Pathophysiology: Chapter 33: Alterations of Cardiovascular Function Flashcards

1
Q

What is the initiating event that leads to the development of atherosclerosis?

a. Release of the inflammatory cytokines
b. Macrophages adhere to vessel walls.
c. Injury to the endothelial cells that line the artery walls
d. Release of the platelet-deprived growth factor

A

ANS: C
Atherosclerosis begins with an injury to the endothelial cells that line the arterial walls.
Possible causes of endothelial injury include the common risk factors for atherosclerosis,
such as smoking, hypertension, diabetes, increased levels of low-density lipoprotein
(LDL), decreased levels of high-density lipoprotein (HDL), and autoimmunity. The
remaining options occur only after the endothelial cells are injured.

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2
Q

What is the effect of oxidized low-density lipoproteins (LDLs) in atherosclerosis?

a. LDLs cause smooth muscle proliferation.
b. LDLs cause regression of atherosclerotic plaques.
c. LDLs increase levels of inflammatory cytokines.
d. LDLs direct macrophages to the site in the endothelium.

A

ANS: A
Oxidized LDLs are toxic to endothelial cells, cause smooth muscle proliferation, and
activate further immune and inflammatory responses. This selection is the only option that
accurately identifies the effects of LDLs.

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3
Q

Which inflammatory cytokines are released when endothelial cells are injured?
a. Granulocyte-macrophage colony-stimulating factor (GM-CSF)
b. Interferon-beta (IFN-), interleukin 6 (IL-6), and granulocyte colony-stimulating
factor (G-CSF)
c. Tumor necrosis factor–alpha (TNF-), interferon-gamma (IFN-), and interleukin
1 (IL-1)
d. Interferon-alpha (IFN-), interleukin-12 (IL-12), and macrophage
colony-stimulating factor (M-CSF)

A

ANS: C
Numerous inflammatory cytokines are released, including TNF-, IFN-, IL-1, toxic
oxygen radicals, and heat shock proteins. This selection is the only option that accurately
identifies which inflammatory cytokines are associated with endothelial cell injury.

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4
Q

When endothelia cells are injured, what alteration contributes to atherosclerosis?

a. The release of toxic oxygen radicals that oxidize low-density lipoproteins (LDLs).
b. Cells are unable to make the normal amount of vasodilating cytokines.
c. Cells produce an increased amount of antithrombotic cytokines.
d. Cells develop a hypersensitivity to homocysteine and lipids.

A

ANS: B
Injured endothelial cells become inflamed and cannot make normal amounts of
antithrombotic and vasodilating cytokines. This selection is the only option that accurately
identifies the factor that contributes to atherosclerosis

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5
Q

Which factor is responsible for the hypertrophy of the myocardium associated with
hypertension?
a. Increased norepinephrine c. Angiotensin II
b. Adducin d. Insulin resistance

A

ANS: C
Of the available options, only angiotensin II is responsible for the hypertrophy of the
myocardium and much of the renal damage associated with hypertension.

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6
Q

What pathologic change occurs to the kidney’s glomeruli as a result of hypertension?

a. Compression of the renal tubules
b. Ischemia of the tubule
c. Increased pressure from within the tubule
d. Obstruction of the renal tubule

A

ANS: B
In the kidney, vasoconstriction and resultant decreased renal perfusion cause tubular
ischemia and preglomerular arteriopathy. This selection is the only option that accurately
identifies the pathologic change to the kidney that occurs as a result of hypertension.

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7
Q

What effect does atherosclerosis have on the development of an aneurysm?

a. Atherosclerosis causes ischemia of the intima.
b. It increases nitric oxide.
c. Atherosclerosis erodes the vessel wall.
d. It obstructs the vessel.

A

ANS: C
Atherosclerosis is a common cause of aneurysms because plaque formation erodes the
vessel wall. This selection is the only option that accurately identifies the effect that
atherosclerosis has on aneurysm development.

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8
Q

Regarding the endothelium, what is the difference between healthy vessel walls and those
that promote clot formation?
a. Inflammation and roughening of the endothelium of the artery are present.
b. Hypertrophy and vasoconstriction of the endothelium of the artery are present.
c. Excessive clot formation and lipid accumulation in the endothelium of the artery
are present.
d. Evidence of age-related changes that weaken the endothelium of the artery are
present.

A

ANS: A
Invasion of the tunica intima by an infectious agent also roughens the normally smooth
lining of the artery, causing platelets to adhere readily. This selection is the only option
that accurately describes the mechanism that supports abnormal clot formation.

