NUR 2063 / NUR2063:
Essentials of Pathophysiology Exam 2
Latest Update 2026/2027 | Rasmussen College |
100% Correct
Section 1: Cardiovascular Pathophysiology
Q1: What is the underlying pathophysiology of atherosclerosis?
A. Degeneration of the arterial media layer due to chronic hypertension, leading to vessel thickening.
B. Endothelial injury, lipid infiltration, and inflammatory response leading to plaque formation in
the intima. [CORRECT]
C. Spasm of the vascular smooth muscle triggered by autonomic imbalances.
D. Infection of the arterial wall by bacteria, causing abscess formation and weakening.
Correct Answer: B
Rationale: Atherosclerosis begins with endothelial injury, which allows low-density lipoproteins (LDLs)
to infiltrate the tunica intima. Macrophages ingest these lipids, becoming foam cells, which trigger a
chronic inflammatory response and the formation of an atherosclerotic plaque. Options A and C describe
elements of other vascular diseases (arteriosclerosis and vasospasm, respectively), while option D
describes a mycotic aneurysm or infectious arteritis.
Q2: Which mechanism explains the finding of left ventricular hypertrophy (LVH) in a patient with
chronic, untreated primary hypertension?
A. Increased preload causes excessive stretching of the myocardial fibers, leading to chamber dilation.
B. Decreased afterload reduces oxygen demand, causing myocardial cells to atrophy and stiffen.
C. Increased afterload forces the left ventricle to work harder against higher systemic resistance,
causing concentric muscle hypertrophy. [CORRECT]
D. Sympathetic overdrive directly stimulates myocardial cell hyperplasia without increasing workload.
Correct Answer: C
Rationale: Chronic hypertension increases systemic vascular resistance (afterload). To overcome this
higher pressure and maintain adequate cardiac output, the left ventricle must generate more tension during
systole, leading to concentric hypertrophy (thickening of the ventricular wall). Option A describes volume
,overload (high preload), which causes eccentric hypertrophy. Options B and D contain incorrect
physiological responses to pressure overload.
Q3: A patient is diagnosed with systolic heart failure. What is the primary underlying pathophysiological
mechanism of this condition?
A. Impaired diastolic filling due to a stiff, noncompliant left ventricle.
B. Impaired contractility and a reduced ejection fraction due to damaged myocardial muscle.
[CORRECT]
C. Backward failure of the right ventricle leading to systemic venous congestion.
D. Obstruction of blood flow out of the left ventricle due to aortic stenosis.
Correct Answer: B
Rationale: Systolic heart failure is characterized by a problem with pumping (contractility). Damage to
the myocardial muscle—often from ischemia or infarction—reduces the force of contraction, leading to a
decreased ejection fraction (typically less than 40%). Option A describes diastolic heart failure (heart
failure with preserved ejection fraction). Option C describes right-sided heart failure, and option D
describes a valvular disorder.
Q4: A patient with a history of long-standing hypertension presents with shortness of breath, but
echocardiography shows a normal left ventricular ejection fraction (LVEF of 55%). Which mechanism
explains this patient's heart failure symptoms?
A. The ventricle has excellent contractility but cannot relax properly during diastole, leading to
decreased stroke volume and pulmonary congestion. [CORRECT]
B. The ventricle is severely dilated, which artificially keeps the ejection fraction percentage normal
despite poor contractile force.
C. The right ventricle is failing first, which masks the drop in left ventricular ejection fraction.
D. The patient has pericardial tamponade, which limits overall cardiac output but preserves intrinsic
muscle function.
Correct Answer: A
Rationale: This patient has diastolic heart failure (HFpEF). Chronic hypertension causes left ventricular
hypertrophy, making the myocardium stiff and noncompliant. Consequently, the ventricle cannot relax
and fill adequately during diastole, reducing preload and stroke volume, causing fluid to back up into the
lungs despite a normal LVEF. Option B describes eccentric hypertrophy, and options C and D do not fit
the clinical scenario of long-standing HTN.
Q5: What is the primary cellular consequence of prolonged ischemia during a myocardial infarction (MI)
that leads to irreversible myocardial cell death?
, A. Depletion of ATP leads to failure of the sodium-potassium pump, causing massive cellular
swelling and rupture of lysosomal membranes. [CORRECT]
B. Rapid influx of calcium into the cell causes prolonged, uncontrolled hypercontractility of the
sarcomeres.
