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120 Cards in this Set
- Front
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Essential hypertension therapy |
Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs) , calcium channel blockers. |
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HTN + CHF therapy |
Diuretics, ACE inhibitors/ARBs, beta-blockers (in compensated CHF), K+ sparing diuretics |
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contra-indicated in cardiogenic shock: |
beta-blockers |
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HTN + Diabetes mellitus |
ACE inhibitors/ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers |
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Calcium channel blocker names |
Nifedipine, verapamil , diltiazem, amlodipine. |
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MOA of Nifedipine, verapamil , diltiazem, amlodipine. |
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility. |
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Most effective Ca channel blockers for heart |
verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle) |
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Most effective Ca channel blockers for Vascular smooth muscle |
amlodipine = nifedipine > diltiazem > verapamil . |
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adv. effects of Ca channel blockers |
Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation |
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adv effects of which drugs: Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation |
Ca channel blockers |
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Hydralazine clinical use |
Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa.Frequently co-administered with a beta-blocker to prevent reflex tachycardia . |
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Hydralazine MOA |
inc. cGMP -> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction . |
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Hydralazine adverse effects |
Compensatory tachycardia (contraindicated in angina/CAD ) , fluid retention, nausea , headache,angina. Lupus-like syndrome |
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adverse effects of what drug: Compensatory tachycardia (contraindicated in angina/CAD ) , fluid retention, nausea , headache,angina. Lupus-like syndrome |
Hydralazine |
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use which drug?: Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a beta-blocker to prevent reflex tachycardia |
Hydralazine |
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use which drugs in this clinical situation?: Hypertension, angina, arrhythmias, Prinzmetal 's angina, Raynaud's |
Ca channel blockers: nifedipine, verapamil, diltiazem, amlodipine |
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Treatment for malignant Hypertension: |
nitroprusside, fenoldopam |
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fenoldopam MOA: |
Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. dec. BP and inc. natriuresis (Na excretion). |
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Nitroprusside MOA: |
Short acting; t cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide) |
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which drug's MOA: Short acting; inc. cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide) |
nitroprusside |
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which drug's MOA: Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. dec. BP and inc. natriuresis (Na excretion). |
fenoldopam |
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MOA Nitroglycerin, isosorbide dinitrate: |
Vasodilate by releasing nitric oxide in smooth muscle, causing inc in cGMP and smooth musclerelaxation . Dilate veins >> arteries. dec. preload. |
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which drug's MOA: Vasodilate by releasing nitric oxide in smooth muscle, causing inc in cGMP and smooth musclerelaxation . Dilate veins >> arteries. dec. preload. |
Nitroglycerin, isosorbide dinitrate |
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Nitroglycerin, isosorbide dinitrate, CLINICAL USE: |
Angina, pulmonary oedema |
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Nitroglycerin, isosorbide dinitrate adverse effect |
Reflex tachycardia, hypotension, flushing, headache, " Monday disease" in industrial exposure:development of tolerance for the vasodilating action during the workweek and loss of toleranceover the weekend results in tachycardia, dizziness, and headache upon re-exposure . |
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which drug's adverse effect?: Reflex tachycardia, hypotension, flushing, headache |
Nitroglycerin, isosorbide dinitrate |
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HMG -CoA reductase inhibitors |
Lovastatin, pravastatin,simvastatin, atorvastatin,rosuvastatin |
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adv. effects of: lovastatin, pravastatin,simvastatin, atorvastatin,rosuvastatin |
Hepatotoxicity (inc. LFTs), rhabdomyolysis |
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which drugs have this adv. effect?: Hepatotoxicity(inc. LFTs),rhabdomyolysis |
lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin |
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desirable effects lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin |
+++ dec LDL, + inc HDL, + dec triglycerides |
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MOA: lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin |
Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor |
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Which drug's MOA: Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor |
Lovastatin, pravastatin,simvastatin, atorvastatin, rosuvastatin |
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MOA: Niacin (vitamin b3) |
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation |
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Which drug's MOA: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation |
Niacin (vit. B3) |
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Adv. effects of Niacin (vit B3) |
Red, flushed face, which is dec. by aspirin or long-term use. Hyperglycemia (acanthosis nigricans) Hyperuricemia (exacerbates gout) |
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Adv effects of which drug: Red, flushed face,which is dec. by aspirinor long-term use. Hyperglycemia (therefore acanthosis nigricans) Hyperuricemia (exacerbates gout) |
Niacin aka vit b3 |
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desirable effects of Niacin: |
++ dec. LDL, ++ inc HDL, + dec triglycerides |
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Bile acid resins (cholestyramine, colestipol, colesevelam) MOA: |
Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more |
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Which drug's MOA: Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more |
Bile acid resins (cholestyramine, colestipol, colesevelam) |
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Bile acid resin names: |
cholestyramine, colestipol, colesevelam |
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cholestyramine, colestipol, colesevelam adv. effects: |
Patients hate it - tastesbad and causes GI discomfort, dec. absorption of fat-soluble vitamins, Cholesterol gallstones |
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adv effects of which drug: Patients hate it - tastes bad and causes GI discomfort, dec. absorption of fat-soluble vitamins, Cholesterol gallstones |
cholestyramine, colestipol, colesevelam |
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5x Lipid lowering agents: |
HMG - CoA reductase inhibitors, Niacin (vitamin B3), Bile acid resins, Cholesterol absorption blockers, Fibrates |
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desirable effects: cholestyramine, colestipol, colesevelam |
++ dec. LDL, + inc HDL, + inc triglycerides |
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name of the cholesterol absorption blocker: |
ezetimibe |
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ezetimibe class |
cholesterol absorption blocker |
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ezetimibe desirable effect: |
++ dec. LDL. (no effect on HDL/triglycerides) |
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LDL lowering drug that has no effect on HDL of triglyceride levels: |
ezetimibe; cholestrol absorption blocker |
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ezetimibe MOA |
Prevent cholesterol reabsorption at small intestine brush border |
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MOA of what drug: Prevent cholesterol reabsorption at small intestine brush border |
ezetimibe |
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name of fibrates: |
gemfibrozil, clofibrate, bezafibrate, fenofibrate |
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gemfibrozil, clofibrate, bezafibrate, fenofibrate: class and MOA |
Fibrates, Upregulate LPL -> TG clearance |
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MOA of what drug: Upregulate LPL -> TG clearance |
fibrates: gemfibrozil, clofibrate, bezafibrate, fenofibrate |
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ezetimibe adverse effects: |
(Rare): inc. LFTs, diarrhea |
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what drug's adverse effects: Rare inc. LFTs, diarrhea |
ezetimibe: cholestrol reabsorption blockers |
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Fibrates adverse effects: |
Myositis, hepatotoxicity (inc. LFTs), cholesterol gallstones |
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what drug's adverse effects: Myositis, hepatotoxicity (inc. LFTs), cholesterol gallstones |
fibrates: gemfibrozil,clofibrate, bezafibrate,fenofibrate |
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effect of nitrates (Nitroglycerin, isosorbide dinitrate) on contractility and HR |
increased: as a reflex response to decreased preload |
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Treatment of Angina: |
nitrates/beta-blockers/Ca channel blockers (Nifedipine acts like nitrates, verapamil acts like beta-blockers) |
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Cardiac Glycosides name: |
Digoxin |
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Digoxin's pharmacokinetics |
75% bioavailable. 20-40% is protein bound. half life: 40 hours |
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Digoxin Clinical use: |
CHF (inc. contractility); atrial fibrillation (dec. conduction at AV node and depression of SA node). |
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Digoxin's class: |
cardiac glycoside |
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Clinical use of what drug?: |
