RASMUSSEN UNIVERSITY · EXAM 2 REVIEW GUIDE
ESSENTIALS OF
PATHOPHYSIOLOGY
A comprehensive examination review featuring 100 verified
questions with detailed rationales across cardiovascular,
respiratory, renal, endocrine, gastrointestinal, neurological,
and multisystem pathophysiology — aligned with the NUR
2063 course syllabus and NCLEX-RN standards.
100 Questions · 7 Sections · Verified Answers
With Detailed Rationales
NUR2063 / NUR 2063 · Latest Update · Grade A
N U R 2 0 6 3 · E SSE N TIA LS O F PATH O PH Y SIO LO G Y · 2 0 2 0 2 7 E DITIO N
,NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
EXAM 2: NUR2063 / NUR 2063 (LATEST UPDATE)
ESSENTIALS OF PATHOPHYSIOLOGY
REVIEW GUIDE QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT | GRADE A -
RASMUSSEN
Comprehensive Examination - Aligned with the NUR 2063 Course Syllabus, NCLEX-RN Pathophysiology
Standards, and Essentials of Pathophysiology Competencies (2026/2027 Edition)
100 Questions | 7 Sections | 4 Options (A-D) | One Correct Answer | Verified Answers with Rationales
75% Scenario-Based Clinical Items | 25% Direct Knowledge | Cognitive Mix: 20% Recall, 50% Application, 30% Analysis
Section 1: Cardiovascular Pathophysiology Questions 1-20
Q1. Which sequence of events best describes the initial pathogenesis of an atherosclerotic plaque
according to the injury-response model emphasized in NUR 2063?
A. Smooth muscle calcification of the tunica media occurs first, followed later by LDL oxidation and
macrophage recruitment
B. Endothelial injury allows LDL entry into the intima; LDL is oxidized, engulfed by macrophages to
form foam cells, and a fatty streak develops [CORRECT]
C. A mural thrombus forms on intact endothelium and organizes into a lipid-rich plaque within the vessel
media
D. Neutrophils invade the adventitia and release proteolytic enzymes that dissolve the internal elastic
lamina
Correct Answer: B
Rationale: Atherosclerosis begins with endothelial injury or dysfunction from risk factors such as
hypertension, smoking, and hyperlipidemia. Increased permeability allows LDL into the intima, where
oxidation attracts macrophages that become foam cells, forming the fatty streak. Calcification and thrombus
formation are late events, and the neutrophil-driven adventitial process in option D is not part of early plaque
biology.
Q2. A 45-year-old client with a BMI of 31 and a strong family history has had blood pressures of 146 to
152 over 90 to 96 mm Hg at three separate visits. No secondary cause is identified on evaluation. Which
finding most strongly supports a diagnosis of primary (essential) hypertension?
A. Abrupt onset of severe hypertension accompanied by an audible abdominal bruit
B. Hypokalemia with metabolic alkalosis on the basic metabolic panel
C. Gradual onset linked to heredity, obesity, high sodium intake, and aging-related vascular changes
[CORRECT]
D. Elevated midnight salivary cortisol with central obesity and purple striae
Correct Answer: C
Rationale: Primary hypertension develops gradually from interacting genetic, lifestyle, and environmental
factors such as obesity and sodium sensitivity. Abrupt severe onset with an abdominal bruit suggests
renovascular disease, hypokalemia with alkalosis suggests primary hyperaldosteronism, and cortisol excess
with striae suggests Cushing syndrome. All three are secondary causes that the evaluation has excluded in this
client.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 1
,NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
Q3. A client with hypertension is found to have elevated plasma renin activity. Which mechanism
explains how activation of the renin-angiotensin-aldosterone system (RAAS) raises arterial pressure?
