NUR 2063 Exam 3 - Essentials of Pathophysiology | Rasmussen University
Exam 3: NUR2063 / NUR 2063 (Latest
Update)
Essentials of Pathophysiology | Review Guide Questions and Verified Answers | 100% Correct
Rasmussen University - College of Nursing
2026/2027 Academic Year | Modules 7-9
Total Questions Cognitive Levels Question Style
25% Recall / 55% Application / 20% 70% Scenario / 20% Recall / 10%
75 Multiple Choice
Analysis Clinical Reasoning
Instructions: Select the single best answer for each question. Each question provides a rationale explaining the
correct response and why alternative options are incorrect, integrating Rasmussen University NUR 2063 Modules
7-9 pathophysiology concepts, disease mechanisms, clinical manifestations, and evidence-based practice.
Section 1: Cardiovascular Disorders (Q1-Q25)
Atherosclerosis pathophysiology, CAD (stable/unstable angina, MI), hypertension (primary/secondary, target organ damage),
heart failure (left/right, HFrEF/HFpEF), valvular disease (AS, AR, MS, MR), arrhythmias (AFib, VT, VF, blocks),
peripheral vascular disease (PAD, AAA, DVT).
Q1: A 56-year-old male presents with substernal chest pain that occurs predictably when walking
uphill, is relieved by rest after 5 minutes, and responds to sublingual nitroglycerin. Which
pathophysiologic process best explains his symptoms?
A. Complete coronary artery occlusion with myocardial necrosis
B. Fixed atherosclerotic plaque causing partial coronary obstruction with demand-supply
mismatch during exertion [CORRECT]
C. Plaque rupture with non-occlusive thrombus causing ischemia at rest
D. Dissection of the coronary artery wall causing dynamic obstruction
Correct Answer: B
Rationale: Stable angina is caused by a fixed atherosclerotic plaque that produces a partial (typically 70% or
greater) coronary obstruction. At rest, blood flow is adequate, but during exertion oxygen demand exceeds
supply (demand-supply mismatch), causing ischemic pain that is relieved by rest or nitroglycerin. Complete
occlusion with necrosis = MI. Plaque rupture at rest = unstable angina. Dissection is a different mechanism
entirely.
Q2: A patient with an acute MI develops myocardial necrosis. At what point after coronary artery
occlusion does irreversible myocardial cell death begin?
A. 1-5 minutes
B. 20-30 minutes [CORRECT]
C. 2-4 hours
D. 6-12 hours
Correct Answer: B
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 1
,NUR 2063 Exam 3 - Essentials of Pathophysiology | Rasmussen University
Rationale: Irreversible myocardial cell death begins after approximately 20-30 minutes of coronary occlusion.
The ischemic zone expands in a wavefront from subendocardium to epicardium, with complete transmural
necrosis occurring by 6 hours. This is why rapid reperfusion (PCI within 90 min door-to-balloon or
thrombolytics within 30 min door-to-needle) is critical to salvage ischemic but not yet necrotic myocardium
(the ischemic penumbra).
Q3: Which cardiac biomarker is MOST specific for myocardial necrosis and remains elevated for
7-10 days after an acute MI?
A. Creatine kinase-MB (CK-MB)
B. Myoglobin
C. Troponin I and T [CORRECT]
D. Lactate dehydrogenase (LDH)
Correct Answer: C
Rationale: Troponin I and T are the most specific biomarkers for myocardial necrosis because they are found
exclusively in cardiac muscle. They rise within 3-4 hours, peak at 24 hours, and remain elevated for 7-10 days,
making them useful for detecting late presentations. CK-MB rises in 4-6 hours but returns to normal in 48-72
hours (useful for detecting reinfarction). Myoglobin is early but not cardiac-specific. LDH is rarely used today.
Q4: A 62-year-old male with a history of hypertension presents with crushing chest pain for 1
hour. ECG reveals ST elevation in leads V2-V4. Which type of acute coronary syndrome is this,
and what is the underlying pathophysiology?
