NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
NSG 530 Exam 2 - Advanced Pathophysiology
Complete Guide with Verified Answers | 100% Correct
Latest 2026/2027
Wilkes University - Graduate Nursing Program
Total Questions 125 Multiple Choice (100% Verified)
Format Single Best Answer with Comprehensive Pathophysiologic Rationales
Cognitive Mix 30% Recall | 50% Application | 20% Analysis
Question Style 70% Scenario-Based | 30% Direct Mechanism Recall
Sections 9 Pathophysiologic Content Domains
Reference Standard Current Pathophysiology Research & Clinical Correlations (2026/2027)
Audience Wilkes University Graduate Nursing Students (NSG 530)
Use Exam 2 Preparation | Complete Verified Solutions Guide
Exam Instructions: This comprehensive 125-question exam is designed for Wilkes University NSG 530 Advanced
Pathophysiology Exam 2 preparation, aligned with the latest 2026/2027 graduate nursing curriculum standards. The exam
is organized into 9 sections covering cellular injury and death, inflammation and immunity, immunodeficiency and
autoimmune disorders, infection pathogenesis, fluid and electrolyte balance, acid-base pathophysiology, cardiac and
vascular function, respiratory function, and genetic/neoplastic pathophysiology. Each question emphasizes
mechanism-focused reasoning rather than symptom recall, using 'Which pathophysiologic mechanism BEST explains...'
format and lab value correlation. The correct response is highlighted in green and labeled [CORRECT]; a rationale box
follows with advanced pathophysiologic reasoning including specific mechanisms, cellular processes, compensatory
responses, and clinical correlation. All answers are 100% verified against current pathophysiologic research and clinical
practice standards.
Section 1: Cellular Injury, Adaptation, and Death
Hypoxia, Ischemia, Oxidative Stress, Necrosis, & Apoptosis (Q1 - Q15)
Q1: A 65-year-old with chronic hypertension has enlarged cardiac myocytes with increased cell size but no
increase in cell number. This cellular adaptation is best described as:
A. Hyperplasia, an increase in cell number
B. Hypertrophy, an increase in cell size without an increase in cell number [CORRECT]
Page 1 | 125 Questions | Complete Advanced Pathophysiology Guide
,NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
C. Metaplasia, replacement of one cell type with another
D. Dysplasia, disordered cellular growth
Correct Answer: B — Hypertrophy, an increase in cell size without an increase in cell n...
Rationale: Hypertrophy is an increase in cell size (not number) in response to increased workload or hormonal stimulation;
cardiac myocytes, which cannot divide, respond to chronic pressure overload via hypertrophy. (A) hyperplasia is increased cell
number. (C) metaplasia is reversible replacement of one cell type with another. (D) dysplasia is disordered growth. The
mechanism is increased protein synthesis and cellular organelles.
Q2: A 55-year-old chronic smoker has bronchial epithelium replaced by stratified squamous epithelium.
Which cellular adaptation is this?
A. Hypertrophy
B. Metaplasia, reversible replacement of one adult cell type with another [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B — Metaplasia, reversible replacement of one adult cell type with another
Rationale: Metaplasia is the reversible replacement of one adult cell type (columnar) with another (squamous) better suited to
withstand chronic irritation (smoking). (A) is increased cell size. (C) is increased cell number. (D) anaplasia is loss of cell
differentiation in malignancy. Squamous metaplasia is adaptive but may lose protective mucus production and predispose to
malignancy.
Q3: A 50-year-old with uterine fibroids has increased smooth muscle cells in the uterus due to hormonal
stimulation. This adaptation is:
A. Hypertrophy
B. Hyperplasia, an increase in cell number in response to hormonal stimulation [CORRECT]
C. Metaplasia
D. Atrophy
Correct Answer: B — Hyperplasia, an increase in cell number in response to hormonal sti...
Rationale: Hyperplasia is an increase in cell number in response to hormonal or growth factor stimulation, as in uterine fibroids
(leiomyomas) from estrogen stimulation. (A) is increased cell size. (C) is cell type replacement. (D) is decreased cell size.