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9
Q

What is the usual source of pulmonary emboli?

a. Deep venous thrombosis
b. Endocarditis
c. Valvular disease
d. Left heart failure

A

ANS: A
Pulmonary emboli originate in the venous circulation (mostly from the deep veins of the
legs) or in the right heart. This selection is the only option that accurately identifies the
usual source of pulmonary emboli.

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10
Q
Which factor can trigger an immune response in the bloodstream that may result in an
embolus?
a. Amniotic fluid 
b. Fat 
c. Bacteria
d. Air
A

ANS: A
Of the options available, only amniotic fluid displaces blood, thereby reducing oxygen,
nutrients, and waste exchange; however, it also introduces antigens, cells, and protein
aggregates that trigger inflammation, coagulation, and the immune response in the
bloodstream.

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11
Q

Which statement best describes thromboangiitis obliterans (Buerger disease)?
a. Inflammatory disorder of small- and medium-size arteries in the feet and
sometimes in the hands
b. Vasospastic disorder of the small arteries and arterioles of the fingers and, less
commonly, of the toes
c. Autoimmune disorder of the large arteries and veins of the upper and lower
extremities
d. Neoplastic disorder of the lining of the arteries and veins of the upper extremities

A

ANS: A
Buerger disease is an inflammatory disease of the peripheral arteries. Inflammation,
thrombus formation, and vasospasm can eventually occlude and obliterate portions of
small- and medium-size arteries. The digital, tibial, and plantar arteries of the feet and the
digital, palmar, and ulnar arteries of the hands are typically affected. This selection is the
only option that accurately describes Buerger disease

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12
Q

Which statement best describes Raynaud disease?
a. Inflammatory disorder of small- and medium-size arteries in the feet and
sometimes in the hands
b. Neoplastic disorder of the lining of the arteries and veins of the upper extremities
c. Vasospastic disorder of the small arteries and arterioles of the fingers and, less
commonly, of the toes
d. Autoimmune disorder of the large arteries and veins of the upper and lower
extremities

A

ANS: C
Attacks of vasospasm in the small arteries and arterioles of the fingers and, less
commonly, of the toes characterize Raynaud phenomenon and Raynaud disease and is the
only option that accurately describes this disease.

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13
Q

What change in a vein supports the development of varicose veins?

a. Increase in osmotic pressure c. Damage to the venous endothelium
b. Damage to the valves in veins d. Increase in hydrostatic pressure

A

ANS: B
If a valve is damaged, permitting backflow, then a section of the vein is subjected to the
pressure exerted by a larger volume of blood under the influence of gravity. The vein
swells as it becomes engorged, and the surrounding tissue becomes edematous because
increased hydrostatic pressure pushes plasma through the stretched vessel wall. This
selection is the only option that accurately describes the development of varicose veins.

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14
Q

Superior vena cava syndrome is a result of a progressive increase of which process?

a. Inflammation c. Distention
b. Occlusion d. Sclerosis

A

ANS: B
Superior vena cava syndrome (SVCS) is a progressive occlusion of the superior vena cava
(SVC) that leads to venous distention in the upper extremities and head. The remaining
options are not associated with this disorder.

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15
Q

What term is used to identify when a cell is temporarily deprived of blood supply?

a. Infarction c. Necrosis
b. Ischemia d. Inflammation

A

ANS: B
Coronary artery disease (CAD) can diminish the myocardial blood supply until deprivation
impairs myocardial metabolism enough to cause ischemia, a local state in which the cells
are temporarily deprived of blood supply. This term is the only option that is used to
identify a temporarily deprived blood supply.

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16
Q

The risk of developing coronary artery disease is increased up to threefold by which
factor?
a. Diabetes mellitus c. Obesity
b. Hypertension d. High alcohol consumption

A

ANS: B
Hypertension is the only factor responsible for a twofold-to-threefold increased risk of
atherosclerotic cardiovascular disease.

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17
Q

Which risk factor is associated with coronary artery disease (CAD) because of its
relationship with the alteration of hepatic lipoprotein?
a. Diabetes mellitus c. Obesity
b. Hypertension d. High alcohol consumption

A

ANS: A
Of the available options, only diabetes mellitus is associated with CAD because of the
resulting alteration of hepatic lipoprotein synthesis; it increases triglyceride levels and is
involved in low-density lipoprotein oxidation.

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18
Q

Nicotine increases atherosclerosis by the release of which neurotransmitter?

a. Histamine c. Angiotensin II
b. Nitric oxide d. Epinephrine

A

ANS: D
Nicotine stimulates the release of catecholamines (e.g., epinephrine, norepinephrine),
which increases the heart rate and causes peripheral vascular constriction. As a result,
blood pressure increases, as do both cardiac workload and oxygen demand. None of the
other options are associated with this mechanism.

