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NSG 3280 PATHOPHYSIOLOGY FOR NURSES I GALEN COLLEGE OF NURSING EXAM STUDY RESOURCE ACCURATE ITEMS MASTER
NSG 3280 PATHOPHYSIOLOGY FOR NURSES I GALEN COLLEGE OF NURSING EXAM STYLE FINAL SCRIPT CORRECT ANSWERS
EXPLANATIONS
NSG3280 Pathophysiology for NursesGRADED
I Review A+
| Galen College of Nursing | 2025/2026
NSG 3280 PATHOPHYSIOLOGY FOR 3280
NSG3280 / NSG NURSES I REVIEW GALEN
Pathophysiology forCOLLEGE OF NURSING EXAM STYLE
Nurses I Review
COMPLETE CORRECT ANSWERS GRADED A+
Galen College of Nursing
2025/2026 Academic Year Update
100% Verified | Exam-Style Questions with Detailed Rationales | Graded A+
Total Questions: 100 MCQ
Testing Time: 120 Minutes (2 hours)
Passing Score: 75% (75 correct)
Format: Computer-based, proctored
Item Types: Standard MCQ, Clinical Scenario, Prioritization,
SATA
Version: 2025/2026 Update
Content Distribution
• Cellular Adaptation & Injury (12%)
• Inflammation & Repair (10%)
• Fluid & Electrolyte Balance (12%)
• Acid-Base Balance (8%)
• Genetics & Neoplasia (10%)
• Immune System Disorders (12%)
• Infectious Diseases (10%)
• Cardiovascular Pathophysiology (12%)
• Respiratory Pathophysiology (8%)
• Neurologic Pathophysiology (6%)
Introduction
The NSG3280 Pathophysiology for Nurses I Review examination assesses the nursing student's foundational
understanding of disease processes, cellular mechanisms, and systemic alterations that affect human health.
This comprehensive review covers key domains including cellular adaptation and injury, inflammation and
tissue repair, fluid and electrolyte imbalances, acid-base disturbances, genetic and neoplastic disorders,
immune system dysfunction, infectious disease processes, and the pathophysiology of cardiovascular,
respiratory, and neurologic systems. This practice exam is designed to mirror the official Galen College testing
environment, offering 100% verified, exam-style questions with detailed rationales to reinforce clinical
reasoning and prepare students for success on the proctored examination.
Section: Cellular Adaptation & Injury
1. A patient with chronic hypertension is found to have left ventricular hypertrophy. Which
cellular adaptation best describes this change?
A. Hyperplasia B. Hypertrophy
C. Atrophy D. Metaplasia
Correct Answer: B. Hypertrophy
Rationale: Hypertrophy is an increase in cell size resulting from increased workload or hormonal
stimulation. In chronic hypertension, the left ventricular myocardium enlarges to compensate for
increased afterload. Hyperplasia refers to an increase in cell number, atrophy is a decrease in cell size, and
metaplasia is the replacement of one mature cell type with another.
2. A long-time smoker undergoes bronchoscopy, which reveals columnar ciliated epithelium
being replaced by stratified squamous epithelium in the large airways. This cellular change is
best described as:
A. Dysplasia B. Hyperplasia
C. Metaplasia D. Anaplasia
1
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Correct Answer: C. Metaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type with another. Chronic
exposure to cigarette smoke irritates the respiratory epithelium, causing transformation from columnar
ciliated to stratified squamous epithelium, which is more resistant to irritation. Dysplasia refers to
abnormal cell maturation, hyperplasia is increased cell number, and anaplasia refers to undifferentiated,
rapidly dividing cells typical of malignancy.
3. A patient with a cast on the leg for 6 weeks presents with noticeable muscle wasting. Which
cellular adaptation has occurred?
A. Hypertrophy B. Hyperplasia
C. Atrophy D. Metaplasia
Correct Answer: C. Atrophy
Rationale: Atrophy is a decrease in cell size due to reduced workload, disuse, inadequate blood supply, or
nutritional deficiency. Immobilization from a cast leads to disuse atrophy of skeletal muscle. Hypertrophy
is an increase in cell size, hyperplasia is increased cell number, and metaplasia is conversion of one cell
type to another.
