NU606/NU 606 Advanced Pathophysiology Review
Actual Exam 2026/2027 with Detailed Rationales | 100%
Verified | Pass Guaranteed
SECTION 1: CELLULAR & MOLECULAR PATHOPHYSIOLOGY
(Questions 1–15)
Q1: Which cellular adaptation allows the liver to regenerate after partial hepatectomy?
A. Metaplasia
B. Dysplasia
C. Hyperplasia [CORRECT]
D. Hypertrophy
Correct Answer: C
Rationale: Correct because hyperplasia is an increase in cell number that allows tissues
with labile or stable cells, such as the liver, to regenerate after injury or partial removal.
This matches the normal physiologic response of hepatocyte proliferation.
Q2: A 58-year-old patient presents with tissue infarction following prolonged ischemia.
Microscopic examination reveals cell swelling, loss of membrane integrity, and nuclear
fragmentation with release of intracellular contents. Which type of cell death is most
likely?
A. Apoptosis
B. Necrosis [CORRECT]
C. Autophagy
D. Pyroptosis
Correct Answer: B
Rationale: Correct because necrosis is characterized by cell swelling, membrane
rupture, and release of intracellular contents triggering inflammation, which occurs
secondary to ischemic injury and ATP depletion. This matches the classic pathologic
findings of irreversible cell injury.
Q3: Which of the following is the primary mechanism by which hypoxia causes cellular
injury?
,A. Direct DNA damage
B. Failure of oxidative phosphorylation and ATP depletion [CORRECT]
C. Activation of caspase enzymes
D. Lysosomal membrane rupture
Correct Answer: B
Rationale: Correct because hypoxia deprives cells of oxygen required for oxidative
phosphorylation in mitochondria, leading to ATP depletion, which is the central event in
hypoxic cell injury. This matches the fundamental pathophysiology of ischemic cell
damage.
Q4: A patient with chronic bronchitis demonstrates replacement of normal ciliated
columnar epithelium with stratified squamous epithelium in the bronchi. This adaptive
change is best described as:
A. Hyperplasia
B. Hypertrophy
C. Metaplasia [CORRECT]
D. Dysplasia
Correct Answer: C
Rationale: Correct because metaplasia is the reversible replacement of one
differentiated cell type with another, as seen when chronic irritation causes squamous
metaplasia in respiratory epithelium. This matches the protective but potentially
premalignant adaptive response.
Q5: Which of the following best describes the role of p53 in normal cellular function?
A. Promotes cell cycle progression
B. Inhibits apoptosis
C. Arrests cell cycle and initiates DNA repair or apoptosis [CORRECT]
D. Stimulates angiogenesis
Correct Answer: C
Rationale: Correct because p53 is a tumor suppressor gene that functions as the
"guardian of the genome" by arresting the cell cycle at G1/S checkpoint, enabling DNA
repair, or triggering apoptosis if damage is irreparable. This matches its critical role in
preventing malignant transformation.
,Q6: A mutation in the BRCA1 gene increases susceptibility to breast and ovarian cancer.
This gene functions primarily as a:
A. Proto-oncogene
B. Tumor suppressor gene [CORRECT]
C. Oncogene
D. Growth factor receptor
Correct Answer: B
Rationale: Correct because BRCA1 is a tumor suppressor gene involved in DNA repair
and maintenance of genomic stability; loss-of-function mutations require both alleles to
be affected (Knudson's two-hit hypothesis) to promote carcinogenesis. This matches
the recessive nature of tumor suppressor gene inactivation.
Q7: Which epigenetic modification is most commonly associated with gene silencing in
cancer cells?
A. Histone acetylation
B. DNA hypomethylation
C. DNA hypermethylation of CpG islands [CORRECT]
D. Histone phosphorylation
Correct Answer: C
Rationale: Correct because hypermethylation of CpG islands in promoter regions is a
key epigenetic mechanism that silences tumor suppressor genes, contributing to
carcinogenesis without altering the DNA sequence. This matches the reversible nature
of epigenetic gene regulation.