CHF (inc. contractility) ; atrial fibrillation (dec. conduction at AV node and depression of SA node). |
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Digoxin's MOA |
Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. inc. i.cellular [Ca2+] -> positive inotropy. Also stimulates vagus nerve -> dec. HR |
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MOA of what drug: Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. inc. i.cellular [Ca2+] -> positive inotropy. Also stimulates vagus nerve -> dec. HR |
digoxin |
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adverse effects of digoxin: |
Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG - inc PR, dec. QT, ST scooping (Salvador Dali), T-wave inversion, arrhythmia , AV block. Can lead to hyperkalemia (das bad). |
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factors that predispose to digoxin toxicity: |
Factors predisposing to toxicity- renal failure (dec. excretion ), hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase), quinidine (dec. digoxin clearance; displaces digoxin from tissue-binding sites) |
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antidote to digoxin toxicity: |
Slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab (fragment antigen binding) fragments, Mg2+. mech: (Magnesium suppresses digoxin-induced ventricular arrhythmias while phenytoin and lidocaine suppresses digoxin-induced ventricular automaticity and delay after-depolarizations) |
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Class one antiarrythmics MOA |
- Na+channel blockers. - Local anesthetics. - Slow or block (dec.) conduction (especially in depolarized cells). - dec. slope of phase 0 depolarization and inc. threshold for firing in abnormal pacemaker cells. - Are state dependent(therefore selectively depress tissue that is frequently depolarized [e.g., tachycardia]) |
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factors increasing toxicity of class one antiarrythmics: |
hyperkalaemia |
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names of class 1A antiarrythmics: |
Quinidine, Procainamide, Disopyramide - "The Queen Proclaims Diso's pyramid ." |
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quinidine toxicity: |
cinchonism- headache,tinnitus; thrombocytopenia; torsades de pointes due to inc QT interval |
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procainamide toxicity: |
reversible SLE-like syndrome; thrombocytopenia; torsades de pointes due to inc QT interval |
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disopyramide toxicity: |
heart failure; thrombocytopenia; torsades de pointes due to inc QT interval |
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adv. effects of which drug: cinchonism- headache,tinnitus; thrombocytopenia; torsades de pointes due to inc QT interval |
quinidine |
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adv. effects of which drug: reversible SLE-like syndrome; thrombocytopenia; torsades de pointes due to inc QT interval |
procainamide |
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adv. effects of which drug: heart failure; thrombocytopenia; torsades de pointes due to inc QT interval |
disopyramide |
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quinidine, procainamide, disopyramide desirable effects: |
class 1a anti-arrythmic: inc. AP duration, inc. effective refractory period (ERP), inc. QT interval. Affect both atrial and ventricular arrhythmias, especially re-entrantand ectopic supraventricular and ventricular tachycardia. |
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desirable effects of which drug: inc. AP duration, inc. effective refractory period (ERP), inc. QT interval. Affect both atrial andventricular arrhythmias, especially re-entrant and ectopic supraventricular and ventricular tachycardia. |
quinidine, procainamide, disopyramide (class 1a antiarrythmics) |
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class 1B anti-arrythmics names and primary use: |
lidocaine, mexiletine, tocainide. (+phenytoin) - "1'd Buy LIDO's MEXIcan Tacos" Use: post MI. "1B is Best post MI" |
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lidocaine, mexiletine, tocainide. Desirable effects: |
dec. AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. therefore useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias |
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desirable effects of which drugs: dec. AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. |
class 1b anti-a.ics: lidocaine, mexiletine, tocainide |
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lidocaine, mexiletine, tocainide: adverse effects |
local anesthetic. CS stimulation/depression, cardiovascular depression |
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adv. FX of which drugs: local anesthetic. CS stimulation/depression, cardiovascular depression. |
lidocaine tocainide, mexiletine |
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class 1c antiarrymics names: |
Flecainide, propafenone |
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Flecainide, propafenone: desirable effects: |
class 1c a-a: No effect on AP duration. Useful in ventricular tachycardias that progress to VF and inintractable SVT. Usually used only as last resort in refractory tachyarrhythmias |
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contraindication of Flecainide, propafenone: |