A. Unstable angina; partial thrombus without necrosis
B. NSTEMI; subendocardial infarction with ST depression
C. STEMI; transmural infarction from complete coronary occlusion [CORRECT]
D. Prinzmetal angina; vasospasm of coronary artery
Correct Answer: C
Rationale: ST elevation in V2-V4 indicates an acute anterior STEMI (ST-elevation myocardial infarction),
caused by complete occlusion of the left anterior descending (LAD) artery producing transmural
(full-thickness) infarction. NSTEMI involves subendocardial infarction without ST elevation. Unstable angina
causes ischemia without necrosis (no troponin elevation). Prinzmetal (variant) angina is caused by coronary
vasospasm and may cause transient ST elevation.
Q5: A 48-year-old female has BP 152/98 mmHg on three separate visits. She has no identified
secondary cause. Which form of hypertension does she have, and what percentage of all HTN
cases does this represent?
A. Secondary hypertension; 5-10% of cases
B. Primary (essential) hypertension; 90-95% of cases [CORRECT]
C. White coat hypertension; 20-30% of cases
D. Malignant hypertension; <1% of cases
Correct Answer: B
Rationale: Primary (essential) hypertension accounts for 90-95% of all hypertension cases and has no
identifiable cause, attributed to genetic, environmental, and lifestyle factors (obesity, sodium intake, stress,
alcohol). Secondary hypertension (5-10%) has an identifiable cause such as renal disease, endocrine disorders
(Cushing, pheochromocytoma, primary aldosteronism), coarctation of the aorta, or obstructive sleep apnea.
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 2
, NUR 2063 Exam 3 - Essentials of Pathophysiology | Rasmussen University
Q6: A patient with longstanding hypertension develops left ventricular hypertrophy (LVH),
chronic kidney disease, and hypertensive retinopathy. Which pathophysiologic mechanisms
primarily contribute to target organ damage in hypertension?
A. Decreased systemic vascular resistance and low cardiac output
B. Increased systemic vascular resistance, RAAS activation, and SNS activation causing
endothelial injury and increased afterload [CORRECT]
C. Vasodilation from decreased sympathetic tone
D. Decreased renin secretion reducing angiotensin II
Correct Answer: B
Rationale: Hypertension pathophysiology involves increased systemic vascular resistance (SVR), RAAS
activation (angiotensin II vasoconstriction and aldosterone sodium retention), and SNS activation. The elevated
pressure causes endothelial injury, accelerated atherosclerosis, increased afterload (causing LVH), and damage
to small arteries in target organs (kidneys, brain, eyes, heart). LVH is a compensatory response to chronic
pressure overload.
Q7: A 55-year-old male presents with BP 220/130, severe headache, blurred vision, chest pain, and
shortness of breath. Papilledema is present on funduscopic exam. Which finding distinguishes
hypertensive emergency from hypertensive urgency?
A. BP > 180/120 mmHg
B. Presence of end-organ damage (encephalopathy, pulmonary edema, renal failure,
papilledema) [CORRECT]
C. Headache and dizziness
D. Duration of hypertension > 10 years
Correct Answer: B
Rationale: Hypertensive emergency is defined by severe BP elevation (typically > 180/120) WITH acute
end-organ damage (hypertensive encephalopathy, papilledema, acute pulmonary edema, acute renal failure,
aortic dissection, stroke, MI). Hypertensive urgency is severe BP elevation WITHOUT end-organ damage.
Emergency requires immediate IV antihypertensive therapy (goal: reduce MAP by 10-25% in first 1-2 hours);
urgency can be managed with oral agents over 24-48 hours.
Q8: A 68-year-old female with heart failure presents with dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, bilateral basilar crackles, and an S3 gallop. Which pathophysiologic process
best explains these findings?
A. Right ventricular failure causing systemic venous congestion
B. Left ventricular failure causing pulmonary congestion from increased pulmonary capillary
pressure [CORRECT]
C. Biventricular failure with peripheral edema as primary feature
D. Diastolic dysfunction with preserved ejection fraction
Correct Answer: B
Rationale: Left-sided heart failure causes decreased left ventricular output and increased left atrial and
pulmonary venous pressure, leading to pulmonary congestion. Classic manifestations include dyspnea,
orthopnea (worse lying flat), paroxysmal nocturnal dyspnea, bilateral basilar crackles, and S3 gallop (rapid
ventricular filling into stiff, volume-overloaded ventricle). Right-sided HF causes systemic congestion
(peripheral edema, JVD, hepatomegaly, ascites).
