, NSG 5140 ADVANCED PATHOPHYSIOLOGY – MIDTERM
EXAM REVIEW
250 Questions with Verified Answers & Detailed Rationales
South College | 2026 Edition | Graded A+
📘 EXAM OVERVIEW
NSG 5140 Advanced Pathophysiology is a graduate-level course at South College that
provides an in-depth exploration of the pathophysiological mechanisms underlying
disease processes across the lifespan. This comprehensive review contains 250 practice
questions covering all major content areas tested on the midterm examination,
including:
• Cellular Adaptation & Injury
• Inflammation & Wound Healing
• Fluid, Electrolyte & Acid-Base Balance
• Genetics & Genomics
• Neoplasia & Oncologic Pathophysiology
• Immunopathology & Hypersensitivity
• Cardiovascular Pathophysiology
• Respiratory Pathophysiology
• Renal Pathophysiology
• Endocrine Pathophysiology
• Neurological Pathophysiology
• Gastrointestinal Pathophysiology
• Multisystem & Complex Disease Processes
,SECTION I: CELLULAR ADAPTATION & INJURY (Questions
1–40)
Question 1
Which of the following best describes the primary mechanism of cellular injury in
hypoxia?
A. Free radical damage
B. ATP depletion leading to loss of ion homeostasis
C. DNA mutation
D. Lipid peroxidation
Correct Answer: B
Rationale: Hypoxia limits oxidative phosphorylation, decreasing ATP production. This
leads to failure of the Na⁺/K⁺ ATPase pump, causing cellular swelling and eventual cell
death.
Question 2
A researcher studying pressure overload in cardiac myocytes observes that sustained
mechanical stretch leads to increased protein synthesis and cell enlargement without
cell division. Which intracellular signaling pathway is most directly responsible for this
adaptive response?
A. Activation of the PI3K/Akt/mTOR pathway leading to increased translation
B. Induction of p53-mediated cell cycle arrest and senescence
C. Upregulation of caspases and initiation of apoptosis
D. Activation of the unfolded protein response (UPR) due to ER stress
Correct Answer: A
Rationale: Cardiac myocytes respond to increased workload by undergoing
hypertrophy, which is driven by the PI3K/Akt/mTOR pathway that enhances protein
synthesis. p53 activation would promote apoptosis or senescence, not hypertrophy.
Caspase activation leads to apoptosis. UPR is triggered by ER stress, not directly by
mechanical stretch.
, Question 3
A pathologist examines a biopsy from the bronchial epithelium of a chronic smoker. The
normal pseudostratified ciliated columnar epithelium is replaced by stratified squamous
epithelium. Which molecular event is most likely initiating this change?
A. Increased expression of anti-apoptotic Bcl-2 in basal cells
B. Reprogramming of stem cells due to chronic irritation and altered transcription factor
signaling
C. Somatic mutation in the p53 gene leading to loss of cell cycle control
D. Epigenetic silencing of E-cadherin promoting epithelial-mesenchymal transition
Correct Answer: B
Rationale: Metaplasia results from reprogramming of tissue-resident stem cells in
response to chronic stress, often involving changes in transcription factors. Increased
Bcl-2 would inhibit apoptosis, not cause metaplasia. p53 mutation is associated with
dysplasia/cancer. E-cadherin silencing is more related to invasion in carcinoma.
Question 4
In a patient with prolonged ischemia due to renal artery stenosis, proximal tubular
epithelial cells exhibit swelling of mitochondria and dilation of the endoplasmic
reticulum on electron microscopy. Which phase of cell injury does this morphology
represent, and what is the primary underlying biochemical defect?
A. Irreversible injury; massive calcium influx into mitochondria
B. Reversible injury; depletion of ATP leading to failure of ion pumps
C. Necroptosis; activation of receptor-interacting protein kinases (RIPK1/RIPK3)
D. Apoptosis; cytochrome c release from mitochondria
Correct Answer: B
Rationale: Mitochondrial swelling and ER dilation are hallmarks of reversible injury. ATP
depletion leads to failure of ion pumps, causing water influx and organelle swelling.
