NUR 634 Final Exam Actual Exam QUESTIONS
AND ANSWERS 2026 | Advanced
Pathophysiology | Complete Q&A Graded A+ |
Pass Guaranteed - A+ Graded
SECTION 1: CELLULAR ADAPTATION, INJURY, AND INFLAMMATION
Questions 1-10
Question 1 A 58-year-old male smoker presents with a persistent cough. A lung biopsy reveals
replacement of normal ciliated columnar epithelium with stratified squamous epithelium. This
cellular adaptation is best described as:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is a reversible change in which one mature, differentiated cell type is
replaced by another mature cell type, typically as an adaptive response to chronic irritation or
stress. In smokers, chronic exposure to irritants causes ciliated pseudostratified columnar
epithelium to transform to stratified squamous epithelium (squamous metaplasia). This
represents a protective adaptation—squamous epithelium is more resistant to irritants but loses
mucociliary clearance function. Importantly, metaplasia is reversible if irritant is removed,
though it can progress to dysplasia.
Why distractors are incorrect:
• A (Dysplasia): Disordered growth with loss of uniformity and architectural orientation;
cells show pleomorphism, hyperchromatism, and loss of polarity. This is pre-neoplastic,
not a benign adaptive change.
• C (Hyperplasia): Increase in cell number (proliferation) causing tissue enlargement, not
change in cell type. Would show more ciliated columnar cells, not squamous
transformation.
, • D (Anaplasia): Loss of differentiation and orientation characteristic of malignant
neoplasms; cells appear primitive/undifferentiated with nuclear pleomorphism and high
nuclear-to-cytoplasmic ratio.
Question 2 A patient with prolonged hypotension develops acute tubular necrosis. The primary
mechanism of cellular injury is:
A. Chemical injury
B. Hypoxic injury [CORRECT]
C. Infectious injury
D. Immunologic injury
Correct Answer: B
Rationale: Prolonged hypotension causes decreased renal perfusion, leading to
ischemic/hypoxic injury of renal tubular epithelial cells. The sequence involves: (1) Decreased
oxygen delivery → switch to anaerobic glycolysis; (2) ATP depletion → failure of Na⁺/K⁺-
ATPase pump; (3) Cellular swelling (hydropic change) due to water influx following sodium
influx; (4) Calcium influx activating phospholipases and proteases; (5) Reactive oxygen species
generation upon reperfusion; (6) Membrane damage and cell death. The proximal tubule (S3
segment) and thick ascending limb are particularly vulnerable due to high metabolic demand.
Why distractors are incorrect:
• A (Chemical injury): Would require nephrotoxic agents (aminoglycosides, contrast dye,
heavy metals), not hemodynamic compromise.
• C (Infectious injury): Would show inflammatory infiltrates, abscess formation, or
specific pathogen-induced damage (e.g., pyelonephritis).
• D (Immunologic injury): Would involve immune complex deposition (e.g.,
glomerulonephritis) or antibody-mediated attack, not ischemic pattern.
Question 3 Which type of necrosis is characterized by preservation of tissue architecture for
several days after cell death?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
,Rationale: Coagulative necrosis results from ischemia in solid organs (heart, kidney, spleen,
liver) and is characterized by denaturation of structural proteins and enzymes, leading to "ghost"
outlines of cells without nuclei. The tissue architecture is preserved for days because lysosomal
enzymes are denatured and cannot digest the tissue. Ultimately, inflammatory cells infiltrate and
remove debris. Grossly appears pale, firm, and dry. Microscopically shows eosinophilic
cytoplasm without nuclei.
Why distractors are incorrect:
• A (Liquefactive necrosis): Enzymatic digestion dominates, creating soft, liquefied tissue
(abscess in bacterial infections) or cystic cavities (brain infarcts). Architecture completely
lost.
• C (Caseous necrosis): Combination of coagulative and liquefactive; cheesy, friable
material with amorphous granular debris and no architecture preservation (characteristic
of TB).
• D (Fat necrosis): Lipase action on triglycerides creates fatty acids that combine with
calcium (saponification), forming chalky white deposits; occurs in breast or pancreas.
Question 4 A patient with rheumatoid arthritis has autoantibodies against which self-antigen?
A. Acetylcholine receptors
B. IgG Fc portion (rheumatoid factor) and citrullinated peptides [CORRECT]
C. Thyroid peroxidase
D. Islet cells
Correct Answer: B
Rationale: Rheumatoid arthritis is characterized by: (1) Rheumatoid factor (RF) – IgM (or
IgA/IgG) autoantibodies against Fc portion of IgG; present in 70-80% of cases; (2) Anti-
citrullinated protein antibodies (ACPAs) against citrullinated peptides (citrullination by
peptidylarginine deiminase); more specific for RA (95% specificity). These immune complexes
activate complement, recruit neutrophils, and drive synovial inflammation, pannus formation,
and joint destruction via cytokines (TNF-α, IL-1, IL-6).
