NURS 6501
NURS 6501 Midterm Exam (4 Versions, 400 Q & A, Latest-
2025/ 2026) / NURS 6501N Midterm Exam / NURS6501
Midterm Exam / NURS6501N Midterm Exam: Walden
University | 100% Correct Q & A |
1: CELLULAR BIOLOGY & GENETIC MECHANISMS (1-20)
1. A patient with chronic hypoxia develops polycythemia. The cellular
adaptation is:
A. Hyperplasia
B. Metaplasia
C. Atrophy
D. Dysplasia
Answer: A. Hyperplasia
Rationale: Hypoxia stimulates renal erythropoietin (EPO) production, causing
erythroid hyperplasia in bone marrow. This compensatory mechanism increases
RBC mass to improve oxygen delivery .
2. In apoptosis, which enzyme executes programmed cell death?
A. Caspase-3
B. Cytochrome c
C. Bcl-2
D. p53
Answer: A. Caspase-3
Rationale: Caspase-3 is the effector caspase that cleaves nuclear lamins, DNA
repair enzymes, and cytoskeletal proteins, leading to characteristic apoptotic
changes. It is activated by both intrinsic and extrinsic pathways .
3. A smoker develops squamous cell carcinoma from chronic bronchial
irritation. This is:
A. Metaplasia → Dysplasia → Neoplasia
B. Hyperplasia → Atrophy
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,NURS 6501
C. Apoptosis → Necrosis
D. Hypertrophy → Metaplasia
Answer: A. Metaplasia → Dysplasia → Neoplasia
Rationale: Chronic irritation causes ciliated pseudostratified columnar
epithelium to transform to stratified squamous epithelium (metaplasia). With
persistent injury, dysplasia develops, progressing to carcinoma in situ and
invasive cancer .
4. Free radical injury primarily damages:
A. Membrane lipids
B. Nuclear DNA
C. Mitochondrial RNA
D. Golgi apparatus
Answer: A. Membrane lipids
Rationale: Reactive oxygen species (ROS) initiate lipid peroxidation, a chain
reaction damaging unsaturated fatty acids in cell membranes, disrupting
integrity and function .
5. In hereditary spherocytosis, the defect is in:
A. Spectrin
B. Band 3
C. Ankyrin
D. All of the above
Answer: D. All of the above
Rationale: Hereditary spherocytosis involves mutations in cytoskeletal proteins
(spectrin, ankyrin, band 3), reducing membrane stability, causing spherical RBCs
that are sequestered and destroyed in the spleen .
6. A mutation in CFTR ΔF508 causes:
A. Misfolding and ER retention
B. Premature truncation
C. Gain of function
D. Nuclear translocation
Answer: A. Misfolding and ER retention
Rationale: ΔF508 is a class II CFTR mutation causing protein misfolding,
retention in the endoplasmic reticulum, and degradation by proteasomes,
preventing chloride channels from reaching the apical membrane .
7. Telomerase reactivation is required for:
A. Immortalization of cancer cells
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,NURS 6501
B. Senescence
C. Apoptosis
D. Differentiation
Answer: A. Immortalization of cancer cells
Rationale: Telomerase maintains telomere length, allowing unlimited replication
(bypassing the Hayflick limit). This is a hallmark of cancer cells, enabling
immortality .
8. In reperfusion injury, damage is mediated by:
A. Neutrophil-derived ROS
B. Anaerobic glycolysis
C. Lactic acid
D. ATP depletion
Answer: A. Neutrophil-derived ROS
Rationale: Reperfusion injury involves the "oxygen paradox" – rapid
reintroduction of oxygen generates ROS via xanthine oxidase, and infiltrating
neutrophils release additional ROS and inflammatory mediators .
9. Amyloidosis is characterized by:
A. Beta-pleated sheet conformation
B. Alpha-helical structure
C. Random coil
D. Triple helix
Answer: A. Beta-pleated sheet conformation
Rationale: Amyloid fibrils have a characteristic beta-pleated sheet structure,
showing Congo red birefringence and green apple birefringence under
polarized light, representing protein misfolding diseases .