19
Q
Which substance is manufactured by the liver and primarily contains cholesterol and
protein?
a. Very low–density lipoproteins (VLDLs)
b. Low-density lipoproteins (LDLs)
c. High-density lipoproteins (HDLs)
d. Triglycerides
A

ANS: B
A series of chemical reactions in the liver results in the production of several lipoproteins
that vary in density and function. These include VLDLs, primarily triglycerides and
protein; LDLs, mostly cholesterol and protein; and HDLs, mainly phospholipids and
protein. LDLs are the only lipoproteins that are manufactured by the liver and primarily
contain cholesterol and protein.

20
Q

Which elevated value may be protective of the development of atherosclerosis?

a. Very low–density lipoproteins (VLDLs)
b. Low-density lipoproteins (LDLs)
c. High-density lipoproteins (HDLs
d. Triglycerides

A

ANS: C
Low levels of HDL cholesterol are also a strong indicator of coronary risk, whereas high
levels of HDLs may be more protective for the development of atherosclerosis than low
levels of LDLs. Neither VLDLs nor elevated triglycerides are associated with a protective
mechanism.

21
Q

Which laboratory test is an indirect measure of atherosclerotic plaque?

a. Homocysteine
b. Low-density lipoprotein (LDL)
c. Erythrocyte sedimentation rate (ESR)
d. C-reactive protein (CRP)

A

ANS: D
Highly sensitive CRP (hs-CRP) is an acute phase reactant or protein mostly synthesized in
the liver and, of the available options, is an indirect measure of atherosclerotic
plaque-related inflammation.

22
Q

Cardiac cells can withstand ischemic conditions and still return to a viable state for how
many minutes?
a. 10 c. 20
b. 15 d. 25

A

ANS: C
Cardiac cells remain viable for approximately 20 minutes under ischemic conditions. If
blood flow is restored, then aerobic metabolism resumes, contractility is restored, and
cellular repair begins. If the coronary artery occlusion persists beyond 20 minutes, then
myocardial infarction (MI) occurs.

23
Q

Which form of angina occurs most often during sleep as a result of vasospasms of one or
more coronary arteries?
a. Unstable c. Silent
b. Stable d. Prinzmetal

A

ANS: D
Of the options available, only Prinzmetal angina (also called variant angina) is chest pain
attributable to transient ischemia of the myocardium that occurs unpredictably and almost
exclusively at rest.

24
Q

When is the scar tissue that is formed after a myocardial infarction (MI) most vulnerable to
injury?
a. Between 5 and 9 days c. Between 15 and 20 days
b. Between 10 and 14 days d. Between 20 and 30 days

A

ANS: B
During the recovery period (10 to 14 days after infarction), individuals feel more capable
of increasing activities and thus may stress the newly formed scar tissue. After 6 weeks,
the necrotic area is completely replaced by scar tissue, which is strong but unable to
contract and relax like healthy myocardial tissue.

25
Q

An individual who is demonstrating elevated levels of troponin, creatine
kinase–isoenzyme MB (CK-MB), and lactic dehydrogenase (LDH) is exhibiting indicators
associated with which condition?
a. Myocardial ischemia c. Myocardial infarction (MI)
b. Hypertension d. Coronary artery disease (CAD)

A

ANS: C
Cardiac troponins (troponin I and troponin T) are the most specific indicators of MI. Other
biomarkers released by myocardial cells include CK-MB and LDH, but they are not
associated with the other options.

26
Q

What is the expected electrocardiogram (ECG) pattern when a thrombus in a coronary
artery permanently lodges in the vessel and the infarction extends through the myocardium
from the endocardium to the epicardium?
a. Prolonged QT interval
b. ST elevation myocardial infarction (STEMI)
c. ST depression myocardial infarction (STDMI)
d. Non-ST elevation myocardial infarction (non-STEMI)

A

ANS: B
Individuals with this pattern on an ECG usually have significant elevations in the ST
segments and are categorized as having STEMI. The other options are not associated with
the described pathologic condition.