Q8: Proto-oncogenes differ from oncogenes in that proto-oncogenes:
A. Are viral in origin
B. Promote uncontrolled cell growth
C. Are normal cellular genes that regulate growth and differentiation [CORRECT]
D. Require both alleles to be mutated for expression
Correct Answer: C
Rationale: Correct because proto-oncogenes are normal cellular genes that regulate cell
growth, differentiation, and survival; they become oncogenes only after gain-of-function
mutations or amplification. This matches the fundamental distinction between normal
and mutated growth-regulatory genes.
, Q9: Which of the following is a characteristic feature of apoptosis rather than necrosis?
A. Cell swelling and membrane rupture
B. Inflammation in surrounding tissue
C. Chromatin condensation and cell shrinkage without inflammation [CORRECT]
D. Release of intracellular enzymes into circulation
Correct Answer: C
Rationale: Correct because apoptosis is programmed cell death characterized by
chromatin condensation, cell shrinkage, membrane blebbing, and phagocytosis without
inflammation, in contrast to the inflammatory response seen in necrosis. This matches
the controlled, energy-dependent nature of apoptotic cell death.
Q10: A patient with chronic alcohol abuse develops fatty changes in hepatocytes. This
cellular adaptation is classified as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Steatosis [CORRECT]
Correct Answer: D
Rationale: Correct because steatosis (fatty change) is the abnormal accumulation of
triglycerides within parenchymal cells, commonly seen in hepatocytes due to alcohol
metabolism, obesity, or diabetes. This matches the reversible intracellular accumulation
pattern.
Q11: Which mechanism is primarily responsible for cellular aging at the molecular level?
A. Decreased protein synthesis
B. Telomere shortening with each cell division [CORRECT]
C. Increased mitochondrial biogenesis
D. Enhanced DNA repair capacity
Correct Answer: B
Rationale: Correct because telomere shortening with each cell division (the "end
replication problem") leads to cellular senescence when telomeres become critically
short, limiting the replicative lifespan of somatic cells. This matches the Hayflick limit
concept of cellular aging.
Actual Exam 2026/2027 with Detailed Rationales | 100%
Verified | Pass Guaranteed
SECTION 1: CELLULAR & MOLECULAR PATHOPHYSIOLOGY
(Questions 1–15)
Q1: Which cellular adaptation allows the liver to regenerate after partial hepatectomy?
A. Metaplasia
B. Dysplasia
C. Hyperplasia [CORRECT]
D. Hypertrophy
Correct Answer: C
Rationale: Correct because hyperplasia is an increase in cell number that allows tissues
with labile or stable cells, such as the liver, to regenerate after injury or partial removal.
This matches the normal physiologic response of hepatocyte proliferation.
Q2: A 58-year-old patient presents with tissue infarction following prolonged ischemia.
Microscopic examination reveals cell swelling, loss of membrane integrity, and nuclear
fragmentation with release of intracellular contents. Which type of cell death is most
likely?
A. Apoptosis
B. Necrosis [CORRECT]
C. Autophagy
D. Pyroptosis
Correct Answer: B
Rationale: Correct because necrosis is characterized by cell swelling, membrane
rupture, and release of intracellular contents triggering inflammation, which occurs
secondary to ischemic injury and ATP depletion. This matches the classic pathologic
findings of irreversible cell injury.
Q3: Which of the following is the primary mechanism by which hypoxia causes cellular
injury?
,A. Direct DNA damage
B. Failure of oxidative phosphorylation and ATP depletion [CORRECT]
C. Activation of caspase enzymes
D. Lysosomal membrane rupture
Correct Answer: B
Rationale: Correct because hypoxia deprives cells of oxygen required for oxidative
phosphorylation in mitochondria, leading to ATP depletion, which is the central event in
hypoxic cell injury. This matches the fundamental pathophysiology of ischemic cell
damage.
