NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
NSG5003 / NSG 5003: Advanced Pathophysiology Final Exam
Week 10 (Latest ) | South University
Aligned with NSG 5003 Course Syllabus, AACN Essentials of Master's Education, and Advanced
Pathophysiology Competencies (2026/2027 Edition)
Instructions: This comprehensive examination consists of 150 multiple-choice questions divided across
11 content sections. Each question has four options (A–D) with ONE best answer. The correct answer is
marked with *[CORRECT]*. Review the rationale provided for each item, which integrates NSG 5003
curriculum objectives, AACN Master's Essentials, and advanced pathophysiology principles. Cognitive
distribution: 20% recall, 50% application, 30% analysis. Question style: 75% scenario-based (patient
presentations, clinical situations, case studies) and 25% direct knowledge.
Section 1: Cellular & Molecular Pathophysiology
Q1: A 68-year-old male with a long history of hypertension presents with an echocardiogram
demonstrating increased left ventricular wall thickness without an increase in cell number. Which cellular
adaptation best describes this finding?
A. Hyperplasia
B. Hypertrophy *[CORRECT]*
C. Metaplasia
D. Dysplasia
Correct Answer: B
Rationale: Hypertrophy is an increase in cell size, classically seen in cardiac myocytes in response to
pressure overload such as chronic hypertension. Hyperplasia is an increase in cell number and does not occur
in terminally differentiated cardiac muscle. Metaplasia and dysplasia involve cell-type replacement and
disordered growth, respectively, neither of which matches this presentation. NSG 5003 emphasizes
adaptation as a reversible, compensatory response to stress.
Q2: A 55-year-old chronic smoker undergoes bronchoscopy with biopsy of the bronchial epithelium. The
pathology report describes replacement of the normal pseudostratified ciliated columnar epithelium with
stratified squamous epithelium. What is the most likely cellular adaptation, and what is its primary clinical
significance?
A. Hypertrophy; loss of ciliary function
B. Metaplasia; precursor that may progress to dysplasia and malignancy *[CORRECT]*
C. Hyperplasia; benign increase in cell number
D. Anaplasia; definitive evidence of invasive carcinoma
Correct Answer: B
Rationale: Squamous metaplasia is a reversible substitution of one differentiated cell type (ciliated columnar)
for another (stratified squamous) better suited to withstand chronic irritation from tobacco smoke. It is a known
precursor lesion that, with continued injury, can progress to dysplasia and squamous cell carcinoma. NSG
5003 stresses that metaplasia is adaptive but carries malignant potential.
Q3: Which of the following clinical scenarios is the BEST example of physiologic hyperplasia rather than
pathologic hyperplasia?
A. Endometrial hyperplasia secondary to unopposed estrogen therapy
Page 1 | NSG 5003 Final Exam | South University
,NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
B. Benign prostatic hyperplasia in a 72-year-old male
C. Glandular epithelial hyperplasia of the breast during pregnancy *[CORRECT]*
D. Thyroid hyperplasia in a patient with Graves disease
Correct Answer: C
Rationale: Glandular hyperplasia of the breast during pregnancy is hormone-driven physiologic hyperplasia
enabling lactation. Endometrial hyperplasia from unopposed estrogen, benign prostatic hyperplasia, and
thyroid hyperplasia in Graves disease are pathologic because they result from abnormal hormonal signaling or
autoimmunity. NSG 5003 distinguishes physiologic (compensatory/hormonal) from pathologic hyperplasia.
Q4: A 45-year-old female has had a cast on her right lower extremity for 8 weeks following tibial fracture.
Upon cast removal, the gastrocnemius muscle appears markedly reduced in size. What cellular process
explains this finding, and what is its underlying mechanism?
