PATHOPHYSIOLOGY · OBJECTIVE ASSESSMENT A+ VERIFIED
NSG 3280 Exams 1–4 Pathophysiology
Tested Questions (2026/2027) PDF
Nursing | Galen College — Complete
Official Exam
A+ Verified Questions Full Rationales Verified Answers
A+ 5 100%
QUESTIONS SECTIONS RATIONALES
Complete coverage Core exam domains Every answer explained
WHAT THIS COVERS
01 Cellular Injury, Inflammation & Genetics
02 Fluid, Electrolyte & Acid-Base Balance
03 Immunity, Inflammation & Hypersensitivity
04 Cardiovascular & Hematologic Pathophysiology
05 Respiratory, Renal & Endocrine Disorders
ABOUT THIS ASSESSMENT
Build mastery in pathophysiology — from cellular injury, inflammation, and genetics to fluid and electrolyte imbalances, immune
responses, and disorders of all major body systems. This assessment targets application and analysis skills required for the NSG 3280
exams, with full rationales for every answer. Content aligns with core domains tested across Exams 1 through 4 at the advanced
upper-division nursing level.
PASSING SCORE LEVEL FORMAT
80% Advanced (Upper-Division Nursing) Application / Analysis
STUVIA ACTUAL EXAM Page 1
,SECTION 1: Cellular Injury, Inflammation & Genetics
Q1. A 68-year-old patient with long-standing hypertension develops progressive left ventricular hypertrophy. The nurse recognizes
that the cardiac myocytes have adapted through which cellular process to reduce wall stress?
A. Hypertrophy of cardiac myocytes
B. Atrophy of myocardial fibers
C. Hyperplasia of the ventricular wall
D. Metaplasia of endocardial tissue
Correct Answer: A
Rationale:
Sustained pressure overload causes individual cardiac myocytes to enlarge (hypertrophy), increasing contractile force and normalizing wall tension
according to Laplace’s law. Atrophy would decrease size, hyperplasia is limited in adult cardiac muscle, and metaplasia is not the primary adaptation
in this setting.
Q2. During a myocardial infarction, a region of myocardium becomes irreversibly injured. Which microscopic finding best indicates
that the cells have progressed beyond reversible injury?
A. Cellular swelling and fatty change
B. Nuclear pyknosis, karyorrhexis, and karyolysis
C. Membrane blebbing with loss of microvilli
D. Dilated endoplasmic reticulum
Correct Answer: B
Rationale:
Nuclear changes—pyknosis, karyorrhexis, and karyolysis—are hallmarks of irreversible cell death (necrosis). Cellular swelling, fatty change,
membrane blebbing, and ER dilation can occur in reversible injury and may resolve if perfusion is restored promptly.
Q3. A patient receives a chemotherapy agent known to generate free radicals. Which cellular structure is most vulnerable to
free-radical–mediated lipid peroxidation?
A. Mitochondrial DNA
B. Nuclear histone proteins
C. Plasma membrane phospholipids
D. Ribosomal RNA
Correct Answer: C
Rationale:
Free radicals preferentially attack polyunsaturated fatty acids in membrane phospholipids, initiating lipid peroxidation that damages membrane
integrity. Although DNA and proteins can also be injured, lipid peroxidation of the plasma membrane is the classic and earliest membrane lesion.
Q4. A pathologist examining tissue from a healing surgical wound notes the presence of granulation tissue. Which combination of
cells and matrix is most characteristic of this stage of healing?
A. Dense collagen bundles and few vessels
B. Mature scar with parallel collagen fibers
C. Predominant neutrophils and fibrin
D. Proliferating fibroblasts, new capillaries, and loose extracellular matrix
Correct Answer: D
Rationale:
Granulation tissue is defined by proliferating fibroblasts, newly formed capillaries (angiogenesis), and a loose provisional extracellular matrix. Dense
collagen characterizes later remodeling; neutrophils dominate acute inflammation; mature scar shows organized collagen with reduced vascularity.
Q5. A newborn is diagnosed with a lysosomal storage disease caused by deficiency of an enzyme that degrades sphingolipids.
Accumulation of undegraded substrate within lysosomes is an example of which cellular mechanism of injury?
A. Accumulation of endogenous material
B. Defect in membrane permeability
C. ATP depletion
D. Free-radical damage
Correct Answer: A
Rationale:
Lysosomal storage disorders result in progressive accumulation of the undegraded endogenous substrate inside lysosomes, leading to cellular
dysfunction. This is distinct from ATP depletion, primary membrane defects, or free-radical injury.
