splanchnic arteries
Decreases BP and increases natriuresis
What is the MOA of nitroglycerin?
Vaso and venodilator by releasing NO in smooth muscle causing an increase cGMP
Decreases preload and afterload
What is the clinical use of nitroglycerin?
What is the toxicity of nitroglycerin?
Monday disease - due to build up of tolerance during the week, lose it over the weekend (because not using it) and then come Monday causes side effects: tachycardia, dizziness, headache
Which beta blockers are contraindicated in angina?
Pindolol and acebutolol - Partial B agonist
Which calcium channel blocker is similar to beta blockers in effect?
What is the mech of action of a statin?
HMG-CoA reductase inhibitors - inhibit conversion of HMG-CoA to mevalonate
What are the side effects of statins?
What is the effect of niacin on lipids?
Inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation
Effect: decreases circulating lipids
What are the side effects of niacin?
Flushing (counteract with aspirin because due to prostaglandins)
What are the bile acid resins?
What is the MOA of bile acid resin?
Prevents intestinal reabsorption of bile acids
Liver must use cholesterol to make more!
What is the side effect?
Decrease absorption of fat soluble vitamins
What is ezetimibe?
Cholesterol absorption blocker - prevents absorption at small intestine brush border
What are the side effects of ezetimibe?
Increase in LFTs
What is the MOA of fibrates?
Upregulates LPL to increase TG clearance
What are the fibrates?
What are the side effects of fibrates?
What lipid med had the best effect on LDL?
HMG- CoA reductase
What lipid med has the greatest effect on TGs?
Which med has the most effect on HDL?
What is half life of digoxin?
What is the bioavailability of digoxin?
What percent of digoxin is protein bound?
What is the MOA of digoxin?
Inhibition of the Na/K pump leading to indirect inhibition of Na/Ca exchanger --> increase intracellular calcium (not pumping it out anymore because no more ATP to run antiport)
Stimulates vagus --> decrease HR, depresses SA node and decreases conduction at AV node
What is the digoxin used for?
What is the toxicity of digoxin?
Cholinergic - N/V, diarrhea, blurry yellow vision
ECG - increased PR interval, decreased QT interval, ST scooping, T-wave inversion, arrhythmias, AV block
What conditions predispose to digoxin toxicity?
Renal failure (because excreted in urine)
Quinidine (displaces digoxin from tissue binding sites, decreases clearance)
What is the antidote for digoxin?
Anti-digoxin Fab fragments
What are the class I anti arrhythmics?
Quinidine, procainamide, disopyramide
What are the effects of the class I anti arrhythmics?
Increase action potential duration
Increase effective refractory period
Affect atrial and ventricular arrhythmias especially reentrant and ectopic SVC and VT
What is the tox of quinidine?
Cinchonism - tinnitus, headache
What is the tox of procainamide?
Reversible SLE-like syndrome
What is the tox of disopyramide?
What are the toxicities of class I?
Torsades de pointes
Hyperkalemia increases the toxicity of these drugs
What are the class b anti-arrythmics?
What are the effects of class b?
Decrease action potential duration
Affect ischemic or de polarized Purkinje and ventricular tissue
What are class b used for?
Post MI arrhythmias
What are the toxicities of class b?
Local anesthetic, CNS stimulation/depression, CV depression
What are the class c antiarrythmics?
What are class c used for?
VT that progresses to VF
Last resort - only for patients without structural abnormalities
What are the tox of class c?
Pro arrhythmic especially post MI
Significantly prolongs refractory period in AV node
What are the class II antiarrythmics?
What do beta blockers do?
Decrease SA and AV nodal activity by decreasing camp and calcium.
Decrease slope of phase 4
Increase PR interval. Esmolol is short acting
What are class II used for?
slowing ventricular rate during a-fib, a-flutter
What is the tox of class II?
Impotence, exacerbation of Asthma, bradycardia , AV nodal block, CHF, sedation, masks hypoglycemia
What can metoprolol cause?