A. Atrophy; decreased protein synthesis and increased proteasomal degradation
*[CORRECT]*
B. Necrosis; irreversible cell membrane damage
C. Apoptosis; programmed cell death of myocytes
D. Metaplasia; transformation to fibroblasts
Correct Answer: A
Rationale: Disuse atrophy results from reduced mechanical load leading to decreased protein synthesis and
increased ubiquitin-proteasome-mediated protein degradation. Necrosis is irreversible cell death, not seen in
disuse. Apoptosis is programmed death of individual cells, not whole-organ shrinkage. NSG 5003 highlights
atrophy as a reversible adaptation to reduced workload, denervation, or inadequate nutrition.
Q5: A cervical biopsy in a 31-year-old female shows disordered cellular proliferation with pleomorphic,
hyperchromatic nuclei and loss of normal tissue architecture, but no invasion through the basement
membrane. Which term best describes this finding?
A. Metaplasia
B. Anaplasia
C. Dysplasia *[CORRECT]*
D. Hyperplasia
Correct Answer: C
Rationale: Dysplasia is disordered growth characterized by pleomorphism, hyperchromasia, increased
mitoses, and loss of polarity, but it remains confined by the basement membrane (pre-invasive). Metaplasia is
cell-type substitution without atypia, anaplasia implies lack of differentiation typical of frank malignancy, and
hyperplasia is an increase in cell number without atypia. NSG 5003 frames dysplasia as a precursor lesion
that may regress or progress to carcinoma in situ.
Q6: A 59-year-old male sustains an acute myocardial infarction and dies 18 hours later. Autopsy reveals
a firm, pale, wedge-shaped lesion in the left ventricle. Which type of necrosis is most consistent with this
finding?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis *[CORRECT]*
D. Fat necrosis
Correct Answer: C
Page 2 | NSG 5003 Final Exam | South University
,NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
Rationale: Coagulative necrosis is characteristic of ischemic injury in most solid organs except the brain;
tissue architecture is preserved but the cells are dead, producing the firm pale appearance. Liquefactive
necrosis is typical of CNS infarcts and bacterial abscesses. Caseous necrosis is associated with TB, and fat
necrosis occurs in pancreatic and breast tissue. NSG 5003 emphasizes the pattern of necrosis as a clue to
underlying etiology.
Q7: Which cellular process is the hallmark of apoptosis and distinguishes it from necrosis?
A. Cell swelling and membrane rupture with release of cellular contents
B. Energy-dependent, programmed cell death without significant inflammation *[CORRECT]*
C. Random DNA fragmentation by lysosomal enzymes
D. Massive calcium influx triggering necrosis
Correct Answer: B
Rationale: Apoptosis is an energy-dependent, gene-regulated process resulting in cell shrinkage, chromatin
condensation, and apoptotic bodies that are phagocytosed without eliciting an inflammatory response.
Necrosis is unregulated, characterized by cell swelling, membrane rupture, and inflammation. NSG 5003
emphasizes apoptosis in embryogenesis, hormone-regulated involution, and DNA-damage responses
mediated by p53.
Q8: A 50-year-old male with severe burns develops cloudy swelling of renal tubular cells on biopsy.
Which cellular change best describes this finding, and what is its reversibility?
A. Irreversible coagulative necrosis
B. Reversible hydropic degeneration due to Na/K pump failure *[CORRECT]*
C. Irreversible apoptosis
D. Reversible metaplasia
Correct Answer: B
Rationale: Cloudy swelling or hydropic degeneration is a reversible form of cell injury caused by impaired
Na/K ATPase, allowing sodium and water to enter the cell and produce vacuolation. If hypoxia persists, injury
progresses to irreversible necrosis. NSG 5003 frames cellular swelling as an early, reversible indicator of
membrane pump failure.
Q9: Reperfusion injury after thrombolytic therapy for acute MI is mediated in large part by the generation
of reactive oxygen species (ROS). Which intracellular enzyme system is a major enzymatic source of
these ROS during reperfusion?