4. Which statement best describes reversible cellular injury?
A. Mitochondrial function is permanently lost B. Cell membrane integrity is destroyed
C. ATP depletion occurs but cellular D. Nuclear pyknosis and karyorrhexis are
homeostasis can be restored if the present
injurious agent is removed
Correct Answer: C. ATP depletion occurs but cellular homeostasis can be restored if the
injurious agent is removed
Rationale: Reversible cellular injury occurs when an injurious agent causes cellular stress but does not
permanently damage organelles or the cell membrane. ATP depletion is an early event in both reversible
and irreversible injury; however, in reversible injury, removing the insult allows restoration of cellular
ATP production and homeostasis. Permanent mitochondrial damage, cell membrane rupture, and nuclear
changes (pyknosis, karyorrhexis) are hallmarks of irreversible injury and cell death.
5. A patient presents with severe chest pain and elevated cardiac biomarkers. Laboratory
findings reveal elevated serum potassium, decreased intracellular potassium, and swelling of
the myocardial cells. These findings are most consistent with:
A. Apoptosis B. Coagulative necrosis
C. Liquefactive necrosis D. Caseous necrosis
Correct Answer: B. Coagulative necrosis
Rationale: Coagulative necrosis typically results from ischemia, as seen in myocardial infarction. The
cellular architecture is preserved but the cells are dead. Early features include intracellular sodium and
water accumulation (cell swelling), potassium leakage from cells, and eventual coagulation of cellular
proteins. Apoptosis is programmed cell death without inflammation, liquefactive necrosis involves
enzymatic liquefaction (typical of brain infarcts), and caseous necrosis is characteristic of tuberculosis.
6. Free radicals cause cellular injury through which primary mechanism?
A. Inhibition of DNA synthesis only B. Lipid peroxidation of cell membranes
C. Activation of anti-inflammatory cytokines D. Stimulation of cellular repair mechanisms
Correct Answer: B. Lipid peroxidation of cell membranes
Rationale: Free radicals, including reactive oxygen species (ROS), cause cellular injury primarily
through lipid peroxidation of cell membranes. This process damages the phospholipid bilayer, disrupting
membrane integrity and leading to increased cell membrane permeability. Free radicals can also damage
proteins and DNA, but the primary mechanism of acute cellular injury is membrane damage through lipid
peroxidation.
7. A biopsy specimen from a patient with chronic liver disease shows hepatocytes with large
accumulations of lipids, pushing the nucleus to the periphery. This pathologic change is
called:
A. Fatty change (steatosis) B. Hyaline droplet degeneration
C. Amyloidosis D. Melanosis
Correct Answer: A. Fatty change (steatosis)
2
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Rationale: Fatty change, or steatosis, occurs when triglycerides accumulate within hepatocytes, often due
to alcohol abuse, diabetes mellitus, obesity, or starvation. The fat vacuoles push the nucleus to the
periphery of the cell, creating a signet-ring appearance. Hyaline droplet degeneration involves
accumulation of abnormal proteins, amyloidosis involves extracellular protein deposition, and melanosis
refers to abnormal melanin accumulation.
8. Which of the following is the most common cause of hypoxic cellular injury?
A. Nutritional deficiency B. Ischemia
C. Genetic mutation D. Radiation exposure
Correct Answer: B. Ischemia
Rationale: Ischemia, or reduced blood supply, is the most common cause of hypoxic cellular injury.
Ischemia not only reduces oxygen delivery but also impairs the delivery of nutrients and removal of
metabolic waste products, making it more damaging than hypoxia alone. The most common cause of
ischemia is arterial obstruction due to thrombosis or atherosclerosis.
9. Apoptosis differs from necrosis in which fundamental way?
A. Apoptosis causes inflammation in B. Apoptosis requires energy (ATP) and
surrounding tissues does not trigger an inflammatory
response
C. Necrosis is a programmed process regulated D. Apoptosis only occurs in pathological
by specific genes conditions
Correct Answer: B. Apoptosis requires energy (ATP) and does not trigger an inflammatory
response
Rationale: Apoptosis is a form of programmed cell death that requires ATP and activates specific caspase
enzymes. Unlike necrosis, apoptosis does not cause inflammation because the dying cells are phagocytosed
before releasing intracellular contents into the extracellular space. Apoptosis occurs both physiologically
(embryonic development, immune cell selection) and pathologically (viral infections, DNA damage).