STUVIA ACTUAL EXAM · Page 2
,Q6. A patient with severe burns develops systemic inflammatory response syndrome. Elevated circulating levels of which cytokine are
most responsible for the fever, acute-phase response, and induction of adhesion molecules on endothelium?
A. Interleukin-10
B. Tumor necrosis factor-alpha and interleukin-1
C. Transforming growth factor-beta
D. Interleukin-4
Correct Answer: B
Rationale:
TNF-α and IL-1 are the principal pro-inflammatory cytokines that mediate fever, hepatic acute-phase protein synthesis, and endothelial activation with
up-regulation of adhesion molecules. IL-10 and TGF-β are largely anti-inflammatory; IL-4 promotes Th2 responses.
Q7. In a patient with chronic venous stasis ulcers, histologic examination of the ulcer base shows persistent inflammation and
incomplete re-epithelialization. Which factor most strongly impairs healing in this setting?
A. Excessive angiogenesis
B. Overproduction of growth factors
C. Local tissue hypoxia and bacterial colonization
D. Premature collagen remodeling
Correct Answer: C
Rationale:
Chronic venous ulcers are characterized by local hypoxia from impaired perfusion and frequent bacterial colonization, both of which prolong
inflammation and prevent orderly progression to proliferation and remodeling. Excess angiogenesis or growth factors are not the primary impediments.
Q8. A 45-year-old woman is found to have a BRCA1 germline mutation. Which molecular consequence of this mutation most directly
increases her lifetime risk of breast and ovarian cancer?
A. Constitutive activation of a tyrosine kinase receptor
B. Loss of a cell-cycle checkpoint kinase
C. Overexpression of an anti-apoptotic protein
D. Impaired DNA double-strand break repair by homologous recombination
Correct Answer: D
Rationale:
BRCA1 is essential for homologous recombination repair of double-strand DNA breaks. Loss of this function leads to genomic instability and markedly
elevated cancer risk. The other options describe different oncogenic mechanisms (e.g., HER2, BCL2, or ATM/CHK2 pathways).
Q9. During the acute inflammatory response, neutrophils migrate from the bloodstream into tissue. Which sequence of events
correctly describes the process of extravasation?
A. Rolling → firm adhesion → diapedesis → chemotaxis
B. Diapedesis → rolling → firm adhesion → chemotaxis
C. Chemotaxis → rolling → diapedesis → firm adhesion
D. Firm adhesion → rolling → chemotaxis → diapedesis
Correct Answer: A
Rationale:
Leukocyte extravasation proceeds through sequential steps: selectin-mediated rolling, integrin-mediated firm adhesion, transmigration (diapedesis)
across the endothelium, and directed migration (chemotaxis) along a chemokine gradient toward the site of injury.
Q10. A patient develops a sterile abscess after intramuscular injection of an irritating medication. The dominant cell type within the
abscess cavity is the neutrophil. Which chemical mediator is most responsible for the sustained recruitment of these cells?
A. Histamine
B. Leukotriene B4 and C5a
C. Nitric oxide
D. Prostaglandin E2
Correct Answer: B
Rationale:
Leukotriene B4 and complement fragment C5a are potent neutrophil chemoattractants that maintain the influx of neutrophils into an abscess.
Histamine primarily increases vascular permeability; NO is a vasodilator; PGE2 mediates pain and fever.
STUVIA ACTUAL EXAM · Page 3
, Q11. A biopsy of a healing fracture callus at three weeks shows woven bone and cartilage. Which cellular process is primarily
responsible for the eventual conversion of this provisional matrix into mature lamellar bone?
A. Apoptosis of osteoblasts
B. Metaplasia of chondrocytes into osteocytes
C. Remodeling by osteoclasts and osteoblasts under mechanical stress
D. Hyperplasia of periosteal fibroblasts
Correct Answer: C
Rationale:
Bone remodeling involves coordinated osteoclastic resorption of woven bone and osteoblastic deposition of organized lamellar bone, guided by
mechanical loading (Wolff’s law). Chondrocytes do not simply metaplastically convert; apoptosis and fibroblast hyperplasia are not the dominant
mechanisms of maturation.
Q12. A researcher is studying cells undergoing apoptosis. Which feature distinguishes apoptotic cell death from necrotic cell death?
