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Drugs > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Cardiovascular

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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2
Q

Cardiovascular

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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3
Q

Cardiovascular

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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4
Q

Cardiovascular

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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5
Q

Cardiovascular

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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6
Q

Cardiovascular

Nitroprusside

A

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

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7
Q

Cardiovascular

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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8
Q

Cardiovascular

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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9
Q

Cardiovascular

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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10
Q

Cardiovascular

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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11
Q

Cardiovascular

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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12
Q

Cardiovascular

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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13
Q

Cardiovascular

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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14
Q

Cardiovascular

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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15
Q

Cardiovascular

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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16
Q

Cardiovascular

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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17
Q

Cardiovascular

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

18
Q

Cardiovascular

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

19
Q

Cardiovascular

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

20
Q

Cardiovascular

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

21
Q

Cardiovascular

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

22
Q

Cardiovascular

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

23
Q

Cardiovascular

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+

24
Q

Cardiovascular

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

25
Q

Cardiovascular

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

26
Q

Cardiovascular

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

27
Q

Cardiovascular

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

28
Q

Cardiovascular

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

29
Q

Cardiovascular

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

30
Q

Cardiovascular

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

31
Q

Cardiovascular

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

32
Q

Cardiovascular

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

33
Q

Cardiovascular

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

34
Q

Cardiovascular

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

35
Q

Cardiovascular

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

36
Q

Cardiovascular

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

37
Q

Cardiovascular

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

38
Q

Cardiovascular

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

39
Q

Cardiovascular

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

40
Q

Cardiovascular

Mg2+

A

1)Torsades de Pointes, Digoxin toxicity

Drugs (16 decks)

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