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piggy > Cardio - Pharmacology > Flashcards

Cardio - Pharmacology Flashcards

1
Q

Which pharmacologic agents are used to treat essential hypertension?

A

Diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blocks

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2
Q

Which pharmacologic agents are used to treat hypertension in patients with congestive heart failure?

A

Diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blocks, blockers (in compensated congested heart failure only) and potassium-sparing diuretics

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3
Q

Which pharmacologic agents are used to treat hypertension in patients with diabetes mellitus?

A

Angiotensin-converting enzyme inhibitors/angiotensin II receptor blocks, calcium-channel blockers, diuretics, blockers, and -blockers

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4
Q

Why are angiotensin-converting enzyme inhibitors especially important in patients with diabetes mellitus?

A

They have been shown to delay progression to diabetic nephropathy

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5
Q

Which does hydralazine reduce: afterload or preload?

A

Afterload

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6
Q

When hydralazine is administered, which vessels dilate more: veins or arterioles?

A

Arterioles

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7
Q

Hydralazine causes smooth muscle relaxation by increasing concentrations of which substance in endothelial cells?

A

cGMP

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8
Q

Which cardiac adverse effect results from the drop in blood pressure induced by hydralazine?

A

Tachycardia (compensatory)

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9
Q

Does hydralazine cause fluid excretion or retention?

A

Retention

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10
Q

Hydralazine can induce which autoimmune complication in patients?

A

SLE

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11
Q

Why is hydralazine contraindicated in patients with angina or coronary artery disease?

A

Because it can cause compensatory tachycardia

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12
Q

What two agents are first-line therapies for hypertension in pregnancy?

A

Hydralazine with methyldopa

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13
Q

How can the reflex tachycardia that is associated with hydralazine be prevented?

A

By administering it with a blocker

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14
Q

What is the mechanism of action of minoxidil?

A

Minoxidil opens potassium channels on the cell membrane, which causes hyperpolarization and subsequent relaxation of vascular smooth muscle

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15
Q

What are the toxicities of minoxidil?

A

Hypertrichosis, reflex tachycardia, angina, salt retention, and pericardial effusion

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16
Q

A 60-year-old man with severe hypertension presents with complaints of increased hair growth and new chest pain. Toxicity of which antihypertensive drug is most likely causing these symptoms?

A

Minoxidil

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17
Q

Which calcium channel blocker is the most selective for vascular smooth muscle?

A

Nifedipine

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18
Q

Which calcium channel blocker is the most cardio-selective?

A

Verapamil

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19
Q

Which calcium channel blocker cannot be used as an anti-arrhythmic?

A

Nifedipine

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20
Q

What are the clinical indications for the use of calcium channel blockers?

A

Hypertension, angina, arrhythmias (except nifedipine), Prinzmetals angina, and Raynauds disease

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21
Q

Name three pharmaceutical agents that are in the class of calcium channel blockers.

A

Nifedipine, diltiazem, and verapamil

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22
Q

What is the ultimate function of calcium channel blockers?

A

To decrease cardiac and smooth muscle contractility

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23
Q

A patient is started on antihypertensive therapy. One week later he returns complaining of swollen ankles and flushed skin. Which class of medication was he likely prescribed?

A

Calcium channel blockers

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24
Q

Are nitrates more effective as preload or afterload reducers?

A

Preload reducers

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25
Q

Does isosorbide dinitrate dilate veins or arteries more?

A

Veins

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26
Q

How does nitric oxide cause smooth muscle relaxation?

A

By increasing cGMP concentration

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27
Q

Vasodilation using nitroglycerin is caused by the release of what chemical in smooth muscle?

A

Nitric Oxide

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28
Q

What are two indications for the use of nitroglycerin?

A

Angina and pulmonary edema

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29
Q

Name four adverse effects of nitroglycerin.

A

Reflex tachycardia, hypotension, flushing, and headache

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30
Q

Name three medications indicated to treat malignant hypertension.

A

Nitroprusside, fenoldopam, and diazoxide

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31
Q

Nitroprusside increases the concentration of which substance via direct release of nitric oxide?

A

cGMP

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32
Q

Nitroprusside is a _____ (short/long) -acting drug.

A

Short

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33
Q

Fenoldopam is an agonist of which receptor?

A

Dopamine D1; D1 activity relaxes renal vasculature

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34
Q

Diazoxide causes relaxation of vascular smooth muscle by opening which membrane channel?

A

Potassium

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35
Q

Name an adverse effect of diazoxide.

A

Hyperglycemia, secondary to a reduction in insulin release

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36
Q

What is the mechanism by which pharmacologic treatments can reduce angina?

A

The reduction of myocardial oxygen consumption by decreasing one or more of the determinants of oxygen consumption: end diastolic volume, blood pressure, heart rate, contractility, and/or ejection time

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37
Q

Among the calcium channel blocker, which acts most like nitrates in treating angina? Which acts like a blocker?

