Term
| class I antiarrhythmic drugs |
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Definition
| sodium channel blockers (CAB in order of potency) --> slow conduction velocity |
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Term
| class II antiarrhythmic drugs |
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Definition
| beta blockers --> blunt sympathetic events |
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Term
| class III antiarrhythmic drugs |
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Definition
| prolong AP duration by blocking K+ channels (increase refractory period) |
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Term
| class IV antiarrythmic drugs |
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Definition
| calcium channel blockers --> affect primarily SA and AV nodes |
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Term
| paradoxical side effect of anti-arrhythmic drugs |
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Definition
| proarrhythmia (esp in people with structural heart disease, LV systolic dysfunction, MI, age, females, and class Ic agents) |
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Term
| what's so bad about class Ic drugs? |
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Definition
| changes the electrophysiological properties of the heart in such a way that around the scar from an MI, they developed incessant ventricular tachycardia --> can lead to sudden cardiac death in people with abnormal hearts. CONTRAINDICATED in patients with structurally abnormal hearts |
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Term
| procainamide - what class drug is it, what does it do, and what are the AE |
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Definition
| class Ia drug; used to suppress atrial fibrillation; too much procainamide (and slow acetylator, means procainamide doesnt get metabolized quickly enough by liver, so it accumulates) --> hypotension, N/V, agranulocytosis, drug-induced-LUPUS!!!; too much procainamide in a FAST acetylator --> accumulation of metabolite NAPA --> functions as a class III drug (k+ blocker, prolongs repolarization, prolongs relative refractory period, can get an EAD and torsades ventricular tachycardia) |
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Term
| what are the 2 class IB drugs and their difference? |
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Definition
| lidocaine (IV) and mexilitine (oral); same drug other than route of admin |
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Term
| what is lidocaine indicated for? |
|
Definition
| suppressing ventricular fibrillation or ventricular tachycardia due to ischemia, no use/effect at all on atrial tissue and no effect on hemodynamics/BP |
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Term
| side effects of lidocaine |
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Definition
| CNS tremulousness, altered mental status, NAUSEA, slurred speech, dizziness, seizures, numbness; acts as a negative inotrope so probably dont want to give to someone with CHF because it will prevent the heart from squeezing |
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Term
| which class of antiarrhythmic drugs are negative inotropic drugs? |
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Definition
| class I drugs. do not give to people with CHF |
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Term
| what are class Ic drugs good for? |
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Definition
| suppressing supraventricular arrhythmias, including atrial fibrillation and flutter in people who are young with structurally normal hearts (remember contraindicated in people with structurally abnormal hearts bc it causes ventricular tachycardia and sudden cardiac death) |
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Term
| what is the Ic drug we need to know? |
|
Definition
|
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Term
|
Definition
| dizziness, lightheadedness, ataxia, paresthesias, constipation, elevated LFTs, nausea, metallic aftertaste (not as much of a risk of proarrhthmia as other Ic drugs, but risk of proarrhythmia in pt with underlying heart disease) |
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Term
| what's the difference between reverse-use dependence drugs and use-dependence drugs? |
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Definition
| reverse-use-dependence drugs work best at rest (i.e. class III drugs, prolong repolarization/QT interval, and QT interval will be longest at REST, so these drugs will therefore have maximal effect at REST); use-dependence drugs work best at a higher heart rate (i.e. class I drugs, esp Ic drugs, block Na channels and prolong depolarization/QRS, and QRS will be largest during exertion, therefore test major effect of drug with exercise) |
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Term
| what are the 2 class III drugs we need to know? |
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Definition
| amiodarone and sotalol (and ibutilide is the IV form of sotalol) |
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Term
| what is important to remember about sotalol? |
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Definition
| it's a class III drug at higher doses and also a beta blocker at low doses (but wouldn't give to someone in lieu of a beta blocker bc its not as strong) |
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|
Term
| sotalol is indicated for? |
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Definition
| adjunctive therapy in treating arrhythmias in patients that have received defibrillators; to treat supraventricular arrhythmias, in particular to treat fibrillation |
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|
Term
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Definition
| class III drug, so torsade; its also a beta blocker so asthma exacerbation, slows the heart beat, RENALLY excreted (CI in people with kidney failure) |
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|
Term
| two drugs to remember that are renally excreted? |
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Definition
|
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Term
| what is amiodarone used for |
|
Definition