post-MI, Structural heart disease "1C is Contraindicated in structural heart diseaseand post-MI." |
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adverse effect of Flecainide, propafenone |
Proarrhythmic, especially post-MI (contraindicated) . Significantly prolongs refractory period in AV node |
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desirable effects of which drug: Useful in ventricular tachycardias that progress to VF and inintractable SVT. Usually used only as last resort in refractory tachyarrhythmias |
Flecainide, propafenone; class 1c antiarrythmics |
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class 2 antiarrythmics: names and what they block: |
beta blockers: Metoprolol, propranolol, esmolol, atenolol, timolol. |
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metaprolol selectivity: |
B1 selective blocker |
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propanolol selectivity: |
B non-sel blocker |
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esmolol selectivity: |
B1 selective. particularly short acting |
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atenolol selectivity |
B1-selective blocker |
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timolol selectivity |
B-non selective blocker |
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class 2 antiarrythmics' MOA: |
B blockers: Decreases SA and AV nodal activity by dec. cAMP, dec. Ca2 + currents. Suppress abnormal pacemakers by dec. slope of phase 4. AV node particularly sensitive: inc. PR interval |
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B1 selective class 2 a-a drugs: |
atenolol, esmolol, metoprolol |
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B non-sel class 2 a-a drugs: |
propanolol, timolol |
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Metoprolol, propranolol, esmolol, atenolol , timolol adverse effects: |
class 2 a-as: B blockers: Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNSeffects (sedation, sleep alterations). + May mask the signs of hypoglycemia. |
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metoprolol specific adverse effect: |
dyslipidemia. Treat overdose with glucagon |
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propanolol specific adverse effect: |
exacerbate vasospasm in Prinzmetal's angina |
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which drug has this adverse effect?: exacerbate vasospasm in Prinzmetal's angina |
propanolol |
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which drug has this adverse effect?: dyslipidemia |
metoprolol: treat overdose with glucagon |
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class 3 anti-arrythmics: names and what they block: |
Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS). K channel blockers. |
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Amiodarone, Ibutilide, Dofetilide, Sotalol. class and MOA: |
class 3 a-as: K channel blockers: inc AP duration, inc ERP. Used when other anti-arrhythmics fail. inc QT interval. |
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sotalol class and toxicity: |
class 3 a-a: torsades de pointes, excessive beta block |
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ibutilide class and toxicity: |
class 3 a-a: torsades de pointes |
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amiodarone class and toxicity: |
mostly class 3 a-a but has class 1, 2, 3, and 4, effects. pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF). |
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tests that are necessary to monitor for a patient on amiodarone: |
PFT, LFT, TFT. can cause hyper/hypothyroidism, hepatotoxicity, pulm. fibrosis amongst other adv. effects |
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class four a-as: names and MOA: |
verapamil and diltiazem (Ca2+ blockers with cardiac selectivity) |
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diltiazem MOA as an a-a: |
Ca2+ channel blocker: dec. conduction velocity, inc. ERP, inc. PR interval. Used in prevention of nodal arrhythmias (e.g., SVT) |
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class four a-a names and toxicity: |
verapamil, and diltiazem: Constipation, flushing, oedema, CV effects (CHF, AV block, sinus node depression). |
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adverse effects of which drugs: Constipation, flushing, oedema, CV effects (CHF, AV block, sinus node depression). |
class 4 a-as: verapamil and diltiazem |
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a-a Used in prevention of nodal arrhythmias (e.g., SVT |
class 4: verapamil and diltiazem Adenosine |
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Adenosine MOA: |
inc. K+ out of cells -> hyperpolarizing the cell + dec. i.cellular Ca2+. |
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Adenosine desirable effects and half life: |
Drug of choice in diagnosing/abolishingsupraventricular tachycardia. Very short acting (15 sec) |
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Adenosine toxicity and antidote: |
Toxicity includes flushing, hypotension,chest pain. Effects blocked by theophylline and caffeine |
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Mg2+ desirable effects |
Effective in torsades de pointes and digoxin toxicity. |
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therapy for torsades de pointes and dig. toxicity: |
Mg2+ |