Necrosis is unprogrammed cell death that always triggers an inflammatory response.
10. A patient who ingested a large amount of acetaminophen develops fulminant liver failure.
Which type of necrosis is most likely present in the liver?
A. Coagulative necrosis B. Liquefactive necrosis
C. Caseous necrosis D. Fat necrosis
Correct Answer: B. Liquefactive necrosis
Rationale: Acetaminophen overdose causes massive hepatocyte necrosis through the formation of the
toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). The necrosis in the liver progresses to
liquefactive necrosis due to the release of intracellular digestive enzymes. The high lipid and water content
of the liver tissue also contributes to liquefaction. Coagulative necrosis is typical of ischemic injury in most
solid organs, caseous necrosis is characteristic of tuberculosis, and fat necrosis occurs with pancreatic
injury.
11. Calcium plays a central role in irreversible cell injury. Which of the following best
describes the mechanism?
A. Calcium depletion prevents apoptotic B. Intracellular calcium accumulation
signaling activates destructive enzymes including
phospholipases, proteases, and
endonucleases
C. Calcium binds to free radicals and neutralizes D. Calcium stabilizes the mitochondrial
them membrane
Correct Answer: B. Intracellular calcium accumulation activates destructive enzymes
including phospholipases, proteases, and endonucleases
Rationale: In irreversible cell injury, persistent ischemia leads to failure of the sodium-potassium pump
and calcium pump, causing intracellular accumulation of calcium. Elevated cytosolic calcium activates
phospholipases (damaging cell membranes), proteases (degrading cytoskeletal and membrane proteins),
ATPases (depleting energy stores), and endonucleases (fragmenting DNA). This calcium-mediated
enzymatic cascade is a critical pathway in the progression from reversible to irreversible cellular injury.
12. Which cellular organelle is most susceptible to damage during ischemic injury?
A. Nucleus B. Ribosome
3
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NSG 3280 PATHOPHYSIOLOGY FOR NURSES I GALEN COLLEGE OF NURSING EXAM STUDY RESOURCE ACCURATE ITEMS MASTER
NSG 3280 PATHOPHYSIOLOGY FOR NURSES I GALEN COLLEGE OF NURSING EXAM STYLE FINAL SCRIPT CORRECT ANSWERS
EXPLANATIONS
NSG3280 Pathophysiology for NursesGRADED
I Review A+
| Galen College of Nursing | 2025/2026
NSG 3280 PATHOPHYSIOLOGY FOR 3280
NSG3280 / NSG NURSES I REVIEW GALEN
Pathophysiology forCOLLEGE OF NURSING EXAM STYLE
Nurses I Review
COMPLETE CORRECT ANSWERS GRADED A+
Galen College of Nursing
2025/2026 Academic Year Update
100% Verified | Exam-Style Questions with Detailed Rationales | Graded A+
Total Questions: 100 MCQ
Testing Time: 120 Minutes (2 hours)
Passing Score: 75% (75 correct)
Format: Computer-based, proctored
Item Types: Standard MCQ, Clinical Scenario, Prioritization,
SATA
Version: 2025/2026 Update
Content Distribution
• Cellular Adaptation & Injury (12%)
• Inflammation & Repair (10%)
• Fluid & Electrolyte Balance (12%)
• Acid-Base Balance (8%)
• Genetics & Neoplasia (10%)
• Immune System Disorders (12%)
• Infectious Diseases (10%)
• Cardiovascular Pathophysiology (12%)
• Respiratory Pathophysiology (8%)
• Neurologic Pathophysiology (6%)
Introduction
The NSG3280 Pathophysiology for Nurses I Review examination assesses the nursing student's foundational
understanding of disease processes, cellular mechanisms, and systemic alterations that affect human health.
This comprehensive review covers key domains including cellular adaptation and injury, inflammation and
tissue repair, fluid and electrolyte imbalances, acid-base disturbances, genetic and neoplastic disorders,
immune system dysfunction, infectious disease processes, and the pathophysiology of cardiovascular,
respiratory, and neurologic systems. This practice exam is designed to mirror the official Galen College testing
environment, offering 100% verified, exam-style questions with detailed rationales to reinforce clinical
reasoning and prepare students for success on the proctored examination.
