1
NURS 6501 ADVANCED PATHOPHYSIOLOGY MIDTERM
EXAM 2026/2027 | Walden University MSN/NP | Questions
& Verified Answers | Pass Guaranteed - A+ Graded
[Section 1: Cellular & Genetic Mechanisms (Q1-12)]
Q1. A 55-year-old man with long-standing hypertension has left ventricular wall
thickening on echocardiogram. The cardiomyocytes demonstrate increased protein
synthesis and organelle production. Which cellular adaptation is present?
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Correct Answer: B Rationale: B. Hypertrophy [CORRECT] — Hypertrophy is an
increase in cell size (not number) due to increased protein synthesis and organelle
production, typically in response to mechanical stress such as hypertension-induced
pressure overload. Hyperplasia involves increased cell number, atrophy is decreased
cell size, and metaplasia is the reversible replacement of one differentiated cell type
with another.
Q2. A smoker has respiratory epithelium in the bronchi replaced by stratified
squamous epithelium. Which cellular adaptation is described?
A. Dysplasia
B. Metaplasia
C. Hyperplasia
D. Anaplasia
Correct Answer: B Rationale: B. Metaplasia [CORRECT] — Metaplasia is the
reversible replacement of one mature differentiated cell type by another, often in
response to chronic irritation (smoking, acid reflux). While metaplasia is adaptive, it
can be a precursor to dysplasia and neoplasia. Dysplasia involves disordered cellular
development, and anaplasia is loss of differentiation in malignancy.
,2
Q3. A patient with cervical intraepithelial neoplasia (CIN III) has disordered epithelial
maturation, nuclear hyperchromasia, and increased mitotic figures extending through
the full thickness of the epithelium. Which term best describes these changes?
A. Metaplasia
B. Dysplasia
C. Hyperplasia
D. Hypertrophy
Correct Answer: B Rationale: B. Dysplasia [CORRECT] — Dysplasia is characterized
by disordered cellular development with nuclear atypia, loss of polarity, and
increased mitotic activity. CIN III represents severe dysplasia/carcinoma in situ where
these changes involve the full epithelial thickness. Dysplasia is considered pre-
neoplastic and may progress to invasive cancer if not treated.
Q4. During myocardial ischemia, which intracellular event occurs first and triggers the
cascade of cell injury?
A. Lysosomal enzyme release
B. Mitochondrial permeability transition pore opening
C. Decreased ATP production and failure of the Na+/K+-ATPase pump
D. Nuclear chromatin clumping
Correct Answer: C Rationale: C. Decreased ATP production and failure of the
Na+/K+-ATPase pump [CORRECT] — Ischemia causes anaerobic metabolism and
rapid ATP depletion. The Na+/K+-ATPase pump fails, leading to cellular swelling,
calcium influx, and organelle dysfunction. This is the earliest reversible event.
Mitochondrial damage, lysosomal rupture, and nuclear changes occur later and
represent progression to irreversible injury.
Q5. Reperfusion of ischemic tissue paradoxically worsens cell injury through
generation of reactive oxygen species. Which mechanism is primarily responsible?
A. Activation of caspase-3
B. Conversion of xanthine dehydrogenase to xanthine oxidase with superoxide
generation
C. Upregulation of Bcl-2
D. Inhibition of cyclooxygenase
,3
Correct Answer: B Rationale: B. Conversion of xanthine dehydrogenase to xanthine
oxidase with superoxide generation [CORRECT] — During ischemia, ATP is degraded
to hypoxanthine. Upon reperfusion, xanthine oxidase (converted from xanthine
dehydrogenase during ischemia) metabolizes hypoxanthine in the presence of
oxygen, generating superoxide and hydrogen peroxide. This oxidative burst causes
lipid peroxidation, protein denaturation, and DNA damage.
Q6. A patient with acute pancreatitis has areas of necrosis where tissue architecture is
lost and cellular outlines are replaced by amorphous debris. Which type of necrosis is
present?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Caseous necrosis
Correct Answer: C Rationale: C. Fat necrosis [CORRECT] — Acute pancreatitis
causes enzymatic fat necrosis through lipase release, which hydrolyzes triglycerides
into fatty acids that combine with calcium to form soap (saponification). This appears
as chalky white deposits. Coagulative necrosis preserves architecture (heart, kidney),
liquefactive occurs in brain/abscesses, and caseous is characteristic of tuberculosis.
Q7. A patient with tuberculosis has necrotic granulomas with cheese-like appearance
on gross examination. Microscopically, the necrotic center appears granular and
eosinophilic without preserved cellular architecture. Which type of necrosis is
present?