Pathologic hyperplasia can be a substrate for neoplasia (endometrial hyperplasia → endometrial cancer).
Q4: A 70-year-old with prolonged immobilization has decreased muscle mass and cell size in the lower
extremities. This cellular adaptation is:
A. Atrophy, decreased cell size due to decreased workload or disuse [CORRECT]
B. Apoptosis
C. Hyperplasia
D. Metaplasia
Correct Answer: A — Atrophy, decreased cell size due to decreased workload or disuse
Page 2 | 125 Questions | Complete Advanced Pathophysiology Guide
,NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
Rationale: Atrophy is decreased cell size and substance due to decreased workload, denervation, ischemia, or inadequate
nutrition, as in disuse atrophy from immobilization. (B) apoptosis is programmed cell death. (C) is increased cell number. (D) is
cell type replacement. Mechanism: decreased protein synthesis, increased protein degradation (ubiquitin-proteasome).
Q5: A 60-year-old with myocardial infarction has cardiac cell death with release of cellular contents, intense
inflammation, and rupture of plasma membranes. This cell death mechanism is:
A. Apoptosis, programmed cell death
B. Necrosis, with enzymatic digestion, protein denaturation, and inflammation [CORRECT]
C. Autophagy
D. Ischemic preconditioning
Correct Answer: B — Necrosis, with enzymatic digestion, protein denaturation, and infla...
Rationale: Necrosis is characterized by cell swelling, membrane rupture, release of contents, and intense inflammation, as seen
in myocardial infarction. (A) apoptosis is programmed cell death with cell shrinkage, no inflammation. (C) autophagy is
self-digestion. (D) ischemic preconditioning is protective. The release of cardiac enzymes (troponin) is a clinical marker of
necrosis.
Q6: A 45-year-old has cell death with chromatin condensation, cell shrinkage, apoptotic bodies, and no
inflammation. This mechanism is:
A. Necrosis
B. Apoptosis, energy-dependent programmed cell death without inflammation [CORRECT]
C. Ischemia
D. Hydropic degeneration
Correct Answer: B — Apoptosis, energy-dependent programmed cell death without inflammation
Rationale: Apoptosis is energy-dependent programmed cell death with chromatin condensation, cell shrinkage, apoptotic bodies,
and phagocytosis without inflammation. (A) necrosis has cell swelling and inflammation. (C) ischemia causes ATP depletion. (D)
hydropic degeneration is cellular swelling. Apoptosis is mediated by caspases and Bcl-2 family proteins.
Q7: Which pathophysiologic mechanism BEST explains cellular injury during hypoxia?
A. Increased ATP production and aerobic metabolism
B. ATP depletion, failure of Na/K ATPase, cellular swelling, and anaerobic metabolism with lactic
acidosis [CORRECT]
C. Increased protein synthesis and organelle proliferation
D. Activation of antioxidant defenses with decreased reactive oxygen species
Correct Answer: B — ATP depletion, failure of Na/K ATPase, cellular swelling, and anaer...
Rationale: Hypoxia causes ATP depletion, failure of Na/K ATPase (sodium and water enter cell, causing swelling), and
anaerobic metabolism with lactic acidosis. (A) is wrong; ATP production falls. (C) is incorrect; protein synthesis decreases. (D) is
wrong; ROS increases. Reversible injury becomes irreversible when membrane damage and mitochondrial failure persist.
Q8: Reperfusion injury after thrombolytic therapy for MI is BEST explained by:
Page 3 | 125 Questions | Complete Advanced Pathophysiology Guide
, NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
A. Restoration of oxygen causing further damage through reactive oxygen species, calcium overload, and
inflammation [CORRECT]
B. Prevention of further cell death by restoring ATP
C. Decreased calcium influx into cells
D. Decreased neutrophil activation
Correct Answer: A — Restoration of oxygen causing further damage through reactive oxyge...
Rationale: Reperfusion injury is damage that occurs when blood supply returns after ischemia, caused by reactive oxygen
species, calcium overload, complement activation, neutrophil infiltration, and mitochondrial permeability transition. (B) is true
but doesn't explain the injury. (C) and (D) are the opposite of what occurs. Reperfusion paradoxically worsens injury despite
restoring oxygen.
