Copy of Cardiovascular Rx - Sheet1

Question 1

Nifedipine

Answer 1

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

Question 2

Verapamil

Answer 2

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

Question 3

Diltiazem

Answer 3

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

Question 4

Amlodipine

Answer 4

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

Question 5

Hydralazine

Answer 5

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

Question 6

Nitroprusside

Answer 6

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

Question 7

Fenoldopam

Answer 7

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

Question 8

Nitroglycerin, isosorbide dinitrate

Answer 8

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

Question 9

Lovastatin

Answer 9

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

Question 10

Pravastatin

Answer 10

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

Question 11

Simvastatin

Answer 11

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

Question 12

Atorvastatin

Answer 12

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

Question 13

Rosuvastatin

Answer 13

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

Question 14

Niacin (B3)

Answer 14

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), Hepatitis

Question 15

Cholestyramine

Answer 15

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

Question 16

Colestipol

Answer 16

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

Question 17

Colesevelam

Answer 17

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

Question 18

Ezetimibe

Answer 18

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

Question 19

Gemfibrozil

Answer 19

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

Question 20

Clofibrate

Answer 20

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

Question 21

Bezafibrate

Answer 21

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

Question 22

Fenofibrate

Answer 22

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

Question 23

Digoxin

Answer 23

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+

Question 24

Quinidine

Answer 24

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

Question 25

Procainamide

Answer 25

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

Question 26

Disopyramide

Answer 26

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

Question 27

Lidocaine

Answer 27

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

Question 28

Mexiletine

Answer 28

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

Question 29

Tocainide

Answer 29

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

Question 30

Flecainide

Answer 30

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

Question 31

Propafenone

Answer 31

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

Question 32

Metoprolol

Answer 32

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

Question 33

Propranolol

Answer 33

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

Question 34

Esmolol

Answer 34

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

Question 35

Amiodarone

Answer 35

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

Question 36

Ibutilide

Answer 36

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

Question 37

Dofetilide

Answer 37

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

Question 38

Sotalol

Answer 38

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

Question 39

Adenosine

Answer 39

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

Question 40

Mg2+

Answer 40

1)Torsades de Pointes, Digoxin toxicity