NURSING EXAM PREP
NSG 3280 EXAM 2
PATHOPHYSIOLOGY FOR NURSES I REVIEW
2026/2027 ACTUAL EXAM TEST BANK
WITH REAL EXAM QUESTIONS AND A+
100% CORRECT VERIFIED ANSWERS
(GUARANTEED PASS!!)
Aligned to Galen College NSG 3280 Pathophysiology for Nurses I Objectives • Intermediate Nursing Course Level
A+ QUESTIONS 5 SECTIONS 100%
VERIFIED COMPLETE RATIONALES
CATEGORIES
Cellular Adaptation, Injury & Inflammation
Cardiovascular Pathophysiology
Respiratory & Renal Pathophysiology
Endocrine & Neurological Pathophysiology
Gastrointestinal, Hematologic & Multisystem Disorders
STUVIAACTUALEXAM
,NSG 3280 Exam 2 | Pathophysiology for Nurses I | 2026/2027 Page 2
SECTION 1: Cellular Adaptation, Injury & Inflammation
Q1. A 68-year-old man with longstanding hypertension undergoes echocardiography that reveals left-ventricular
wall thickening without chamber dilation. The nurse recognizes this change as a compensatory response to
chronic pressure overload. Which cellular adaptation best explains the observed myocardial change?
A. Hypertrophy of cardiac myocytes
B. Hyperplasia of cardiac myocytes
C. Metaplasia of myocardial tissue
D. Atrophy of the left ventricular wall
Correct Answer: A
Rationale: Chronic pressure overload stimulates existing cardiac myocytes to increase in size (hypertrophy) because adult
cardiac myocytes have limited capacity for hyperplasia. This adaptive thickening helps maintain stroke volume against
elevated afterload.
Q2. A patient with chronic gastroesophageal reflux develops replacement of stratified squamous epithelium by
columnar epithelium in the distal esophagus. The nurse identifies this tissue change as a known risk factor for
adenocarcinoma. Which adaptive process has occurred?
A. Dysplasia of squamous cells
B. Metaplasia of the esophageal epithelium
C. Hyperplasia of the esophageal mucosa
D. Hypertrophy of esophageal smooth muscle
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another better suited to a chronic
stressor. In Barrett esophagus, squamous epithelium is replaced by columnar epithelium in response to acid exposure.
Q3. After a myocardial infarction, laboratory results show elevated serum troponin and creatine kinase-MB.
Histologic examination of the infarcted zone later reveals loss of nuclei, eosinophilic cytoplasm, and infiltration by
neutrophils. Which form of cell death is primarily responsible for the tissue damage?
A. Apoptosis of myocytes with intact membranes
B. Liquefactive necrosis from bacterial invasion
C. Coagulative necrosis secondary to ischemia
D. Caseous necrosis typical of granulomatous disease
Correct Answer: C
Rationale: Ischemic injury to solid organs such as the heart produces coagulative necrosis, characterized by protein
denaturation, preservation of tissue architecture for days, and subsequent neutrophilic infiltration. Elevated cardiac enzymes
reflect membrane rupture of necrotic myocytes.
STUVIAACTUALEXAM
, NSG 3280 Exam 2 | Pathophysiology for Nurses I | 2026/2027 Page 3
Q4. A 45-year-old woman develops acute pain, redness, and swelling at the site of a surgical incision three days
postoperatively. The nurse notes local heat and a small amount of purulent drainage. Which sequence of vascular
and cellular events best characterizes this acute inflammatory response?
A. Lymphocyte-dominated infiltration with granuloma formation
B. Delayed hypersensitivity with eosinophil predominance
C. Complement-independent mast-cell degranulation only
D. Immediate vasoconstriction followed by prolonged vasodilation and neutrophil margination
Correct Answer: D
Rationale: Acute inflammation begins with transient vasoconstriction, then sustained vasodilation and increased permeability
that produce the classic signs of redness and swelling. Neutrophils marginate, emigrate, and predominate in the first 24–48
hours.