27
Q

How does angiotensin II increase the workload of the heart after a myocardial infarction
(MI)?
a. By increasing the peripheral vasoconstriction
b. By causing dysrhythmias as a result of hyperkalemia
c. By reducing the contractility of the myocardium
d. By stimulating the sympathetic nervous system

A

ANS: A
Angiotensin II is released during myocardial ischemia and contributes to the pathogenesis
of a myocardial infarction (MI) in several ways. First, it results in the systemic effects of
peripheral vasoconstriction and fluid retention. These homeostatic responses are
counterproductive in that they increase myocardial work and thus exacerbate the effects of
the loss of myocyte contractility. Angiotensin II is also locally released, where it is a
growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts;
promotes catecholamine release; and causes coronary artery spasm. This selection is the
only option that accurately describes how angiotensin II increases workload after a MI.

28
Q

The pulsus paradoxus that occurs as a result of pericardial effusion is caused by a
dysfunction in which mechanism?
a. Diastolic filling pressures of the right ventricle and reduction of blood volume in
both ventricles
b. Blood ejected from the right atrium and reduction of blood volume in the right
ventricle
c. Blood ejected from the left atrium and reduction of blood volume in the left
ventricle
d. Diastolic filling pressures of the left ventricle and reduction of blood volume in all
four heart chambers.

A

ANS: D
Pulsus paradoxus means that the arterial blood pressure during expiration exceeds arterial
pressure during inspiration by more than 10 mm Hg. This clinical finding reflects
impairment of diastolic filling of the left ventricle plus a reduction of blood volume within
all four cardiac chambers. This selection is the only option that accurately describes the
mechanism.

29
Q

A patient reports sudden onset of severe chest pain that radiates to the back and worsens
with respiratory movement and when lying down. These clinical manifestations describe:
a. Myocardial infarction (MI) c. Restrictive pericarditis
b. Pericardial effusion d. Acute pericarditis

A

ANS: D
Most individuals with acute pericarditis describe several days of fever, myalgias, and
malaise, followed by the sudden onset of severe chest pain that worsens with respiratory
movements and with lying down. Although the pain may radiate to the back, it is generally
felt in the anterior chest and may be initially confused with the pain of an acute MI.
Individuals with acute pericarditis also may report dysphagia, restlessness, irritability,
anxiety, and weakness. This selection is the only option with these symptoms.

30
Q

Ventricular dilation and grossly impaired systolic function, leading to dilated heart failure,
characterize which form of cardiomyopathy?
a. Congestive c. Septal
b. Hypertrophic d. Dystrophic

A

ANS: A
Only dilated cardiomyopathy (congestive cardiomyopathy) is characterized by ventricular
dilation and grossly impaired systolic function, leading to dilated heart failure.

31
Q

A disproportionate thickening of the interventricular septum is the hallmark of which form
of cardiomyopathy?
a. Dystrophic c. Restrictive
b. Hypertrophic d. Dilated

A

ANS: B
Only hypertrophic cardiomyopathy is characterized by a thickening of the septal wall,
which may cause outflow obstruction to the left ventricle outflow tract.

32
Q

Amyloidosis, hemochromatosis, or glycogen storage disease usually causes which form of
cardiomyopathy?
a. Infiltrative c. Septal
b. Restrictive d. Hypertrophic

A

ANS: B
Restrictive cardiomyopathy may occur idiopathically or as a cardiac manifestation of
systemic diseases, such as scleroderma, amyloidosis, sarcoidosis, lymphoma, and
hemochromatosis, or a number of inherited storage diseases. This characterization is not
true of the other forms of cardiomyopathy.

33
Q

Which condition is a cause of acquired aortic regurgitation?

a. Congenital malformation c. Rheumatic fever
b. Cardiac failure d. Coronary artery disease (CAD)

A

ANS: C
Rheumatic heart disease, bacterial endocarditis, syphilis, hypertension, connective tissue
disorders (e.g., Marfan syndrome, ankylosing spondylitis), appetite suppressing
medications, trauma, or atherosclerosis can cause acquired aortic regurgitation. This
selection is the only available option that is known to cause acquired aortic regurgitation.

34
Q

Which predominantly female valvular disorder is thought to have an autosomal dominant
inheritance pattern, as well as being associated with connective tissue disease?
a. Mitral valve prolapse c. Tricuspid valve prolapse
b. Tricuspid stenosis d. Aortic insufficiency

A

ANS: A
Mitral valve prolapse tends to be most prevalent in young women. Studies suggest an
autosomal dominant and X-linked inheritance pattern. Because mitral valve prolapse often
is associated with other inherited connective tissue disorders (e.g., Marfan syndrome,
Ehlers-Danlos syndrome, osteogenesis imperfecta), it is thought to result from a genetic or
environmental disruption of valvular development during the fifth or sixth week of
gestation. This provided history is not associated with any of the other options.