Why distractors are incorrect:
• A (Acetylcholine receptors): Target in myasthenia gravis (neuromuscular junction
disorder).
• C (Thyroid peroxidase): Target in Hashimoto's thyroiditis (autoimmune
hypothyroidism).
, • D (Islet cells/GAD65): Target in Type 1 diabetes mellitus (autoimmune destruction of β-
cells).
Question 5 A patient experiences anaphylaxis after receiving penicillin. Which type of
hypersensitivity reaction is this?
A. Type I (Immediate) [CORRECT]
B. Type II (Cytotoxic)
C. Type III (Immune Complex)
D. Type IV (Delayed-Type)
Correct Answer: A
Rationale: Anaphylaxis is the classic Type I hypersensitivity reaction: (1) Sensitization phase –
penicillin (hapten) binds to carrier protein; processed by APCs to Th2 cells; B cells produce IgE
specific for penicillin; IgE binds FcεRI receptors on mast cells/basophils; (2) Effector phase – re-
exposure causes cross-linking of IgE, mast cell degranulation within minutes; release of
histamine, leukotrienes (C4, D4, E4), prostaglandin D2; causes vasodilation, increased vascular
permeability, bronchospasm, hypotension, and potentially fatal cardiovascular collapse.
Why distractors are incorrect:
• B (Type II): Antibody-mediated cytotoxicity (e.g., hemolytic anemia, Goodpasture's,
myasthenia gravis); involves IgG/IgM against cell surface or matrix antigens.
• C (Type III): Immune complex deposition causing inflammation (e.g., serum sickness,
SLE, post-streptococcal glomerulonephritis, Arthus reaction).
• D (Type IV): T-cell mediated, delayed 24-72 hours (e.g., contact dermatitis, TB skin test,
granuloma formation, type 1 diabetes, MS).
Question 6 Granulomatous inflammation is characteristic of which condition?
A. Acute appendicitis
B. Tuberculosis [CORRECT]
C. Viral hepatitis
D. Bacterial pneumonia (lobar)
Correct Answer: B
Rationale: Granulomatous inflammation is a specialized chronic inflammatory response to
persistent, poorly degradable pathogens or foreign material. Tuberculosis causes caseating
granulomas: central necrosis (caseous), surrounded by epithelioid macrophages (activated
AND ANSWERS 2026 | Advanced
Pathophysiology | Complete Q&A Graded A+ |
Pass Guaranteed - A+ Graded
SECTION 1: CELLULAR ADAPTATION, INJURY, AND INFLAMMATION
Questions 1-10
Question 1 A 58-year-old male smoker presents with a persistent cough. A lung biopsy reveals
replacement of normal ciliated columnar epithelium with stratified squamous epithelium. This
cellular adaptation is best described as:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is a reversible change in which one mature, differentiated cell type is
replaced by another mature cell type, typically as an adaptive response to chronic irritation or
stress. In smokers, chronic exposure to irritants causes ciliated pseudostratified columnar
epithelium to transform to stratified squamous epithelium (squamous metaplasia). This
represents a protective adaptation—squamous epithelium is more resistant to irritants but loses
mucociliary clearance function. Importantly, metaplasia is reversible if irritant is removed,
though it can progress to dysplasia.
Why distractors are incorrect:
• A (Dysplasia): Disordered growth with loss of uniformity and architectural orientation;
cells show pleomorphism, hyperchromatism, and loss of polarity. This is pre-neoplastic,
not a benign adaptive change.
• C (Hyperplasia): Increase in cell number (proliferation) causing tissue enlargement, not
change in cell type. Would show more ciliated columnar cells, not squamous
transformation.
, • D (Anaplasia): Loss of differentiation and orientation characteristic of malignant
neoplasms; cells appear primitive/undifferentiated with nuclear pleomorphism and high
nuclear-to-cytoplasmic ratio.
Question 2 A patient with prolonged hypotension develops acute tubular necrosis. The primary
mechanism of cellular injury is:
A. Chemical injury
B. Hypoxic injury [CORRECT]
C. Infectious injury
D. Immunologic injury
Correct Answer: B
Rationale: Prolonged hypotension causes decreased renal perfusion, leading to
ischemic/hypoxic injury of renal tubular epithelial cells. The sequence involves: (1) Decreased
oxygen delivery → switch to anaerobic glycolysis; (2) ATP depletion → failure of Na⁺/K⁺-
ATPase pump; (3) Cellular swelling (hydropic change) due to water influx following sodium
influx; (4) Calcium influx activating phospholipases and proteases; (5) Reactive oxygen species
generation upon reperfusion; (6) Membrane damage and cell death. The proximal tubule (S3
segment) and thick ascending limb are particularly vulnerable due to high metabolic demand.