A. Extensive inflammation in surrounding tissue
B. Rupture of the plasma membrane with release of contents
C. Marked cellular swelling and organelle breakdown
D. Formation of apoptotic bodies that are phagocytosed without inflammation
Correct Answer: D
Rationale:
Apoptosis produces membrane-bound apoptotic bodies that are rapidly cleared by phagocytes without eliciting inflammation. Necrosis is characterized
by membrane rupture, content release, and secondary inflammation, often preceded by cellular swelling.
Q13. A patient with α1-antitrypsin deficiency develops early-onset emphysema. The pathophysiologic mechanism involves unchecked
proteolytic activity against which pulmonary structure?
A. Alveolar septal elastic fibers
B. Type II pneumocyte surfactant production
C. Bronchial cartilage rings
D. Pulmonary capillary endothelium
Correct Answer: A
Rationale:
α1-Antitrypsin normally inhibits neutrophil elastase. Its deficiency allows elastase to degrade alveolar septal elastic fibers, leading to loss of elastic
recoil and emphysema. Surfactant, cartilage, and endothelium are not the primary targets of this protease imbalance.
Q14. After a period of ischemia, reperfusion of tissue paradoxically worsens injury. Which mechanism contributes most to reperfusion
injury?
A. Immediate restoration of ATP stores
B. Generation of reactive oxygen species and neutrophil influx
C. Rapid clearance of inflammatory mediators
D. Inhibition of the complement cascade
Correct Answer: B
Rationale:
Reperfusion delivers oxygen that fuels formation of reactive oxygen species and also allows neutrophils to enter the previously ischemic tissue,
amplifying damage. ATP restoration is beneficial; clearance of mediators and complement inhibition would be protective, not injurious.
Q15. A 32-year-old woman has a first-degree relative with familial adenomatous polyposis. Genetic testing reveals a germline
mutation in the APC gene. Which cellular pathway is most directly disrupted by loss of APC function?
A. Receptor tyrosine kinase signaling
B. DNA mismatch repair
C. Wnt/β-catenin signaling leading to uncontrolled proliferation
D. p53-mediated apoptosis
Correct Answer: C
Rationale:
APC is a negative regulator of the Wnt pathway; its loss allows β-catenin to accumulate and drive transcription of proliferative genes. This is distinct
from RTK signaling, mismatch repair (Lynch syndrome), or p53 pathways.
STUVIA ACTUAL EXAM · Page 4
NSG 3280 Exams 1–4 Pathophysiology
Tested Questions (2026/2027) PDF
Nursing | Galen College — Complete
Official Exam
A+ Verified Questions Full Rationales Verified Answers
A+ 5 100%
QUESTIONS SECTIONS RATIONALES
Complete coverage Core exam domains Every answer explained
WHAT THIS COVERS
01 Cellular Injury, Inflammation & Genetics
02 Fluid, Electrolyte & Acid-Base Balance
03 Immunity, Inflammation & Hypersensitivity
04 Cardiovascular & Hematologic Pathophysiology
05 Respiratory, Renal & Endocrine Disorders
ABOUT THIS ASSESSMENT
Build mastery in pathophysiology — from cellular injury, inflammation, and genetics to fluid and electrolyte imbalances, immune
responses, and disorders of all major body systems. This assessment targets application and analysis skills required for the NSG 3280
exams, with full rationales for every answer. Content aligns with core domains tested across Exams 1 through 4 at the advanced
upper-division nursing level.
PASSING SCORE LEVEL FORMAT
80% Advanced (Upper-Division Nursing) Application / Analysis
STUVIA ACTUAL EXAM Page 1
,SECTION 1: Cellular Injury, Inflammation & Genetics
Q1. A 68-year-old patient with long-standing hypertension develops progressive left ventricular hypertrophy. The nurse recognizes
that the cardiac myocytes have adapted through which cellular process to reduce wall stress?
A. Hypertrophy of cardiac myocytes
B. Atrophy of myocardial fibers
C. Hyperplasia of the ventricular wall
D. Metaplasia of endocardial tissue
Correct Answer: A
Rationale:
Sustained pressure overload causes individual cardiac myocytes to enlarge (hypertrophy), increasing contractile force and normalizing wall tension
according to Laplace’s law. Atrophy would decrease size, hyperplasia is limited in adult cardiac muscle, and metaplasia is not the primary adaptation
in this setting.
Q2. During a myocardial infarction, a region of myocardium becomes irreversibly injured. Which microscopic finding best indicates
that the cells have progressed beyond reversible injury?