Dyslipidemia - tx OD with glucagon
What can propranolol do?
Exacerbate spasm in Prinzmetal's
What are the class III?
What is the MOA of class III?
Increase AP duration
Increase QT interval
Used when other antiarrythmics
What is the tox of sotalol?
Torsades de pointes
Excessive beta block
What is the tox of ibutilide?
What is the tox of amiodarone?
Blue/gray Skin deposits
AV nodal block
What is unique about amiodarone?
Has class I-iV effects because it alters the lipid membrane
What are the class IV?
Calcium channel blockers: verapamil, diltiazem
What is the MOA of class IV?
Decreases conduction velocity, increases ERP, increase PR,
What are class IV used for?
In prevention of nodal arrythmias
What is the MOA of adenosine as an antiarrythmic?
Increase K efflux hyper polarizing the cell and decreases spontaneous calcium channels
Short acting (15 seconds)
What is the DOC for diagnosing/taxing SVT?
What is the tox of adenosine?
What blocks adenosine?
What is magnesium used for?
Effective in torsades and digoxin tox
Which antiarrythmic causes bradycardia and QT prolongation?
Sotalol - class 3 K-blocking and beta blocker
How do beta blockers work as antiarrythmics?
Slow AV nodal conduction and phase 4 depolarization of cardiac pacemaker cells
Phase 4 is mediated by sodium channels that depolarize spontaneously
What phase do calcium channel blockers slow?
Phase 0 of pacemaker cells - the opening of voltage gated calcium channels
Phase 2 of myocyte action potential - calcium influx through calcium channels that balances K efflux
What side effects is verapamil associated with?
AV nodal block
What is ergonovine?
An ergot alkaloid that stimulates serotonin and alpha adrenergic receptors
What is ergonovine used for?
Testing for Prinzmetal's angina by provoking an attack
How is procainamide metabolized?
What is the MOA of an ARB?
Blocks Ang I receptors thereby blocking the effects of angiotensin II
Will have increased renin and Ang I and Ang II but decreased aldosterone and vasodilation. No change in bradykinin
How does metoprolol work in lowering bp?
Blocks B1 in heart and in Jg apparatus thereby decreasing the level of circulating renin.
What is the MOA of nesirtide?
Recombinant form of BNP - dilates arterioles and venules by activating guanylate cycle and increasing cGMP. Also causes diuresis/natriuresis and decreases bp
What can nesirtide be used for?
Decompensated left ventricular dysfunction leading to CHF
On which part of the EKG do beta blockers act?
Increase the PR interval
Which phase of the ventricular depolarization graph do class IA agents act on?
Prolong phase 0 - decrease sodium influx so that the upstroke isn't as rapid
Prolong phase 3 - slow K efflux for slow repolarization
Increase AP duration, ERP, and QT interval
What effects do class IB agents have on the ventricular action potential graph?
Shorten phase 3 - so increase efflux of K and repolarization, also decreases ERP
Decreases duration of the action potential
Have affinity for rapidly de polarizing cells (best for ischemic cells)
What effect do class IC agents have on the ventricular action potential curve?
Slows phase 0 - slow the opening of sodium channels so the upstroke isn't as rapid.
Has no effect on action potential duration
Works within the QRS interval
May significantly prolong the refractory period in the AV node (PR interval)
Have highest affinity for non-resting sodium channel - have more effect on normal myocardium
What phase do beta blockers act in?
Prolong phase 4 - decreases current through funny sodium channels so decreases rate of depolarization
Also decreases calcium influx thru channels that usually augment phase 4 by decreasing camp
Slows conduction through the SA and AV node (increases PR interval)
What effects do class 3 agents have on the ventricular action potential curve?
Increase phase 3 - decrease potassium efflux
Increases AP duration, QT interval and ERP
What is the toxicity of sotalol?
Torsades and excessive beta block
What is the toxicity of ibutilide?