1
NURS 6501 ADVANCED PATHOPHYSIOLOGY 4 VERSION
MIDTERM EXAM BANK 2026/2027 | 400 Total Questions
with Verified Correct Answers | Latest Edition | Pass
Guaranteed - A+ Graded
[ [VERSION 1 - 100 QUESTIONS] [V1S1: Cellular & Genetic Pathophysiology
(Q1-20)]
Q1. A 45-year-old patient with chronic alcohol use presents with hepatomegaly. Liver
biopsy reveals Mallory-Denk bodies and ballooning degeneration of hepatocytes.
Which cellular adaptation process is primarily occurring?
A. Hypertrophy
B. Hyperplasia
C. Steatosis with reversible injury
D. Apoptosis
Correct Answer: C. Steatosis with reversible injury [CORRECT]
Rationale: Mallory-Denk bodies and hepatocyte ballooning are hallmarks of alcoholic
steatohepatitis, representing reversible cellular injury with fat accumulation.
Apoptosis would show Councilman bodies; hypertrophy and hyperplasia do not
produce these specific findings.
Correct Answer: C
Q2. A child with cystic fibrosis has a mutation in the CFTR gene. Which
pathophysiologic mechanism explains the multi-organ involvement?
A. Gain-of-function mutation causing constitutive channel activation
B. Loss-of-function mutation impairing chloride ion transport
C. Mitochondrial DNA mutation disrupting oxidative phosphorylation
D. Genomic imprinting defect affecting paternal allele expression
Correct Answer: B. Loss-of-function mutation impairing chloride ion transport
[CORRECT]
,2
Rationale: CFTR gene mutations cause loss of chloride channel function, leading to
thick mucus secretions in lungs, pancreas, and sweat glands. It is an autosomal
recessive disorder, not imprinting or mitochondrial.
Correct Answer: B
Q3. During myocardial ischemia, which intracellular event occurs first in the
progression from reversible to irreversible injury?
A. Lysosomal rupture
B. Mitochondrial swelling with calcium overload
C. Nuclear pyknosis
D. Plasma membrane phospholipid loss
Correct Answer: B. Mitochondrial swelling with calcium overload [CORRECT]
Rationale: Mitochondrial dysfunction with calcium accumulation and ATP depletion
marks the transition point to irreversible injury. Lysosomal rupture and nuclear
pyknosis occur later; phospholipid loss is a consequence, not the initial trigger.
Correct Answer: B
Q4. A patient with Li-Fraumeni syndrome develops multiple primary malignancies.
Which gene is mutated in this disorder?
A. RB1
B. TP53
C. BRCA1
D. APC
Correct Answer: B. TP53 [CORRECT]
Rationale: Li-Fraumeni syndrome results from germline TP53 mutations, causing loss
of cell cycle checkpoint control and apoptosis regulation. RB1 causes retinoblastoma;
BRCA1 is breast/ovarian cancer; APC is familial adenomatous polyposis.
Correct Answer: B
,3
Q5. Which mechanism best explains cellular atrophy in a patient with prolonged
corticosteroid use?
A. Increased protein synthesis via mTOR activation
B. Ubiquitin-proteasome pathway activation and autophagy
C. Decreased apoptosis with cellular senescence
D. Hypertrophy of adjacent compensatory cells
Correct Answer: B. Ubiquitin-proteasome pathway activation and autophagy
[CORRECT]
Rationale: Corticosteroid-induced atrophy involves increased protein breakdown via
the ubiquitin-proteasome system and autophagy-lysosomal pathways. mTOR
activation promotes growth; apoptosis decrease does not explain atrophy.
Correct Answer: B
Q6. In pyroptosis, which inflammatory caspase is primarily activated?
A. Caspase-3
B. Caspase-8
C. Caspase-1
D. Caspase-9
Correct Answer: C. Caspase-1 [CORRECT]
Rationale: Pyroptosis is a pro-inflammatory programmed cell death mediated by
caspase-1 (and caspase-4/5/11) activation of gasdermin D. Caspase-3 mediates
apoptosis; caspase-8 and -9 are initiator caspases in extrinsic/intrinsic apoptosis.
Correct Answer: C
Q7. A newborn with Prader-Willi syndrome demonstrates hypotonia and failure to
thrive. Which genetic mechanism is responsible?
, 4
A. Mitochondrial DNA deletion
B. Paternal chromosome 15q11-q13 deletion or maternal uniparental disomy
C. Trinucleotide repeat expansion on X chromosome
D. Autosomal dominant point mutation in the leptin receptor
Correct Answer: B. Paternal chromosome 15q11-q13 deletion or maternal
uniparental disomy [CORRECT]
Rationale: Prader-Willi syndrome results from loss of paternally expressed genes at
15q11-q13 via deletion or maternal uniparental disomy (imprinting disorder). It is not
mitochondrial, trinucleotide repeat, or leptin receptor-related.
Correct Answer: B
Q8. Which reactive oxygen species is generated primarily during the respiratory burst
in neutrophils?
A. Hydrogen peroxide
B. Superoxide anion
C. Hydroxyl radical
D. Peroxynitrite
Correct Answer: B. Superoxide anion [CORRECT]
Rationale: NADPH oxidase in neutrophils converts O2 to superoxide anion (O2•-) as
the initial ROS in respiratory burst. Hydrogen peroxide and hydroxyl radicals are
downstream products; peroxynitrite forms from superoxide and nitric oxide.
Correct Answer: B
Q9. A patient with xeroderma pigmentosum develops multiple skin cancers. Which
cellular process is defective?