A. Cyclooxygenase-2
B. Xanthine oxidase *[CORRECT]*
C. Lactate dehydrogenase
D. Hexokinase
Correct Answer: B
Rationale: During ischemia, ATP is degraded to hypoxanthine, and xanthine dehydrogenase is converted to
xanthine oxidase. On reperfusion, xanthine oxidase uses oxygen to generate superoxide anions, driving
reperfusion injury. COX-2 produces prostaglandins, LDH converts pyruvate to lactate, and hexokinase
phosphorylates glucose. NSG 5003 highlights ROS-mediated lipid peroxidation, protein denaturation, and
DNA damage as key mechanisms of reperfusion injury.
Q10: A patient with cholera develops profuse watery diarrhea. The pathogenesis involves persistent
activation of adenylate cyclase in intestinal epithelial cells, resulting in elevated intracellular cAMP. Which
cellular mechanism is directly responsible for the massive fluid secretion?
Page 3 | NSG 5003 Final Exam | South University
, NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
A. Activation of phospholipase C and release of IP3
B. Opening of chloride channels (CFTR) with inhibition of sodium reabsorption *[CORRECT]*
C. Direct damage to tight junctions by bacterial toxins
D. Stimulation of Na/K ATPase leading to potassium loss
Correct Answer: B
Rationale: Cholera toxin ADP-ribosylates the Gs protein, locking adenylate cyclase in the active state. The
resulting rise in cAMP opens CFTR chloride channels, causing massive chloride efflux into the lumen,
followed by sodium and water. This is an example of altered signal transduction and membrane transport.
NSG 5003 uses cholera as the classic model of G-protein-coupled receptor dysregulation.
Q11: A 60-year-old male with chronic hepatitis C develops a hepatocellular carcinoma. The tumor exhibits
a mutation in a gene that normally downregulates cellular proliferation. Which gene is most likely
affected?
A. RAS
B. MYC
C. TP53 (p53) *[CORRECT]*
D. BCL-2
Correct Answer: C
Rationale: TP53 encodes the p53 protein, a tumor suppressor that arrests the cell cycle at G1/S for DNA
repair or triggers apoptosis when repair is impossible. Loss-of-function mutations in TP53 are among the most
common alterations in human cancers. RAS and MYC are proto-oncogenes (gain-of-function), and BCL-2
inhibits apoptosis. NSG 5003 emphasizes tumor suppressor genes as 'brakes' on proliferation whose loss
permits malignant progression.
Q12: A 72-year-old female's cardiac biopsy reveals accumulation of a golden-brown, finely granular
pigment within myocardial cells that does not elicit inflammation. What is this pigment, and what does its
accumulation indicate?
A. Hemosiderin; iron overload from hemochromatosis
B. Lipofuscin; 'wear-and-tear' pigment from lysosomal lipid peroxidation *[CORRECT]*
C. Melanin; increased melanocyte activity
D. Bilirubin; hepatic dysfunction
Correct Answer: B
Rationale: Lipofuscin is an insoluble, golden-brown, lipid-containing pigment that accumulates in postmitotic
cells (cardiac myocytes, neurons) as a byproduct of lysosomal lipid peroxidation, often called the
'wear-and-tear' or aging pigment. Hemosiderin derives from hemoglobin breakdown and indicates iron excess,
melanin is produced by melanocytes, and bilirubin reflects heme catabolism. NSG 5003 distinguishes
lipofuscin as benign accumulation of aging cells.
Q13: A 35-year-old female undergoes partial hepatectomy as a living donor for liver transplantation.
Within 6 months, her liver regrows to near-original size. Which cellular mechanism primarily accounts for
this restoration?
