NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Rasmussen University
NUR 2063 / NUR2063: Essentials of
Pathophysiology
Exam 2 — Comprehensive Examination
Latest Edition
Format: Multiple Choice Cognitive Levels: Recall /
Course: NUR 2063 Questions: 100
(A–D) Application / Analysis
Examination Instructions. This comprehensive examination consists of 100
multiple-choice questions distributed across nine (9) content sections aligned with the
Rasmussen University NUR 2063 Essentials of Pathophysiology syllabus, NCLEX-RN
Pathophysiology Standards, and the Essentials of Pathophysiology Competencies
(2026/2027 Edition). Approximately 75% of items are scenario-based (patient
presentations, clinical situations, case studies) and 25% assess direct knowledge.
Cognitive level distribution: ~20% recall, ~50% application, ~30% analysis. Each item
has four options (A–D), with exactly one correct answer. Each item is followed by a 2–4
sentence rationale that explains why the correct option is right and why the distractors
are wrong, grounded in NUR 2063 curriculum, NCLEX-RN standards, and core
pathophysiology principles.
Section Topic Questions
1 Cellular Injury, Adaptation, & Death Q1 – Q12
2 Inflammation & Wound Healing Q13 – Q24
3 Immunity & Immunopathology Q25 – Q36
4 Infection & Infectious Disease Q37 – Q46
5 Fluid, Electrolyte, & Acid-Base Imbalances Q47 – Q58
6 Cardiovascular Pathophysiology Q59 – Q70
7 Respiratory Pathophysiology Q71 – Q82
8 Renal & Genitourinary Pathophysiology Q83 – Q91
9 Endocrine & Metabolic Pathophysiology Q92 – Q100
TOTAL 100 Questions
Section 1: Cellular Injury, Adaptation, & Death
Rasmussen University • NUR 2063 Comprehensive Examination Page 1
,NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q1. A 65-year-old male with longstanding hypertension has an
echocardiogram showing increased left ventricular wall thickness without an
increase in chamber size. Which cellular adaptation best explains this
finding?
A. Atrophy of myocardial fibers
B. Hyperplasia of cardiomyocytes
C. Hypertrophy of cardiac muscle cells [CORRECT]
D. Metaplasia of endocardial epithelium
Correct Answer: C
Rationale: Hypertrophy is an increase in cell size and is the classic adaptation of cardiac
myocytes to chronic pressure overload from hypertension. Cardiac muscle cells are
terminally differentiated and cannot undergo hyperplasia. Atrophy is a decrease in cell
size, and metaplasia is replacement of one adult cell type by another. The NUR 2063
curriculum emphasizes that increased workload on cardiac muscle produces concentric
hypertrophy.
Q2. A 54-year-old male with chronic GERD undergoes endoscopy. Biopsy of
the distal esophagus shows columnar epithelium replacing the normal
squamous epithelium. Which cellular adaptation is described?
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Barrett esophagus represents metaplasia, the reversible replacement of
normal squamous epithelium by intestinal-type columnar epithelium as an adaptive
response to chronic acid exposure. Dysplasia is disordered cell growth within a
population; hyperplasia is increased cell number; anaplasia is loss of differentiation seen
in malignancy. This metaplastic change predisposes the patient to adenocarcinoma.
Rasmussen University • NUR 2063 Comprehensive Examination Page 2
,NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q3. A 42-year-old female has an abnormal Pap smear. Cervical biopsy shows
disordered epithelial cells with increased nuclear-to-cytoplasmic ratio,
hyperchromatic nuclei, and loss of polarity, but the basement membrane is
intact. Which cellular alteration is present?
A. Atrophy
B. Metaplasia
C. Dysplasia [CORRECT]
D. Hypertrophy
Correct Answer: C
Rationale: Dysplasia is characterized by abnormal, disordered cell growth with
pleomorphism, hyperchromatic nuclei, increased mitotic figures, and loss of normal
polarity, often representing a preneoplastic change. In cervical dysplasia (CIN),
HPV-driven changes produce atypical squamous cells. Metaplasia is a reversible cell-type
substitution; atrophy and hypertrophy are size changes, not abnormalities of
differentiation.