35
Q

Which disorder causes a transitory truncal rash that is nonpruritic and pink with
erythematous macules that may fade in the center, making them appear as a ringworm?
a. Fat emboli
b. Rheumatic fever
c. Bacterial endocarditis
d. Myocarditis of acquired immunodeficiency syndrome

A

ANS: B
Erythema marginatum is a distinctive truncal rash that often accompanies acute rheumatic
fever. It consists of nonpruritic, pink erythematous macules that never occur on the face or
hands. This presentation is not associated with any of the other options.

36
Q

What is the most common cause of infective endocarditis?

a. Virus c. Bacterium
b. Fungus d. Rickettsiae

A

ANS: C
Infective endocarditis is a general term used to describe infection and inflammation of the
endocardium—especially the cardiac valves. Bacteria are the most common cause of
infective endocarditis, especially streptococci, staphylococci, or enterococci.

37
Q

What is the most common cardiac disorder associated with acquired immunodeficiency
syndrome (AIDS)
a. Cardiomyopathy c. Left heart failure
b. Myocarditis d. Heart block

A

ANS: C
Pericardial effusion and left heart failure are the most common complications of human
immunodeficiency virus (HIV) infection. Other conditions include cardiomyopathy,
myocarditis, tuberculous pericarditis, infective and nonbacterial endocarditis, heart block,
pulmonary hypertension, and nonantiretroviral drug-related cardiotoxicity.

38
Q

A patient is diagnosed with pulmonary disease and elevated pulmonary vascular
resistance. Which form of heart failure may result from pulmonary disease and elevated
pulmonary vascular resistance?
a. Right heart failure c. Low-output failure
b. Left heart failure d. High-output failure

A

ANS: A
Right heart failure is defined as the inability of the right ventricle to provide adequate
blood flow into the pulmonary circulation at a normal central venous pressure. This
condition is often a result of pulmonary disease and the resulting elevated pulmonary
vascular resistance.

39
Q

What cardiac pathologic condition contributes to ventricular remodeling?

a. Left ventricular hypertrophy c. Myocardial ischemia
b. Right ventricular failure d. Contractile dysfunction

A

ANS: C
Of the options available, myocardial ischemia contributes to inflammatory, immune, and
neurohumoral changes that mediate a process called ventricular remodeling.

40
Q

In systolic heart failure, what effect does the renin-angiotensin-aldosterone system
(RAAS) have on stroke volume?
a. Increases preload and decreases afterload.
b. Increases preload and increases afterload.
c. Decreases preload and increases afterload.
d. Decreases preload and decreases afterload.

A

ANS: B
Activation of the RAAS not only causes an increase in preload and afterload, but it also
causes direct toxicity to the myocardium. This selection is the only option that accurately
identifies the effect that the RAAS has on stroke volume in this situation.

41
Q

What is the cause of the dyspnea resulting from a thoracic aneurysm?

a. Pressure on surrounding organs c. Formation of atherosclerotic lesions
b. Poor oxygenation d. Impaired blood flow

A

ANS: A
Clinical manifestations depend on the location of the aneurysm. Pressure of a thoracic
aneurysm on surrounding organs cause symptoms of dysphagia (difficulty in swallowing)
and dyspnea (breathlessness). This selection is the only option that accurately describes the
cause of dyspnea resulting from a thoracic aneurysm.

42
Q

Which statement is true concerning the cells’ ability to synthesize cholesterol?

a. Cell production of cholesterol is affected by the aging process.
b. Cells produce cholesterol only when dietary fat intake is low.
c. Most body cells are capable of producing cholesterol.
d. Most cholesterol produced by the cells is converted to the low-density form.

A

ANS: C
Although cholesterol can easily be obtained from dietary fat intake, most body cells can
also manufacture cholesterol. This selection is the only option that accurately describes the
cellular role in cholesterol synthesis.

43
Q

What is the trigger for angina pectoris?

a. Atherosclerotic lesions c. Myocardial necrosis
b. Hyperlipidemia d. Myocardial ischemia

A

ANS: D
Angina pectoris is chest pain caused by myocardial ischemia. None of the other options
are considered triggers for angina pectoris.

44
Q

Individuals being effectively managed for type 2 diabetes mellitus often experience a
healthy decline in blood pressure as a result of what intervention?
a. Managed carbohydrate intake
b. Appropriate exercise
c. Insulin-sensitivity medication therapy
d. Introduction of minimal doses of insulin

A

ANS: C
Many people with type 2 diabetes mellitus, who are treated with drugs that increase insulin
sensitivity, experience a decline in their blood pressure without taking antihypertensive
drugs. Although the other medications may be included in the management plan, the other
options are not associated with a decrease in hypertension.