A. Cellular swelling and fatty change
B. Nuclear pyknosis, karyorrhexis, and karyolysis
C. Membrane blebbing with loss of microvilli
D. Dilated endoplasmic reticulum
Correct Answer: B
Rationale:
Nuclear changes—pyknosis, karyorrhexis, and karyolysis—are hallmarks of irreversible cell death (necrosis). Cellular swelling, fatty change,
membrane blebbing, and ER dilation can occur in reversible injury and may resolve if perfusion is restored promptly.
Q3. A patient receives a chemotherapy agent known to generate free radicals. Which cellular structure is most vulnerable to
free-radical–mediated lipid peroxidation?
A. Mitochondrial DNA
B. Nuclear histone proteins
C. Plasma membrane phospholipids
D. Ribosomal RNA
Correct Answer: C
Rationale:
Free radicals preferentially attack polyunsaturated fatty acids in membrane phospholipids, initiating lipid peroxidation that damages membrane
integrity. Although DNA and proteins can also be injured, lipid peroxidation of the plasma membrane is the classic and earliest membrane lesion.
Q4. A pathologist examining tissue from a healing surgical wound notes the presence of granulation tissue. Which combination of
cells and matrix is most characteristic of this stage of healing?
A. Dense collagen bundles and few vessels
B. Mature scar with parallel collagen fibers
C. Predominant neutrophils and fibrin
D. Proliferating fibroblasts, new capillaries, and loose extracellular matrix
Correct Answer: D
Rationale:
Granulation tissue is defined by proliferating fibroblasts, newly formed capillaries (angiogenesis), and a loose provisional extracellular matrix. Dense
collagen characterizes later remodeling; neutrophils dominate acute inflammation; mature scar shows organized collagen with reduced vascularity.
Q5. A newborn is diagnosed with a lysosomal storage disease caused by deficiency of an enzyme that degrades sphingolipids.
Accumulation of undegraded substrate within lysosomes is an example of which cellular mechanism of injury?
A. Accumulation of endogenous material
B. Defect in membrane permeability
C. ATP depletion
D. Free-radical damage
Correct Answer: A
Rationale:
Lysosomal storage disorders result in progressive accumulation of the undegraded endogenous substrate inside lysosomes, leading to cellular
dysfunction. This is distinct from ATP depletion, primary membrane defects, or free-radical injury.
STUVIA ACTUAL EXAM · Page 2
,Q6. A patient with severe burns develops systemic inflammatory response syndrome. Elevated circulating levels of which cytokine are
most responsible for the fever, acute-phase response, and induction of adhesion molecules on endothelium?
A. Interleukin-10
B. Tumor necrosis factor-alpha and interleukin-1
C. Transforming growth factor-beta
D. Interleukin-4
Correct Answer: B
Rationale:
TNF-α and IL-1 are the principal pro-inflammatory cytokines that mediate fever, hepatic acute-phase protein synthesis, and endothelial activation with
up-regulation of adhesion molecules. IL-10 and TGF-β are largely anti-inflammatory; IL-4 promotes Th2 responses.
Q7. In a patient with chronic venous stasis ulcers, histologic examination of the ulcer base shows persistent inflammation and
incomplete re-epithelialization. Which factor most strongly impairs healing in this setting?
A. Excessive angiogenesis
B. Overproduction of growth factors
C. Local tissue hypoxia and bacterial colonization
D. Premature collagen remodeling
Correct Answer: C
Rationale:
Chronic venous ulcers are characterized by local hypoxia from impaired perfusion and frequent bacterial colonization, both of which prolong
inflammation and prevent orderly progression to proliferation and remodeling. Excess angiogenesis or growth factors are not the primary impediments.
Q8. A 45-year-old woman is found to have a BRCA1 germline mutation. Which molecular consequence of this mutation most directly
increases her lifetime risk of breast and ovarian cancer?
A. Constitutive activation of a tyrosine kinase receptor
B. Loss of a cell-cycle checkpoint kinase
C. Overexpression of an anti-apoptotic protein
D. Impaired DNA double-strand break repair by homologous recombination
Correct Answer: D
Rationale:
BRCA1 is essential for homologous recombination repair of double-strand DNA breaks. Loss of this function leads to genomic instability and markedly
elevated cancer risk. The other options describe different oncogenic mechanisms (e.g., HER2, BCL2, or ATM/CHK2 pathways).
Q9. During the acute inflammatory response, neutrophils migrate from the bloodstream into tissue. Which sequence of events
correctly describes the process of extravasation?