A

Nifedipine; verapamil

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38
Q

What are the effects of nitrates, blockers, and a combination of both on end diastolic volume?

A

Blockers increase end diastolic volume, nitrates decrease end diastolic volume, and a combination of both either has no effect or decreases end diastolic volume

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39
Q

What are the effects of nitrates, blockers, and a combination of both on blood pressure?

A

Blockers, nitrates, and a combination of both all decrease blood pressure

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40
Q

What are the effects of nitrates, beta blockers, and a combination of both on contractility?

A

Blockers decrease contractility, nitrates increase contractility (as a reflex response), and a combination of both has little/no effect on contractility

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41
Q

What are the effects of nitrates, blockers, and a combination of both on heart rate?

A

Blockers decrease heart rate, nitrates increase heart rate (as a reflex response), and a combination of both decreases heart rate

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42
Q

What are the effects of nitrates, blockers, and a combination of both on ejection time?

A

Blockers increase ejection time, nitrates decrease ejection time, and a combination of both has little/no effect on ejection time

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43
Q

What are the effects of nitrates, blockers, and a combination of both on myocardial oxygen consumption?

A

Blockers and nitrates decrease myocardial oxygen consumption, but a combination of both severely decreases myocardial oxygen consumption

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44
Q

Which two beta-blockers are contraindicated in angina and why?

A

Pindolol and acebutolol because they are partial beta-agonists and can increase myocardial oxygen consumption

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45
Q

Which drugs have the most powerful low-density lipoprotein-lowering effects?

A

Statins have the strongest reducing effect of all of the lipid-lowering drugs

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46
Q

Other than statins, which drugs are indicated for lowering low-density lipoprotein levels?

A

Niacin, which lowers low-density lipoprotein levels, although less than statins

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47
Q

Which lipid-lowering agent causes the greatest increase in high-density lipoprotein levels? Which agents cause a more modest increase?

A

Niacin causes the greatest increase in high-density lipoprotein levels; statins have a moderate effect on high-density lipoprotein levels

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48
Q

Which lipid-lowering agents cause the most significant reduction in triglycerides? Which have a more modest benefit?

A

Fibrates reduce triglycerides most significantly; statins, bile acid resins, and niacin have a moderate effect in this regard

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49
Q

What adverse effects do HMG-CoA reductase inhibitors (eg, lovastatin, atorvastatin) have?

A

Elevated liver enzymes (which is reversible) and rhabdomyolysis

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50
Q

What adverse effects does niacin have?

A

Facial flushing, which can be reduced with the use of aspirin and decreases over time; hyperglycemia; and hyperuricemia

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51
Q

What adverse effects do bile acid resins (cholestyramine) have?

A

Bad taste, gastrointestinal discomfort, a decreased effect on the absorption of fat-soluble vitamins, and the production of cholesterol gallstones

52
Q

What adverse effects do fibrates (eg, gemfibrozil, clofibrate) have?

A

Elevated liver enzymes and myositis

53
Q

Which category of lipid-lowering agents works by inhibiting the formation of the cholesterol precursor mevalonate?

A

HMG-CoA reductase inhibitors; this is the rate-limiting step in cholesterol synthesis

54
Q

Which lipid-lowering agent works by inhibiting lipolysis in adipose tissue and reducing hepatic very-low-density lipoprotein secretion into circulation?

A

Niacin

55
Q

Which category of lipid-lowering agents works by preventing the intestinal reabsorption of bile acids, causing increased hepatic usage of cholesterol to replenish the bile acids?

A

Bile acid resins (cholestyramine, colestipol)

56
Q

Which category of lipid-lowering agents works by preventing cholesterol reabsorption at the small intestine brush border?

A

Cholesterol absorption blockers (ezetimibe)

57
Q

Which category of lipid-lowering agents works by upregulating lipoprotein lipase, causing increased triglyceride clearance from the blood?

A

Fibrates (gemfibrozil, clofibrate, fenofibrate, bezafibrate)

58
Q

A 50-year-old man with hypercholesterolemia is deficient in vitamins A, D, E and K. He also complains of gastrointestinal discomfort since starting a lipid-lowering agent. Which lipid-lowering agent is the most likely cause?

A

Bile acid resins

59
Q

Which class of lipid-lowering agents is contraindicated in patients with gallstones?

A

Bile acid resins

60
Q

A patient has recently started taking lovastatin. He presents with diffuse muscle pain and weakness. Which lab test should be ordered?

A

Creatine kinase to test for rhabdomyolysis

61
Q

Which poison inhibits the calcium release channel in the sarcoplasmic reticulum?

A

Ryanodine

62
Q

Digoxin inhibits which mechanism of transport in the cell membrane?

