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NURS6501 Advanced Pathophysiology Master Quiz Bank - 2026/2027 | Complete Assessment Collection & Practice Questions

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Master NURS 6501 Advanced Pathophysiology with this comprehensive Master Quiz Bank for 2026/2027. This complete assessment collection features practice questions covering all course topics including cellular injury, genetic disorders, immune pathologies, system-specific diseases, and clinical case studies. Perfect for Walden University MSN students seeking extensive practice and thorough preparation for all pathophysiology assessments.

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Uploaded on
January 12, 2026
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Written in
2025/2026
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NURS6501 Advanced Pathophysiology Master
Quiz Bank - 2026/2027 | Complete Assessment
Collection & Practice Questions


150 Questions & 100 % Correct Answers

Module 1 – Cellular, Genetic, and Immunologic Foundations (15 Q)

Q1

A 60-year-old man with chronic alcohol use disorder presents with jaundice and ascites.
A liver biopsy reveals hepatocytes with large, fatty vacuoles pushing the nucleus to the
periphery. Which pathologic process best explains this morphology?

A. Apoptosis

B. Caseous necrosis

C. Coagulative necrosis

D. Steatosis (fatty change)

Correct Answer: D

Rationale: Steatosis reflects reversible accumulation of triglyceride within the
cytoplasm; alcohol impairs hepatocyte β-oxidation and lipoprotein export. Apoptosis (A)
produces shrunken, eosinophilic cells without fat. Caseous (B) and coagulative (C)
necrosis are irreversible and lack vacuolation.

,Q2

A child with sickle-cell trait experiences high-altitude hypoxia and develops painless
hematuria. Which cellular adaptation predisposes to the observed red-cell sickling under
hypoxic stress?

A. Decreased 2,3-BPG production

B. Increased HbA affinity for oxygen

C. Mutation causing valine substitution at position 6 of β-globin

D. Up-regulation of fetal hemoglobin (HbF)

Correct Answer: C

Rationale: HbS results from βGlu6Val, creating a hydrophobic “sticky patch” that
polymerizes when deoxygenated. 2,3-BPG (A) increases in hypoxia and promotes
sickling by lowering O₂ affinity. HbF (D) protects, not predisposes.

Q3

A 45-year-old woman receives doxorubicin for breast cancer. Three weeks later her
ejection fraction falls from 60 % to 35 %. Electron microscopy shows myocyte
mitochondrial DNA depletion and loss of cristae. Which type of cellular injury
predominates?

A. Reversible hypoxic injury

B. Apoptosis triggered by oxidative stress

C. Oncotic (necrotic) myocyte death via membrane lysis

D. Autophagic vacuolization

,Correct Answer: B

Rationale: Anthracyclines generate ROS that trigger intrinsic (mitochondrial) apoptosis;
DNA depletion and cristae loss are hallmarks. Membrane lysis (C) would indicate
necrosis, not seen here. Autophagy (D) produces double-membrane vacuoles, not DNA
loss.

Q4

A newborn exhibits coarse facial features, hepatosplenomegaly, and cherry-red spot on
fundus. Enzyme assay shows absent α-L-iduronidase. Which pathophysiologic process
best describes the accumulated material in lysosomes?

A. Misfolded protein aggregation

B. Glycogen branching deficiency

C. Incomplete glycosaminoglycan degradation

D. Sphingomyelin accumulation

Correct Answer: C

Rationale: Hurler syndrome (MPS I) lacks α-L-iduronidase → dermatan & heparan
sulfate accumulate in lysosomes. Sphingomyelin (D) is Niemann-Pick; glycogen (B) is
Pompe; misfolded proteins (A) are seen in α-1 antitrypsin deficiency.

Q5

A 30-year-old man with BRCA1 mutation develops triple-negative breast cancer. Which
molecular mechanism links the mutated BRCA1 to the observed genomic instability?

A. Impaired homologous recombination DNA repair

, B. Defective nucleotide-excision repair of thymine dimers

C. Microsatellite instability from mismatch-repair failure

D. Increased telomerase activity

Correct Answer: A

Rationale: BRCA1 is essential for error-free homologous recombination; loss causes
double-strand breaks and chromosomal rearrangements. Microsatellite instability (C) is
Lynch syndrome; NER (B) is xeroderma pigmentosum.

Q6

A 25-year-old woman presents with recurrent venous thrombosis and spontaneous
miscarriages. Lab shows prolonged PTT that corrects with normal plasma. Which
autoantibody produces the observed hyper-coagulability?

A. Anti-β₂-glycoprotein-I

B. Anti-factor VIII

C. Anti-protein C

D. Lupus anticoagulant

Correct Answer: A

Rationale: Anti-β₂-GPI (with anti-cardiolipin & lupus anticoagulant) defines
antiphospholipid syndrome; antibody disrupts annexin A5 shield → ↑ thrombin
generation. Anti-factor VIII (B) causes bleeding, not thrombosis.

Q7
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