A. Rolling → firm adhesion → diapedesis → chemotaxis
B. Diapedesis → rolling → firm adhesion → chemotaxis
C. Chemotaxis → rolling → diapedesis → firm adhesion
D. Firm adhesion → rolling → chemotaxis → diapedesis
Correct Answer: A
Rationale:
Leukocyte extravasation proceeds through sequential steps: selectin-mediated rolling, integrin-mediated firm adhesion, transmigration (diapedesis)
across the endothelium, and directed migration (chemotaxis) along a chemokine gradient toward the site of injury.
Q10. A patient develops a sterile abscess after intramuscular injection of an irritating medication. The dominant cell type within the
abscess cavity is the neutrophil. Which chemical mediator is most responsible for the sustained recruitment of these cells?
A. Histamine
B. Leukotriene B4 and C5a
C. Nitric oxide
D. Prostaglandin E2
Correct Answer: B
Rationale:
Leukotriene B4 and complement fragment C5a are potent neutrophil chemoattractants that maintain the influx of neutrophils into an abscess.
Histamine primarily increases vascular permeability; NO is a vasodilator; PGE2 mediates pain and fever.
STUVIA ACTUAL EXAM · Page 3
, Q11. A biopsy of a healing fracture callus at three weeks shows woven bone and cartilage. Which cellular process is primarily
responsible for the eventual conversion of this provisional matrix into mature lamellar bone?
A. Apoptosis of osteoblasts
B. Metaplasia of chondrocytes into osteocytes
C. Remodeling by osteoclasts and osteoblasts under mechanical stress
D. Hyperplasia of periosteal fibroblasts
Correct Answer: C
Rationale:
Bone remodeling involves coordinated osteoclastic resorption of woven bone and osteoblastic deposition of organized lamellar bone, guided by
mechanical loading (Wolff’s law). Chondrocytes do not simply metaplastically convert; apoptosis and fibroblast hyperplasia are not the dominant
mechanisms of maturation.
Q12. A researcher is studying cells undergoing apoptosis. Which feature distinguishes apoptotic cell death from necrotic cell death?
A. Extensive inflammation in surrounding tissue
B. Rupture of the plasma membrane with release of contents
C. Marked cellular swelling and organelle breakdown
D. Formation of apoptotic bodies that are phagocytosed without inflammation
Correct Answer: D
Rationale:
Apoptosis produces membrane-bound apoptotic bodies that are rapidly cleared by phagocytes without eliciting inflammation. Necrosis is characterized
by membrane rupture, content release, and secondary inflammation, often preceded by cellular swelling.
Q13. A patient with α1-antitrypsin deficiency develops early-onset emphysema. The pathophysiologic mechanism involves unchecked
proteolytic activity against which pulmonary structure?
A. Alveolar septal elastic fibers
B. Type II pneumocyte surfactant production
C. Bronchial cartilage rings
D. Pulmonary capillary endothelium
Correct Answer: A
Rationale:
α1-Antitrypsin normally inhibits neutrophil elastase. Its deficiency allows elastase to degrade alveolar septal elastic fibers, leading to loss of elastic
recoil and emphysema. Surfactant, cartilage, and endothelium are not the primary targets of this protease imbalance.
Q14. After a period of ischemia, reperfusion of tissue paradoxically worsens injury. Which mechanism contributes most to reperfusion
injury?
A. Immediate restoration of ATP stores
B. Generation of reactive oxygen species and neutrophil influx
C. Rapid clearance of inflammatory mediators
D. Inhibition of the complement cascade
Correct Answer: B
Rationale:
Reperfusion delivers oxygen that fuels formation of reactive oxygen species and also allows neutrophils to enter the previously ischemic tissue,
amplifying damage. ATP restoration is beneficial; clearance of mediators and complement inhibition would be protective, not injurious.
Q15. A 32-year-old woman has a first-degree relative with familial adenomatous polyposis. Genetic testing reveals a germline
mutation in the APC gene. Which cellular pathway is most directly disrupted by loss of APC function?
A. Receptor tyrosine kinase signaling
B. DNA mismatch repair
C. Wnt/β-catenin signaling leading to uncontrolled proliferation
D. p53-mediated apoptosis
Correct Answer: C
Rationale:
APC is a negative regulator of the Wnt pathway; its loss allows β-catenin to accumulate and drive transcription of proliferative genes. This is distinct
from RTK signaling, mismatch repair (Lynch syndrome), or p53 pathways.
STUVIA ACTUAL EXAM · Page 4