C. Lack of oxygen causes a sudden shift to anaerobic metabolism, generating excessive heat that
denatures cellular proteins.
D. Accumulation of carbon dioxide directly poisons the mitochondria, halting the electron transport chain.
Correct Answer: A
Rationale: Prolonged ischemia depletes cellular ATP. Without ATP, the Na+/K+ pump fails, allowing
sodium to accumulate inside the cell, which draws water in and causes severe cellular swelling (oncotic
necrosis). Additionally, the lack of ATP allows lysosomal membranes to rupture, releasing digestive
enzymes that destroy the cell from the inside out. Option B occurs earlier in ischemia (reperfusion injury)
but is not the primary mechanism of prolonged ischemic necrosis. Options C and D are
misrepresentations of cellular hypoxia.
Q6: A patient presents with cool, clammy skin, tachycardia, hypotension, and a cardiac output of 3.0
L/min following a massive anterior myocardial infarction. Which type of shock is this patient
experiencing, and what is the primary mechanism?
A. Hypovolemic shock; massive internal bleeding has reduced venous return.
B. Distributive shock; systemic vasodilation is causing blood to pool peripherally.
C. Cardiogenic shock; severe pump failure has drastically reduced cardiac output and tissue
perfusion. [CORRECT]
D. Obstructive shock; a pulmonary embolism is blocking blood return to the left heart.
Correct Answer: C
Rationale: The patient's recent massive MI directly implicates damage to the heart muscle, leading to
pump failure. This results in a profound drop in cardiac output (3.0 L/min is severely low), causing
hypotension and systemic hypoperfusion (cool, clammy skin due to sympathetic vasoconstriction). This is
the hallmark of cardiogenic shock. Option A lacks evidence of bleeding; option B lacks fever or signs of
sepsis/anaphylaxis; option D lacks evidence of a pulmonary embolism.
Q7: Which mechanism explains the development of tachycardia in a patient experiencing acute
hypovolemic shock secondary to massive hemorrhage?
A. Direct stimulation of the sinoatrial node by circulating catecholamines released from the adrenal
medulla.
B. Activation of the renin-angiotensin-aldosterone system (RAAS) causing direct positive chronotropy.
Essentials of Pathophysiology Exam 2
Latest Update 2026/2027 | Rasmussen College |
100% Correct
Section 1: Cardiovascular Pathophysiology
Q1: What is the underlying pathophysiology of atherosclerosis?
A. Degeneration of the arterial media layer due to chronic hypertension, leading to vessel thickening.
B. Endothelial injury, lipid infiltration, and inflammatory response leading to plaque formation in
the intima. [CORRECT]
C. Spasm of the vascular smooth muscle triggered by autonomic imbalances.
D. Infection of the arterial wall by bacteria, causing abscess formation and weakening.
Correct Answer: B
Rationale: Atherosclerosis begins with endothelial injury, which allows low-density lipoproteins (LDLs)
to infiltrate the tunica intima. Macrophages ingest these lipids, becoming foam cells, which trigger a
chronic inflammatory response and the formation of an atherosclerotic plaque. Options A and C describe
elements of other vascular diseases (arteriosclerosis and vasospasm, respectively), while option D
describes a mycotic aneurysm or infectious arteritis.
Q2: Which mechanism explains the finding of left ventricular hypertrophy (LVH) in a patient with
chronic, untreated primary hypertension?
A. Increased preload causes excessive stretching of the myocardial fibers, leading to chamber dilation.
B. Decreased afterload reduces oxygen demand, causing myocardial cells to atrophy and stiffen.
C. Increased afterload forces the left ventricle to work harder against higher systemic resistance,
causing concentric muscle hypertrophy. [CORRECT]
D. Sympathetic overdrive directly stimulates myocardial cell hyperplasia without increasing workload.
Correct Answer: C
Rationale: Chronic hypertension increases systemic vascular resistance (afterload). To overcome this
higher pressure and maintain adequate cardiac output, the left ventricle must generate more tension during
systole, leading to concentric hypertrophy (thickening of the ventricular wall). Option A describes volume
,overload (high preload), which causes eccentric hypertrophy. Options B and D contain incorrect
physiological responses to pressure overload.
Q3: A patient is diagnosed with systolic heart failure. What is the primary underlying pathophysiological
mechanism of this condition?
