Pathophysiology 5th Edition Copstead Banasik Test Bank
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Chapter 18: Alterations in Cardiac Function
- The most reliable indicator that a person is experiencing an acute myocardial infarction (MI) is
|a.||severe, crushing chest pain.|
|d.||pain radiating to the lower legs.|
Injuries to cardiac tissue caused by myocardial ischemia and infarction are indicated on the ECG by ST-segment changes. ST-segment elevation on the ECG indicates that ischemic injury is ongoing and that efforts to improve perfusion or reduce oxygen demand may be effective in preserving myocardial muscle. In some instances, an MI is entirely asymptomatic. Dysrhythmias that accompany MI are attributed to injured and ischemic cells that have not yet become necrotic. Pain radiating to the jaw and neck, not the lower legs, is symptomatic of an MI.
REF: Pg. 388
- Primary treatment for myocardial infarction (MI) is directed at
|a.||protecting the heart from further ischemia.|
|b.||decreasing myocardial oxygen demands.|
|c.||reducing heart rate and blood pressure.|
|d.||activating the parasympathetic system.|
Reducing oxygen demand may be effective in preserving myocardial muscle. Decreasing demand increases myocardial oxygen supply. Once the cardiac muscle has been damaged, it is more important to preserve remaining muscle and prevent further loss of the myocardium. Reduction in the heart rate and blood pressure is not the primary treatment goal in MI care. Parasympathetic activation is not the primary treatment for myocardial infarction.
REF: Pg. 390
- Rheumatic heart disease is most often a consequence of
|a.||chronic intravenous drug abuse.|
|b.||viral infection with herpes virus.|
|c.||b-hemolytic streptococcal infection.|
Rheumatic heart disease is an uncommon but serious consequence of rheumatic fever. Rheumatic fever is an acute inflammatory disease that follows infection with group A b-hemolytic streptococci. Rheumatic heart disease is not associated with chronic IV drug abuse. Rheumatic fever is an acute inflammatory infectious disease. Cardiomyopathy does not cause rheumatic heart disease.
REF: Pg. 395
- Patients presenting with symptoms of unstable angina and no ST segment elevation are treated with
|c.||acute reperfusion therapy.|
|d.||cardiac biomarkers only.|
Patients presenting with symptoms of unstable angina and no ST elevation on the ECG would be treated with antiplatelet drugs as a cornerstone of therapy. Coronary angiography may be used as an additional method of diagnosis but would not be the primary option. The patient with symptoms of unstable angina would not benefit from reperfusion strategies. Cardiac biomarkers may be assessed in the unstable angina patient, but are not the primary indicator.
REF: Pg. 386
- An example of an acyanotic heart defect is
|a.||tetralogy of Fallot.|
|b.||transposition of the great arteries.|
|c.||ventricular septal defect.|
|d.||all right-to-left shunt defects.|
An example of an acyanotic heart defect is a ventricular septal defect. In this condition, blood from the left ventricle leaks into the right ventricle due to a defect in the ventricular wall. This leakage causes extra pressure in the right ventricle resulting in pulmonary hypertension. Tetralogy of Fallot is a cyanotic congenital defect. Transposition of the great vessels is a cyanotic congenital defect. The category of cyanotic congenital defects refers to those that are right-to-left shunts.
REF: Pgs. 403-404
- Patent ductus arteriosus is accurately described as a(n)
|a.||opening between the atria.|
|b.||stricture of the aorta that impedes blood flow.|
|c.||communication between the aorta and the pulmonary artery.|
|d.||cyanotic heart defect associated with right-to-left shunt.|
A patent ductus arteriosus is a normal channel between the pulmonary artery and the aorta that remains open during intrauterine life. A patent ductus arteriosus is not an opening or a stricture in the atria. Patent ductus arteriosus is an acyanotic congenital defect.
REF: Pgs. 404-405
- Hypotension, distended neck veins, and muffled heart sounds are classic manifestations of
|c.||congestive heart failure (CHF).|
The three classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. There are many other manifestations as well. Myocardial infarction is not exhibited by the symptoms described. Classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. Symptoms of CHF may include jugular venous distention. Cardiomyopathy is not exhibited by the symptoms described.
REF: Pg. 399
- Constrictive pericarditis is associated with
|a.||impaired cardiac filling.|
|c.||increased cardiac preload.|
|d.||elevated myocardial oxygen consumption.|
Constrictive pericarditis results in a fibrous scarred pericardium that restricts cardiac filling. Chronic pericarditis may be the result of a previous cardiac surgery. Pericarditis is associated with increased workload of the heart because contraction is opposed by the surrounding structures. The constrictive process includes symptoms of exercise intolerance, weakness, and fatigue.