A

Na+/K+/adenosine triphosphatase

63
Q

Why is external calcium referred to as trigger calcium in the cardiac myocyte?

A

Because it is the trigger for release of intracellular calcium stores from the sarcoplasmic reticulum

64
Q

What is the mechanism by which 1 activation increases cardiac contractility?

A

1 activation causes protein kinase A to phosphorylate L-type calcium channels, increasing intracellular calcium and strengthening contraction

65
Q

Digoxin is removed from the body by _____ excretion.

A

Urinary; as a result, renal failure can cause digoxin toxicity

66
Q

What is the mechanism of action of digoxin?

A

By inhibiting the cardiac myocyte sodium/potassium pump, digoxin also prevents sodium/calcium exchange, increasing intracellular calcium concentration

67
Q

What is the effect of increased intracellular calcium on cardiac function?

A

Positive inotropy

68
Q

Because it can increase contractility, digoxin is used to treat what condition?

A

Congestive heart failure

69
Q

By what mechanism is digoxin beneficial in atrial fibrillation?

A

Digoxin decreases conduction at the atrioventricular node and causes depression of the sinoatrial node

70
Q

What are three common gastrointestinal complaints that occur with digoxin use?

A

Nausea, vomiting, and diarrhea

71
Q

What vision complaint can occur with digoxin use?

A

Blurry yellow vision

72
Q

What potential heart problem can arise with the use of digoxin?

A

Arrhythmia

73
Q

What factors increase the likelihood of digoxin toxicity?

A

Kidney failure (because of decreased excretion), hypokalemia, and quinidine (due to displacement of tissue-binding sites)

74
Q

What is the approach to treatment of digoxin toxicity?

A

Slow normalization of potassium levels, lidocaine, a cardiac pacer, anti-digoxin antibodies, and magnesium

75
Q

How does hypokalemia increase the toxicities of digoxin?

A

Potassium competes with digoxin at the same binding site in sodium/potassium adenosine triphosphatase, so hypokalemia allows for increased digoxin binding, and thus increased digoxin toxicities

76
Q

What are some potential electrocardiogram findings in a patient who has digoxin toxicity?

A

Prolonged PR interval, shortened QT interval, scooping, T-wave inversion, arrhythmia, and signs of hyperkalemia

77
Q

What is the ultimate mechanism of action of cardiac glycosides?

A

To increase intracellular calcium (thereby acting as a positive inotrope), and to stimulate the vagus nerve

78
Q

A patient on procainamide for an arrhythmia develops facial rash and joint pain. She is found to have antihistone antibodies in her serum. What is the diagnosis?

A

Reversible systemic lupus erythematosus-like syndrome

79
Q

Quinidine causes symptoms of headache and tinnitus, which are collectively known as what?

A

Cinchonism; which can occur with all quinine derivatives

80
Q

What effect do class IC antiarrhythmics have on action potential duration?

A

They have no effect on action potential duration

81
Q

Which antiarrhythmics are indicated to prevent arrhythmia after myocardial infarction? Which are contraindicated?

A

Class IB antiarrhythmics are indicated to prevent arrhythmia after myocardial infarction, but class IC antiarrhythmics are contraindicated

82
Q

What is the toxicity of class IC antiarrhythmics?

A

They are proarrhythmic because they increase the refractory period of the atrioventricular node; especially in patients who have recently had a myocardial infarction; these drugs are only used as a last resort

83
Q

Name the class IB antiarrhythmic drugs.

A

Class IB antiarrhythmics are Lidocaine, Mexiletine, and Tocainide (remember: Id Buy Lidys Mexican Tacos)

84
Q

What electrolyte abnormality increases the toxicity of class I antiarrhythmics?

A

Hyperkalaemia

85
Q

Which antiarrhythmics belong to class IA?

A

Quinidine, Procainamide, and Disopyramide; remember the mnemonic The Queen Proclaims Disos pyramid

86
Q

Which antiepileptic drug can also act as a class IB antiarrhythmic?

A

Phenytoin

87
Q

How do sodium channel blocker antiarrhythmics work?

A

They act as local anesthetics, in that they slow or block conduction by decreasing the slope of phase 4 depolarization and increasing the threshold for firing in abnormal pacemaker cells

88
Q

What does it mean when sodium channel blockers are described as state dependent?

A

State dependent means that the antiarrhythmics act only on tissue that is frequently depolarized (eg, fast tachycardia)

89
Q

What effect do class IA antiarrhythmics have on the electrical activity of the heart?

A

They increase the action potential duration, increase the effective refractory period, and increase the QT interval

90
Q

What are class IA antiarrhythmics used for?

A

To treat atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia

91
Q

What are the adverse effects of quinidine?

