Rasmussen Pathophysiology NUR 2063 Essentials
Exam 2 ACTUAL EXAM 2026/2027 | Rasmussen
NUR 2063 Patho Exam 2 | Verified Q&A | Pass
Guaranteed - A+ Graded
Total Questions: 60 | Time Suggested: 90 minutes
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1–15)
Q1. A client with chronic untreated hypertension presents with shortness of breath, peripheral edema,
and fatigue. Which pathophysiological mechanism best explains the development of heart failure in this
client?
A. Decreased systemic vascular resistance leading to reduced afterload
B. Increased left ventricular workload causing compensatory hypertrophy and eventual remodeling
C. Decreased blood viscosity resulting in reduced oxygen delivery to the myocardium
D. Increased baroreceptor sensitivity causing inappropriate bradycardia
Correct Answer: B
Rationale: Chronic hypertension increases systemic afterload, forcing the left ventricle to work harder to
eject blood. Over time, the myocardium undergoes concentric hypertrophy as a compensatory
response. Persistent pressure overload leads to maladaptive remodeling, ventricular dilation, decreased
contractility, and ultimately heart failure with reduced ejection fraction (HFrEF). This progression
explains the presenting symptoms of dyspnea (pulmonary congestion) and peripheral edema (systemic
venous congestion).
Q2. A client with atherosclerosis has plaque rupture in a coronary artery, leading to platelet aggregation
and thrombus formation. Which substance is primarily responsible for platelet activation and
aggregation at the site of plaque rupture?
A. Tissue plasminogen activator (tPA)
B. Adenosine diphosphate (ADP) and thromboxane A2
C. Nitric oxide
D. Prostacyclin
,Correct Answer: B
Rationale: When plaque rupture exposes subendothelial collagen, platelets adhere via von Willebrand
factor and become activated. Activated platelets release ADP and thromboxane A2, which recruit
additional platelets and promote aggregation, forming a platelet-rich thrombus. ADP binds P2Y12
receptors, and thromboxane A2 amplifies the activation cascade. This platelet plug is the initial
hemostatic response that, combined with the coagulation cascade, produces an occlusive thrombus
causing acute coronary syndrome.
Q3. [SELECT ALL THAT APPLY] A client with heart failure has decreased cardiac output. Which
compensatory mechanisms does the body activate to maintain perfusion? (Select all that apply.)
A. Activation of the renin-angiotensin-aldosterone system (RAAS)
B. Increased sympathetic nervous system activity
C. Release of atrial natriuretic peptide (ANP)
D. Vasodilation of systemic arterioles
E. Increased release of antidiuretic hormone (ADH)
F. Decreased heart rate to reduce myocardial oxygen demand
Correct Answers: A, B, C, E
Rationale: In heart failure, decreased cardiac output activates multiple compensatory mechanisms:
RAAS (A) increases sodium/water retention and vasoconstriction to maintain perfusion pressure.
Sympathetic activation (B) increases heart rate and contractility via catecholamines. ANP (C) is released
from stretched atria as a counter-regulatory hormone promoting vasodilation and natriuresis. ADH (E)
increases free water reabsorption. Systemic vasodilation (D) does not occur—vasoconstriction is the
compensatory response. Bradycardia (F) would further reduce cardiac output; tachycardia is the
compensatory response.
Q4. A client with mitral stenosis develops pulmonary edema. Which hemodynamic change is the primary
cause of this complication?
A. Increased preload to the right ventricle
B. Obstruction of left ventricular outflow
C. Elevated left atrial pressure transmitted backward to pulmonary circulation
D. Decreased pulmonary vascular resistance
Correct Answer: C
Rationale: Mitral stenosis narrows the mitral valve orifice, impeding blood flow from left atrium to left
ventricle during diastole. This causes pressure buildup in the left atrium, which is transmitted backward
through the pulmonary veins into the pulmonary capillary bed. Elevated pulmonary capillary hydrostatic
pressure (>25 mm Hg) forces fluid into the interstitium and alveoli, producing pulmonary edema
, (dyspnea, orthopnea, crackles). This is a classic example of cardiogenic pulmonary edema due to left-
sided heart obstruction.