| primary therapy for atrial arrhythmias; adjunctive therapy for ventricular arrhythmias in patients with defibrillators; most effective drug to suppress arrhythmias in patients with CHF |
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Term
|
Definition
| pulmonary toxicity/fibrosis (most serious compliation), hyperthyroidism (thyroid repletion to treat), hypothyroidism (ablate or remove the thyroid to treat), corneal deposits in the eyes, blindness, changes color of skin, optic RETINITIS (most serious eye complication) |
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Term
| what is important to know about amioderone's interaction with other drugs? |
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Definition
| increases the digoxin and coumadin levels therefore if giving both to a ptient, decrease the digoxin and coumadin levels by 1/2. when you increase digoxin concentration --> digoxin toxicity --> DADs (frequent VPDs) |
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Term
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Definition
| only IV form of class III drug we have; metabolized by kidney so make sure their K+ and Mg2+ is okaybe |
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|
Term
| beta blockers very useful in what? |
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Definition
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Term
| why should we know adenosine? |
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Definition
| naturally occurring purine, given via IV with a half life of 30 seconds, stops 99% of supraventricular arrhythmias (most potent, short-life drug we have to suppress the AV node, so any arrhythmia that uses the AV node to propagate itself will be suppressed by adenosine) |
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|
Term
| what is digoxin used for? |
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Definition
| as a positive inotrope, also works during phase 3 of AP |
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Term
| what is the mainstay of therapy for reentry? |
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Definition
| beta blockers (get rid of an initiating event, need to slow down one of the paths); class IV drugs can also be used (moreso used as antihypertensives) |
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|
Term
| what prevents triggered activity? |
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Definition
| beta blockers (successful with medications 40-50% of the time, but bc of side effects most often use other methods, ablations etc) |
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Term
| describe polygenic hypercholesterolemia |
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Definition
| polygenic = caused by interaction of several defective genes (diet-induced defective receptors - eating saturated fats cause LDL receptors to not work as well; people are cholesterol hyperabsorbers - 80-90% vs 40-60%) patients are VERY treatable by change in diet, exercise and cholesterol lowering agents; is most prevalent form of hypercholesterolemia |
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Term
| describe monogenic hypercholesterolemia |
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Definition
| familial, only accounts for 5-10% of pts with high cholesterol. caused by a single defective gene --> abn LDL receptor (either totally missing aka null, which is rare, or abnormal LDL apoB100) --> LDL which carries the bulk of the cholesterol is not recognized --> abundance of LDL is now in circulation --> elevated plasma cholesterol, family hx of CAD, coronary events at young age, tendonous xanthoma (extensor tendon nodules), planar xanthoma (scaly yellow lesions), most rapid form of atherosclerosis |
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|
Term
|
Definition
| high TG --> elevated levels of VLDL --> generates LDL and HDL --> LDL becomes oxidiezed and contributes to fatty streak --> HDL taken up by prox tubule of kidney and removed from blood |
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Term
|
Definition
|
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Term
|
Definition
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|
Term
| how do we calculate the non-HDL goal from the LDL goal? |
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Definition
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Term
| what is the highest risk category of coronary heart disease risk? |
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Definition
| established CHD and CHD risk equivalents (risk of having a major coronary event >20% per 10 years): peripheral arterial disease, abdominal aortic aneurysm, symptomatic carotid artery disease, diabetes, multiple risk factors >20% over 10 years |
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Term
| what is the second CHD risk category |
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Definition
| people with multiple CHD risk factors in whom 10 year risk for CHD < or = 20% |
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|
Term
| what is the third CHD risk category |
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Definition
| 0-1 risk factor, 10 year risk of <10% |
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Term
| which drug is contraindicated in combination with statins? |
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Definition
| gemfibrozil; if need to combine statin + fibric acid derivative, use fenofibrate |
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Term
| which hyperlipidemia drug shouldn't be used as monotherapy in people with kidney disease (serum creatinine >1.5 mg/dL)? |
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Definition
| fenofibrate bc it increases serum creatinine; use gemfibrozil |
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|
Term
| which drug shoul not be used in someone with baseline hyper-TG? |
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Definition
| bile acid sequestrant bc it increases TG |
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Term
| what is the mechanism for cholestyramine |
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Definition
| binds bile acid and prevents its reabsorption. increases excretion of bile acids in stool and reduces bile acid pool. --> liver makes more cholesterol and turns it into bile acid and makes more LDL receptors |
