Term
| Which five drug types are used to prevent myocardial infacts? |
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Definition
| Prevent MI's with: ASA, B-blockers, ACE Inhibitors, Anti-platelets and anti-coagulants |
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Term
| Which five drugs can be used to treat dyslipidemia? |
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Definition
| Treat dyslipidemia with: Bile-acid binding resin, statins, cholesterol absorption inhibitors, fibrates and Niacin |
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Term
| Bile Acid Binding Resins (ex. Cholestyramine and colestipol) |
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Definition
| Bile acids excreted, so LDL removed from blood. Decent at lowering LDL and increasing HDL, but not great. Interferes with absorptions of many other drugs. Adjunt to Statins. |
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Term
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Definition
| Most efficacious for dyslipidemia. Inhibit HMG-CoA reductase. May cause myopathy and hepatotoxicity, also improves endothelial cell Fx, increases plaque stability and reduces inflammation |
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Term
| Cholesterol absorption blocker (Ezetimibe) |
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Definition
| Ezetimibe, only modest effect vs. dyslipidemia, but very few side effects. Combine with statins, do not mix with bile acid binding resins. |
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Term
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Definition
| Best increase in HDLs. Use for hypertriglyceridemia w/ low HDL. Flushing and hepatotoxicity are major problems, may increase myopathy of Statins. |
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Term
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Definition
| Very good against TG's, and for Type II Diabetes. Binds to PPAR-alpha. May cause hair loss, or even increase LDLs in some patients. For dyslipidemia. |
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Term
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Definition
| Stable angina: Due to increase O2 demand and coronary atherosclerosis. Precipitated by exercise, eating, stress. Lasts 1-5 minutes, relieved by rest or nitroglycerin. |
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Term
|
Definition
| Variant angina: occurs at rest, often at night, due to coronary vasospasm. |
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Term
| What four drugs could you use to treat stable angina? |
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Definition
| Treat stable angina with: B-blockers, Ranolazine, Nitrates and Calcium Channel blockers |
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Term
| What two drugs would you use to treat Variant Angina? |
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Definition
| Variant Angina: Nitrates, Calcium Channel blockers |
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Term
| Nitrates (nitroglycerin, isosorbide dinitrates) |
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Definition
| Nitrates: Form NO, which stimulates cGMP -> vasodilation and decreased platelet aggregation. Causes severe headaches. Tolerance is a problem. Potentiated by PDE5 inhibitors (ex. Sildenafil.) Good for acute decompensation and stable angina. |
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Term
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Definition
| B-Blockers: Prophylaxis for stable angina (unpredictable for variant angina). Treat STABLE heart failure, prolong survival by 35%! Sx worsen initially, then improve. Abrupt withdrawl is bad, can cause broncho-constriction. |
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Term
Calcium Channel Blockers
("-dipines")
(Diltiazem, Verapamil) |
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Definition
| Relax vasculature. (D,V) also decrease HR and contractility. For stable or variant angina. Should not be combined with B-blockers...many drug interactions. Can cause headache, leg edema, dizziness. |
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Term
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Definition
| Ranolazine: Blocks "late" Na+ current -> heart uses more Glc. Prophylaxis for stable angina. Very safe, use with all other angina drugs. |
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Term
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Definition
| Unstable Angina is "acute coronary syndrome". Angina > 20 min. Due to inadequate O2 supply to myocardium. Thrombosis plays a major role in causing unstable angina- often non-occlusive thrombus. |
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Term
| What two drug classes are used to treat unstable angina? |
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Definition
| Unstable angina (usually from non-occlusive thrombi) can be treated with anti-platelets or anti-coagulants |
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Term
| Name three anti-platelet drugs |
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Definition
| ASA, ADP Inhibitors, GP IIb/IIIa receptor inhibitors |
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Term
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Definition
| Permanently acetylates COX1, decreases TA2 production. 50% reduction in risk of death or MI. Risk of bleeding, 5-8% of people resist anti-platelet effects. |
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Term
| ADP Inhibitors (clopidogrel, ticlopidine) |
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Definition
| ADP Inhibitors: Inhibit binding of ADP to Platelets. 20-35% risk reduction. Use with ASA. Can cause Neutropenia or thrombocytopenic purpura. Less bleeding than ASA. |
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Term
| GP IIb/IIIa Receptor Inhibitor (Abciximab, eptifibatide, tirofiban) |
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Definition
| Antibodies that prevent fibrinogen mediated x-linking of platelets. 9% risk reduction. Given IV, used with ASA and heparin. Risk of thrombocytopenia and bleeding. Short duration, good for percutaneous coronary interventions. |
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Term
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Definition
| Catalyzes action of anti-thrombin, prevents coagulation. LMWH works on factor Xa. Heparin = 33% risk reduction, LMWH = 66% reduction. Heparin is given IV, LMWH is given SubQ. LMWH has better pharmacokinetics. Some risk of bleeding. |
