NURS 6501 ADVANCED PATHOPHYSIOLOGY MIDTERM
2026/2027 | Official Practice Exam | Pass Guaranteed - A+
Graded
Total Questions: 50 | Time: 90 min | Pass: 80%
TABLE OF CONTENTS
Section 1 | Cellular Function & Genetics | Q1 – Q10
Section 2 | Inflammation & Immunity | Q11 – Q20
Section 3 | Cardiovascular & Hematologic Pathophysiology | Q21 – Q30
Section 4 | Respiratory & Renal Pathophysiology | Q31 – Q40
Section 5 | Endocrine & Neurologic Pathophysiology | Q41 – Q50
Instructions: Choose the single best answer. Pass: 40 in 90 minutes.
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SECTION 1: CELLULAR FUNCTION & GENETICS Q1 – Q10
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Question 1 of 50
A 62-year-old man with a 40-pack-year smoking history presents for a routine
physical. Bronchoscopy reveals that the pseudostratified ciliated columnar
epithelium lining his distal bronchi has been replaced by stratified squamous
epithelium. The pathologist notes this change is reversible if the irritant is
removed.
A. Atrophy from chronic hypoxia
B. Hypertrophy of existing columnar cells
,2
C. Metaplasia with replacement by a different cell type ✓ CORRECT
D. Dysplasia with disordered nuclear maturation
Correct Answer: C
Rationale: Metaplasia is the reversible substitution of one differentiated cell
type for another, typically in response to chronic irritation such as smoking.
Dysplasia involves disordered maturation and is considered pre-neoplastic,
which is not the case here. In clinical practice, this finding should prompt
smoking cessation counseling to allow potential reversal.
Question 2 of 50
A 28-year-old woman with a history of systemic lupus erythematosus has
developed progressive fatigue over the past six months. Laboratory studies
reveal a hemoglobin of 8.2 g/dL with a mean corpuscular volume of 108 fL. Her
peripheral blood smear shows macro-ovalocytes and hypersegmented
neutrophils.
A. Iron deficiency from chronic disease
B. Pernicious anemia from autoimmune destruction of parietal cells ✓
CORRECT
C. Folate deficiency from dietary insufficiency
D. Hemolytic anemia from complement activation
Correct Answer: B
Rationale: Pernicious anemia involves autoimmune destruction of gastric
parietal cells, leading to intrinsic factor deficiency and vitamin B12
malabsorption, which produces macrocytic anemia with hypersegmented
neutrophils. Folate deficiency also causes macrocytosis but lacks the
autoimmune association and neurologic complications seen with B12
,3
deficiency. Patients with SLE have higher rates of autoimmune comorbidities,
making pernicious anemia a more likely diagnosis than isolated nutritional
deficiency.
Question 3 of 50
During a liver biopsy, a pathologist identifies hepatocytes with single-cell
necrosis showing cell shrinkage, chromatin condensation, and formation of
apoptotic bodies without significant inflammatory infiltrate.
A. Coagulative necrosis from ischemic injury
B. Liquefactive necrosis from bacterial infection
C. Apoptosis via intrinsic and extrinsic caspase pathways ✓ CORRECT
D. Fat necrosis from enzymatic digestion
Correct Answer: C
Rationale: Apoptosis is characterized by cell shrinkage, chromatin
condensation, and apoptotic body formation without inflammation, mediated
by caspase cascades. Coagulative necrosis shows preserved architecture with
loss of nuclei; liquefactive necrosis involves enzymatic digestion typical of
abscesses; fat necrosis occurs in adipose tissue with calcium saponification.
Recognizing apoptosis is important because it represents programmed cell
death rather than injury, which has different therapeutic implications.
Question 4 of 50
A 45-year-old woman with chronic hepatitis C has developed cirrhosis. Liver
biopsy shows widespread cellular swelling and mitochondrial vacuolization in
hepatocytes near the portal tracts, but the plasma membranes remain intact.
, 4
A. Irreversible injury with karyolysis and membrane rupture
B. Reversible injury from ATP depletion and Na+/K+ pump failure ✓ CORRECT
C. Apoptosis with caspase activation and cell shrinkage
D. Metaplasia with replacement by fibroblasts
Correct Answer: B
Rationale: In reversible injury, ATP depletion causes Na+/K+ pump failure,
leading to cellular swelling and mitochondrial dysfunction without membrane
rupture. Irreversible injury would show karyolysis and membrane disruption;
apoptosis involves programmed cell shrinkage; metaplasia is an adaptive
change, not acute ischemic injury. Distinguishing reversible from irreversible
injury guides clinical decisions about whether hepatocellular damage can be
reversed with treatment.
Question 5 of 50
A 38-year-old woman with a strong family history of breast and ovarian cancer
undergoes genetic testing. The results identify a mutation in the BRCA1 gene,
which significantly increases her lifetime risk of developing these malignancies.
A. Defective mismatch repair causing microsatellite instability
B. Impaired homologous recombination DNA repair and genomic instability ✓
CORRECT
C. Enhanced telomerase activity preventing replicative senescence
D. Upregulation of tumor suppressor p53
Correct Answer: B
Rationale: BRCA1 is critical for homologous recombination repair of double-
strand DNA breaks; loss causes genomic instability and increased cancer risk.