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|
Term
| what effect does cholestyramine have on levels of lipids? |
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Definition
| -15-20% LDL, -15% total cholesterol, increase in TG |
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Term
| mechanism for fibric acid derivatives? |
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Definition
| interfere with VLDL synthesis, may increase lipoprotein lipase and may upregulate LDL receptors. work thorugh PPAR. when we increase VLDL metabolism --> increase LDL (but this LDL is large and buoyant, less likely to be oxidized and atherogenic) |
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|
Term
| what effect do fibric acid derivatives have on lipid levels |
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Definition
| -8% LDL and total cholesterol, +8% HDL, -30% trigs |
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|
Term
| what is cholestyramine indicated for? |
|
Definition
| second line drug for managing hypercholesterolemia (used with statins) |
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|
Term
| what are fibric acid derivatives used for? |
|
Definition
| mixed dyslipidemia (elevated LDL and TG, low HDL) |
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|
Term
|
Definition
| constipation, diarrhea, bloating, increase in TG |
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|
Term
| AE of fibric acid derivatives |
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Definition
| gall stones, myopathy, increase LFTs |
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Term
| what are the 2 drugs that are nicotinic acids? |
|
Definition
| niacin (fast acting) and niospan (intermediate release) |
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Term
| mechanism of nicotinic acids? |
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Definition
| inhibit hepatic production of VLDL (almost same as fibric acid derivatives, but SUPER) |
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Term
| what effect do nicotinic acids have on lipid levels? |
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Definition
| -30-60% VLDL-TG, -15-25% LDL, +25-50% HDL |
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|
Term
| how is cholestyramine metabolized |
|
Definition
| not absorbed, passed in stools |
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|
Term
| how is fibric acid derivative metabolized? |
|
Definition
|
|
Term
| how is nicotinic acid metabolized? |
|
Definition
|
|
Term
|
Definition
| LOTS, limits clinical use, must start with a low does and slowly increase. glucose intolerance, gout, rash, flushing, itching, peptic ulcer, hepatotoxicity, arrhythmias |
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|
Term
| what are nicotinic acids used for? |
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Definition
| mixed dyslipidemia, hyperTG |
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|
Term
|
Definition
| selectively inhibits GI absorption of cholesterol by acting at the brush border of the small intestine |
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|
Term
| what effect does ezetimibe have on lipid levels? |
|
Definition
| moderate decrease in LDL, best if used with a statin |
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|
Term
| ezetimibe is contraindicated in people with? |
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Definition
|
|
Term
| ezetimibe is indicated for? |
|
Definition
| people with polygenic hypercholesterolemia |
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|
Term
| statin + cholestyramine =? |
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Definition
| double stimulation for LDL receptor upregulation |
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|
Term
| cholestyramine + nicotinic acid = ? |
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Definition
| upregulate LDL receptor and decrease VLDL production |
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|
Term
|
Definition
| best combination, starting dose of statin + 10mg ezetimibe = like a high dose statin |
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|
Term
| what are the best statins (big ones)? |
|
Definition
| atorvostatin, simvastatin, rosuvastatin |
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|
Term
| what are mid-level statins? |
|
Definition
|
|
Term
| what are low-level statins? |
|
Definition
|
|
Term
| mechanism of statin action? |
|
Definition
| inhibit HMG-COA reductase, block hepatic cholesterol synthesis. upregulation of LDL receptors, enhances VLDL uptake, lowers LDL, lowers TG, raises HDL |
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|
Term
| what does statin do to lipid levels? |
|
Definition
| -40-60% LDL, -16-20% VLDL and TG, +10% HDL |
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|
Term
| what happens when we increase [statin]? |
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Definition
| get a stepwise decrease in cholesterol. every time we double [statin], get -6% LDL |
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|
Term
| which statins are metabolized by CYP3A4? |
|
Definition
| atorvostatin, simvastatin, lovastatin |
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|
Term
| which statins are metabolized by CYP 2C9? |
|
Definition
| rosuvastatin, fluvastatin |
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|
Term
| drugs that inhibit CYP3A4...? |
|
Definition
| increase plasma concentration of statins! ex: antibiotics like clarithromycin, erythromycin, cyclosporine, GRAPEFRUIT juice |
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|
Term
| drugs that induce CYP 3A4...? |
|
Definition
| decrease plasma concentration of statins; ex: phenobarbital, phenytoin, rifampin |
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|
Term
| drugs that inhibit CYP2C9...? |
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Definition
| increase plasma concentration of statins; ex: warfarin, NSAIDs, diazepam |
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|
Term
|
Definition
| rare myopathy, abnormal LFTs, GI distress |
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|
Term
| what are statins used for? |
|
Definition
| first line therapy in treating hypercholesteremia, mixed dyslipidemia at higher doses |
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