NURS 6501 ADVANCED PATHOPHYSIOLOGY
WALDEN UNIVERSITY MIDTERM EXAM
(2025/2026)
Actual Midterm Exam + Practice Test Bank (120 Questions)
Verified | Detailed Rationales | Cellular Mechanisms | Clinical Correlations
DOMAIN 1: CELLULAR BIOLOGY & GENETIC MECHANISMS
(Questions 1–15)
1. A patient with chronic hypoxia develops polycythemia. The cellular
adaptation is:
a) Hyperplasia
b) Metaplasia
c) Atrophy
d) Dysplasia
a) Hyperplasia
Rationale: EPO-mediated erythroid hyperplasia in renal juxtaglomerular cells →
increased RBC mass. Compensatory adaptation to hypoxia.
2. In apoptosis, which enzyme executes programmed cell death?
a) Caspase-3
b) Cytochrome c
c) Bcl-2
d) p53
a) Caspase-3
Rationale: Effector caspase cleaves nuclear lamina, DNA, and cytoskeletal proteins.
Intrinsic/extrinsic pathway convergence.
3. A smoker develops squamous cell carcinoma from chronic bronchial
irritation. This is:
a) Metaplasia → Dysplasia → Neoplasia
b) Hyperplasia → Atrophy
c) Apoptosis → Necrosis
d) Hypertrophy → Metaplasia
a) Metaplasia → Dysplasia → Neoplasia
Rationale: Ciliated → squamous metaplasia → loss of polarity → carcinoma in situ.
Stepwise carcinogenesis.
4. Free radical injury primarily damages:
a) Membrane lipids
b) Nuclear DNA
c) Mitochondrial RNA
,d) Golgi apparatus
a) Membrane lipids
Rationale: Lipid peroxidation → chain reaction → loss of membrane integrity. ROS
mechanism.
5. In hereditary spherocytosis, the defect is in:
a) Spectrin
b) Band 3
c) Ankyrin
d) All of the above
d) All of the above
Rationale: Cytoskeletal proteins → loss of biconcave shape → splenic sequestration.
Membrane disorder.
6. A mutation in CFTR ΔF508 causes:
a) Misfolding and ER retention
b) Premature truncation
c) Gain of function
d) Nuclear translocation
a) Misfolding and ER retention
Rationale: Class II mutation → degradation by proteasome → absent apical Cl⁻ channel.
Protein trafficking defect.
7. Telomerase reactivation is required for:
a) Immortalization of cancer cells
b) Senescence
c) Apoptosis
d) Differentiation
a) Immortalization of cancer cells
Rationale: Hayflick limit bypassed → unlimited replication. Hallmark of cancer.
8. In reperfusion injury, damage is mediated by:
a) Neutrophil-derived ROS
b) Anaerobic glycolysis
c) Lactic acid
d) ATP depletion
a) Neutrophil-derived ROS
Rationale: Oxygen paradox → xanthine oxidase → superoxide. Inflammatory amplification.
9. Amyloidosis is characterized by:
a) Beta-pleated sheet conformation
b) Alpha-helical structure
c) Random coil
d) Triple helix
a) Beta-pleated sheet conformation
Rationale: Congo red birefringence → insoluble fibrils. Protein misfolding disease.
, 10. Oncogene activation in cancer is due to:
a) Gain-of-function mutation
b) Loss-of-function mutation
c) Epigenetic silencing
d) Telomere shortening
a) Gain-of-function mutation
Rationale: RAS, MYC → constitutive signaling. Driver mutation.
11. In Huntington’s disease, the mutation is:
a) CAG repeat expansion
b) Point mutation in APP
c) Trinucleotide deletion
d) Frameshift
a) CAG repeat expansion
Rationale: Polyglutamine tract → neuronal intranuclear inclusions. Anticipation
phenomenon.
12. Autophagy is activated in response to:
a) Nutrient deprivation
b) Oxidative stress
c) DNA damage
d) All of the above
d) All of the above
Rationale: mTOR inhibition → LC3 lipidation → autophagosome formation. Cellular
recycling.
13. In lysosomal storage disease (Gaucher), the deficient enzyme is:
a) Glucocerebrosidase
b) Hexosaminidase A
c) Sphingomyelinase
d) Galactosidase
a) Glucocerebrosidase
Rationale: Glucocerebroside accumulation → macrophage engorgement. Lipidosis.
14. Necroptosis is regulated by:
a) RIPK3 and MLKL
b) Caspase-8
c) Bcl-2
d) p53
a) RIPK3 and MLKL
Rationale: Programmed necrosis → plasma membrane rupture. Inflammatory cell death.