REF: Pg. 400
- Mitral stenosis is associated with
|a.||a prominent S4 heart sound.|
|b.||a pressure gradient across the mitral valve.|
|c.||left ventricular hypertrophy.|
|d.||a muffled second heart sound (S2).|
Mitral stenosis is characterized by an abnormal left atrial–left ventricular pressure gradient during ventricular diastole. Mitral stenosis is not associated with an S4 heart sound. Mitral stenosis is associated with left atrial hypertrophy, not left ventricular hypertrophy. Mitral stenosis does not have a symptom of a muffled second heart sound.
REF: Pg. 392
- Aortic regurgitation is associated with
|b.||elevated left ventricular/aortic systolic pressure gradient.|
|c.||elevated systemic diastolic blood pressure.|
|d.||shortened ventricular ejection phase.|
Aortic regurgitation results from an incompetent aortic valve that allows blood to leak back from the aorta into the left ventricle during diastole. In aortic regurgitation, there is not an elevated left ventricular/aortic pressure gradient. Diastolic blood pressure is generally lower because of rapid runoff of blood into the ventricle. Aortic regurgitation is associated with a longer ventricular ejection phase.
REF: Pg. 394
- Angina due to coronary artery spasm is called _____ angina.
Variant, or Prinzmetal, angina is the term applied to vasospasm-initiated anginal symptoms due to significant atherosclerotic plaques. These spasms usually respond promptly to vasodilating agents. Coronary artery spasm does not produce stable angina. Classic or typical angina is often associated with physical exertion. Unstable angina presents a similar clinical picture as myocardial infarction.
REF: Pgs. 384-386
- While hospitalized, an elderly patient with a history of myocardial infarction was noted to have high levels of low-density lipoproteins (LDLs). What is the significance of this finding?
|a.||Increased LDL levels are associated with increased risk of coronary artery disease.|
|b.||Measures to decrease LDL levels in the elderly would be unlikely to affect the progression of this disease.|
|c.||Increased LDL levels are indicative of moderate alcohol intake, and patients should be advised to abstain.|
|d.||Elevated LDL levels are an expected finding in the elderly and therefore are not particularly significant.|
High levels of low-density lipoproteins (LDLs), which are high in cholesterol, have been associated with the highest risk of coronary atherosclerosis. Even when lipid metabolism is normal, a high-fat diet can overwhelm the liver’s ability to clear LDL cholesterol from the circulation and result in hyperlipidemia. Dietary fat restriction may be beneficial in reducing cholesterol in this case. Increased LDL levels are not indicative of alcohol intake. Elevated LDL levels are not an expected finding in the elderly and should be treated.
REF: Pg. 381
- What compensatory sign would be expected during periods of physical exertion in a patient with limited ventricular stroke volume?
An individual with reduced stroke volume would exhibit compensatory increases in heart rate. Hypertension associated with decreased ventricular stroke volume. An individual with reduced stroke volume would exhibit compensatory increases in heart rate; therefore, bradycardia would not be expected. Aortic regurgitation would not be an expected compensatory sign of limited stroke volume.
REF: Pg. 390
- An elderly patient’s blood pressure is measured at 160/98. How would the patient’s left ventricular function be affected by this level of blood pressure?
|a.||This is an expected blood pressure in the elderly and has little effect on left ventricular function.|
|b.||Left ventricular workload is increased with high afterload.|
|c.||High blood pressure enhances left ventricular perfusion during systole.|
|d.||High-pressure workload leads to left ventricular atrophy.|
Activation of the sympathetic nervous system increases the heart rate, contractility, blood pressure, and fluid retention by the kidney. Unfortunately, these compensatory efforts impose a greater workload on the heart. A blood pressure of 160/90 mm Hg is a higher than expected blood pressure in an elderly patient. High blood pressure does not enhance ventricular perfusion. Greater workload on the heart may contribute to further ischemic damage.
REF: Pg. 390
- A patient with a history of myocardial infarction continues to complain of intermittent chest pain brought on by exertion and relieved by rest. The likely cause of this pain is
Stable angina is the most common form of chest pain and is characterized by pain that is caused under conditions of increased myocardial workload, such as physical exertion or emotional strain. Pain related to myocardial infarction is not relieved by rest. Coronary vasospasm is characterized by unpredictable attacks of angina pain. A patient with unstable angina presents with symptoms similar to myocardial infarction.
REF: Pg. 385
- The majority of cardiac cells that die after myocardial infarction do so because of
MI results when prolonged or total disruption of blood flow to the myocardium causes cellular death by necrosis or apoptosis. Cardiac cells do not die as a result of cellular rupture. Insufficient glucose is not associated with myocardial death. The initiating event of MI is believed to be related to thrombus, but the resulting disruption of flow to the myocardium is due to necrosis or apoptosis.