Q5. [ORDERED RESPONSE – PATHOPHYSIOLOGICAL SEQUENCE] A client experiences an acute
myocardial infarction (MI). Place the following cellular events in the correct sequence from initial insult
to cell death.
1. Ischemia causes switch from aerobic to anaerobic metabolism
2. ATP depletion leads to failure of Na⁺/K⁺-ATPase pumps
3. Calcium influx activates phospholipases and proteases
4. Loss of membrane integrity causes cell swelling and necrosis
Correct Answer: 1, 2, 3, 4
Rationale: Coronary occlusion causes myocardial ischemia (1), forcing cells to switch to inefficient
anaerobic glycolysis. ATP production drops by 90% within minutes, failing the Na⁺/K⁺-ATPase pump (2).
Intracellular sodium rises, causing cellular edema. The Na⁺/Ca²⁺ exchanger reverses, pumping calcium
into the cell. Calcium overload (3) activates phospholipases (membrane damage), proteases
(cytoskeletal breakdown), and ATPases (further ATP consumption). Within 20–40 minutes, irreversible
membrane damage occurs (4), releasing intracellular enzymes (troponin, CK-MB) into circulation.
Q6. A client with atrial fibrillation has an irregularly irregular rhythm with no discernible P waves. Which
pathophysiological mechanism explains the thromboembolic risk in this condition?
A. Increased ventricular contractility causing blood stasis in the ventricles
B. Loss of organized atrial contraction causing blood stasis and thrombus formation in the atrial
appendage
C. Increased heart rate causing endothelial damage and platelet activation
D. Decreased cardiac output causing hypercoagulability through hemoconcentration
Correct Answer: B
Rationale: In atrial fibrillation, disorganized atrial electrical activity replaces coordinated contraction
with quivering. The loss of effective atrial systole causes blood stasis, particularly in the left atrial
appendage where flow is already sluggish. Stasis activates the coagulation cascade, promoting thrombus
formation. These thrombi can embolize to the brain (stroke), limbs, or viscera. This mechanism explains
why anticoagulation (warfarin, DOACs) is essential for stroke prevention in atrial fibrillation, regardless
of rate control.
Exam 2 ACTUAL EXAM 2026/2027 | Rasmussen
NUR 2063 Patho Exam 2 | Verified Q&A | Pass
Guaranteed - A+ Graded
Total Questions: 60 | Time Suggested: 90 minutes
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1–15)
Q1. A client with chronic untreated hypertension presents with shortness of breath, peripheral edema,
and fatigue. Which pathophysiological mechanism best explains the development of heart failure in this
client?
A. Decreased systemic vascular resistance leading to reduced afterload
B. Increased left ventricular workload causing compensatory hypertrophy and eventual remodeling
C. Decreased blood viscosity resulting in reduced oxygen delivery to the myocardium
D. Increased baroreceptor sensitivity causing inappropriate bradycardia
Correct Answer: B
Rationale: Chronic hypertension increases systemic afterload, forcing the left ventricle to work harder to
eject blood. Over time, the myocardium undergoes concentric hypertrophy as a compensatory
response. Persistent pressure overload leads to maladaptive remodeling, ventricular dilation, decreased
contractility, and ultimately heart failure with reduced ejection fraction (HFrEF). This progression
explains the presenting symptoms of dyspnea (pulmonary congestion) and peripheral edema (systemic
venous congestion).
Q2. A client with atherosclerosis has plaque rupture in a coronary artery, leading to platelet aggregation
and thrombus formation. Which substance is primarily responsible for platelet activation and
aggregation at the site of plaque rupture?
A. Tissue plasminogen activator (tPA)
B. Adenosine diphosphate (ADP) and thromboxane A2
C. Nitric oxide
D. Prostacyclin
,Correct Answer: B
Rationale: When plaque rupture exposes subendothelial collagen, platelets adhere via von Willebrand
factor and become activated. Activated platelets release ADP and thromboxane A2, which recruit
additional platelets and promote aggregation, forming a platelet-rich thrombus. ADP binds P2Y12
receptors, and thromboxane A2 amplifies the activation cascade. This platelet plug is the initial
hemostatic response that, combined with the coagulation cascade, produces an occlusive thrombus
causing acute coronary syndrome.