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Term
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Definition
| Synthetic drug that blocks factor Xa. Similar effect as Heparin, 100% bioavailable. Maybe better than Heparin, but very expensive. Risk of bleeding. |
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Term
| Direct thrombin inhibitors (ex. lepirudin, argatroban) |
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Definition
| Leech based- bind thrombin and prevent substrate access. Given IV, stable anticoagulation, but not yet proven beneficial in unstable angina. Some risk of bleeding. |
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Term
| Name three drug classes important in treating acute myocardial infaction |
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Definition
| Treat acute MI with: Fibrinolytics, Analgesics and Renin-angiotensin inhibitors |
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Term
| Fibrinolytics (alteplase, reteplase, tenecteplase) |
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Definition
| Fibrinolytics, used for acute MI: activate bound plasminogen. Recanalize thrombotic occlusions. Increase survival by 18%, reduces infarct size. Given IV, ASAP. Risk of bleeding, stroke (esp. if given w/ Heparin). Best for ppl w/ Diabetes, least in elderly or ppl w/ hypertension. |
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Term
| Analgesics (morphine, meperidine, pentazocine) |
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Definition
| Stimulate mu-type receptors, reduce pain, anxiety and autonomics. Given IV. Can cause hypotension, vomiting, depression of respiration. For acute MI or unstable angina. |
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Term
| Renin-Angiotensin Inhibitors (ACE Inhibitors: enalapril, lisinopril) and (ARBs: valsartan, candesartan) |
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Definition
| ACEI: block angiotensin formation and ARBs: block access of angiotension to receptor. Increases Na/H2O excretion, but also REDUCES VENTRICULAR REMODELING, give following ASA and B-blockers. Very good for elderly, ppl w/ previous MI or CHF. In CHF improves survival 5-25%. ACEI can cause cough or angioedema. |
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Term
| What class of drugs are used to prevent a secondary MI? |
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Definition
| Oral anticoagulants (ex. Warfarin), B-blockers, ASA, anti-platelets, ACEI or ARBs, lipid-lowering drugs. |
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Term
| Oral anticoagulants (ex. Warfarin) |
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Definition
| Block synthesis of reduced form of Vit. K, interferes with clotting cascade. Risk of bleeding, skin necrosis, drug-drug interactions. |
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Term
| What are the characteristics of systolic dysfuncion in heart failure? |
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Definition
| Systolic dysfunction: Decreased ejection fraction, decreased contractility, and ventricular dilation. |
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Term
| What are the characteristics of diastolic dysfunction in heart failure? |
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Definition
| Diastolic dysfunction: Preserves ejection fraction, ventricles become stiff and fibrous, decreased ventricular filling. Associated with diabetes and hypertension. No good Tx. |
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Term
| Name the four main drug classes used to treat stable chronic heart failure |
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Definition
| Stable chronic heart failure: Diuretics, Renin-angiotensin inhibitors, B-blockers, aldosterone antagonists |
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Term
| Name four major drug classes used to treat acutely decompensated heart failure |
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Definition
| Acutely decompensated heart failure: diuretics, nitrates, B-agonists, Phosphodiesterase inhibitors |
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Term
| Loop diuretics (ex. furosamide) |
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Definition
| Inhibits Na/K/Cl transporter on ASCENDING loop of Henle. Good at clearing edema and dyspnea, most effective diuretic. Good for acute decompensation or CHF. Beware hypokalemia. Potentiated by renin-angiotensin inhibitors. Does not prolong survival. |
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Term
| Thiazide diuretics (Metolazone, hydrochlorothiazide) |
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Definition
| Good for hypertension or chronic stable heart failure. Inhibits Na/Cl transport on distal tubule. No effect on survival. Increases uric acid (gout!) and blood Glc (diabetes!), often used w/ K+ sparing diuretic. Potentiated by Renin-angiotensin Inhibitors. |
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Term
| K+ sparing diuretics (Amiloride, triamterene) |
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Definition
| Blocks Na+ channels in distal tubule and collecting ducts. Very low efficacy alone, but helps prevent K+ loss- use with other diuretics. Risk of hyperkalemia. |
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Term
| Aldosterone antagonists (spironolactone, eplerenone) |
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Definition
| Block EXPRESSION of Na+ channels in distal tuble and collecting ducts, antagonist for aldosterone receptor in kidney. Saves k+, low efficacy diuretic, also PREVENTS VENTRICULAR REMODELING. Prolongs survival up to 25%, for severe CHF. Risk of hyperkalemia and gynecomastia. |
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Term
| Direct Arterial Vasodilators (Hydralazine) |
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Definition
| Hydralazine: mechanism unknown. Doesn't improve survival. Part of Bidil for blacks. |
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Term
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Definition
| Good for severe heart failure, increases contracticlity & PNS, decreases SNS, improves exercise tolerance. No effect on survival. Very low therapeutic index, many drug-drug interactions. |
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Term
| B-adronergic agonists (dopamine, dobutamine) |