A. Homologous recombination repair
B. Nucleotide excision repair
NURS 6501 ADVANCED PATHOPHYSIOLOGY 4 VERSION
MIDTERM EXAM BANK 2026/2027 | 400 Total Questions
with Verified Correct Answers | Latest Edition | Pass
Guaranteed - A+ Graded
[ [VERSION 1 - 100 QUESTIONS] [V1S1: Cellular & Genetic Pathophysiology
(Q1-20)]
Q1. A 45-year-old patient with chronic alcohol use presents with hepatomegaly. Liver
biopsy reveals Mallory-Denk bodies and ballooning degeneration of hepatocytes.
Which cellular adaptation process is primarily occurring?
A. Hypertrophy
B. Hyperplasia
C. Steatosis with reversible injury
D. Apoptosis
Correct Answer: C. Steatosis with reversible injury [CORRECT]
Rationale: Mallory-Denk bodies and hepatocyte ballooning are hallmarks of alcoholic
steatohepatitis, representing reversible cellular injury with fat accumulation.
Apoptosis would show Councilman bodies; hypertrophy and hyperplasia do not
produce these specific findings.
Correct Answer: C
Q2. A child with cystic fibrosis has a mutation in the CFTR gene. Which
pathophysiologic mechanism explains the multi-organ involvement?
A. Gain-of-function mutation causing constitutive channel activation
B. Loss-of-function mutation impairing chloride ion transport
C. Mitochondrial DNA mutation disrupting oxidative phosphorylation
D. Genomic imprinting defect affecting paternal allele expression
Correct Answer: B. Loss-of-function mutation impairing chloride ion transport
[CORRECT]
,2
Rationale: CFTR gene mutations cause loss of chloride channel function, leading to
thick mucus secretions in lungs, pancreas, and sweat glands. It is an autosomal
recessive disorder, not imprinting or mitochondrial.
Correct Answer: B
Q3. During myocardial ischemia, which intracellular event occurs first in the
progression from reversible to irreversible injury?
A. Lysosomal rupture
B. Mitochondrial swelling with calcium overload
C. Nuclear pyknosis
D. Plasma membrane phospholipid loss
Correct Answer: B. Mitochondrial swelling with calcium overload [CORRECT]
Rationale: Mitochondrial dysfunction with calcium accumulation and ATP depletion
marks the transition point to irreversible injury. Lysosomal rupture and nuclear
pyknosis occur later; phospholipid loss is a consequence, not the initial trigger.
Correct Answer: B
Q4. A patient with Li-Fraumeni syndrome develops multiple primary malignancies.
Which gene is mutated in this disorder?
A. RB1
B. TP53
C. BRCA1
D. APC
Correct Answer: B. TP53 [CORRECT]
Rationale: Li-Fraumeni syndrome results from germline TP53 mutations, causing loss
of cell cycle checkpoint control and apoptosis regulation. RB1 causes retinoblastoma;
BRCA1 is breast/ovarian cancer; APC is familial adenomatous polyposis.
Correct Answer: B
,3
Q5. Which mechanism best explains cellular atrophy in a patient with prolonged
corticosteroid use?
A. Increased protein synthesis via mTOR activation
B. Ubiquitin-proteasome pathway activation and autophagy
C. Decreased apoptosis with cellular senescence
D. Hypertrophy of adjacent compensatory cells
Correct Answer: B. Ubiquitin-proteasome pathway activation and autophagy
[CORRECT]
Rationale: Corticosteroid-induced atrophy involves increased protein breakdown via
the ubiquitin-proteasome system and autophagy-lysosomal pathways. mTOR
activation promotes growth; apoptosis decrease does not explain atrophy.
Correct Answer: B
Q6. In pyroptosis, which inflammatory caspase is primarily activated?
A. Caspase-3
B. Caspase-8
C. Caspase-1
D. Caspase-9
Correct Answer: C. Caspase-1 [CORRECT]
Rationale: Pyroptosis is a pro-inflammatory programmed cell death mediated by
caspase-1 (and caspase-4/5/11) activation of gasdermin D. Caspase-3 mediates
apoptosis; caspase-8 and -9 are initiator caspases in extrinsic/intrinsic apoptosis.
Correct Answer: C
Q7. A newborn with Prader-Willi syndrome demonstrates hypotonia and failure to
thrive. Which genetic mechanism is responsible?
, 4
A. Mitochondrial DNA deletion
B. Paternal chromosome 15q11-q13 deletion or maternal uniparental disomy
C. Trinucleotide repeat expansion on X chromosome
D. Autosomal dominant point mutation in the leptin receptor
Correct Answer: B. Paternal chromosome 15q11-q13 deletion or maternal
uniparental disomy [CORRECT]
Rationale: Prader-Willi syndrome results from loss of paternally expressed genes at
15q11-q13 via deletion or maternal uniparental disomy (imprinting disorder). It is not
mitochondrial, trinucleotide repeat, or leptin receptor-related.
Correct Answer: B
Q8. Which reactive oxygen species is generated primarily during the respiratory burst
in neutrophils?
A. Hydrogen peroxide
B. Superoxide anion
C. Hydroxyl radical
D. Peroxynitrite
Correct Answer: B. Superoxide anion [CORRECT]
Rationale: NADPH oxidase in neutrophils converts O2 to superoxide anion (O2•-) as
the initial ROS in respiratory burst. Hydrogen peroxide and hydroxyl radicals are
downstream products; peroxynitrite forms from superoxide and nitric oxide.
Correct Answer: B
Q9. A patient with xeroderma pigmentosum develops multiple skin cancers. Which
cellular process is defective?
A. Homologous recombination repair
B. Nucleotide excision repair