Q3. [SELECT ALL THAT APPLY] A client with heart failure has decreased cardiac output. Which
compensatory mechanisms does the body activate to maintain perfusion? (Select all that apply.)
A. Activation of the renin-angiotensin-aldosterone system (RAAS)
B. Increased sympathetic nervous system activity
C. Release of atrial natriuretic peptide (ANP)
D. Vasodilation of systemic arterioles
E. Increased release of antidiuretic hormone (ADH)
F. Decreased heart rate to reduce myocardial oxygen demand
Correct Answers: A, B, C, E
Rationale: In heart failure, decreased cardiac output activates multiple compensatory mechanisms:
RAAS (A) increases sodium/water retention and vasoconstriction to maintain perfusion pressure.
Sympathetic activation (B) increases heart rate and contractility via catecholamines. ANP (C) is released
from stretched atria as a counter-regulatory hormone promoting vasodilation and natriuresis. ADH (E)
increases free water reabsorption. Systemic vasodilation (D) does not occur—vasoconstriction is the
compensatory response. Bradycardia (F) would further reduce cardiac output; tachycardia is the
compensatory response.
Q4. A client with mitral stenosis develops pulmonary edema. Which hemodynamic change is the primary
cause of this complication?
A. Increased preload to the right ventricle
B. Obstruction of left ventricular outflow
C. Elevated left atrial pressure transmitted backward to pulmonary circulation
D. Decreased pulmonary vascular resistance
Correct Answer: C
Rationale: Mitral stenosis narrows the mitral valve orifice, impeding blood flow from left atrium to left
ventricle during diastole. This causes pressure buildup in the left atrium, which is transmitted backward
through the pulmonary veins into the pulmonary capillary bed. Elevated pulmonary capillary hydrostatic
pressure (>25 mm Hg) forces fluid into the interstitium and alveoli, producing pulmonary edema
, (dyspnea, orthopnea, crackles). This is a classic example of cardiogenic pulmonary edema due to left-
sided heart obstruction.
Q5. [ORDERED RESPONSE – PATHOPHYSIOLOGICAL SEQUENCE] A client experiences an acute
myocardial infarction (MI). Place the following cellular events in the correct sequence from initial insult
to cell death.
1. Ischemia causes switch from aerobic to anaerobic metabolism
2. ATP depletion leads to failure of Na⁺/K⁺-ATPase pumps
3. Calcium influx activates phospholipases and proteases
4. Loss of membrane integrity causes cell swelling and necrosis
Correct Answer: 1, 2, 3, 4
Rationale: Coronary occlusion causes myocardial ischemia (1), forcing cells to switch to inefficient
anaerobic glycolysis. ATP production drops by 90% within minutes, failing the Na⁺/K⁺-ATPase pump (2).
Intracellular sodium rises, causing cellular edema. The Na⁺/Ca²⁺ exchanger reverses, pumping calcium
into the cell. Calcium overload (3) activates phospholipases (membrane damage), proteases
(cytoskeletal breakdown), and ATPases (further ATP consumption). Within 20–40 minutes, irreversible
membrane damage occurs (4), releasing intracellular enzymes (troponin, CK-MB) into circulation.
Q6. A client with atrial fibrillation has an irregularly irregular rhythm with no discernible P waves. Which
pathophysiological mechanism explains the thromboembolic risk in this condition?
A. Increased ventricular contractility causing blood stasis in the ventricles
B. Loss of organized atrial contraction causing blood stasis and thrombus formation in the atrial
appendage
C. Increased heart rate causing endothelial damage and platelet activation
D. Decreased cardiac output causing hypercoagulability through hemoconcentration
Correct Answer: B
Rationale: In atrial fibrillation, disorganized atrial electrical activity replaces coordinated contraction
with quivering. The loss of effective atrial systole causes blood stasis, particularly in the left atrial
appendage where flow is already sluggish. Stasis activates the coagulation cascade, promoting thrombus
formation. These thrombi can embolize to the brain (stroke), limbs, or viscera. This mechanism explains
why anticoagulation (warfarin, DOACs) is essential for stroke prevention in atrial fibrillation, regardless
of rate control.