Q5. A patient receives a second dose of intravenous penicillin and within minutes develops urticaria,
bronchospasm, and hypotension. The nurse recognizes a type I hypersensitivity reaction. Which immunologic
mechanism is primarily responsible?
A. IgE-mediated mast-cell degranulation and histamine release
B. IgG-mediated cytotoxicity against penicillin-coated cells
C. Immune-complex deposition in vessel walls
D. T-cell-mediated delayed cytotoxicity
Correct Answer: A
Rationale: Type I (immediate) hypersensitivity is driven by antigen cross-linking of IgE bound to Fcε receptors on mast cells
and basophils, triggering rapid release of histamine and other mediators that produce the observed anaphylactic features.
Q6. A laboratory report for a patient with systemic lupus erythematosus shows high titers of antinuclear antibodies
and low serum complement levels. The nurse understands that tissue injury in this disease is produced mainly by
which hypersensitivity mechanism?
A. Type I IgE-mediated mast-cell activation
B. Type III immune-complex deposition and complement activation
C. Type II antibody-dependent cellular cytotoxicity
D. Type IV delayed T-cell-mediated inflammation
Correct Answer: B
Rationale: SLE is a classic type III hypersensitivity disorder in which circulating immune complexes deposit in tissues,
activate complement, and generate inflammation. Hypocomplementemia reflects consumption of complement components
during this process.
Q7. A patient with advanced HIV infection presents with a CD4 count of 80 cells/µL and oral thrush. The nurse
attributes the opportunistic infection to which primary immune defect?
A. Defective neutrophil chemotaxis
B. Absence of circulating B lymphocytes
C. Profound depletion of CD4+ T-helper lymphocytes
D. Excessive production of IgE
Correct Answer: C
Rationale: HIV preferentially infects and destroys CD4+ T-helper cells. When the count falls below approximately 200
cells/µL, cell-mediated immunity is severely compromised, allowing opportunistic infections such as oral candidiasis.
STUVIAACTUALEXAM
NSG 3280 EXAM 2
PATHOPHYSIOLOGY FOR NURSES I REVIEW
2026/2027 ACTUAL EXAM TEST BANK
WITH REAL EXAM QUESTIONS AND A+
100% CORRECT VERIFIED ANSWERS
(GUARANTEED PASS!!)
Aligned to Galen College NSG 3280 Pathophysiology for Nurses I Objectives • Intermediate Nursing Course Level
A+ QUESTIONS 5 SECTIONS 100%
VERIFIED COMPLETE RATIONALES
CATEGORIES
Cellular Adaptation, Injury & Inflammation
Cardiovascular Pathophysiology
Respiratory & Renal Pathophysiology
Endocrine & Neurological Pathophysiology
Gastrointestinal, Hematologic & Multisystem Disorders
STUVIAACTUALEXAM
,NSG 3280 Exam 2 | Pathophysiology for Nurses I | 2026/2027 Page 2
SECTION 1: Cellular Adaptation, Injury & Inflammation
Q1. A 68-year-old man with longstanding hypertension undergoes echocardiography that reveals left-ventricular
wall thickening without chamber dilation. The nurse recognizes this change as a compensatory response to
chronic pressure overload. Which cellular adaptation best explains the observed myocardial change?
A. Hypertrophy of cardiac myocytes
B. Hyperplasia of cardiac myocytes
C. Metaplasia of myocardial tissue
D. Atrophy of the left ventricular wall
Correct Answer: A
Rationale: Chronic pressure overload stimulates existing cardiac myocytes to increase in size (hypertrophy) because adult
cardiac myocytes have limited capacity for hyperplasia. This adaptive thickening helps maintain stroke volume against
elevated afterload.
Q2. A patient with chronic gastroesophageal reflux develops replacement of stratified squamous epithelium by
columnar epithelium in the distal esophagus. The nurse identifies this tissue change as a known risk factor for
adenocarcinoma. Which adaptive process has occurred?