A. Renin directly constricts peripheral arterioles and increases heart rate through cardiac beta-1
receptors
B. Angiotensin I stimulates the adrenal medulla to release aldosterone, promoting sodium and water
retention
C. Aldosterone converts circulating angiotensinogen to angiotensin I within the hepatic circulation
D. Angiotensin II produces intense vasoconstriction, stimulates aldosterone secretion from the adrenal
cortex, promotes sodium and water retention, and triggers ADH release and thirst [CORRECT]
Correct Answer: D
Rationale: Renin enzymatically cleaves angiotensinogen to angiotensin I, which is converted by ACE,
primarily in the pulmonary endothelium, to angiotensin II. Angiotensin II raises blood pressure through potent
vasoconstriction, aldosterone-mediated sodium and water retention, and stimulation of ADH and thirst. Renin
has no direct vascular effect, aldosterone is secreted by the adrenal cortex rather than the medulla, and the
liver, not aldosterone, supplies angiotensinogen.
Q4. A 72-year-old client with chronic heart failure reports awakening from sleep two hours after going to
bed with sudden severe dyspnea and a desire to sit upright or stand by an open window. Which
pathophysiologic mechanism best explains this paroxysmal nocturnal dyspnea?
A. Reabsorption of interstitial fluid from dependent extremities into the circulation when lying flat
increases venous return and pulmonary capillary pressure, producing transient pulmonary edema during
sleep [CORRECT]
B. Right ventricular afterload rises during sleep because of position-dependent compression of the
pulmonary artery
C. Nocturnal glycosuria creates an osmotic diuresis that concentrates the blood and thickens pulmonary
secretions
D. Sleep-related lymphatic obstruction prevents drainage of the lower lung lobes
Correct Answer: A
Rationale: In left-sided heart failure, lying supine redistributes edema fluid from the legs into the central
circulation, raising preload and pulmonary capillary hydrostatic pressure; the resulting interstitial pulmonary
edema awakens the client with dyspnea that improves on sitting or standing. Right ventricular afterload
changes, glycosuria, and lymphatic obstruction are not involved in this classic orthopnea-to-PND sequence.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 2
, NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
Q5. Which description accurately distinguishes heart failure with preserved ejection fraction (HFpEF)
from heart failure with reduced ejection fraction (HFrEF)?
A. HFpEF is caused by acute pulmonary embolus, whereas HFrEF is caused by chronic anemia
B. In HFpEF the ventricle is stiff and noncompliant with impaired diastolic filling and an ejection
fraction of 50 percent or higher, while in HFrEF the ventricle dilates and contracts poorly with an
ejection fraction below 40 percent [CORRECT]
C. HFpEF produces a dilated, hypokinetic ventricle, whereas HFrEF produces a thickened, small-cavity
ventricle
D. Both conditions share an ejection fraction below 35 percent and differ only in the presence of jugular
venous distention
Correct Answer: B
Rationale: HFpEF, or diastolic dysfunction, is characterized by a preserved ejection fraction with filling
impairment from a stiff, often hypertrophied ventricle, common in hypertension and diabetes. HFrEF, or
systolic dysfunction, involves weakened contractility with ventricular dilation and an ejection fraction below
40 percent. The two disorders differ in ejection fraction and ventricular geometry, not merely in venous
findings.
Q6. A 68-year-old client with chronic heart failure presents with a 2.7 kg (6 lb) weight gain over three
days, bilateral ankle edema, jugular venous distention of 10 cm, bibasilar crackles, and new dyspnea at
rest. Which interpretation best integrates these findings for the plan of care?
A. The findings represent isolated right-sided congestion; the lungs remain unaffected and no provider
notification is needed
B. The findings are expected effects of diuretic therapy and indicate the current medication regimen is
working
C. Systemic and pulmonary venous congestion from fluid retention indicate acute decompensated heart
failure, warranting prompt provider notification, strict intake and output monitoring, daily weights, and
anticipated diuretic adjustment [CORRECT]
D. The findings indicate isolated hypoalbuminemia from malnutrition rather than cardiac
decompensation
Correct Answer: C
Rationale: Rapid weight gain, jugular venous distention, and peripheral edema reflect systemic venous
congestion, while bibasilar crackles and dyspnea at rest indicate pulmonary congestion; together they signal
acute decompensated heart failure. Recognizing this combined biventricular pattern and escalating care
reflects NCLEX-level clinical judgment. Attributing the findings to diuretic success, isolated right-sided
congestion, or malnutrition misses the decompensation.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 3
ESSENTIALS OF
PATHOPHYSIOLOGY
A comprehensive examination review featuring 100 verified
questions with detailed rationales across cardiovascular,
respiratory, renal, endocrine, gastrointestinal, neurological,
and multisystem pathophysiology — aligned with the NUR
2063 course syllabus and NCLEX-RN standards.