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 3
Exam 3: NUR2063 / NUR 2063 (Latest
Update)
Essentials of Pathophysiology | Review Guide Questions and Verified Answers | 100% Correct
Rasmussen University - College of Nursing
2026/2027 Academic Year | Modules 7-9
Total Questions Cognitive Levels Question Style
25% Recall / 55% Application / 20% 70% Scenario / 20% Recall / 10%
75 Multiple Choice
Analysis Clinical Reasoning
Instructions: Select the single best answer for each question. Each question provides a rationale explaining the
correct response and why alternative options are incorrect, integrating Rasmussen University NUR 2063 Modules
7-9 pathophysiology concepts, disease mechanisms, clinical manifestations, and evidence-based practice.
Section 1: Cardiovascular Disorders (Q1-Q25)
Atherosclerosis pathophysiology, CAD (stable/unstable angina, MI), hypertension (primary/secondary, target organ damage),
heart failure (left/right, HFrEF/HFpEF), valvular disease (AS, AR, MS, MR), arrhythmias (AFib, VT, VF, blocks),
peripheral vascular disease (PAD, AAA, DVT).
Q1: A 56-year-old male presents with substernal chest pain that occurs predictably when walking
uphill, is relieved by rest after 5 minutes, and responds to sublingual nitroglycerin. Which
pathophysiologic process best explains his symptoms?
A. Complete coronary artery occlusion with myocardial necrosis
B. Fixed atherosclerotic plaque causing partial coronary obstruction with demand-supply
mismatch during exertion [CORRECT]
C. Plaque rupture with non-occlusive thrombus causing ischemia at rest
D. Dissection of the coronary artery wall causing dynamic obstruction
Correct Answer: B
Rationale: Stable angina is caused by a fixed atherosclerotic plaque that produces a partial (typically 70% or
greater) coronary obstruction. At rest, blood flow is adequate, but during exertion oxygen demand exceeds
supply (demand-supply mismatch), causing ischemic pain that is relieved by rest or nitroglycerin. Complete
occlusion with necrosis = MI. Plaque rupture at rest = unstable angina. Dissection is a different mechanism
entirely.
Q2: A patient with an acute MI develops myocardial necrosis. At what point after coronary artery
occlusion does irreversible myocardial cell death begin?
A. 1-5 minutes
B. 20-30 minutes [CORRECT]
C. 2-4 hours
D. 6-12 hours
Correct Answer: B
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 1
,NUR 2063 Exam 3 - Essentials of Pathophysiology | Rasmussen University
Rationale: Irreversible myocardial cell death begins after approximately 20-30 minutes of coronary occlusion.
The ischemic zone expands in a wavefront from subendocardium to epicardium, with complete transmural
necrosis occurring by 6 hours. This is why rapid reperfusion (PCI within 90 min door-to-balloon or
thrombolytics within 30 min door-to-needle) is critical to salvage ischemic but not yet necrotic myocardium
(the ischemic penumbra).
Q3: Which cardiac biomarker is MOST specific for myocardial necrosis and remains elevated for
7-10 days after an acute MI?
A. Creatine kinase-MB (CK-MB)
B. Myoglobin
C. Troponin I and T [CORRECT]
D. Lactate dehydrogenase (LDH)
Correct Answer: C
Rationale: Troponin I and T are the most specific biomarkers for myocardial necrosis because they are found
exclusively in cardiac muscle. They rise within 3-4 hours, peak at 24 hours, and remain elevated for 7-10 days,
making them useful for detecting late presentations. CK-MB rises in 4-6 hours but returns to normal in 48-72
hours (useful for detecting reinfarction). Myoglobin is early but not cardiac-specific. LDH is rarely used today.
Q4: A 62-year-old male with a history of hypertension presents with crushing chest pain for 1
hour. ECG reveals ST elevation in leads V2-V4. Which type of acute coronary syndrome is this,
and what is the underlying pathophysiology?