Section: Cellular Adaptation & Injury
1. A patient with chronic hypertension is found to have left ventricular hypertrophy. Which
cellular adaptation best describes this change?
A. Hyperplasia B. Hypertrophy
C. Atrophy D. Metaplasia
Correct Answer: B. Hypertrophy
Rationale: Hypertrophy is an increase in cell size resulting from increased workload or hormonal
stimulation. In chronic hypertension, the left ventricular myocardium enlarges to compensate for
increased afterload. Hyperplasia refers to an increase in cell number, atrophy is a decrease in cell size, and
metaplasia is the replacement of one mature cell type with another.
2. A long-time smoker undergoes bronchoscopy, which reveals columnar ciliated epithelium
being replaced by stratified squamous epithelium in the large airways. This cellular change is
best described as:
A. Dysplasia B. Hyperplasia
C. Metaplasia D. Anaplasia
1
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NSG3280 Pathophysiology for Nurses I Review | Galen College of Nursing | 2025/2026
Correct Answer: C. Metaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type with another. Chronic
exposure to cigarette smoke irritates the respiratory epithelium, causing transformation from columnar
ciliated to stratified squamous epithelium, which is more resistant to irritation. Dysplasia refers to
abnormal cell maturation, hyperplasia is increased cell number, and anaplasia refers to undifferentiated,
rapidly dividing cells typical of malignancy.
3. A patient with a cast on the leg for 6 weeks presents with noticeable muscle wasting. Which
cellular adaptation has occurred?
A. Hypertrophy B. Hyperplasia
C. Atrophy D. Metaplasia
Correct Answer: C. Atrophy
Rationale: Atrophy is a decrease in cell size due to reduced workload, disuse, inadequate blood supply, or
nutritional deficiency. Immobilization from a cast leads to disuse atrophy of skeletal muscle. Hypertrophy
is an increase in cell size, hyperplasia is increased cell number, and metaplasia is conversion of one cell
type to another.
4. Which statement best describes reversible cellular injury?
A. Mitochondrial function is permanently lost B. Cell membrane integrity is destroyed
C. ATP depletion occurs but cellular D. Nuclear pyknosis and karyorrhexis are
homeostasis can be restored if the present
injurious agent is removed
Correct Answer: C. ATP depletion occurs but cellular homeostasis can be restored if the
injurious agent is removed
Rationale: Reversible cellular injury occurs when an injurious agent causes cellular stress but does not
permanently damage organelles or the cell membrane. ATP depletion is an early event in both reversible
and irreversible injury; however, in reversible injury, removing the insult allows restoration of cellular
ATP production and homeostasis. Permanent mitochondrial damage, cell membrane rupture, and nuclear
changes (pyknosis, karyorrhexis) are hallmarks of irreversible injury and cell death.
5. A patient presents with severe chest pain and elevated cardiac biomarkers. Laboratory
findings reveal elevated serum potassium, decreased intracellular potassium, and swelling of
the myocardial cells. These findings are most consistent with:
A. Apoptosis B. Coagulative necrosis
C. Liquefactive necrosis D. Caseous necrosis
Correct Answer: B. Coagulative necrosis
Rationale: Coagulative necrosis typically results from ischemia, as seen in myocardial infarction. The
cellular architecture is preserved but the cells are dead. Early features include intracellular sodium and
water accumulation (cell swelling), potassium leakage from cells, and eventual coagulation of cellular
proteins. Apoptosis is programmed cell death without inflammation, liquefactive necrosis involves
enzymatic liquefaction (typical of brain infarcts), and caseous necrosis is characteristic of tuberculosis.
6. Free radicals cause cellular injury through which primary mechanism?
A. Inhibition of DNA synthesis only B. Lipid peroxidation of cell membranes
C. Activation of anti-inflammatory cytokines D. Stimulation of cellular repair mechanisms
Correct Answer: B. Lipid peroxidation of cell membranes
Rationale: Free radicals, including reactive oxygen species (ROS), cause cellular injury primarily
through lipid peroxidation of cell membranes. This process damages the phospholipid bilayer, disrupting
membrane integrity and leading to increased cell membrane permeability. Free radicals can also damage
proteins and DNA, but the primary mechanism of acute cellular injury is membrane damage through lipid
peroxidation.