Q9: A 50-year-old with acute tubular necrosis has renal tubular cells with cloudy swelling and vacuolation.
This early reversible cellular injury is:
A. Fatty change
B. Hydropic degeneration (vacuolar degeneration), reversible cellular swelling from water influx
[CORRECT]
C. Necrosis
D. Apoptosis
Correct Answer: B — Hydropic degeneration (vacuolar degeneration), reversible cellular ...
Rationale: Hydropic (vacuolar) degeneration is reversible cellular swelling due to water influx from Na/K pump failure, seen in
acute tubular necrosis, hepatitis, and ischemia. (A) fatty change is lipid accumulation. (C) necrosis is irreversible. (D) apoptosis is
programmed. The Na/K ATPase failure from ATP depletion causes Na accumulation and water influx.
Q10: Free radical injury causes cellular damage primarily through:
A. Activation of protein synthesis
B. Lipid peroxidation of membranes, protein modification, and DNA damage [CORRECT]
C. Increased ATP production
D. Decreased calcium influx
Correct Answer: B — Lipid peroxidation of membranes, protein modification, and DNA damage
Rationale: Free radicals (superoxide, hydroxyl, hydrogen peroxide) cause cellular injury through lipid peroxidation of
membranes, protein modification (fragmentation, cross-linking), and DNA damage. (A), (C), and (D) are wrong. Antioxidant
defenses (SOD, catalase, glutathione, vitamins E and C) limit damage. Free radical injury occurs in ischemia-reperfusion,
inflammation, chemical injury, and aging.
Q11: A 40-year-old has hepatic steatosis with accumulation of triglycerides in hepatocytes. The most likely
cause is:
A. Increased protein synthesis
B. Increased triglyceride synthesis or decreased apoprotein synthesis impairing lipid export [CORRECT]
C. Increased glycogen storage
D. Decreased lipogenesis
Page 4 | 125 Questions | Complete Advanced Pathophysiology Guide
NSG 530 Exam 2 - Advanced Pathophysiology
Complete Guide with Verified Answers | 100% Correct
Latest 2026/2027
Wilkes University - Graduate Nursing Program
Total Questions 125 Multiple Choice (100% Verified)
Format Single Best Answer with Comprehensive Pathophysiologic Rationales
Cognitive Mix 30% Recall | 50% Application | 20% Analysis
Question Style 70% Scenario-Based | 30% Direct Mechanism Recall
Sections 9 Pathophysiologic Content Domains
Reference Standard Current Pathophysiology Research & Clinical Correlations (2026/2027)
Audience Wilkes University Graduate Nursing Students (NSG 530)
Use Exam 2 Preparation | Complete Verified Solutions Guide
Exam Instructions: This comprehensive 125-question exam is designed for Wilkes University NSG 530 Advanced
Pathophysiology Exam 2 preparation, aligned with the latest 2026/2027 graduate nursing curriculum standards. The exam
is organized into 9 sections covering cellular injury and death, inflammation and immunity, immunodeficiency and
autoimmune disorders, infection pathogenesis, fluid and electrolyte balance, acid-base pathophysiology, cardiac and
vascular function, respiratory function, and genetic/neoplastic pathophysiology. Each question emphasizes
mechanism-focused reasoning rather than symptom recall, using 'Which pathophysiologic mechanism BEST explains...'
format and lab value correlation. The correct response is highlighted in green and labeled [CORRECT]; a rationale box
follows with advanced pathophysiologic reasoning including specific mechanisms, cellular processes, compensatory
responses, and clinical correlation. All answers are 100% verified against current pathophysiologic research and clinical
practice standards.
Section 1: Cellular Injury, Adaptation, and Death
Hypoxia, Ischemia, Oxidative Stress, Necrosis, & Apoptosis (Q1 - Q15)
Q1: A 65-year-old with chronic hypertension has enlarged cardiac myocytes with increased cell size but no
increase in cell number. This cellular adaptation is best described as:
A. Hyperplasia, an increase in cell number
B. Hypertrophy, an increase in cell size without an increase in cell number [CORRECT]
Page 1 | 125 Questions | Complete Advanced Pathophysiology Guide
,NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
C. Metaplasia, replacement of one cell type with another
D. Dysplasia, disordered cellular growth
Correct Answer: B — Hypertrophy, an increase in cell size without an increase in cell n...