A. Hypertrophy of remaining hepatocytes only
B. Compensatory hyperplasia of remaining hepatocytes driven by growth factors
*[CORRECT]*
C. Metaplasia of stellate cells into hepatocytes
D. Stem cell differentiation from bone marrow
Page 4 | NSG 5003 Final Exam | South University
NSG5003 / NSG 5003: Advanced Pathophysiology Final Exam
Week 10 (Latest ) | South University
Aligned with NSG 5003 Course Syllabus, AACN Essentials of Master's Education, and Advanced
Pathophysiology Competencies (2026/2027 Edition)
Instructions: This comprehensive examination consists of 150 multiple-choice questions divided across
11 content sections. Each question has four options (A–D) with ONE best answer. The correct answer is
marked with *[CORRECT]*. Review the rationale provided for each item, which integrates NSG 5003
curriculum objectives, AACN Master's Essentials, and advanced pathophysiology principles. Cognitive
distribution: 20% recall, 50% application, 30% analysis. Question style: 75% scenario-based (patient
presentations, clinical situations, case studies) and 25% direct knowledge.
Section 1: Cellular & Molecular Pathophysiology
Q1: A 68-year-old male with a long history of hypertension presents with an echocardiogram
demonstrating increased left ventricular wall thickness without an increase in cell number. Which cellular
adaptation best describes this finding?
A. Hyperplasia
B. Hypertrophy *[CORRECT]*
C. Metaplasia
D. Dysplasia
Correct Answer: B
Rationale: Hypertrophy is an increase in cell size, classically seen in cardiac myocytes in response to
pressure overload such as chronic hypertension. Hyperplasia is an increase in cell number and does not occur
in terminally differentiated cardiac muscle. Metaplasia and dysplasia involve cell-type replacement and
disordered growth, respectively, neither of which matches this presentation. NSG 5003 emphasizes
adaptation as a reversible, compensatory response to stress.
Q2: A 55-year-old chronic smoker undergoes bronchoscopy with biopsy of the bronchial epithelium. The
pathology report describes replacement of the normal pseudostratified ciliated columnar epithelium with
stratified squamous epithelium. What is the most likely cellular adaptation, and what is its primary clinical
significance?
A. Hypertrophy; loss of ciliary function
B. Metaplasia; precursor that may progress to dysplasia and malignancy *[CORRECT]*
C. Hyperplasia; benign increase in cell number
D. Anaplasia; definitive evidence of invasive carcinoma
Correct Answer: B
Rationale: Squamous metaplasia is a reversible substitution of one differentiated cell type (ciliated columnar)
for another (stratified squamous) better suited to withstand chronic irritation from tobacco smoke. It is a known
precursor lesion that, with continued injury, can progress to dysplasia and squamous cell carcinoma. NSG
5003 stresses that metaplasia is adaptive but carries malignant potential.
Q3: Which of the following clinical scenarios is the BEST example of physiologic hyperplasia rather than
pathologic hyperplasia?
A. Endometrial hyperplasia secondary to unopposed estrogen therapy
Page 1 | NSG 5003 Final Exam | South University
,NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
B. Benign prostatic hyperplasia in a 72-year-old male
C. Glandular epithelial hyperplasia of the breast during pregnancy *[CORRECT]*
D. Thyroid hyperplasia in a patient with Graves disease
Correct Answer: C
Rationale: Glandular hyperplasia of the breast during pregnancy is hormone-driven physiologic hyperplasia
enabling lactation. Endometrial hyperplasia from unopposed estrogen, benign prostatic hyperplasia, and
thyroid hyperplasia in Graves disease are pathologic because they result from abnormal hormonal signaling or
autoimmunity. NSG 5003 distinguishes physiologic (compensatory/hormonal) from pathologic hyperplasia.
Q4: A 45-year-old female has had a cast on her right lower extremity for 8 weeks following tibial fracture.
Upon cast removal, the gastrocnemius muscle appears markedly reduced in size. What cellular process
explains this finding, and what is its underlying mechanism?