10. Oncogene activation in cancer is due to:
A. Gain-of-function mutation
B. Loss-of-function mutation
C. Epigenetic silencing
D. Telomere shortening
Answer: A. Gain-of-function mutation
Rationale: Oncogenes (e.g., RAS, MYC, HER2) are activated by gain-of-function
mutations (point mutations, amplification, translocation), leading to constitutive
growth signaling. Tumor suppressor genes involve loss-of-function .
11. In Huntington's disease, the mutation is:
A. CAG repeat expansion
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, NURS 6501
B. Point mutation in APP
C. Trinucleotide deletion
D. Frameshift
Answer: A. CAG repeat expansion
Rationale: Huntington's is caused by autosomal dominant CAG trinucleotide
repeat expansion in the HTT gene, producing polyglutamine tracts that form
neuronal intranuclear inclusions. Anticipation occurs with increasing repeat
length in successive generations .
12. Autophagy is activated in response to:
A. Nutrient deprivation
B. Oxidative stress
C. DNA damage
D. All of the above
Answer: D. All of the above
Rationale: Autophagy is a cellular recycling process activated by stressors
including nutrient deprivation, oxidative stress, and DNA damage. mTOR
inhibition triggers LC3 lipidation and autophagosome formation .
13. In lysosomal storage disease (Gaucher), the deficient enzyme is:
A. Glucocerebrosidase
B. Hexosaminidase A
C. Sphingomyelinase
D. Galactosidase
Answer: A. Glucocerebrosidase
Rationale: Gaucher disease (most common lysosomal storage disorder) results
from glucocerebrosidase deficiency, causing glucocerebroside accumulation in
macrophages (Gaucher cells) .
14. Necroptosis is regulated by:
A. RIPK3 and MLKL
B. Caspase-8
C. Bcl-2
D. p53
Answer: A. RIPK3 and MLKL
Rationale: Necroptosis is programmed necrosis regulated by RIPK3 and MLKL,
leading to plasma membrane rupture and inflammatory cell death. It is caspase-
independent .
P a g e 4 | 55
NURS 6501 Midterm Exam (4 Versions, 400 Q & A, Latest-
2025/ 2026) / NURS 6501N Midterm Exam / NURS6501
Midterm Exam / NURS6501N Midterm Exam: Walden
University | 100% Correct Q & A |
1: CELLULAR BIOLOGY & GENETIC MECHANISMS (1-20)
1. A patient with chronic hypoxia develops polycythemia. The cellular
adaptation is:
A. Hyperplasia
B. Metaplasia
C. Atrophy
D. Dysplasia
Answer: A. Hyperplasia
Rationale: Hypoxia stimulates renal erythropoietin (EPO) production, causing
erythroid hyperplasia in bone marrow. This compensatory mechanism increases
RBC mass to improve oxygen delivery .
2. In apoptosis, which enzyme executes programmed cell death?
A. Caspase-3
B. Cytochrome c
C. Bcl-2
D. p53
Answer: A. Caspase-3
Rationale: Caspase-3 is the effector caspase that cleaves nuclear lamins, DNA
repair enzymes, and cytoskeletal proteins, leading to characteristic apoptotic
changes. It is activated by both intrinsic and extrinsic pathways .
3. A smoker develops squamous cell carcinoma from chronic bronchial
irritation. This is:
A. Metaplasia → Dysplasia → Neoplasia
B. Hyperplasia → Atrophy
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,NURS 6501
C. Apoptosis → Necrosis
D. Hypertrophy → Metaplasia
Answer: A. Metaplasia → Dysplasia → Neoplasia
Rationale: Chronic irritation causes ciliated pseudostratified columnar
epithelium to transform to stratified squamous epithelium (metaplasia). With
persistent injury, dysplasia develops, progressing to carcinoma in situ and
invasive cancer .
4. Free radical injury primarily damages:
A. Membrane lipids
B. Nuclear DNA
C. Mitochondrial RNA
D. Golgi apparatus
Answer: A. Membrane lipids
Rationale: Reactive oxygen species (ROS) initiate lipid peroxidation, a chain
reaction damaging unsaturated fatty acids in cell membranes, disrupting
integrity and function .