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Correct Answer: C Rationale: C. Caseous [CORRECT] — Caseous necrosis is
characteristic of granulomatous inflammation, particularly tuberculosis. It appears
soft, white, and cheese-like grossly, with amorphous granular debris microscopically.
Unlike coagulative necrosis, tissue architecture is completely lost. It results from cell-
mediated immune responses against intracellular pathogens.
, 4
Q8. A tumor suppressor gene on chromosome 17 is mutated, leading to loss of cell
cycle checkpoint control and increased genomic instability. Which gene is most likely
involved?
A. RAS
B. TP53
C. MYC
D. BCR-ABL
Correct Answer: B Rationale: B. TP53 [CORRECT] — TP53 (located on chromosome
17p13.1) is the most commonly mutated tumor suppressor gene in human cancers. It
encodes p53, the "guardian of the genome," which arrests the cell cycle at G1/S to
allow DNA repair or initiates apoptosis if damage is irreparable. Loss of p53 function
leads to uncontrolled proliferation and genomic instability. RAS, MYC, and BCR-ABL
are oncogenes, not tumor suppressors.
Q9. A patient with chronic myeloid leukemia has the Philadelphia chromosome
t(9;22)(q34;q11). Which molecular consequence drives the malignant transformation?
A. Loss of tumor suppressor function
B. Formation of a constitutively active tyrosine kinase fusion protein (BCR-ABL)
C. Overexpression of a growth factor receptor
D. Epigenetic silencing of a DNA repair gene
Correct Answer: B Rationale: B. Formation of a constitutively active tyrosine kinase
fusion protein (BCR-ABL) [CORRECT] — The Philadelphia chromosome translocation
fuses the BCR gene on chromosome 22 with the ABL1 gene on chromosome 9,
creating the BCR-ABL fusion protein. This fusion has constitutively active tyrosine
kinase activity that drives uncontrolled myeloid proliferation, independent of normal
growth factor signaling.
Q10. A patient with Li-Fraumeni syndrome develops multiple primary cancers at a
young age (breast cancer at 28, sarcoma at 35). Which genetic mechanism explains
this predisposition?
A. Germline mutation in a tumor suppressor gene (TP53)
B. Somatic mutation in an oncogene
C. Chromosomal translocation
D. Epigenetic hypermethylation
NURS 6501 ADVANCED PATHOPHYSIOLOGY MIDTERM
EXAM 2026/2027 | Walden University MSN/NP | Questions
& Verified Answers | Pass Guaranteed - A+ Graded
[Section 1: Cellular & Genetic Mechanisms (Q1-12)]
Q1. A 55-year-old man with long-standing hypertension has left ventricular wall
thickening on echocardiogram. The cardiomyocytes demonstrate increased protein
synthesis and organelle production. Which cellular adaptation is present?
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Correct Answer: B Rationale: B. Hypertrophy [CORRECT] — Hypertrophy is an
increase in cell size (not number) due to increased protein synthesis and organelle
production, typically in response to mechanical stress such as hypertension-induced
pressure overload. Hyperplasia involves increased cell number, atrophy is decreased
cell size, and metaplasia is the reversible replacement of one differentiated cell type
with another.
Q2. A smoker has respiratory epithelium in the bronchi replaced by stratified
squamous epithelium. Which cellular adaptation is described?
A. Dysplasia
B. Metaplasia
C. Hyperplasia
D. Anaplasia
Correct Answer: B Rationale: B. Metaplasia [CORRECT] — Metaplasia is the
reversible replacement of one mature differentiated cell type by another, often in
response to chronic irritation (smoking, acid reflux). While metaplasia is adaptive, it
can be a precursor to dysplasia and neoplasia. Dysplasia involves disordered cellular
development, and anaplasia is loss of differentiation in malignancy.
,2
Q3. A patient with cervical intraepithelial neoplasia (CIN III) has disordered epithelial
maturation, nuclear hyperchromasia, and increased mitotic figures extending through
the full thickness of the epithelium. Which term best describes these changes?
A. Metaplasia
B. Dysplasia
C. Hyperplasia
D. Hypertrophy
Correct Answer: B Rationale: B. Dysplasia [CORRECT] — Dysplasia is characterized
by disordered cellular development with nuclear atypia, loss of polarity, and
increased mitotic activity. CIN III represents severe dysplasia/carcinoma in situ where
these changes involve the full epithelial thickness. Dysplasia is considered pre-
neoplastic and may progress to invasive cancer if not treated.
Q4. During myocardial ischemia, which intracellular event occurs first and triggers the
cascade of cell injury?