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Definition
| Increase HR and contractility, increase renal blood flow. Increase CO, decrease filling pressure. No effect on survival, may cause tachycardia. |
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Term
| Phosphodiesterase Inhibitors (amrinone, milrinone, enoximone) |
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Definition
| Increases cAMP, intracellular Ca2+, increases contractility. Use only for acute decompensation. Good when you can't give DA b/c patient on a B-blocker. May DECREASE survival. |
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Term
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Definition
| Recombinant form of BNP. Increases cardiac output, decreases filling pressure. Only for acute decompensation, no effect on survival. |
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Term
| Name three factors that can cause arrhythmias |
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Definition
| 1) alterations in extracellular electrolyte concentrations, 2) neural, hormonal or drug actions on heart, 3) intrinsic changes (ex. ischemic damage) |
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Term
| Class IA antiarrhthmics (quinidine, procainamide) |
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Definition
| Blocks Na and K channels. Prolongs QRS and QT waves. "broad spectrum" antiarrhythmics. May cause arrhythmias. |
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Term
| Class IB antiarrhythmics (lidocaine, mexiletine, phenytoin) |
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Definition
| Blocks Na channels when HR is high or in ischemic damage. "Selective" for abnormal tissue. Decreases QT interval. Useful for digoxin-induced arrhythmias, or ischemia induced arrythmias. Little effect on ECG of normal hearts. |
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Term
| Class IC antiarrhythmic (flecainide, moricizine) |
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Definition
| Blocks Na channels. Decreases conduction, increases QRS interval. Good for SERIOUS ventricular arrhythmias and AV node re-entry tachycardia. Prone to cause arrhythmias. |
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Term
| Class II antiarrhythmic drugs (B-blockers) |
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Definition
| Increase PR interval (reflects delay of AV node), controls ventricular rate in atrial flutter/fibrilation. Good at decreasing sudden cardiac death after MI |
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Term
| Class III antiarrhythmic drugs (amiodarone, bretylium, sotalol) |
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Definition
| Widely used, block K channel. Increase refractoriness, increase QT interval and decrease PR interval. Good for a wide range of arrhythmias- less likely to cause arrhythmias. |
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Term
| Class IV antiarrhythmic drugs (verapamil, diltiazem- Ca2+ channel blockers) |
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Definition
| decrease AV node conduction. Increase PR interval. Good for AV nodal re-entry tachycardia or ventricular rate control in A-Fib (similar effect as B-blockers) |
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Term
| Digoxin as an anti-arrhythmic |
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Definition
| Blocks Na/K ATPase, decreases AV conduction, increases PR interval. For ventricular rate control, but prone to cause arrhythmias. |
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Term
|
Definition
| Opens K channels and decreases cAMP levels. Decreases sinus node rate, increases PR interval. For AV node reenetry tachycardia. Short duration of action, given IV. |
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Term
| What three physiological mechanisms oppose a fall in blood pressure? |
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Definition
| 1) renin-angiotensin-aldosterone system, 2) SNS, 3) fluid retention by the kidney |
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Term
| What anti-hypertensive medication is OK to take with NSAIDs? |
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Definition
| Ca2+ channel blockers are good for BP and can be taken w/ NSAIDs. |
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Term
|
Definition
| Blocks activity of renin. Increases Na/H20 exretion and decreases TPR. Strongly potentiated by a diuretic, can be combined with ACEI or ARB. Not for pregnant women. Expensive. |
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Term
| Alpha adrenergic blockers (doxazosin, terazosin) |
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Definition
| Block alpha-1 receptors. Decrease TPR. Tolerance is a problem. Good with diuretics. Reduce BP. |
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Term
| Centrally acting sympatholytics (clonidine, methyldopa) |
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Definition
| Activate alpha-2 receptors in brainstem. Decrease SNS activity. Limited to resistant hypertension. Can cause dry mouth, bradycardia. Rebound hypertension w/ discontinuation. Methyldopa can be used in pregnant women. |
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Term
| Direct Arterial Vasodilators- for hypertension |
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Definition
| Used in combination w/ diuretics and B-blockers. For resistant hypertension. |
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Term
| What is the antidote for Carbon Monoxide poisoning? |
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Definition
|
|
Term
| What is the antidote for Iron poisoning? |
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Definition
|
|
Term
| How do you treat lead poisoning? |
|
Definition
| Chelate with succimer, EDTA or penicillamine |
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Term
| How do you treat Mercury poisoning? |
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Definition
| Hemodialysis or chelate with succimer, EDTA, or British Anti-lewisite |
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Term
| What is the antidote for Acetaminophen poisoning? |
|
Definition
| N-acetylcysteine (mucomist) |
|
|
Term
| What is the antidote for Cyanide poisoning? |
|
Definition
|
|
Term
| What is the antidote for Nitrite poisoning? |
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Definition
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