5. In hereditary spherocytosis, the defect is in:
A. Spectrin
B. Band 3
C. Ankyrin
D. All of the above
Answer: D. All of the above
Rationale: Hereditary spherocytosis involves mutations in cytoskeletal proteins
(spectrin, ankyrin, band 3), reducing membrane stability, causing spherical RBCs
that are sequestered and destroyed in the spleen .
6. A mutation in CFTR ΔF508 causes:
A. Misfolding and ER retention
B. Premature truncation
C. Gain of function
D. Nuclear translocation
Answer: A. Misfolding and ER retention
Rationale: ΔF508 is a class II CFTR mutation causing protein misfolding,
retention in the endoplasmic reticulum, and degradation by proteasomes,
preventing chloride channels from reaching the apical membrane .
7. Telomerase reactivation is required for:
A. Immortalization of cancer cells
P a g e 2 | 55
,NURS 6501
B. Senescence
C. Apoptosis
D. Differentiation
Answer: A. Immortalization of cancer cells
Rationale: Telomerase maintains telomere length, allowing unlimited replication
(bypassing the Hayflick limit). This is a hallmark of cancer cells, enabling
immortality .
8. In reperfusion injury, damage is mediated by:
A. Neutrophil-derived ROS
B. Anaerobic glycolysis
C. Lactic acid
D. ATP depletion
Answer: A. Neutrophil-derived ROS
Rationale: Reperfusion injury involves the "oxygen paradox" – rapid
reintroduction of oxygen generates ROS via xanthine oxidase, and infiltrating
neutrophils release additional ROS and inflammatory mediators .
9. Amyloidosis is characterized by:
A. Beta-pleated sheet conformation
B. Alpha-helical structure
C. Random coil
D. Triple helix
Answer: A. Beta-pleated sheet conformation
Rationale: Amyloid fibrils have a characteristic beta-pleated sheet structure,
showing Congo red birefringence and green apple birefringence under
polarized light, representing protein misfolding diseases .
10. Oncogene activation in cancer is due to:
A. Gain-of-function mutation
B. Loss-of-function mutation
C. Epigenetic silencing
D. Telomere shortening
Answer: A. Gain-of-function mutation
Rationale: Oncogenes (e.g., RAS, MYC, HER2) are activated by gain-of-function
mutations (point mutations, amplification, translocation), leading to constitutive
growth signaling. Tumor suppressor genes involve loss-of-function .
11. In Huntington's disease, the mutation is:
A. CAG repeat expansion
P a g e 3 | 55
, NURS 6501
B. Point mutation in APP
C. Trinucleotide deletion
D. Frameshift
Answer: A. CAG repeat expansion
Rationale: Huntington's is caused by autosomal dominant CAG trinucleotide
repeat expansion in the HTT gene, producing polyglutamine tracts that form
neuronal intranuclear inclusions. Anticipation occurs with increasing repeat
length in successive generations .
12. Autophagy is activated in response to:
A. Nutrient deprivation
B. Oxidative stress
C. DNA damage
D. All of the above
Answer: D. All of the above
Rationale: Autophagy is a cellular recycling process activated by stressors
including nutrient deprivation, oxidative stress, and DNA damage. mTOR
inhibition triggers LC3 lipidation and autophagosome formation .
13. In lysosomal storage disease (Gaucher), the deficient enzyme is:
A. Glucocerebrosidase
B. Hexosaminidase A
C. Sphingomyelinase
D. Galactosidase
Answer: A. Glucocerebrosidase
Rationale: Gaucher disease (most common lysosomal storage disorder) results
from glucocerebrosidase deficiency, causing glucocerebroside accumulation in
macrophages (Gaucher cells) .
14. Necroptosis is regulated by:
A. RIPK3 and MLKL
B. Caspase-8
C. Bcl-2
D. p53
Answer: A. RIPK3 and MLKL
Rationale: Necroptosis is programmed necrosis regulated by RIPK3 and MLKL,
leading to plasma membrane rupture and inflammatory cell death. It is caspase-
independent .
P a g e 4 | 55
