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NSG 3280 EXAM 1 –
PATHOPHYSIOLOGY FOR NURSES I |
GALEN COLLEGE OF NURSING |
PRACTICE QUESTIONS AND DETAILED
RATIONALES | 2026/2027
Unofficial practice resource. These are original study questions, not verified or reproduced Galen
College of Nursing exam questions. No question bank can guarantee an A+ or a passing grade.
Introduction
NSG 3280 Exam 1 – Pathophysiology for Nurses I focuses on the mechanisms through which
disease disrupts normal cellular and organ function. For nursing students at Galen College of
Nursing, mastering foundational pathophysiology supports clinical reasoning, interpretation of
patient findings, and understanding why particular signs, symptoms, and complications develop.
This practice resource is designed for students who need to move beyond memorizing definitions
and apply concepts to challenging patient scenarios. Questions emphasize cellular adaptation and
injury, inflammation, immune responses, fluid and electrolyte imbalances, acid–base regulation,
hemodynamic changes, infection, neoplasia, and altered metabolism. The exact topics covered
on your Exam 1 may differ according to the current course syllabus, instructor guidance, and
assigned readings.
Each multiple-choice question includes four answer options and a detailed rationale explaining
the correct response and why the alternatives are less appropriate. For effective preparation,
answer each question before reading its rationale, record the concepts you miss, and revisit the
corresponding material in your course resources. This approach can help identify weaknesses,
strengthen clinical reasoning, and improve readiness for the examination, although results
depend on your preparation and the alignment of your review with the official course objectives.
Content area overview — suggested practice blueprint
This is a study allocation for practice, not an official Galen College of Nursing exam blueprint.
Content area Questions Key topics Weight
Cellular adaptation and injury 10 Cell stress, apoptosis, necrosis, ischemia 10%
Inflammatory mediators, immune response,
Inflammation and immunity 10 10%
healing
,2|Page
Genetics and disease
7 Inheritance, mutations, gene regulation 7%
mechanisms
Sodium, potassium, calcium, osmolality,
Fluid and electrolytes 12 12%
edema
Acid–base regulation 10 Acidosis, alkalosis, compensation, ABGs 10%
Hemodynamic disorders 9 Shock, thrombosis, embolism, perfusion 9%
Infection and host response 8 Fever, pathogens, sepsis, immune defense 8%
Neoplasia 8 Tumor behavior, invasion, metastasis 8%
Altered metabolism 8 Diabetes, hypoxia, ATP, catabolism 8%
Cardiovascular
8 Ischemia, heart failure, vascular disease 8%
pathophysiology
Clinical findings, laboratory patterns,
Integrated clinical reasoning 10 10%
mechanisms
Total 100 100%
QUESTIONS 1–100
Section 1: Cellular adaptation and injury
Q1
A patient with chronic aortic stenosis develops thickening of the left ventricular wall. Which
cellular response best explains this finding?
A) Increased number of mature cardiomyocytes through rapid mitosis B) Increased size of
existing cardiomyocytes in response to pressure overload C) Replacement of cardiac muscle by
mature epithelial cells D) Decreased synthesis of contractile proteins with no structural change
Rationale: B is correct because sustained pressure overload causes cardiac hypertrophy. A is
incorrect because adult cardiomyocytes have limited proliferative capacity. C is not a normal
cardiac adaptation. D does not explain ventricular wall thickening.
Q2
A patient’s skeletal muscle mass decreases after prolonged bed rest. Which mechanism is most
likely responsible?
A) Increased protein synthesis exceeding protein breakdown B) Increased cell number in
response to reduced activity C) Conversion of muscle fibers into adipocytes D) Reduced protein
synthesis and increased breakdown associated with disuse
, 3|Page
Rationale: D is correct because disuse shifts muscle protein balance toward loss. A would
preserve or increase muscle mass. B describes hyperplasia, which does not explain the typical
reduction in muscle size. C is not the primary mechanism of disuse atrophy.
Q3
A biopsy from a chronically irritated airway shows replacement of ciliated columnar epithelium
with stratified squamous epithelium. What is the principal consequence?
A) Metaplasia may improve resistance to irritation but impair mucociliary clearance B) The
tissue has necessarily become invasive carcinoma C) All epithelial cells have undergone
coagulative necrosis D) The airway has developed hypertrophy of individual ciliated cells only
Rationale: A is correct because metaplasia changes one mature cell type into another and may
compromise normal function. B is incorrect because metaplasia is not itself cancer, although
persistent injury can increase risk. C describes cell death, not adaptation. D describes increased
cell size and does not explain the cell-type replacement.
Q4
A patient experiences prolonged intestinal ischemia. Cells develop swelling, membrane damage,
and leakage of intracellular enzymes. Which process is most likely?
A) Physiological hyperplasia B) Reversible adaptation without injury C) Irreversible cell injury
progressing toward necrosis D) Normal differentiation into specialized cells
Rationale: C is correct because severe ischemia depletes ATP and disrupts membrane integrity,
leading to cell death. A and D are growth or differentiation processes, not destructive injury. B is
inconsistent with substantial membrane damage and enzyme leakage.
Q5
A tissue sample shows cell shrinkage, chromatin condensation, and membrane-bound fragments
with minimal inflammation. Which process is occurring?
A) Liquefactive necrosis B) Coagulative necrosis C) Apoptosis D) Fat necrosis
Rationale: C is correct because apoptosis is regulated cell death with cell shrinkage and apoptotic
bodies. A involves enzymatic digestion and liquefaction. B is commonly associated with
ischemic injury in solid organs. D involves destruction of adipose tissue.
Q6
A patient sustains an ischemic stroke, and the affected brain tissue undergoes enzymatic
digestion. Which necrosis pattern is expected?