These changes are reversible before membrane damage occurs.
EXAM REVIEW
250 Questions with Verified Answers & Detailed Rationales
South College | 2026 Edition | Graded A+
📘 EXAM OVERVIEW
NSG 5140 Advanced Pathophysiology is a graduate-level course at South College that
provides an in-depth exploration of the pathophysiological mechanisms underlying
disease processes across the lifespan. This comprehensive review contains 250 practice
questions covering all major content areas tested on the midterm examination,
including:
• Cellular Adaptation & Injury
• Inflammation & Wound Healing
• Fluid, Electrolyte & Acid-Base Balance
• Genetics & Genomics
• Neoplasia & Oncologic Pathophysiology
• Immunopathology & Hypersensitivity
• Cardiovascular Pathophysiology
• Respiratory Pathophysiology
• Renal Pathophysiology
• Endocrine Pathophysiology
• Neurological Pathophysiology
• Gastrointestinal Pathophysiology
• Multisystem & Complex Disease Processes
,SECTION I: CELLULAR ADAPTATION & INJURY (Questions
1–40)
Question 1
Which of the following best describes the primary mechanism of cellular injury in
hypoxia?
A. Free radical damage
B. ATP depletion leading to loss of ion homeostasis
C. DNA mutation
D. Lipid peroxidation
Correct Answer: B
Rationale: Hypoxia limits oxidative phosphorylation, decreasing ATP production. This
leads to failure of the Na⁺/K⁺ ATPase pump, causing cellular swelling and eventual cell
death.
Question 2
A researcher studying pressure overload in cardiac myocytes observes that sustained
mechanical stretch leads to increased protein synthesis and cell enlargement without
cell division. Which intracellular signaling pathway is most directly responsible for this
adaptive response?
A. Activation of the PI3K/Akt/mTOR pathway leading to increased translation
B. Induction of p53-mediated cell cycle arrest and senescence
C. Upregulation of caspases and initiation of apoptosis
D. Activation of the unfolded protein response (UPR) due to ER stress
Correct Answer: A
Rationale: Cardiac myocytes respond to increased workload by undergoing
hypertrophy, which is driven by the PI3K/Akt/mTOR pathway that enhances protein
synthesis. p53 activation would promote apoptosis or senescence, not hypertrophy.
Caspase activation leads to apoptosis. UPR is triggered by ER stress, not directly by
mechanical stretch.
, Question 3
A pathologist examines a biopsy from the bronchial epithelium of a chronic smoker. The
normal pseudostratified ciliated columnar epithelium is replaced by stratified squamous
epithelium. Which molecular event is most likely initiating this change?
A. Increased expression of anti-apoptotic Bcl-2 in basal cells
B. Reprogramming of stem cells due to chronic irritation and altered transcription factor
signaling
C. Somatic mutation in the p53 gene leading to loss of cell cycle control
D. Epigenetic silencing of E-cadherin promoting epithelial-mesenchymal transition
Correct Answer: B
Rationale: Metaplasia results from reprogramming of tissue-resident stem cells in
response to chronic stress, often involving changes in transcription factors. Increased
Bcl-2 would inhibit apoptosis, not cause metaplasia. p53 mutation is associated with
dysplasia/cancer. E-cadherin silencing is more related to invasion in carcinoma.
Question 4
In a patient with prolonged ischemia due to renal artery stenosis, proximal tubular
epithelial cells exhibit swelling of mitochondria and dilation of the endoplasmic
reticulum on electron microscopy. Which phase of cell injury does this morphology
represent, and what is the primary underlying biochemical defect?
A. Irreversible injury; massive calcium influx into mitochondria
B. Reversible injury; depletion of ATP leading to failure of ion pumps
C. Necroptosis; activation of receptor-interacting protein kinases (RIPK1/RIPK3)
D. Apoptosis; cytochrome c release from mitochondria
Correct Answer: B
Rationale: Mitochondrial swelling and ER dilation are hallmarks of reversible injury. ATP
depletion leads to failure of ion pumps, causing water influx and organelle swelling.
These changes are reversible before membrane damage occurs.