Rationale: Hypertrophy is an increase in cell size (not number) in response to increased workload or hormonal stimulation;
cardiac myocytes, which cannot divide, respond to chronic pressure overload via hypertrophy. (A) hyperplasia is increased cell
number. (C) metaplasia is reversible replacement of one cell type with another. (D) dysplasia is disordered growth. The
mechanism is increased protein synthesis and cellular organelles.
Q2: A 55-year-old chronic smoker has bronchial epithelium replaced by stratified squamous epithelium.
Which cellular adaptation is this?
A. Hypertrophy
B. Metaplasia, reversible replacement of one adult cell type with another [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B — Metaplasia, reversible replacement of one adult cell type with another
Rationale: Metaplasia is the reversible replacement of one adult cell type (columnar) with another (squamous) better suited to
withstand chronic irritation (smoking). (A) is increased cell size. (C) is increased cell number. (D) anaplasia is loss of cell
differentiation in malignancy. Squamous metaplasia is adaptive but may lose protective mucus production and predispose to
malignancy.
Q3: A 50-year-old with uterine fibroids has increased smooth muscle cells in the uterus due to hormonal
stimulation. This adaptation is:
A. Hypertrophy
B. Hyperplasia, an increase in cell number in response to hormonal stimulation [CORRECT]
C. Metaplasia
D. Atrophy
Correct Answer: B — Hyperplasia, an increase in cell number in response to hormonal sti...
Rationale: Hyperplasia is an increase in cell number in response to hormonal or growth factor stimulation, as in uterine fibroids
(leiomyomas) from estrogen stimulation. (A) is increased cell size. (C) is cell type replacement. (D) is decreased cell size.
Pathologic hyperplasia can be a substrate for neoplasia (endometrial hyperplasia → endometrial cancer).
Q4: A 70-year-old with prolonged immobilization has decreased muscle mass and cell size in the lower
extremities. This cellular adaptation is:
A. Atrophy, decreased cell size due to decreased workload or disuse [CORRECT]
B. Apoptosis
C. Hyperplasia
D. Metaplasia
Correct Answer: A — Atrophy, decreased cell size due to decreased workload or disuse
Page 2 | 125 Questions | Complete Advanced Pathophysiology Guide
,NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
Rationale: Atrophy is decreased cell size and substance due to decreased workload, denervation, ischemia, or inadequate
nutrition, as in disuse atrophy from immobilization. (B) apoptosis is programmed cell death. (C) is increased cell number. (D) is
cell type replacement. Mechanism: decreased protein synthesis, increased protein degradation (ubiquitin-proteasome).
Q5: A 60-year-old with myocardial infarction has cardiac cell death with release of cellular contents, intense
inflammation, and rupture of plasma membranes. This cell death mechanism is:
A. Apoptosis, programmed cell death
B. Necrosis, with enzymatic digestion, protein denaturation, and inflammation [CORRECT]
C. Autophagy
D. Ischemic preconditioning
Correct Answer: B — Necrosis, with enzymatic digestion, protein denaturation, and infla...
Rationale: Necrosis is characterized by cell swelling, membrane rupture, release of contents, and intense inflammation, as seen
in myocardial infarction. (A) apoptosis is programmed cell death with cell shrinkage, no inflammation. (C) autophagy is
self-digestion. (D) ischemic preconditioning is protective. The release of cardiac enzymes (troponin) is a clinical marker of
necrosis.
Q6: A 45-year-old has cell death with chromatin condensation, cell shrinkage, apoptotic bodies, and no
inflammation. This mechanism is:
A. Necrosis
B. Apoptosis, energy-dependent programmed cell death without inflammation [CORRECT]
C. Ischemia
D. Hydropic degeneration
Correct Answer: B — Apoptosis, energy-dependent programmed cell death without inflammation
Rationale: Apoptosis is energy-dependent programmed cell death with chromatin condensation, cell shrinkage, apoptotic bodies,
and phagocytosis without inflammation. (A) necrosis has cell swelling and inflammation. (C) ischemia causes ATP depletion. (D)
hydropic degeneration is cellular swelling. Apoptosis is mediated by caspases and Bcl-2 family proteins.
