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
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
- Beta blockers (in compensated congested heart failure only)
- Potassium-sparing diuretics
3
Q
Which pharmacologic agents are used to treat hypertension in patients with diabetes mellitus?
A
Angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers (ARBs), calcium-channel blockers, diuretics, α-blockers, and β-blockers
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
5
Q
Which does hydralazine reduce: afterload or preload?
A
Afterload
6
Q
When hydralazine is administered, which vessels dilate more: veins or arterioles?
A
Arterioles
7
Q
Hydralazine causes smooth muscle relaxation by increasing concentrations of which substance in endothelial cells?
A
cGMP
8
Q
Which cardiac adverse effect results from the drop in blood pressure induced by hydralazine?
A
Tachycardia (compensatory)
9
Q
Does hydralazine cause fluid excretion or retention?
A
Retention
10
Q
Hydralazine can induce which autoimmune complication in patients?
A
Systemic lupus erythematosus
11
Q
Why is hydralazine contraindicated in patients with angina or coronary artery disease?
A
Because it can cause compensatory tachycardia
12
Q
What two agents are first-line therapies for hypertension in pregnancy?
A
Hydralazine with methyldopa
13
Q
How can the reflex tachycardia that is associated with hydralazine be prevented?
A
By administering it with a β-blocker
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
15
Q
What are the toxicities of minoxidil?
A
Hypertrichosis, reflex tachycardia, angina, salt retention, and pericardial effusion
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
17
Q
Which calcium channel blocker is the most selective for vascular smooth muscle?
A
Nifedipine
18
Q
Which calcium channel blocker is the most cardio-selective?
A
Verapamil
19
Q
Which calcium channel blocker cannot be used as an anti-arrhythmic?
A
Nifedipine
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
21
Q
Name three pharmaceutical agents that are in the class of calcium channel blockers.
A
Nifedipine, diltiazem, and verapamil
22
Q
What is the ultimate function of calcium channel blockers?
A
To decrease cardiac and smooth muscle contractility
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
24
Q
Are nitrates more effective as preload or afterload reducers?
A
Preload reducers
25
Does isosorbide dinitrate dilate veins or arteries more?
Veins
26
How does nitric oxide cause smooth muscle relaxation?
By increasing cGMP concentration
27
Vasodilation using nitroglycerin is caused by the release of what chemical in smooth muscle?
Nitric oxide
28
What are two indications for the use of nitroglycerin?
Angina and pulmonary edema
29
Name four adverse effects of nitroglycerin.
Reflex tachycardia, hypotension, flushing, and headache
30
Name three medications indicated to treat malignant hypertension.
Nitroprusside, fenoldopam, and diazoxide
31
Nitroprusside increases the concentration of which substance via direct release of nitric oxide?
cGMP
32
Nitroprusside is a _____ (short/long) -acting drug.
Short
33
Fenoldopam is an agonist of which receptor?
Dopamine D1; D1 activity relaxes renal vasculature
34
Diazoxide causes relaxation of vascular smooth muscle by opening which membrane channel?
Potassium
35
Name an adverse effect of diazoxide.
Hyperglycemia, secondary to a reduction in insulin release
36
What is the mechanism by which pharmacologic treatments can reduce angina?
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
37
Among the calcium channel blocker, which acts most like nitrates in treating angina? Which acts like a blocker?
Nifedipine; verapamil
38
What are the effects of nitrates, blockers, and a combination of both on end diastolic volume?
Blockers increase end diastolic volume, nitrates decrease end diastolic volume, and a combination of both either has no effect or decreases end diastolic volume
39
What are the effects of nitrates, β-blockers, and a combination of both on blood pressure?
β-blockers, nitrates, and a combination of both all decrease blood pressure
40
What are the effects of nitrates, beta blockers, and a combination of both on contractility?
Blockers decrease contractility, nitrates increase contractility (as a reflex response), and a combination of both has little/no effect on contractility
41
What are the effects of nitrates, blockers, and a combination of both on heart rate?
Blockers decrease heart rate, nitrates increase heart rate (as a reflex response), and a combination of both decreases heart rate
42
What are the effects of nitrates, blockers, and a combination of both on ejection time?
Blockers increase ejection time, nitrates decrease ejection time, and a combination of both has little/no effect on ejection time
43
What are the effects of nitrates, blockers, and a combination of both on myocardial oxygen consumption?
Blockers and nitrates decrease myocardial oxygen consumption, but a combination of both severely decreases myocardial oxygen consumption
44
Which two beta-blockers are contraindicated in angina and why?
Pindolol and acebutolol because they are partial beta-agonists and can increase myocardial oxygen consumption
45
Which drugs have the most powerful low-density lipoprotein-lowering effects?
Statins have the strongest reducing effect of all of the lipid-lowering drugs
46
Other than statins, which drugs are indicated for lowering low-density lipoprotein levels?
Niacin, which lowers low-density lipoprotein levels, although less than statins
47
Which lipid-lowering agent causes the greatest increase in high-density lipoprotein levels? Which agents cause a more modest increase?