100 Questions · 7 Sections · Verified Answers
With Detailed Rationales
NUR2063 / NUR 2063 · Latest Update · Grade A
N U R 2 0 6 3 · E SSE N TIA LS O F PATH O PH Y SIO LO G Y · 2 0 2 0 2 7 E DITIO N
,NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
EXAM 2: NUR2063 / NUR 2063 (LATEST UPDATE)
ESSENTIALS OF PATHOPHYSIOLOGY
REVIEW GUIDE QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT | GRADE A -
RASMUSSEN
Comprehensive Examination - Aligned with the NUR 2063 Course Syllabus, NCLEX-RN Pathophysiology
Standards, and Essentials of Pathophysiology Competencies (2026/2027 Edition)
100 Questions | 7 Sections | 4 Options (A-D) | One Correct Answer | Verified Answers with Rationales
75% Scenario-Based Clinical Items | 25% Direct Knowledge | Cognitive Mix: 20% Recall, 50% Application, 30% Analysis
Section 1: Cardiovascular Pathophysiology Questions 1-20
Q1. Which sequence of events best describes the initial pathogenesis of an atherosclerotic plaque
according to the injury-response model emphasized in NUR 2063?
A. Smooth muscle calcification of the tunica media occurs first, followed later by LDL oxidation and
macrophage recruitment
B. Endothelial injury allows LDL entry into the intima; LDL is oxidized, engulfed by macrophages to
form foam cells, and a fatty streak develops [CORRECT]
C. A mural thrombus forms on intact endothelium and organizes into a lipid-rich plaque within the vessel
media
D. Neutrophils invade the adventitia and release proteolytic enzymes that dissolve the internal elastic
lamina
Correct Answer: B
Rationale: Atherosclerosis begins with endothelial injury or dysfunction from risk factors such as
hypertension, smoking, and hyperlipidemia. Increased permeability allows LDL into the intima, where
oxidation attracts macrophages that become foam cells, forming the fatty streak. Calcification and thrombus
formation are late events, and the neutrophil-driven adventitial process in option D is not part of early plaque
biology.
Q2. A 45-year-old client with a BMI of 31 and a strong family history has had blood pressures of 146 to
152 over 90 to 96 mm Hg at three separate visits. No secondary cause is identified on evaluation. Which
finding most strongly supports a diagnosis of primary (essential) hypertension?
A. Abrupt onset of severe hypertension accompanied by an audible abdominal bruit
B. Hypokalemia with metabolic alkalosis on the basic metabolic panel
C. Gradual onset linked to heredity, obesity, high sodium intake, and aging-related vascular changes
[CORRECT]
D. Elevated midnight salivary cortisol with central obesity and purple striae
Correct Answer: C
Rationale: Primary hypertension develops gradually from interacting genetic, lifestyle, and environmental
factors such as obesity and sodium sensitivity. Abrupt severe onset with an abdominal bruit suggests
renovascular disease, hypokalemia with alkalosis suggests primary hyperaldosteronism, and cortisol excess
with striae suggests Cushing syndrome. All three are secondary causes that the evaluation has excluded in this
client.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 1
,NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
Q3. A client with hypertension is found to have elevated plasma renin activity. Which mechanism
explains how activation of the renin-angiotensin-aldosterone system (RAAS) raises arterial pressure?
A. Renin directly constricts peripheral arterioles and increases heart rate through cardiac beta-1
receptors
B. Angiotensin I stimulates the adrenal medulla to release aldosterone, promoting sodium and water
retention
C. Aldosterone converts circulating angiotensinogen to angiotensin I within the hepatic circulation
D. Angiotensin II produces intense vasoconstriction, stimulates aldosterone secretion from the adrenal
cortex, promotes sodium and water retention, and triggers ADH release and thirst [CORRECT]
Correct Answer: D
Rationale: Renin enzymatically cleaves angiotensinogen to angiotensin I, which is converted by ACE,
primarily in the pulmonary endothelium, to angiotensin II. Angiotensin II raises blood pressure through potent
vasoconstriction, aldosterone-mediated sodium and water retention, and stimulation of ADH and thirst. Renin
has no direct vascular effect, aldosterone is secreted by the adrenal cortex rather than the medulla, and the
liver, not aldosterone, supplies angiotensinogen.