Q4. A cell subjected to hypoxia initially develops reversible injury. Which
finding indicates the cell has crossed into irreversible injury?
A. Cellular swelling
B. Decreased ATP concentration
C. Detachment of ribosomes from rough ER
D. Severe membrane damage with mitochondrial permeability transition
[CORRECT]
Correct Answer: D
Rationale: Irreversible injury is defined by severe damage to the plasma membrane and
mitochondria, including the mitochondrial permeability transition pore (MPTP) opening,
which dissipates the proton-motive force and releases cytochrome c. Cellular swelling,
ATP depletion, and ribosomal detachment are reversible features of early hypoxic injury.
Once the membrane is structurally disrupted, cell death cannot be reversed.
Q5. A 58-year-old male presents with acute chest pain. Cardiac enzymes
confirm an ST-elevation myocardial infarction. What is the primary
mechanism of cardiomyocyte death in the central infarct zone?
A. Hypoxic and ischemic injury [CORRECT]
B. Direct chemical toxicity
C. Cell-mediated immunologic injury
D. Inherited genetic defect
Correct Answer: A
Rationale: Coronary artery occlusion produces hypoxia and ischemia in the downstream
myocardium, leading to ATP depletion, failure of Na⁺/K⁺-ATPase, intracellular swelling,
calcium influx, and mitochondrial injury—the central mechanism of cellular injury.
Chemical, immunologic, and genetic etiologies are not the primary drivers of acute MI.
The NUR 2063 curriculum identifies ischemia/hypoxia as the most common cause of
cellular injury.
Rasmussen University • NUR 2063 Comprehensive Examination Page 3
, NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q6. A patient receives thrombolytic therapy for an acute MI. Although
perfusion is restored, cardiac enzymes continue to rise, and chest pain
worsens. Which mechanism best explains this paradoxical worsening?
A. Apoptosis
B. Reperfusion injury [CORRECT]
C. Coagulative necrosis
D. Caseous necrosis
Correct Answer: B
Rationale: Reperfusion injury occurs when blood flow is restored to ischemic tissue,
generating reactive oxygen species, calcium overload, neutrophil infiltration, and
complement activation that paradoxically worsen injury. Oxidative stress damages
membranes, mitochondria, and DNA beyond the original ischemic insult. Apoptosis is
programmed cell death; necrosis patterns describe morphology of cell death, not the
worsening from revascularization.
Q7. An elderly patient dies of a massive MI. Autopsy reveals the myocardium
in the infarct territory is firm, pale, and wedge-shaped with preservation of
cell outlines. Which pattern of necrosis is described?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis [CORRECT]
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis is characteristic of ischemic injury in most solid organs
except the brain. Protein denaturation preserves cell outlines, giving tissue a firm, pale
appearance; the classic example is myocardial infarction. Liquefactive necrosis occurs in
brain ischemia and abscesses; caseous necrosis is associated with tuberculosis; fat
necrosis occurs with pancreatic injury.
Q8. An 80-year-old female suffers an ischemic stroke. CT scan shows an area
of brain tissue undergoing softening and enzymatic degradation. Which
pattern of necrosis is occurring?
A. Coagulative necrosis
B. Liquefactive necrosis [CORRECT]
C. Caseous necrosis
D. Fibrinoid necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is typical of ischemic injury in the brain, where the lack
of stromal support permits enzymatic digestion by microglia and neutrophils, producing a
cystic, softened lesion. Bacterial abscesses also exhibit this pattern. Coagulative necrosis
is the rule in other solid organs; caseous necrosis occurs in TB; fibrinoid necrosis is seen
in immune-mediated vascular injury.