15. Mitochondrial DNA mutations affect:
a) Oxidative phosphorylation
b) Glycolysis
c) TCA cycle
WALDEN UNIVERSITY MIDTERM EXAM
(2025/2026)
Actual Midterm Exam + Practice Test Bank (120 Questions)
Verified | Detailed Rationales | Cellular Mechanisms | Clinical Correlations
DOMAIN 1: CELLULAR BIOLOGY & GENETIC MECHANISMS
(Questions 1–15)
1. A patient with chronic hypoxia develops polycythemia. The cellular
adaptation is:
a) Hyperplasia
b) Metaplasia
c) Atrophy
d) Dysplasia
a) Hyperplasia
Rationale: EPO-mediated erythroid hyperplasia in renal juxtaglomerular cells →
increased RBC mass. Compensatory adaptation to hypoxia.
2. In apoptosis, which enzyme executes programmed cell death?
a) Caspase-3
b) Cytochrome c
c) Bcl-2
d) p53
a) Caspase-3
Rationale: Effector caspase cleaves nuclear lamina, DNA, and cytoskeletal proteins.
Intrinsic/extrinsic pathway convergence.
3. A smoker develops squamous cell carcinoma from chronic bronchial
irritation. This is:
a) Metaplasia → Dysplasia → Neoplasia
b) Hyperplasia → Atrophy
c) Apoptosis → Necrosis
d) Hypertrophy → Metaplasia
a) Metaplasia → Dysplasia → Neoplasia
Rationale: Ciliated → squamous metaplasia → loss of polarity → carcinoma in situ.
Stepwise carcinogenesis.
4. Free radical injury primarily damages:
a) Membrane lipids
b) Nuclear DNA
c) Mitochondrial RNA
,d) Golgi apparatus
a) Membrane lipids
Rationale: Lipid peroxidation → chain reaction → loss of membrane integrity. ROS
mechanism.
5. In hereditary spherocytosis, the defect is in:
a) Spectrin
b) Band 3
c) Ankyrin
d) All of the above
d) All of the above
Rationale: Cytoskeletal proteins → loss of biconcave shape → splenic sequestration.
Membrane disorder.
6. A mutation in CFTR ΔF508 causes:
a) Misfolding and ER retention
b) Premature truncation
c) Gain of function
d) Nuclear translocation
a) Misfolding and ER retention
Rationale: Class II mutation → degradation by proteasome → absent apical Cl⁻ channel.
Protein trafficking defect.
7. Telomerase reactivation is required for:
a) Immortalization of cancer cells
b) Senescence
c) Apoptosis
d) Differentiation
a) Immortalization of cancer cells
Rationale: Hayflick limit bypassed → unlimited replication. Hallmark of cancer.
8. In reperfusion injury, damage is mediated by:
a) Neutrophil-derived ROS
b) Anaerobic glycolysis
c) Lactic acid
d) ATP depletion
a) Neutrophil-derived ROS
Rationale: Oxygen paradox → xanthine oxidase → superoxide. Inflammatory amplification.
9. Amyloidosis is characterized by:
a) Beta-pleated sheet conformation
b) Alpha-helical structure
c) Random coil
d) Triple helix
a) Beta-pleated sheet conformation
Rationale: Congo red birefringence → insoluble fibrils. Protein misfolding disease.
, 10. Oncogene activation in cancer is due to:
a) Gain-of-function mutation
b) Loss-of-function mutation
c) Epigenetic silencing
d) Telomere shortening
a) Gain-of-function mutation
Rationale: RAS, MYC → constitutive signaling. Driver mutation.
11. In Huntington’s disease, the mutation is:
a) CAG repeat expansion
b) Point mutation in APP
c) Trinucleotide deletion
d) Frameshift
a) CAG repeat expansion
Rationale: Polyglutamine tract → neuronal intranuclear inclusions. Anticipation
phenomenon.
12. Autophagy is activated in response to:
a) Nutrient deprivation
b) Oxidative stress
c) DNA damage
d) All of the above
d) All of the above
Rationale: mTOR inhibition → LC3 lipidation → autophagosome formation. Cellular
recycling.
13. In lysosomal storage disease (Gaucher), the deficient enzyme is:
a) Glucocerebrosidase
b) Hexosaminidase A
c) Sphingomyelinase
d) Galactosidase
a) Glucocerebrosidase
Rationale: Glucocerebroside accumulation → macrophage engorgement. Lipidosis.
14. Necroptosis is regulated by:
a) RIPK3 and MLKL
b) Caspase-8
c) Bcl-2
d) p53
a) RIPK3 and MLKL
Rationale: Programmed necrosis → plasma membrane rupture. Inflammatory cell death.
15. Mitochondrial DNA mutations affect:
a) Oxidative phosphorylation
b) Glycolysis
c) TCA cycle