Q4. A 72-year-old client with chronic heart failure reports awakening from sleep two hours after going to
bed with sudden severe dyspnea and a desire to sit upright or stand by an open window. Which
pathophysiologic mechanism best explains this paroxysmal nocturnal dyspnea?
A. Reabsorption of interstitial fluid from dependent extremities into the circulation when lying flat
increases venous return and pulmonary capillary pressure, producing transient pulmonary edema during
sleep [CORRECT]
B. Right ventricular afterload rises during sleep because of position-dependent compression of the
pulmonary artery
C. Nocturnal glycosuria creates an osmotic diuresis that concentrates the blood and thickens pulmonary
secretions
D. Sleep-related lymphatic obstruction prevents drainage of the lower lung lobes
Correct Answer: A
Rationale: In left-sided heart failure, lying supine redistributes edema fluid from the legs into the central
circulation, raising preload and pulmonary capillary hydrostatic pressure; the resulting interstitial pulmonary
edema awakens the client with dyspnea that improves on sitting or standing. Right ventricular afterload
changes, glycosuria, and lymphatic obstruction are not involved in this classic orthopnea-to-PND sequence.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 2
, NUR 2063 Essentials of Pathophysiology | Exam 2 Review Guide | 100 Questions
Q5. Which description accurately distinguishes heart failure with preserved ejection fraction (HFpEF)
from heart failure with reduced ejection fraction (HFrEF)?
A. HFpEF is caused by acute pulmonary embolus, whereas HFrEF is caused by chronic anemia
B. In HFpEF the ventricle is stiff and noncompliant with impaired diastolic filling and an ejection
fraction of 50 percent or higher, while in HFrEF the ventricle dilates and contracts poorly with an
ejection fraction below 40 percent [CORRECT]
C. HFpEF produces a dilated, hypokinetic ventricle, whereas HFrEF produces a thickened, small-cavity
ventricle
D. Both conditions share an ejection fraction below 35 percent and differ only in the presence of jugular
venous distention
Correct Answer: B
Rationale: HFpEF, or diastolic dysfunction, is characterized by a preserved ejection fraction with filling
impairment from a stiff, often hypertrophied ventricle, common in hypertension and diabetes. HFrEF, or
systolic dysfunction, involves weakened contractility with ventricular dilation and an ejection fraction below
40 percent. The two disorders differ in ejection fraction and ventricular geometry, not merely in venous
findings.
Q6. A 68-year-old client with chronic heart failure presents with a 2.7 kg (6 lb) weight gain over three
days, bilateral ankle edema, jugular venous distention of 10 cm, bibasilar crackles, and new dyspnea at
rest. Which interpretation best integrates these findings for the plan of care?
A. The findings represent isolated right-sided congestion; the lungs remain unaffected and no provider
notification is needed
B. The findings are expected effects of diuretic therapy and indicate the current medication regimen is
working
C. Systemic and pulmonary venous congestion from fluid retention indicate acute decompensated heart
failure, warranting prompt provider notification, strict intake and output monitoring, daily weights, and
anticipated diuretic adjustment [CORRECT]
D. The findings indicate isolated hypoalbuminemia from malnutrition rather than cardiac
decompensation
Correct Answer: C
Rationale: Rapid weight gain, jugular venous distention, and peripheral edema reflect systemic venous
congestion, while bibasilar crackles and dyspnea at rest indicate pulmonary congestion; together they signal
acute decompensated heart failure. Recognizing this combined biventricular pattern and escalating care
reflects NCLEX-level clinical judgment. Attributing the findings to diuretic success, isolated right-sided
congestion, or malnutrition misses the decompensation.
Rasmussen University | NUR 2063 | Verified Answers with Rationales 3
