Cardiovascular Rx Flashcards by Ijeoma Iko | Brainscape

Q

Nifedipine

A

1) HTN, angina, Prinzmetal’s angina, Raynaud’s
2)Ca2+ Channel Blockers/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility
-more vascular sm. muscle effects
3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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Q

Verapamil

A

1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT)
2)Anti-arrhythmics: Ca2+ Channel Blockers(Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility
-more heart effects – decrease conduction velocity, increase ERP and PR interval
3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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Q

Diltiazem

A

1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT)
2)Anti-arrhythmics: Ca2+ Channel Blockers (Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility
-more heart effects – decrease conduction velocity, increase ERP and PR interval
3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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Q

Amlodipine

A

1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s
2)Ca2+ Channel Blockers/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility
-more vascular smooth muscle effects
3)Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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Q

Hydralazine

A

1)Severe HTN (pregnancy), CHF, reflex tachycardia (w/ beta-blocker)
2)Increase cGMP to cause sm. muscle relaxation
-vasodilates arterioles > veins
-Afterload reduction
3) Compensatory tachycardia, fluid retention, nausea, headache, angina, lupus-like syndrome
4) Contraindicated in angina and CAD

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Q

Nitroprusside

A

1)Malignant HTN
2)Increases cGMP via direct release of NO; short acting
3) Cyanide toxicity

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Q

Fenoldopam

A

1)Malignant HTN
2)Dopamine (D1) receptor agonist
-leads to coronary, peripheral, renal, and splanchnic vasodilation
-decreases BP and increases naturesis

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Q

Nitroglycerin, isosorbide dinitrate

A

1)Angina, pulmonary edema
2)Vasodilator – release of NO in sm. muscle –> increases cGMP and sm muscle relaxation
-dilates veins&raquo_space; arteries (decreases preload)
3) reflex tachycardia, hypotension, flushing, headache
4) “Monday Disease” –> devleop tolerance during the week and loss of tolerance during weekend resulting in side effects

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Q

Lovastatin

A

1)Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2)HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3)Hepatotoxicity (increase LFTs), rhabdomyolysis

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Q

Pravastatin

A

1)Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2)HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3)Hepatotoxicity (increase LFTs), rhabdomyolysis

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Q

Simvastatin

A

1)Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2)HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3)Hepatotoxicity (increase LFTs), rhabdomyolysis

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Q

Atorvastatin

A

1)Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2)HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3)Hepatotoxicity (increase LFTs), rhabdomyolysis

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Q

Rosuvastatin

A

1)Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2)HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3)Hepatotoxicity (increase LFTs), rhabdomyolysis

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Q

Niacin (B3)

A

1)Lipid-lowering agent (decreases LDL and TG, sig increases HDL)
2)Inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion into circulation
3)Red flushed face, hyperglycemia (acanthosis nigrans), hyperuricemia (excerbates gout)

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Q

Cholestyramine

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

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Q

Colestipol

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

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Q

Colesevelam

A

1)Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2)Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3)Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones

Q

Ezetimibe

A

1) Lipid-loweing agents (decrease LDL)
2) Cholesterol Absorption Blockers/Prevent cholesterol reabsorption at small intestine brush border
3) Rare increase in LFTs, diarrhea

Q

Gemfibrozil

A

1)Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2)Fibrates/Upregulates LPL –> increases TG clearance
3)Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Q

Clofibrate

A

1)Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2)Fibrates/Upregulates LPL –> increases TG clearance
3)Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Q

Bezafibrate

A

1)Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2)Fibrates/Upregulates LPL –> increases TG clearance
3)Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Q

Fenofibrate

A

1)Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2)Fibrates/Upregulates LPL –> increases TG clearance
3)Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Q

Digoxin

A

1)CHF (increase contractility), A.fib (decrease conduction at AV node, depression of SA node)
2)Cardiac Glycoside/Direct inhibition of Na+/K+ ATPase leads to indirect inhibtion of Na+/Ca2+ exchanger/antiport –> increases Ca2+ concentration(positive inotropy)
-stimulates vagus nerve to decrease HR
3)Cholinergic –> N/V/D, blurry yellow vision, EKG changes (increased PR, decrased QT, ST scooping, T-wave inversion, arrhythmia, AV block), hyperkalemia
-Factors predisposing to toxicity –> renal failure, hypokalemia, quinidine (decreases clearance)
4)Antidote –> slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg2+

Q

Quinidine

A

1)Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2)Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3)Cinchonism – headache, tinnitus; thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity

Q

Procainamide

A

1)Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2)Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3)Reversible SLE-like syndrome, thrombocytopenia, Torsades de Pointes (increased QT),hyperkalemia causes increased toxicity

Q

Disopyramide

A

1)Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2)Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3)Heart failure, thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity

Q

Lidocaine

A

1)Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2)Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3)Local anesthetic, CNS stimulation/depression, cardiovascular depression
4)Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity

Q

Mexiletine

A

1)Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2)Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3)Local anesthetic, CNS stimulation/depression, cardiovascular depression
4)Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity

Q

Tocainide

A

1)Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2)Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3)Local anesthetic, CNS stimulation/depression, cardiovascular depression
4)Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity

Q

Flecainide

A

1)V.tach that progress to V.fib, intractable SVT, last resort in refractory tachyarrhythmias
2)Anti-arrhythmias: Na+ Channel Blocker (Class IC)/ Slow or block conduction – no effect on AP duration
3)Pro-arrhythmic (esp post-MI), prolongs refractory period in AV node
4)Contraindicated post-MI and in pts with structural abnormalities, hyperkalemia causes increased toxicity

Q

Propafenone

A

1)V.tach that progress to V.fib, intractable SVT, last resort in refractory tachyarrhythmias
2)Anti-arrhythmias: Na+ Channel Blocker (Class IC)/ Slow or block conduction – no effect on AP duration
3)Pro-arrhythmic (esp post-MI), prolongs refractory period in AV node
4)Contraindicated post-MI and in pts with structural abnormalities, hyperkalemia causes increased toxicity

Q

Metoprolol

A

1)V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2)Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3)Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia, dyslipidemia
4)Treat overdose with glucagon

Q

Propranolol

A

1)V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2)Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3)Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia
4)Exacerbate vasospasm in Prinzmetal’s angina

Q

Esmolol

A

1)V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2)Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3)Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia
4)Very short-acting

Q

Amiodarone

A

1)When other anti-arrhythmics fail
2)Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3)Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits (blue/grey) – cause photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) – check PFTs, LFTs, TFTs
4) Has Class I, II, III and IV effects – alters the lipid membrane

Q

Ibutilide

A

1)When other anti-arrhythmics fail
2)Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3)Torsades de Pointes

Q

Dofetilide

A

1)When other anti-arrhythmics fail
2)Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval

Q

Sotalol

A

1)When other anti-arrhythmics fail
2)Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3)Torsades de Pointes, excessive beta-block

Q

Adenosine

A

1)Diagnosing/abolishing SVT
2)Increase K+ removal from cell –> hyperpolarize the cell and decrease I(Ca), very short-acting
3)Flushing, hypotension, chest pain
4)Effects blocked by theophylline and caffeine

Q

Mg2+

A

1)Torsades de Pointes, Digoxin toxicity