Q7: Which pathophysiologic mechanism BEST explains cellular injury during hypoxia?
A. Increased ATP production and aerobic metabolism
B. ATP depletion, failure of Na/K ATPase, cellular swelling, and anaerobic metabolism with lactic
acidosis [CORRECT]
C. Increased protein synthesis and organelle proliferation
D. Activation of antioxidant defenses with decreased reactive oxygen species
Correct Answer: B — ATP depletion, failure of Na/K ATPase, cellular swelling, and anaer...
Rationale: Hypoxia causes ATP depletion, failure of Na/K ATPase (sodium and water enter cell, causing swelling), and
anaerobic metabolism with lactic acidosis. (A) is wrong; ATP production falls. (C) is incorrect; protein synthesis decreases. (D) is
wrong; ROS increases. Reversible injury becomes irreversible when membrane damage and mitochondrial failure persist.
Q8: Reperfusion injury after thrombolytic therapy for MI is BEST explained by:
Page 3 | 125 Questions | Complete Advanced Pathophysiology Guide
, NSG 530 Exam 2 - Advanced Pathophysiology - Wilkes University Verified Answers | 100% Correct - Latest 2026/2027
A. Restoration of oxygen causing further damage through reactive oxygen species, calcium overload, and
inflammation [CORRECT]
B. Prevention of further cell death by restoring ATP
C. Decreased calcium influx into cells
D. Decreased neutrophil activation
Correct Answer: A — Restoration of oxygen causing further damage through reactive oxyge...
Rationale: Reperfusion injury is damage that occurs when blood supply returns after ischemia, caused by reactive oxygen
species, calcium overload, complement activation, neutrophil infiltration, and mitochondrial permeability transition. (B) is true
but doesn't explain the injury. (C) and (D) are the opposite of what occurs. Reperfusion paradoxically worsens injury despite
restoring oxygen.
Q9: A 50-year-old with acute tubular necrosis has renal tubular cells with cloudy swelling and vacuolation.
This early reversible cellular injury is:
A. Fatty change
B. Hydropic degeneration (vacuolar degeneration), reversible cellular swelling from water influx
[CORRECT]
C. Necrosis
D. Apoptosis
Correct Answer: B — Hydropic degeneration (vacuolar degeneration), reversible cellular ...
Rationale: Hydropic (vacuolar) degeneration is reversible cellular swelling due to water influx from Na/K pump failure, seen in
acute tubular necrosis, hepatitis, and ischemia. (A) fatty change is lipid accumulation. (C) necrosis is irreversible. (D) apoptosis is
programmed. The Na/K ATPase failure from ATP depletion causes Na accumulation and water influx.
Q10: Free radical injury causes cellular damage primarily through:
A. Activation of protein synthesis
B. Lipid peroxidation of membranes, protein modification, and DNA damage [CORRECT]
C. Increased ATP production
D. Decreased calcium influx
Correct Answer: B — Lipid peroxidation of membranes, protein modification, and DNA damage
Rationale: Free radicals (superoxide, hydroxyl, hydrogen peroxide) cause cellular injury through lipid peroxidation of
membranes, protein modification (fragmentation, cross-linking), and DNA damage. (A), (C), and (D) are wrong. Antioxidant
defenses (SOD, catalase, glutathione, vitamins E and C) limit damage. Free radical injury occurs in ischemia-reperfusion,
inflammation, chemical injury, and aging.
Q11: A 40-year-old has hepatic steatosis with accumulation of triglycerides in hepatocytes. The most likely
cause is:
A. Increased protein synthesis
B. Increased triglyceride synthesis or decreased apoprotein synthesis impairing lipid export [CORRECT]
C. Increased glycogen storage
D. Decreased lipogenesis
Page 4 | 125 Questions | Complete Advanced Pathophysiology Guide