7. A biopsy specimen from a patient with chronic liver disease shows hepatocytes with large
accumulations of lipids, pushing the nucleus to the periphery. This pathologic change is
called:
A. Fatty change (steatosis) B. Hyaline droplet degeneration
C. Amyloidosis D. Melanosis
Correct Answer: A. Fatty change (steatosis)
2
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NSG3280 Pathophysiology for Nurses I Review | Galen College of Nursing | 2025/2026
Rationale: Fatty change, or steatosis, occurs when triglycerides accumulate within hepatocytes, often due
to alcohol abuse, diabetes mellitus, obesity, or starvation. The fat vacuoles push the nucleus to the
periphery of the cell, creating a signet-ring appearance. Hyaline droplet degeneration involves
accumulation of abnormal proteins, amyloidosis involves extracellular protein deposition, and melanosis
refers to abnormal melanin accumulation.
8. Which of the following is the most common cause of hypoxic cellular injury?
A. Nutritional deficiency B. Ischemia
C. Genetic mutation D. Radiation exposure
Correct Answer: B. Ischemia
Rationale: Ischemia, or reduced blood supply, is the most common cause of hypoxic cellular injury.
Ischemia not only reduces oxygen delivery but also impairs the delivery of nutrients and removal of
metabolic waste products, making it more damaging than hypoxia alone. The most common cause of
ischemia is arterial obstruction due to thrombosis or atherosclerosis.
9. Apoptosis differs from necrosis in which fundamental way?
A. Apoptosis causes inflammation in B. Apoptosis requires energy (ATP) and
surrounding tissues does not trigger an inflammatory
response
C. Necrosis is a programmed process regulated D. Apoptosis only occurs in pathological
by specific genes conditions
Correct Answer: B. Apoptosis requires energy (ATP) and does not trigger an inflammatory
response
Rationale: Apoptosis is a form of programmed cell death that requires ATP and activates specific caspase
enzymes. Unlike necrosis, apoptosis does not cause inflammation because the dying cells are phagocytosed
before releasing intracellular contents into the extracellular space. Apoptosis occurs both physiologically
(embryonic development, immune cell selection) and pathologically (viral infections, DNA damage).
Necrosis is unprogrammed cell death that always triggers an inflammatory response.
10. A patient who ingested a large amount of acetaminophen develops fulminant liver failure.
Which type of necrosis is most likely present in the liver?
A. Coagulative necrosis B. Liquefactive necrosis
C. Caseous necrosis D. Fat necrosis
Correct Answer: B. Liquefactive necrosis
Rationale: Acetaminophen overdose causes massive hepatocyte necrosis through the formation of the
toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). The necrosis in the liver progresses to
liquefactive necrosis due to the release of intracellular digestive enzymes. The high lipid and water content
of the liver tissue also contributes to liquefaction. Coagulative necrosis is typical of ischemic injury in most
solid organs, caseous necrosis is characteristic of tuberculosis, and fat necrosis occurs with pancreatic
injury.
11. Calcium plays a central role in irreversible cell injury. Which of the following best
describes the mechanism?
A. Calcium depletion prevents apoptotic B. Intracellular calcium accumulation
signaling activates destructive enzymes including
phospholipases, proteases, and
endonucleases
C. Calcium binds to free radicals and neutralizes D. Calcium stabilizes the mitochondrial
them membrane
Correct Answer: B. Intracellular calcium accumulation activates destructive enzymes
including phospholipases, proteases, and endonucleases
Rationale: In irreversible cell injury, persistent ischemia leads to failure of the sodium-potassium pump
and calcium pump, causing intracellular accumulation of calcium. Elevated cytosolic calcium activates
phospholipases (damaging cell membranes), proteases (degrading cytoskeletal and membrane proteins),
ATPases (depleting energy stores), and endonucleases (fragmenting DNA). This calcium-mediated
enzymatic cascade is a critical pathway in the progression from reversible to irreversible cellular injury.
12. Which cellular organelle is most susceptible to damage during ischemic injury?
A. Nucleus B. Ribosome
3
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