A. Atrophy; decreased protein synthesis and increased proteasomal degradation
*[CORRECT]*
B. Necrosis; irreversible cell membrane damage
C. Apoptosis; programmed cell death of myocytes
D. Metaplasia; transformation to fibroblasts
Correct Answer: A
Rationale: Disuse atrophy results from reduced mechanical load leading to decreased protein synthesis and
increased ubiquitin-proteasome-mediated protein degradation. Necrosis is irreversible cell death, not seen in
disuse. Apoptosis is programmed death of individual cells, not whole-organ shrinkage. NSG 5003 highlights
atrophy as a reversible adaptation to reduced workload, denervation, or inadequate nutrition.
Q5: A cervical biopsy in a 31-year-old female shows disordered cellular proliferation with pleomorphic,
hyperchromatic nuclei and loss of normal tissue architecture, but no invasion through the basement
membrane. Which term best describes this finding?
A. Metaplasia
B. Anaplasia
C. Dysplasia *[CORRECT]*
D. Hyperplasia
Correct Answer: C
Rationale: Dysplasia is disordered growth characterized by pleomorphism, hyperchromasia, increased
mitoses, and loss of polarity, but it remains confined by the basement membrane (pre-invasive). Metaplasia is
cell-type substitution without atypia, anaplasia implies lack of differentiation typical of frank malignancy, and
hyperplasia is an increase in cell number without atypia. NSG 5003 frames dysplasia as a precursor lesion
that may regress or progress to carcinoma in situ.
Q6: A 59-year-old male sustains an acute myocardial infarction and dies 18 hours later. Autopsy reveals
a firm, pale, wedge-shaped lesion in the left ventricle. Which type of necrosis is most consistent with this
finding?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis *[CORRECT]*
D. Fat necrosis
Correct Answer: C
Page 2 | NSG 5003 Final Exam | South University
,NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
Rationale: Coagulative necrosis is characteristic of ischemic injury in most solid organs except the brain;
tissue architecture is preserved but the cells are dead, producing the firm pale appearance. Liquefactive
necrosis is typical of CNS infarcts and bacterial abscesses. Caseous necrosis is associated with TB, and fat
necrosis occurs in pancreatic and breast tissue. NSG 5003 emphasizes the pattern of necrosis as a clue to
underlying etiology.
Q7: Which cellular process is the hallmark of apoptosis and distinguishes it from necrosis?
A. Cell swelling and membrane rupture with release of cellular contents
B. Energy-dependent, programmed cell death without significant inflammation *[CORRECT]*
C. Random DNA fragmentation by lysosomal enzymes
D. Massive calcium influx triggering necrosis
Correct Answer: B
Rationale: Apoptosis is an energy-dependent, gene-regulated process resulting in cell shrinkage, chromatin
condensation, and apoptotic bodies that are phagocytosed without eliciting an inflammatory response.
Necrosis is unregulated, characterized by cell swelling, membrane rupture, and inflammation. NSG 5003
emphasizes apoptosis in embryogenesis, hormone-regulated involution, and DNA-damage responses
mediated by p53.
Q8: A 50-year-old male with severe burns develops cloudy swelling of renal tubular cells on biopsy.
Which cellular change best describes this finding, and what is its reversibility?
A. Irreversible coagulative necrosis
B. Reversible hydropic degeneration due to Na/K pump failure *[CORRECT]*
C. Irreversible apoptosis
D. Reversible metaplasia
Correct Answer: B
Rationale: Cloudy swelling or hydropic degeneration is a reversible form of cell injury caused by impaired
Na/K ATPase, allowing sodium and water to enter the cell and produce vacuolation. If hypoxia persists, injury
progresses to irreversible necrosis. NSG 5003 frames cellular swelling as an early, reversible indicator of
membrane pump failure.
Q9: Reperfusion injury after thrombolytic therapy for acute MI is mediated in large part by the generation
of reactive oxygen species (ROS). Which intracellular enzyme system is a major enzymatic source of
these ROS during reperfusion?