A. Lysosomal enzyme release
B. Mitochondrial permeability transition pore opening
C. Decreased ATP production and failure of the Na+/K+-ATPase pump
D. Nuclear chromatin clumping
Correct Answer: C Rationale: C. Decreased ATP production and failure of the
Na+/K+-ATPase pump [CORRECT] — Ischemia causes anaerobic metabolism and
rapid ATP depletion. The Na+/K+-ATPase pump fails, leading to cellular swelling,
calcium influx, and organelle dysfunction. This is the earliest reversible event.
Mitochondrial damage, lysosomal rupture, and nuclear changes occur later and
represent progression to irreversible injury.
Q5. Reperfusion of ischemic tissue paradoxically worsens cell injury through
generation of reactive oxygen species. Which mechanism is primarily responsible?
A. Activation of caspase-3
B. Conversion of xanthine dehydrogenase to xanthine oxidase with superoxide
generation
C. Upregulation of Bcl-2
D. Inhibition of cyclooxygenase
,3
Correct Answer: B Rationale: B. Conversion of xanthine dehydrogenase to xanthine
oxidase with superoxide generation [CORRECT] — During ischemia, ATP is degraded
to hypoxanthine. Upon reperfusion, xanthine oxidase (converted from xanthine
dehydrogenase during ischemia) metabolizes hypoxanthine in the presence of
oxygen, generating superoxide and hydrogen peroxide. This oxidative burst causes
lipid peroxidation, protein denaturation, and DNA damage.
Q6. A patient with acute pancreatitis has areas of necrosis where tissue architecture is
lost and cellular outlines are replaced by amorphous debris. Which type of necrosis is
present?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Caseous necrosis
Correct Answer: C Rationale: C. Fat necrosis [CORRECT] — Acute pancreatitis
causes enzymatic fat necrosis through lipase release, which hydrolyzes triglycerides
into fatty acids that combine with calcium to form soap (saponification). This appears
as chalky white deposits. Coagulative necrosis preserves architecture (heart, kidney),
liquefactive occurs in brain/abscesses, and caseous is characteristic of tuberculosis.
Q7. A patient with tuberculosis has necrotic granulomas with cheese-like appearance
on gross examination. Microscopically, the necrotic center appears granular and
eosinophilic without preserved cellular architecture. Which type of necrosis is
present?
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Correct Answer: C Rationale: C. Caseous [CORRECT] — Caseous necrosis is
characteristic of granulomatous inflammation, particularly tuberculosis. It appears
soft, white, and cheese-like grossly, with amorphous granular debris microscopically.
Unlike coagulative necrosis, tissue architecture is completely lost. It results from cell-
mediated immune responses against intracellular pathogens.
, 4
Q8. A tumor suppressor gene on chromosome 17 is mutated, leading to loss of cell
cycle checkpoint control and increased genomic instability. Which gene is most likely
involved?
A. RAS
B. TP53
C. MYC
D. BCR-ABL
Correct Answer: B Rationale: B. TP53 [CORRECT] — TP53 (located on chromosome
17p13.1) is the most commonly mutated tumor suppressor gene in human cancers. It
encodes p53, the "guardian of the genome," which arrests the cell cycle at G1/S to
allow DNA repair or initiates apoptosis if damage is irreparable. Loss of p53 function
leads to uncontrolled proliferation and genomic instability. RAS, MYC, and BCR-ABL
are oncogenes, not tumor suppressors.
Q9. A patient with chronic myeloid leukemia has the Philadelphia chromosome
t(9;22)(q34;q11). Which molecular consequence drives the malignant transformation?
A. Loss of tumor suppressor function
B. Formation of a constitutively active tyrosine kinase fusion protein (BCR-ABL)
C. Overexpression of a growth factor receptor
D. Epigenetic silencing of a DNA repair gene
Correct Answer: B Rationale: B. Formation of a constitutively active tyrosine kinase
fusion protein (BCR-ABL) [CORRECT] — The Philadelphia chromosome translocation
fuses the BCR gene on chromosome 22 with the ABL1 gene on chromosome 9,
creating the BCR-ABL fusion protein. This fusion has constitutively active tyrosine
kinase activity that drives uncontrolled myeloid proliferation, independent of normal
growth factor signaling.
Q10. A patient with Li-Fraumeni syndrome develops multiple primary cancers at a
young age (breast cancer at 28, sarcoma at 35). Which genetic mechanism explains
this predisposition?
A. Germline mutation in a tumor suppressor gene (TP53)
B. Somatic mutation in an oncogene
C. Chromosomal translocation
D. Epigenetic hypermethylation