Rasmussen University • NUR 2063 Comprehensive Examination Page 4
Rasmussen University
NUR 2063 / NUR2063: Essentials of
Pathophysiology
Exam 2 — Comprehensive Examination
Latest Edition
Format: Multiple Choice Cognitive Levels: Recall /
Course: NUR 2063 Questions: 100
(A–D) Application / Analysis
Examination Instructions. This comprehensive examination consists of 100
multiple-choice questions distributed across nine (9) content sections aligned with the
Rasmussen University NUR 2063 Essentials of Pathophysiology syllabus, NCLEX-RN
Pathophysiology Standards, and the Essentials of Pathophysiology Competencies
(2026/2027 Edition). Approximately 75% of items are scenario-based (patient
presentations, clinical situations, case studies) and 25% assess direct knowledge.
Cognitive level distribution: ~20% recall, ~50% application, ~30% analysis. Each item
has four options (A–D), with exactly one correct answer. Each item is followed by a 2–4
sentence rationale that explains why the correct option is right and why the distractors
are wrong, grounded in NUR 2063 curriculum, NCLEX-RN standards, and core
pathophysiology principles.
Section Topic Questions
1 Cellular Injury, Adaptation, & Death Q1 – Q12
2 Inflammation & Wound Healing Q13 – Q24
3 Immunity & Immunopathology Q25 – Q36
4 Infection & Infectious Disease Q37 – Q46
5 Fluid, Electrolyte, & Acid-Base Imbalances Q47 – Q58
6 Cardiovascular Pathophysiology Q59 – Q70
7 Respiratory Pathophysiology Q71 – Q82
8 Renal & Genitourinary Pathophysiology Q83 – Q91
9 Endocrine & Metabolic Pathophysiology Q92 – Q100
TOTAL 100 Questions
Section 1: Cellular Injury, Adaptation, & Death
Rasmussen University • NUR 2063 Comprehensive Examination Page 1
,NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q1. A 65-year-old male with longstanding hypertension has an
echocardiogram showing increased left ventricular wall thickness without an
increase in chamber size. Which cellular adaptation best explains this
finding?
A. Atrophy of myocardial fibers
B. Hyperplasia of cardiomyocytes
C. Hypertrophy of cardiac muscle cells [CORRECT]
D. Metaplasia of endocardial epithelium
Correct Answer: C
Rationale: Hypertrophy is an increase in cell size and is the classic adaptation of cardiac
myocytes to chronic pressure overload from hypertension. Cardiac muscle cells are
terminally differentiated and cannot undergo hyperplasia. Atrophy is a decrease in cell
size, and metaplasia is replacement of one adult cell type by another. The NUR 2063
curriculum emphasizes that increased workload on cardiac muscle produces concentric
hypertrophy.
Q2. A 54-year-old male with chronic GERD undergoes endoscopy. Biopsy of
the distal esophagus shows columnar epithelium replacing the normal
squamous epithelium. Which cellular adaptation is described?
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Barrett esophagus represents metaplasia, the reversible replacement of
normal squamous epithelium by intestinal-type columnar epithelium as an adaptive
response to chronic acid exposure. Dysplasia is disordered cell growth within a
population; hyperplasia is increased cell number; anaplasia is loss of differentiation seen
in malignancy. This metaplastic change predisposes the patient to adenocarcinoma.
Rasmussen University • NUR 2063 Comprehensive Examination Page 2
,NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q3. A 42-year-old female has an abnormal Pap smear. Cervical biopsy shows
disordered epithelial cells with increased nuclear-to-cytoplasmic ratio,
hyperchromatic nuclei, and loss of polarity, but the basement membrane is
intact. Which cellular alteration is present?
A. Atrophy
B. Metaplasia
C. Dysplasia [CORRECT]
D. Hypertrophy
Correct Answer: C
Rationale: Dysplasia is characterized by abnormal, disordered cell growth with
pleomorphism, hyperchromatic nuclei, increased mitotic figures, and loss of normal
polarity, often representing a preneoplastic change. In cervical dysplasia (CIN),
HPV-driven changes produce atypical squamous cells. Metaplasia is a reversible cell-type
substitution; atrophy and hypertrophy are size changes, not abnormalities of
differentiation.