A

Cinchonism (headache and tinnitus), thrombocytopenia, and torsades de pointes (due to prolonged QT)

92
Q

What do class IB antiarrhythmics do?

A

They decrease action potential duration and preferentially affect ischemic Purkinje and ventricular tissue

93
Q

What are class IB antiarrhythmics used for?

A

To treat ventricular arrhythmia (especially after myocardial infarction) and in digitalis-induced arrhythmias

94
Q

What are the adverse effects of class IB antiarrhythmics?

A

They can cause central nervous system stimulation or depression and cardiovascular depression

95
Q

What are class IC antiarrhythmics useful for?

A

As a last resort in ventricular tachycardia that may progress to ventricular fibrillation, and in intractable supraventricular tachycardia

96
Q

Which antiarrhythmics belong to class IC?

A

Flecainide, encainide, and propafenone (remember: Chipotles Food has Excellent Produce)

97
Q

Which blocker is shortest acting?

A

Esmolol

98
Q

Which cardiac node is most sensitive to blockers: the sinoatrial node or the atrioventricular node?

A

The atrioventricular node; as a result, the PR interval is lengthened on electrocardiogram

99
Q

Which antiarrhythmics belong in class II?

A

Blockers, such as propranolol, esmolol, timolol, metoprolol, and atenolol

100
Q

What is the mechanism of action of blockers?

A

Blockers decrease cAMP and calcium ion current and suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker action potential

101
Q

What is the clinical use of blockers?

A

To treat ventricular tachycardia and supraventricular tachycardia and to slow ventricular rate during atrial fibrillation and atrial flutter

102
Q

What are the toxicities of blockers?

A

Impotence, asthma exacerbation, cardiovascular effects (bradycardia, atrioventricular block, and congestive heart failure), central nervous system effects (sedation and sleep alterations)

103
Q

Which adverse effect is specific to metoprolol as opposed to other blockers?

A

Dyslipidemia

104
Q

What is the antidote for blocker overdose?

A

Glucagon

105
Q

Why might blockers be dangerous for someone who takes insulin?

A

Because they can mask signs of hypoglycemia

106
Q

What three types of testing must be periodically performed for patients who are taking amiodarone?

A

Pulmonary function testing, liver function testing, and thyroid function testing

107
Q

Which antiarrhythmics belong to class III?

A

Potassium channel blockers, such as sotalol, ibutilide, bretylium, dofetilide, and amiodarone

108
Q

What is the mechanism of action of potassium channel blockers?

A

They increase the action potential duration, increase the effective refractory period, and increase the QT interval

109
Q

Name two toxicities of sotalol.

A

Torsades des pointes and excessive blockade

110
Q

Name a potentially fatal adverse effect of ibutilide.

A

Torsades des pointes

111
Q

What are two toxicities of bretylium?

A

New arrhythmias and hypotension

112
Q

Name eight toxicities of amiodarone.

A

Pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism, corneal deposits, blue-gray skin deposits, neurologic effects, constipation, and cardiovascular effects (bradycardia, heart block, and congestive heart failure)

113
Q

Why does amiodarone have class I, II, III, and IV effects?

A

Because it alters the lipid membrane

114
Q

Why is amiodarone likely to interfere with thyroid function?

A

Because it is 40% iodine by weight

115
Q

Class IV antiarrhythmics primarily affect which cardiac myocytes?

A

Atrioventricular nodal pacemaker cells

116
Q

How do class IV antiarrhythmics affect conduction velocity through the atrioventricular node?

A

Decrease

117
Q

How do class IV antiarrhythmics affect the refractory period of cardiac myocytes?

A

Increase

118
Q

How do class IV antiarrhythmics affect PR intervals on electrocardiogram?

A

Increase; due to slowed conduction through the atrioventricular node

119
Q

Which two antiarrhythmic drugs belong to class IV?

A

Diltiazem and verapamil

120
Q

What is the clinical use of calcium channel blockers?

A

They are used in the prevention of nodal arrhythmias, such as supraventricular tachycardia

121
Q

What are the adverse effects of calcium channel blockers?

A

Constipation, flushing, edema, and cardiovascular effects (congestive heart failure, atrioventricular block, sinus node depression)

122
Q

Which antiarrhythmic is a first-line drug for diagnosing and abolishing supraventricular tachycardia?

A

Adenosine

123
Q

Which ion is infused for treatment of torsades des pointes and digoxin toxicity?

A

Magnesium

124
Q

What is the mechanism of action of adenosine?

A

Adenosine increases the amount of potassium flowing out of cells, leading to hyperpolarization of the cell

125
Q

What is the duration of action of adenosine?

A

Adenosine is a short (about 15 seconds)-acting drug

126
Q

What are three toxicities of the antiarrhythmic drug adenosine?

A

Flushing, hypotension, and chest pain

piggy (83 decks)

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