REF: Pg. 386
- Which serum biomarker(s) are indicative of irreversible damage to myocardial cells?
|a.||Elevated CK-MB, troponin I, and troponin T|
|b.||Markedly decreased CK-MB and troponin I|
|d.||Prolonged coagulation time|
Elevated cardiac biomarkers are one indication of myocardial necrosis. Cardiac biomarkers may not be utilized if a patient presents with chest pain and evidence of acute ischemia on the electrocardiogram. Cardiac biomarkers are elevated in the presence of MI. Elevated LDL is a risk factor for coronary atherosclerosis. Coagulation times are not used to assess myocardial damage.
REF: Pg. 388
- A loud pansystolic murmur that radiates to the axilla is most likely a result of
The murmur of mitral regurgitation usually occurs throughout ventricular systole (pansystolic), radiates toward the left axilla, and has a high-pitched blowing character. Aortic insufficiency is characterized by a high-pitched blowing murmur during ventricular diastole. A characteristic murmur of aortic stenosis occurs during ventricular systole and varies in intensity, progressively getting louder and then diminishing (crescendo-decrescendo). The murmur of aortic stenosis generally radiates to the neck. Blood rushing through the narrowed mitral valve during ventricular diastole can sometimes be heard as a low-pitched, rumbling diastolic murmur at the heart’s apex.
REF: Pg. 394
- A patient with significant aortic stenosis is likely to experience
|c.||increased pulse pressure.|
In the patient with aortic stenosis, syncope and “graying out” episodes may occur when cerebral perfusion is inadequate. Low systolic blood pressure is a common sign of aortic stenosis. Faint pulses are a common sign of aortic stenosis. Peripheral edema is not associated with aortic stenosis.
REF: Pg. 394
- Myocarditis should be suspected in a patient who presents with
|a.||chest pain and ST elevation.|
|b.||acute onset of left ventricular dysfunction.|
|c.||murmur and abnormal valves on echocardiogram.|
|d.||family history of cardiomyopathy.|
Acute myocarditis is commonly characterized by left ventricular dysfunction or general dilation of all four heart chambers. Chest pain and ST elevation is indicative of myocardial infarction. Myocarditis is associated with viral infections. Dilated cardiomyopathy runs in families and has a genetic basis.
REF: Pg. 397
- Atherosclerotic plaques with large lipid cores are prone to
Rupture of atherosclerotic plaques with large lipid cores initiates platelet aggregation and thrombus formation. Dislodgement is not an occurrence of atherosclerotic plaques with large lipid cores. Atherosclerotic plaques with large lipid cores are not prone to binding. Large lipid cores of atherosclerotic plaques are not prone to attachment.
REF: Pg. 382
- Acute coronary syndrome in the presence of thrombosis may present as (Select all that apply.)
|c.||sudden cardiac arrest.|
ANS: A, B, C
Thrombosis occurs suddenly and may partially or completely obstruct the artery and cause acute ischemia. Acute coronary syndrome may present as unstable angina, MI, or sudden cardiac arrest. Bleeding is not a presenting symptom of acute coronary syndrome. Hypovolemia is not a presenting symptom of acute coronary syndrome.
REF: Pg. 383
- Inflammatory disorders that may alter endothelial cell function include
(Select all that apply.)
ANS: B, C, E
Inflammatory disorders that may alter endothelial cell function include lupus erythematosus, Kawasaki syndrome, and polyarteritis nodosa. Multiple sclerosis is not an inflammatory disorder that may alter endothelial cell function. Rheumatoid arthritis is not an inflammatory disorder that may alter endothelial cell function.
REF: Pg. 385
- Diagnostic tests used to diagnose or confirm MI include (Select all that apply.)
ANS: A, B, C, D
Electrocardiogram, cardiac catheterization, echocardiography, and radionuclide scintigraphy are diagnostic tests used to confirm MI. Computed tomography is not used to confirm MI.
REF: Pg. 387
- Atherosclerotic plaque formation is due to injury to the ____________.
coronary artery endothelium
Atherosclerotic plaque formation is due to injury to the coronary artery endothelium.
REF: Pg. 381
- The cause of Prinzmetal angina is ________.
The cause of Prinzmetal angina is vasospasm.
REF: Pg. 383 | Pg. 385
- A reduction in _________ production after birth contributes to the heart’s closure and constriction in patent ductus arteriosus.
A reduction in prostaglandin E production after birth contributes to the heart’s closure and constriction in patent ductus arteriosus.
REF: Pg. 405
- __________ is a congenital malformation that results in the formation of one large vessel that receives blood from both the right and left ventricles.
Truncus arteriosus is a congenital malformation that results in the formation of one large vessel that receives blood from both the right and left ventricles.
REF: Pg. 406