Q4. A cell subjected to hypoxia initially develops reversible injury. Which
finding indicates the cell has crossed into irreversible injury?
A. Cellular swelling
B. Decreased ATP concentration
C. Detachment of ribosomes from rough ER
D. Severe membrane damage with mitochondrial permeability transition
[CORRECT]
Correct Answer: D
Rationale: Irreversible injury is defined by severe damage to the plasma membrane and
mitochondria, including the mitochondrial permeability transition pore (MPTP) opening,
which dissipates the proton-motive force and releases cytochrome c. Cellular swelling,
ATP depletion, and ribosomal detachment are reversible features of early hypoxic injury.
Once the membrane is structurally disrupted, cell death cannot be reversed.
Q5. A 58-year-old male presents with acute chest pain. Cardiac enzymes
confirm an ST-elevation myocardial infarction. What is the primary
mechanism of cardiomyocyte death in the central infarct zone?
A. Hypoxic and ischemic injury [CORRECT]
B. Direct chemical toxicity
C. Cell-mediated immunologic injury
D. Inherited genetic defect
Correct Answer: A
Rationale: Coronary artery occlusion produces hypoxia and ischemia in the downstream
myocardium, leading to ATP depletion, failure of Na⁺/K⁺-ATPase, intracellular swelling,
calcium influx, and mitochondrial injury—the central mechanism of cellular injury.
Chemical, immunologic, and genetic etiologies are not the primary drivers of acute MI.
The NUR 2063 curriculum identifies ischemia/hypoxia as the most common cause of
cellular injury.
Rasmussen University • NUR 2063 Comprehensive Examination Page 3
, NUR 2063 – Essentials of Pathophysiology Exam 2 • 2026/2027 Edition
Q6. A patient receives thrombolytic therapy for an acute MI. Although
perfusion is restored, cardiac enzymes continue to rise, and chest pain
worsens. Which mechanism best explains this paradoxical worsening?
A. Apoptosis
B. Reperfusion injury [CORRECT]
C. Coagulative necrosis
D. Caseous necrosis
Correct Answer: B
Rationale: Reperfusion injury occurs when blood flow is restored to ischemic tissue,
generating reactive oxygen species, calcium overload, neutrophil infiltration, and
complement activation that paradoxically worsen injury. Oxidative stress damages
membranes, mitochondria, and DNA beyond the original ischemic insult. Apoptosis is
programmed cell death; necrosis patterns describe morphology of cell death, not the
worsening from revascularization.
Q7. An elderly patient dies of a massive MI. Autopsy reveals the myocardium
in the infarct territory is firm, pale, and wedge-shaped with preservation of
cell outlines. Which pattern of necrosis is described?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis [CORRECT]
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis is characteristic of ischemic injury in most solid organs
except the brain. Protein denaturation preserves cell outlines, giving tissue a firm, pale
appearance; the classic example is myocardial infarction. Liquefactive necrosis occurs in
brain ischemia and abscesses; caseous necrosis is associated with tuberculosis; fat
necrosis occurs with pancreatic injury.
Q8. An 80-year-old female suffers an ischemic stroke. CT scan shows an area
of brain tissue undergoing softening and enzymatic degradation. Which
pattern of necrosis is occurring?
A. Coagulative necrosis
B. Liquefactive necrosis [CORRECT]
C. Caseous necrosis
D. Fibrinoid necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is typical of ischemic injury in the brain, where the lack
of stromal support permits enzymatic digestion by microglia and neutrophils, producing a
cystic, softened lesion. Bacterial abscesses also exhibit this pattern. Coagulative necrosis
is the rule in other solid organs; caseous necrosis occurs in TB; fibrinoid necrosis is seen
in immune-mediated vascular injury.
Rasmussen University • NUR 2063 Comprehensive Examination Page 4