A. Cyclooxygenase-2
B. Xanthine oxidase *[CORRECT]*
C. Lactate dehydrogenase
D. Hexokinase
Correct Answer: B
Rationale: During ischemia, ATP is degraded to hypoxanthine, and xanthine dehydrogenase is converted to
xanthine oxidase. On reperfusion, xanthine oxidase uses oxygen to generate superoxide anions, driving
reperfusion injury. COX-2 produces prostaglandins, LDH converts pyruvate to lactate, and hexokinase
phosphorylates glucose. NSG 5003 highlights ROS-mediated lipid peroxidation, protein denaturation, and
DNA damage as key mechanisms of reperfusion injury.
Q10: A patient with cholera develops profuse watery diarrhea. The pathogenesis involves persistent
activation of adenylate cyclase in intestinal epithelial cells, resulting in elevated intracellular cAMP. Which
cellular mechanism is directly responsible for the massive fluid secretion?
Page 3 | NSG 5003 Final Exam | South University
, NSG 5003: Advanced Pathophysiology Final Exam (2026/2027) - South University 150 Questions | Week 10
A. Activation of phospholipase C and release of IP3
B. Opening of chloride channels (CFTR) with inhibition of sodium reabsorption *[CORRECT]*
C. Direct damage to tight junctions by bacterial toxins
D. Stimulation of Na/K ATPase leading to potassium loss
Correct Answer: B
Rationale: Cholera toxin ADP-ribosylates the Gs protein, locking adenylate cyclase in the active state. The
resulting rise in cAMP opens CFTR chloride channels, causing massive chloride efflux into the lumen,
followed by sodium and water. This is an example of altered signal transduction and membrane transport.
NSG 5003 uses cholera as the classic model of G-protein-coupled receptor dysregulation.
Q11: A 60-year-old male with chronic hepatitis C develops a hepatocellular carcinoma. The tumor exhibits
a mutation in a gene that normally downregulates cellular proliferation. Which gene is most likely
affected?
A. RAS
B. MYC
C. TP53 (p53) *[CORRECT]*
D. BCL-2
Correct Answer: C
Rationale: TP53 encodes the p53 protein, a tumor suppressor that arrests the cell cycle at G1/S for DNA
repair or triggers apoptosis when repair is impossible. Loss-of-function mutations in TP53 are among the most
common alterations in human cancers. RAS and MYC are proto-oncogenes (gain-of-function), and BCL-2
inhibits apoptosis. NSG 5003 emphasizes tumor suppressor genes as 'brakes' on proliferation whose loss
permits malignant progression.
Q12: A 72-year-old female's cardiac biopsy reveals accumulation of a golden-brown, finely granular
pigment within myocardial cells that does not elicit inflammation. What is this pigment, and what does its
accumulation indicate?
A. Hemosiderin; iron overload from hemochromatosis
B. Lipofuscin; 'wear-and-tear' pigment from lysosomal lipid peroxidation *[CORRECT]*
C. Melanin; increased melanocyte activity
D. Bilirubin; hepatic dysfunction
Correct Answer: B
Rationale: Lipofuscin is an insoluble, golden-brown, lipid-containing pigment that accumulates in postmitotic
cells (cardiac myocytes, neurons) as a byproduct of lysosomal lipid peroxidation, often called the
'wear-and-tear' or aging pigment. Hemosiderin derives from hemoglobin breakdown and indicates iron excess,
melanin is produced by melanocytes, and bilirubin reflects heme catabolism. NSG 5003 distinguishes
lipofuscin as benign accumulation of aging cells.
Q13: A 35-year-old female undergoes partial hepatectomy as a living donor for liver transplantation.
Within 6 months, her liver regrows to near-original size. Which cellular mechanism primarily accounts for
this restoration?
A. Hypertrophy of remaining hepatocytes only
B. Compensatory hyperplasia of remaining hepatocytes driven by growth factors
*[CORRECT]*
C. Metaplasia of stellate cells into hepatocytes
D. Stem cell differentiation from bone marrow
Page 4 | NSG 5003 Final Exam | South University