Q4: A patient with chronic bronchitis demonstrates replacement of normal ciliated
columnar epithelium with stratified squamous epithelium in the bronchi. This adaptive
change is best described as:
A. Hyperplasia
B. Hypertrophy
C. Metaplasia [CORRECT]
D. Dysplasia
Correct Answer: C
Rationale: Correct because metaplasia is the reversible replacement of one
differentiated cell type with another, as seen when chronic irritation causes squamous
metaplasia in respiratory epithelium. This matches the protective but potentially
premalignant adaptive response.
Q5: Which of the following best describes the role of p53 in normal cellular function?
A. Promotes cell cycle progression
B. Inhibits apoptosis
C. Arrests cell cycle and initiates DNA repair or apoptosis [CORRECT]
D. Stimulates angiogenesis
Correct Answer: C
Rationale: Correct because p53 is a tumor suppressor gene that functions as the
"guardian of the genome" by arresting the cell cycle at G1/S checkpoint, enabling DNA
repair, or triggering apoptosis if damage is irreparable. This matches its critical role in
preventing malignant transformation.
,Q6: A mutation in the BRCA1 gene increases susceptibility to breast and ovarian cancer.
This gene functions primarily as a:
A. Proto-oncogene
B. Tumor suppressor gene [CORRECT]
C. Oncogene
D. Growth factor receptor
Correct Answer: B
Rationale: Correct because BRCA1 is a tumor suppressor gene involved in DNA repair
and maintenance of genomic stability; loss-of-function mutations require both alleles to
be affected (Knudson's two-hit hypothesis) to promote carcinogenesis. This matches
the recessive nature of tumor suppressor gene inactivation.
Q7: Which epigenetic modification is most commonly associated with gene silencing in
cancer cells?
A. Histone acetylation
B. DNA hypomethylation
C. DNA hypermethylation of CpG islands [CORRECT]
D. Histone phosphorylation
Correct Answer: C
Rationale: Correct because hypermethylation of CpG islands in promoter regions is a
key epigenetic mechanism that silences tumor suppressor genes, contributing to
carcinogenesis without altering the DNA sequence. This matches the reversible nature
of epigenetic gene regulation.
Q8: Proto-oncogenes differ from oncogenes in that proto-oncogenes:
A. Are viral in origin
B. Promote uncontrolled cell growth
C. Are normal cellular genes that regulate growth and differentiation [CORRECT]
D. Require both alleles to be mutated for expression
Correct Answer: C
Rationale: Correct because proto-oncogenes are normal cellular genes that regulate cell
growth, differentiation, and survival; they become oncogenes only after gain-of-function
mutations or amplification. This matches the fundamental distinction between normal
and mutated growth-regulatory genes.
, Q9: Which of the following is a characteristic feature of apoptosis rather than necrosis?
A. Cell swelling and membrane rupture
B. Inflammation in surrounding tissue
C. Chromatin condensation and cell shrinkage without inflammation [CORRECT]
D. Release of intracellular enzymes into circulation
Correct Answer: C
Rationale: Correct because apoptosis is programmed cell death characterized by
chromatin condensation, cell shrinkage, membrane blebbing, and phagocytosis without
inflammation, in contrast to the inflammatory response seen in necrosis. This matches
the controlled, energy-dependent nature of apoptotic cell death.
Q10: A patient with chronic alcohol abuse develops fatty changes in hepatocytes. This
cellular adaptation is classified as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Steatosis [CORRECT]
Correct Answer: D
Rationale: Correct because steatosis (fatty change) is the abnormal accumulation of
triglycerides within parenchymal cells, commonly seen in hepatocytes due to alcohol
metabolism, obesity, or diabetes. This matches the reversible intracellular accumulation
pattern.
Q11: Which mechanism is primarily responsible for cellular aging at the molecular level?
A. Decreased protein synthesis
B. Telomere shortening with each cell division [CORRECT]
C. Increased mitochondrial biogenesis
D. Enhanced DNA repair capacity
Correct Answer: B
Rationale: Correct because telomere shortening with each cell division (the "end
replication problem") leads to cellular senescence when telomeres become critically
short, limiting the replicative lifespan of somatic cells. This matches the Hayflick limit
concept of cellular aging.