A. Impaired diastolic filling due to a stiff, noncompliant left ventricle.
B. Impaired contractility and a reduced ejection fraction due to damaged myocardial muscle.
[CORRECT]
C. Backward failure of the right ventricle leading to systemic venous congestion.
D. Obstruction of blood flow out of the left ventricle due to aortic stenosis.
Correct Answer: B
Rationale: Systolic heart failure is characterized by a problem with pumping (contractility). Damage to
the myocardial muscle—often from ischemia or infarction—reduces the force of contraction, leading to a
decreased ejection fraction (typically less than 40%). Option A describes diastolic heart failure (heart
failure with preserved ejection fraction). Option C describes right-sided heart failure, and option D
describes a valvular disorder.
Q4: A patient with a history of long-standing hypertension presents with shortness of breath, but
echocardiography shows a normal left ventricular ejection fraction (LVEF of 55%). Which mechanism
explains this patient's heart failure symptoms?
A. The ventricle has excellent contractility but cannot relax properly during diastole, leading to
decreased stroke volume and pulmonary congestion. [CORRECT]
B. The ventricle is severely dilated, which artificially keeps the ejection fraction percentage normal
despite poor contractile force.
C. The right ventricle is failing first, which masks the drop in left ventricular ejection fraction.
D. The patient has pericardial tamponade, which limits overall cardiac output but preserves intrinsic
muscle function.
Correct Answer: A
Rationale: This patient has diastolic heart failure (HFpEF). Chronic hypertension causes left ventricular
hypertrophy, making the myocardium stiff and noncompliant. Consequently, the ventricle cannot relax
and fill adequately during diastole, reducing preload and stroke volume, causing fluid to back up into the
lungs despite a normal LVEF. Option B describes eccentric hypertrophy, and options C and D do not fit
the clinical scenario of long-standing HTN.
Q5: What is the primary cellular consequence of prolonged ischemia during a myocardial infarction (MI)
that leads to irreversible myocardial cell death?
, A. Depletion of ATP leads to failure of the sodium-potassium pump, causing massive cellular
swelling and rupture of lysosomal membranes. [CORRECT]
B. Rapid influx of calcium into the cell causes prolonged, uncontrolled hypercontractility of the
sarcomeres.
C. Lack of oxygen causes a sudden shift to anaerobic metabolism, generating excessive heat that
denatures cellular proteins.
D. Accumulation of carbon dioxide directly poisons the mitochondria, halting the electron transport chain.
Correct Answer: A
Rationale: Prolonged ischemia depletes cellular ATP. Without ATP, the Na+/K+ pump fails, allowing
sodium to accumulate inside the cell, which draws water in and causes severe cellular swelling (oncotic
necrosis). Additionally, the lack of ATP allows lysosomal membranes to rupture, releasing digestive
enzymes that destroy the cell from the inside out. Option B occurs earlier in ischemia (reperfusion injury)
but is not the primary mechanism of prolonged ischemic necrosis. Options C and D are
misrepresentations of cellular hypoxia.
Q6: A patient presents with cool, clammy skin, tachycardia, hypotension, and a cardiac output of 3.0
L/min following a massive anterior myocardial infarction. Which type of shock is this patient
experiencing, and what is the primary mechanism?
A. Hypovolemic shock; massive internal bleeding has reduced venous return.
B. Distributive shock; systemic vasodilation is causing blood to pool peripherally.
C. Cardiogenic shock; severe pump failure has drastically reduced cardiac output and tissue
perfusion. [CORRECT]
D. Obstructive shock; a pulmonary embolism is blocking blood return to the left heart.
Correct Answer: C
Rationale: The patient's recent massive MI directly implicates damage to the heart muscle, leading to
pump failure. This results in a profound drop in cardiac output (3.0 L/min is severely low), causing
hypotension and systemic hypoperfusion (cool, clammy skin due to sympathetic vasoconstriction). This is
the hallmark of cardiogenic shock. Option A lacks evidence of bleeding; option B lacks fever or signs of
sepsis/anaphylaxis; option D lacks evidence of a pulmonary embolism.
Q7: Which mechanism explains the development of tachycardia in a patient experiencing acute
hypovolemic shock secondary to massive hemorrhage?
A. Direct stimulation of the sinoatrial node by circulating catecholamines released from the adrenal
medulla.
B. Activation of the renin-angiotensin-aldosterone system (RAAS) causing direct positive chronotropy.