Why distractors are incorrect:
• A (Chemical injury): Would require nephrotoxic agents (aminoglycosides, contrast dye,
heavy metals), not hemodynamic compromise.
• C (Infectious injury): Would show inflammatory infiltrates, abscess formation, or
specific pathogen-induced damage (e.g., pyelonephritis).
• D (Immunologic injury): Would involve immune complex deposition (e.g.,
glomerulonephritis) or antibody-mediated attack, not ischemic pattern.
Question 3 Which type of necrosis is characterized by preservation of tissue architecture for
several days after cell death?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
,Rationale: Coagulative necrosis results from ischemia in solid organs (heart, kidney, spleen,
liver) and is characterized by denaturation of structural proteins and enzymes, leading to "ghost"
outlines of cells without nuclei. The tissue architecture is preserved for days because lysosomal
enzymes are denatured and cannot digest the tissue. Ultimately, inflammatory cells infiltrate and
remove debris. Grossly appears pale, firm, and dry. Microscopically shows eosinophilic
cytoplasm without nuclei.
Why distractors are incorrect:
• A (Liquefactive necrosis): Enzymatic digestion dominates, creating soft, liquefied tissue
(abscess in bacterial infections) or cystic cavities (brain infarcts). Architecture completely
lost.
• C (Caseous necrosis): Combination of coagulative and liquefactive; cheesy, friable
material with amorphous granular debris and no architecture preservation (characteristic
of TB).
• D (Fat necrosis): Lipase action on triglycerides creates fatty acids that combine with
calcium (saponification), forming chalky white deposits; occurs in breast or pancreas.
Question 4 A patient with rheumatoid arthritis has autoantibodies against which self-antigen?
A. Acetylcholine receptors
B. IgG Fc portion (rheumatoid factor) and citrullinated peptides [CORRECT]
C. Thyroid peroxidase
D. Islet cells
Correct Answer: B
Rationale: Rheumatoid arthritis is characterized by: (1) Rheumatoid factor (RF) – IgM (or
IgA/IgG) autoantibodies against Fc portion of IgG; present in 70-80% of cases; (2) Anti-
citrullinated protein antibodies (ACPAs) against citrullinated peptides (citrullination by
peptidylarginine deiminase); more specific for RA (95% specificity). These immune complexes
activate complement, recruit neutrophils, and drive synovial inflammation, pannus formation,
and joint destruction via cytokines (TNF-α, IL-1, IL-6).
Why distractors are incorrect:
• A (Acetylcholine receptors): Target in myasthenia gravis (neuromuscular junction
disorder).
• C (Thyroid peroxidase): Target in Hashimoto's thyroiditis (autoimmune
hypothyroidism).
, • D (Islet cells/GAD65): Target in Type 1 diabetes mellitus (autoimmune destruction of β-
cells).
Question 5 A patient experiences anaphylaxis after receiving penicillin. Which type of
hypersensitivity reaction is this?
A. Type I (Immediate) [CORRECT]
B. Type II (Cytotoxic)
C. Type III (Immune Complex)
D. Type IV (Delayed-Type)
Correct Answer: A
Rationale: Anaphylaxis is the classic Type I hypersensitivity reaction: (1) Sensitization phase –
penicillin (hapten) binds to carrier protein; processed by APCs to Th2 cells; B cells produce IgE
specific for penicillin; IgE binds FcεRI receptors on mast cells/basophils; (2) Effector phase – re-
exposure causes cross-linking of IgE, mast cell degranulation within minutes; release of
histamine, leukotrienes (C4, D4, E4), prostaglandin D2; causes vasodilation, increased vascular
permeability, bronchospasm, hypotension, and potentially fatal cardiovascular collapse.
Why distractors are incorrect:
• B (Type II): Antibody-mediated cytotoxicity (e.g., hemolytic anemia, Goodpasture's,
myasthenia gravis); involves IgG/IgM against cell surface or matrix antigens.
• C (Type III): Immune complex deposition causing inflammation (e.g., serum sickness,
SLE, post-streptococcal glomerulonephritis, Arthus reaction).
• D (Type IV): T-cell mediated, delayed 24-72 hours (e.g., contact dermatitis, TB skin test,
granuloma formation, type 1 diabetes, MS).
Question 6 Granulomatous inflammation is characteristic of which condition?
A. Acute appendicitis
B. Tuberculosis [CORRECT]
C. Viral hepatitis
D. Bacterial pneumonia (lobar)
Correct Answer: B
Rationale: Granulomatous inflammation is a specialized chronic inflammatory response to
persistent, poorly degradable pathogens or foreign material. Tuberculosis causes caseating
granulomas: central necrosis (caseous), surrounded by epithelioid macrophages (activated