Niacin causes the greatest increase in high-density lipoprotein levels; statins have a moderate effect on high-density lipoprotein levels
48
Which lipid-lowering agents cause the most significant reduction in triglycerides? Which have a more modest benefit?
Fibrates reduce triglycerides most significantly; statins, bile acid resins, and niacin have a moderate effect in this regard
49
What adverse effects do HMG-CoA reductase inhibitors (eg, lovastatin, atorvastatin) have?
Elevated liver enzymes (which is reversible) and rhabdomyolysis
50
What adverse effects does niacin have?
Facial flushing, which can be reduced with the use of aspirin and decreases over time; hyperglycemia; and hyperuricemia
51
What adverse effects do bile acid resins (cholestyramine) have?
Bad taste, gastrointestinal discomfort, a decreased effect on the absorption of fat-soluble vitamins, and the production of cholesterol gallstones
52
What adverse effects do fibrates (eg, gemfibrozil, clofibrate) have?
Elevated liver enzymes and myositis
53
Which category of lipid-lowering agents works by inhibiting the formation of the cholesterol precursor mevalonate?
HMG-CoA reductase inhibitors; this is the rate-limiting step in cholesterol synthesis
54
Which lipid-lowering agent works by inhibiting lipolysis in adipose tissue and reducing hepatic very-low-density lipoprotein secretion into circulation?
Niacin
55
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?
Bile acid resins (cholestyramine, colestipol)
56
Which category of lipid-lowering agents works by preventing cholesterol reabsorption at the small intestine brush border?
Cholesterol absorption blockers (ezetimibe)
57
Which category of lipid-lowering agents works by upregulating lipoprotein lipase, causing increased triglyceride clearance from the blood?
Fibrates (gemfibrozil, clofibrate, fenofibrate, bezafibrate)
58
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?
Bile acid resins
59
Which class of lipid-lowering agents is contraindicated in patients with gallstones?
Bile acid resins
60
A patient has recently started taking lovastatin. He presents with diffuse muscle pain and weakness. Which lab test should be ordered?
Creatine kinase to test for rhabdomyolysis
61
Which poison inhibits the calcium release channel in the sarcoplasmic reticulum?
Ryanodine
62
Digoxin inhibits which mechanism of transport in the cell membrane?
Na+/K+/adenosine triphosphatase
63
Why is external calcium referred to as trigger calcium in the cardiac myocyte?
Because it is the trigger for release of intracellular calcium stores from the sarcoplasmic reticulum
64
What is the mechanism by which β1 activation increases cardiac contractility?
1 activation causes protein kinase A to phosphorylate L-type calcium channels, increasing intracellular calcium and strengthening contraction
65
Digoxin is removed from the body by _____ excretion.
Urinary; as a result, renal failure can cause digoxin toxicity
66
What is the mechanism of action of digoxin?
By inhibiting the cardiac myocyte sodium/potassium pump, digoxin also prevents sodium/calcium exchange, increasing intracellular calcium concentration
67
What is the effect of increased intracellular calcium on cardiac function?
Positive inotropy
68
Because it can increase contractility, digoxin is used to treat what condition?
Congestive heart failure
69
By what mechanism is digoxin beneficial in atrial fibrillation?
Digoxin decreases conduction at the atrioventricular node and causes depression of the sinoatrial node
70
What are three common gastrointestinal complaints that occur with digoxin use?
Nausea, vomiting, and diarrhea
71
What vision complaint can occur with digoxin use?
Blurry yellow vision
72
What potential heart problem can arise with the use of digoxin?
Arrhythmia
73
What factors increase the likelihood of digoxin toxicity?
Kidney failure (because of decreased excretion), hypokalemia, and quinidine (due to displacement of tissue-binding sites)
74
What is the approach to treatment of digoxin toxicity?
Slow normalization of potassium levels, lidocaine, a cardiac pacer, anti-digoxin antibodies, and magnesium
75
How does hypokalemia increase the toxicities of digoxin?
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
What are some potential electrocardiogram findings in a patient who has digoxin toxicity?
Prolonged PR interval, shortened QT interval, scooping, T-wave inversion, arrhythmia, and signs of hyperkalemia
77
What is the ultimate mechanism of action of cardiac glycosides?
To increase intracellular calcium (thereby acting as a positive inotrope), and to stimulate the vagus nerve
78
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?
Reversible systemic lupus erythematosus-like syndrome
79
Quinidine causes symptoms of headache and tinnitus, which are collectively known as what?
Cinchonism; which can occur with all quinine derivatives
80
What effect do class IC antiarrhythmics have on action potential duration?
They have no effect on action potential duration
81
Which antiarrhythmics are indicated to prevent arrhythmia after myocardial infarction? Which are contraindicated?
Class IB antiarrhythmics are indicated to prevent arrhythmia after myocardial infarction, but class IC antiarrhythmics are contraindicated
82
What is the toxicity of class IC antiarrhythmics?
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
Name the class IB antiarrhythmic drugs.
Class **IB** antiarrhythmics are **Lid**ocaine, **Mexi**letine, and **T**ocainide (remember: **I**d **B**uy **Lid**ys **Mexi**can **T**acos)
84
What electrolyte abnormality increases the toxicity of class I antiarrhythmics?