A. Unstable angina; partial thrombus without necrosis
B. NSTEMI; subendocardial infarction with ST depression
C. STEMI; transmural infarction from complete coronary occlusion [CORRECT]
D. Prinzmetal angina; vasospasm of coronary artery
Correct Answer: C
Rationale: ST elevation in V2-V4 indicates an acute anterior STEMI (ST-elevation myocardial infarction),
caused by complete occlusion of the left anterior descending (LAD) artery producing transmural
(full-thickness) infarction. NSTEMI involves subendocardial infarction without ST elevation. Unstable angina
causes ischemia without necrosis (no troponin elevation). Prinzmetal (variant) angina is caused by coronary
vasospasm and may cause transient ST elevation.
Q5: A 48-year-old female has BP 152/98 mmHg on three separate visits. She has no identified
secondary cause. Which form of hypertension does she have, and what percentage of all HTN
cases does this represent?
A. Secondary hypertension; 5-10% of cases
B. Primary (essential) hypertension; 90-95% of cases [CORRECT]
C. White coat hypertension; 20-30% of cases
D. Malignant hypertension; <1% of cases
Correct Answer: B
Rationale: Primary (essential) hypertension accounts for 90-95% of all hypertension cases and has no
identifiable cause, attributed to genetic, environmental, and lifestyle factors (obesity, sodium intake, stress,
alcohol). Secondary hypertension (5-10%) has an identifiable cause such as renal disease, endocrine disorders
(Cushing, pheochromocytoma, primary aldosteronism), coarctation of the aorta, or obstructive sleep apnea.
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 2
, NUR 2063 Exam 3 - Essentials of Pathophysiology | Rasmussen University
Q6: A patient with longstanding hypertension develops left ventricular hypertrophy (LVH),
chronic kidney disease, and hypertensive retinopathy. Which pathophysiologic mechanisms
primarily contribute to target organ damage in hypertension?
A. Decreased systemic vascular resistance and low cardiac output
B. Increased systemic vascular resistance, RAAS activation, and SNS activation causing
endothelial injury and increased afterload [CORRECT]
C. Vasodilation from decreased sympathetic tone
D. Decreased renin secretion reducing angiotensin II
Correct Answer: B
Rationale: Hypertension pathophysiology involves increased systemic vascular resistance (SVR), RAAS
activation (angiotensin II vasoconstriction and aldosterone sodium retention), and SNS activation. The elevated
pressure causes endothelial injury, accelerated atherosclerosis, increased afterload (causing LVH), and damage
to small arteries in target organs (kidneys, brain, eyes, heart). LVH is a compensatory response to chronic
pressure overload.
Q7: A 55-year-old male presents with BP 220/130, severe headache, blurred vision, chest pain, and
shortness of breath. Papilledema is present on funduscopic exam. Which finding distinguishes
hypertensive emergency from hypertensive urgency?
A. BP > 180/120 mmHg
B. Presence of end-organ damage (encephalopathy, pulmonary edema, renal failure,
papilledema) [CORRECT]
C. Headache and dizziness
D. Duration of hypertension > 10 years
Correct Answer: B
Rationale: Hypertensive emergency is defined by severe BP elevation (typically > 180/120) WITH acute
end-organ damage (hypertensive encephalopathy, papilledema, acute pulmonary edema, acute renal failure,
aortic dissection, stroke, MI). Hypertensive urgency is severe BP elevation WITHOUT end-organ damage.
Emergency requires immediate IV antihypertensive therapy (goal: reduce MAP by 10-25% in first 1-2 hours);
urgency can be managed with oral agents over 24-48 hours.
Q8: A 68-year-old female with heart failure presents with dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, bilateral basilar crackles, and an S3 gallop. Which pathophysiologic process
best explains these findings?
A. Right ventricular failure causing systemic venous congestion
B. Left ventricular failure causing pulmonary congestion from increased pulmonary capillary
pressure [CORRECT]
C. Biventricular failure with peripheral edema as primary feature
D. Diastolic dysfunction with preserved ejection fraction
Correct Answer: B
Rationale: Left-sided heart failure causes decreased left ventricular output and increased left atrial and
pulmonary venous pressure, leading to pulmonary congestion. Classic manifestations include dyspnea,
orthopnea (worse lying flat), paroxysmal nocturnal dyspnea, bilateral basilar crackles, and S3 gallop (rapid
ventricular filling into stiff, volume-overloaded ventricle). Right-sided HF causes systemic congestion
(peripheral edema, JVD, hepatomegaly, ascites).
Rasmussen University | Modules 7-9 | Latest 2026/2027 Update Page 3