A. Dysplasia of squamous cells
B. Metaplasia of the esophageal epithelium
C. Hyperplasia of the esophageal mucosa
D. Hypertrophy of esophageal smooth muscle
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another better suited to a chronic
stressor. In Barrett esophagus, squamous epithelium is replaced by columnar epithelium in response to acid exposure.
Q3. After a myocardial infarction, laboratory results show elevated serum troponin and creatine kinase-MB.
Histologic examination of the infarcted zone later reveals loss of nuclei, eosinophilic cytoplasm, and infiltration by
neutrophils. Which form of cell death is primarily responsible for the tissue damage?
A. Apoptosis of myocytes with intact membranes
B. Liquefactive necrosis from bacterial invasion
C. Coagulative necrosis secondary to ischemia
D. Caseous necrosis typical of granulomatous disease
Correct Answer: C
Rationale: Ischemic injury to solid organs such as the heart produces coagulative necrosis, characterized by protein
denaturation, preservation of tissue architecture for days, and subsequent neutrophilic infiltration. Elevated cardiac enzymes
reflect membrane rupture of necrotic myocytes.
STUVIAACTUALEXAM
, NSG 3280 Exam 2 | Pathophysiology for Nurses I | 2026/2027 Page 3
Q4. A 45-year-old woman develops acute pain, redness, and swelling at the site of a surgical incision three days
postoperatively. The nurse notes local heat and a small amount of purulent drainage. Which sequence of vascular
and cellular events best characterizes this acute inflammatory response?
A. Lymphocyte-dominated infiltration with granuloma formation
B. Delayed hypersensitivity with eosinophil predominance
C. Complement-independent mast-cell degranulation only
D. Immediate vasoconstriction followed by prolonged vasodilation and neutrophil margination
Correct Answer: D
Rationale: Acute inflammation begins with transient vasoconstriction, then sustained vasodilation and increased permeability
that produce the classic signs of redness and swelling. Neutrophils marginate, emigrate, and predominate in the first 24–48
hours.
Q5. A patient receives a second dose of intravenous penicillin and within minutes develops urticaria,
bronchospasm, and hypotension. The nurse recognizes a type I hypersensitivity reaction. Which immunologic
mechanism is primarily responsible?
A. IgE-mediated mast-cell degranulation and histamine release
B. IgG-mediated cytotoxicity against penicillin-coated cells
C. Immune-complex deposition in vessel walls
D. T-cell-mediated delayed cytotoxicity
Correct Answer: A
Rationale: Type I (immediate) hypersensitivity is driven by antigen cross-linking of IgE bound to Fcε receptors on mast cells
and basophils, triggering rapid release of histamine and other mediators that produce the observed anaphylactic features.
Q6. A laboratory report for a patient with systemic lupus erythematosus shows high titers of antinuclear antibodies
and low serum complement levels. The nurse understands that tissue injury in this disease is produced mainly by
which hypersensitivity mechanism?
A. Type I IgE-mediated mast-cell activation
B. Type III immune-complex deposition and complement activation
C. Type II antibody-dependent cellular cytotoxicity
D. Type IV delayed T-cell-mediated inflammation
Correct Answer: B
Rationale: SLE is a classic type III hypersensitivity disorder in which circulating immune complexes deposit in tissues,
activate complement, and generate inflammation. Hypocomplementemia reflects consumption of complement components
during this process.
Q7. A patient with advanced HIV infection presents with a CD4 count of 80 cells/µL and oral thrush. The nurse
attributes the opportunistic infection to which primary immune defect?
A. Defective neutrophil chemotaxis
B. Absence of circulating B lymphocytes
C. Profound depletion of CD4+ T-helper lymphocytes
D. Excessive production of IgE
Correct Answer: C
Rationale: HIV preferentially infects and destroys CD4+ T-helper cells. When the count falls below approximately 200
cells/µL, cell-mediated immunity is severely compromised, allowing opportunistic infections such as oral candidiasis.
STUVIAACTUALEXAM