Hyperkalemia
85
Which antiarrhythmics belong to class IA?
Quinidine, Procainamide, and Disopyramide; remember the mnemonic The **Q**ueen **P**roclaims **D**isos **pyramid**
86
Which antiepileptic drug can also act as a class IB antiarrhythmic?
Phenytoin
87
How do sodium channel blocker antiarrhythmics work?
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
What does it mean when sodium channel blockers are described as state dependent?
State dependent means that the antiarrhythmics act only on tissue that is frequently depolarized (eg, fast tachycardia)
89
What effect do class IA antiarrhythmics have on the electrical activity of the heart?
They increase the action potential duration, increase the effective refractory period, and increase the QT interval
90
What are class IA antiarrhythmics used for?
To treat atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia
91
What are the adverse effects of quinidine?
Cinchonism (headache and tinnitus), thrombocytopenia, and torsades de pointes (due to prolonged QT)
92
What do class IB antiarrhythmics do?
They decrease action potential duration and preferentially affect ischemic Purkinje and ventricular tissue
93
What are class IB antiarrhythmics used for?
To treat ventricular arrhythmia (especially after myocardial infarction) and in digitalis-induced arrhythmias
94
What are the adverse effects of class IB antiarrhythmics?
They can cause central nervous system stimulation or depression and cardiovascular depression
95
What are class IC antiarrhythmics useful for?
As a last resort in ventricular tachycardia that may progress to ventricular fibrillation, and in intractable supraventricular tachycardia
96
Which antiarrhythmics belong to class IC?
Flecainide, encainide, and propafenone (remember: Chipotles **F**ood has **E**xcellent **P**roduce)
97
Which blocker is shortest acting?
Esmolol
98
Which cardiac node is most sensitive to blockers: the sinoatrial node or the atrioventricular node?
The atrioventricular node; as a result, the PR interval is lengthened on electrocardiogram
99
Which antiarrhythmics belong in class II?
Beta-blockers, such as propranolol, esmolol, timolol, metoprolol, and atenolol.
100
What is the mechanism of action of beta-blockers?
Beta-blockers decrease cAMP and calcium ion current and suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker action potential.
101
What is the clinical use of β-blockers?
To treat ventricular tachycardia and supraventricular tachycardia and to slow ventricular rate during atrial fibrillation and atrial flutter
102
What are the toxicities of blockers?
Impotence, asthma exacerbation, cardiovascular effects (bradycardia, atrioventricular block, and congestive heart failure), central nervous system effects (sedation and sleep alterations)
103
Which adverse effect is specific to metoprolol as opposed to other blockers?
Dyslipidemia
104
What is the antidote for blocker overdose?
Glucagon
105
Why might blockers be dangerous for someone who takes insulin?
Because they can mask signs of hypoglycemia
106
What three types of testing must be periodically performed for patients who are taking amiodarone?
Pulmonary function testing, liver function testing, and thyroid function testing
107
Which antiarrhythmics belong to class III?
Potassium channel blockers, such as sotalol, ibutilide, bretylium, dofetilide, and amiodarone
108
What is the mechanism of action of potassium channel blockers?
They increase the action potential duration, increase the effective refractory period, and increase the QT interval
109
Name two toxicities of sotalol.
Torsades des pointes and excessive blockade
110
Name a potentially fatal adverse effect of ibutilide.
Torsades des pointes
111
What are two toxicities of bretylium?
New arrhythmias and hypotension
112
Name eight toxicities of amiodarone.
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
Why does amiodarone have class I, II, III, and IV effects?
Because it alters the lipid membrane
114
Why is amiodarone likely to interfere with thyroid function?
Because it is 40% iodine by weight
115
Class IV antiarrhythmics primarily affect which cardiac myocytes?
Atrioventricular nodal pacemaker cells
116
How do class IV antiarrhythmics affect conduction velocity through the atrioventricular node?
Decrease
117
How do class IV antiarrhythmics affect the refractory period of cardiac myocytes?
Increase
118
How do class IV antiarrhythmics affect PR intervals on electrocardiogram?
Increase; due to slowed conduction through the atrioventricular node
119
Which two antiarrhythmic drugs belong to class IV?
Diltiazem and verapamil
120
What is the clinical use of calcium channel blockers?
They are used in the prevention of nodal arrhythmias, such as supraventricular tachycardia
121
What are the adverse effects of calcium channel blockers?
Constipation, flushing, edema, and cardiovascular effects (congestive heart failure, atrioventricular block, sinus node depression)
122
Which antiarrhythmic is a first-line drug for diagnosing and abolishing supraventricular tachycardia?
Adenosine
123
Which ion is infused for treatment of torsades des pointes and digoxin toxicity?
Magnesium
124
What is the mechanism of action of adenosine?
Adenosine increases the amount of potassium flowing out of cells, leading to hyperpolarization of the cell
125
What is the duration of action of adenosine?
Adenosine is a short (about 15 seconds)-acting drug
126
What are three toxicities of the antiarrhythmic drug adenosine?
Flushing, hypotension, and chest pain