NSG 3280 EXAM 1 –
PATHOPHYSIOLOGY FOR NURSES I |
GALEN COLLEGE OF NURSING |
PRACTICE QUESTIONS AND DETAILED
RATIONALES | 2026/2027
Unofficial practice resource. These are original study questions, not verified or reproduced Galen
College of Nursing exam questions. No question bank can guarantee an A+ or a passing grade.
Introduction
NSG 3280 Exam 1 – Pathophysiology for Nurses I focuses on the mechanisms through which
disease disrupts normal cellular and organ function. For nursing students at Galen College of
Nursing, mastering foundational pathophysiology supports clinical reasoning, interpretation of
patient findings, and understanding why particular signs, symptoms, and complications develop.
This practice resource is designed for students who need to move beyond memorizing definitions
and apply concepts to challenging patient scenarios. Questions emphasize cellular adaptation and
injury, inflammation, immune responses, fluid and electrolyte imbalances, acid–base regulation,
hemodynamic changes, infection, neoplasia, and altered metabolism. The exact topics covered
on your Exam 1 may differ according to the current course syllabus, instructor guidance, and
assigned readings.
Each multiple-choice question includes four answer options and a detailed rationale explaining
the correct response and why the alternatives are less appropriate. For effective preparation,
answer each question before reading its rationale, record the concepts you miss, and revisit the
corresponding material in your course resources. This approach can help identify weaknesses,
strengthen clinical reasoning, and improve readiness for the examination, although results
depend on your preparation and the alignment of your review with the official course objectives.
Content area overview — suggested practice blueprint
This is a study allocation for practice, not an official Galen College of Nursing exam blueprint.
Content area Questions Key topics Weight
Cellular adaptation and injury 10 Cell stress, apoptosis, necrosis, ischemia 10%
Inflammatory mediators, immune response,
Inflammation and immunity 10 10%
healing
,2|Page
Genetics and disease
7 Inheritance, mutations, gene regulation 7%
mechanisms
Sodium, potassium, calcium, osmolality,
Fluid and electrolytes 12 12%
edema
Acid–base regulation 10 Acidosis, alkalosis, compensation, ABGs 10%
Hemodynamic disorders 9 Shock, thrombosis, embolism, perfusion 9%
Infection and host response 8 Fever, pathogens, sepsis, immune defense 8%
Neoplasia 8 Tumor behavior, invasion, metastasis 8%
Altered metabolism 8 Diabetes, hypoxia, ATP, catabolism 8%
Cardiovascular
8 Ischemia, heart failure, vascular disease 8%
pathophysiology
Clinical findings, laboratory patterns,
Integrated clinical reasoning 10 10%
mechanisms
Total 100 100%
QUESTIONS 1–100
Section 1: Cellular adaptation and injury
Q1
A patient with chronic aortic stenosis develops thickening of the left ventricular wall. Which
cellular response best explains this finding?
A) Increased number of mature cardiomyocytes through rapid mitosis B) Increased size of
existing cardiomyocytes in response to pressure overload C) Replacement of cardiac muscle by
mature epithelial cells D) Decreased synthesis of contractile proteins with no structural change
Rationale: B is correct because sustained pressure overload causes cardiac hypertrophy. A is
incorrect because adult cardiomyocytes have limited proliferative capacity. C is not a normal
cardiac adaptation. D does not explain ventricular wall thickening.
Q2
A patient’s skeletal muscle mass decreases after prolonged bed rest. Which mechanism is most
likely responsible?
A) Increased protein synthesis exceeding protein breakdown B) Increased cell number in
response to reduced activity C) Conversion of muscle fibers into adipocytes D) Reduced protein
synthesis and increased breakdown associated with disuse
, 3|Page
Rationale: D is correct because disuse shifts muscle protein balance toward loss. A would
preserve or increase muscle mass. B describes hyperplasia, which does not explain the typical
reduction in muscle size. C is not the primary mechanism of disuse atrophy.
Q3
A biopsy from a chronically irritated airway shows replacement of ciliated columnar epithelium
with stratified squamous epithelium. What is the principal consequence?
A) Metaplasia may improve resistance to irritation but impair mucociliary clearance B) The
tissue has necessarily become invasive carcinoma C) All epithelial cells have undergone
coagulative necrosis D) The airway has developed hypertrophy of individual ciliated cells only
Rationale: A is correct because metaplasia changes one mature cell type into another and may
compromise normal function. B is incorrect because metaplasia is not itself cancer, although
persistent injury can increase risk. C describes cell death, not adaptation. D describes increased
cell size and does not explain the cell-type replacement.
Q4
A patient experiences prolonged intestinal ischemia. Cells develop swelling, membrane damage,
and leakage of intracellular enzymes. Which process is most likely?
A) Physiological hyperplasia B) Reversible adaptation without injury C) Irreversible cell injury
progressing toward necrosis D) Normal differentiation into specialized cells
Rationale: C is correct because severe ischemia depletes ATP and disrupts membrane integrity,
leading to cell death. A and D are growth or differentiation processes, not destructive injury. B is
inconsistent with substantial membrane damage and enzyme leakage.
Q5
A tissue sample shows cell shrinkage, chromatin condensation, and membrane-bound fragments
with minimal inflammation. Which process is occurring?
A) Liquefactive necrosis B) Coagulative necrosis C) Apoptosis D) Fat necrosis
Rationale: C is correct because apoptosis is regulated cell death with cell shrinkage and apoptotic
bodies. A involves enzymatic digestion and liquefaction. B is commonly associated with
ischemic injury in solid organs. D involves destruction of adipose tissue.
Q6
A patient sustains an ischemic stroke, and the affected brain tissue undergoes enzymatic
digestion. Which necrosis pattern is expected?
