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NURS6501 Advanced Pathophysiology Midterm Exam - Walden University MSN | Disease Processes & System Pathology

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Prepare for your NURS 6501 Advanced Pathophysiology Midterm Exam with this comprehensive study guide for Walden University's MSN program (). This essential resource covers disease mechanisms, cellular injury processes, genetic disorders, immune system pathologies, and system-specific disorders for advanced practice nursing students. Perfect for mastering pathophysiological concepts and excelling in midterm assessment.

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January 12, 2026
Number of pages
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Written in
2025/2026
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NURS6501 Advanced Pathophysiology Midterm
Exam - Walden University MSN 2026-2027 |
Disease Processes & System Pathology


75 multiple-choice items | Bloom level coded (A = analysis/synthesis, P = application, R
= advanced recall)

MODULE 1 ‑ Cellular Basis of Disease (15 Qs)

Q1. A 55-year-old man with untreated hypertension is found to have a left-ventricular
wall thickness of 1.7 cm (normal ≤1.1 cm) with normal cavity size. Which
pathophysiologic process best explains this change?

A. Pathologic hyperplasia

B. Compensatory hypertrophy (P)

C. Metaplasia

D. Dysplasia

Correct Answer: B

Rationale: Chronic pressure overload increases sarcomeres in parallel → concentric
hypertrophy (adaptive). Not hyperplasia (cell number), metaplasia (cell type), or
dysplasia (atypia).

,Q2. A 42-year-old woman with BRCA1 mutation undergoes prophylactic oophorectomy.
Pathology shows multiple microscopic ovarian cortical inclusion cysts lined by
tubal-type ciliated epithelium. This change is termed:

A. Apocrine metaplasia

B. Squamous metaplasia

C. Tubal metaplasia (P)

D. Dysplastic metaplasia

Correct Answer: C

Rationale: Ciliated tubal epithelium in ovary is tubal metaplasia—benign cell-type switch.
Not apocrine (breast), squamous, or dysplastic.

Q3. A 6-year-old boy ingests iron tablets. Serum markers show lipid peroxidation and
mitochondrial swelling. Which type of cellular injury predominates?

A. Apoptosis

B. Oxidative stress (P)

C. Autophagy

D. Chaperone-mediated proteolysis

Correct Answer: B

Rationale: Iron catalyzes Fenton reaction → ROS → membrane lipid
peroxidation—classic oxidative injury. Not programmed death or proteostasis.

,Q4. A 68-year-old smoker develops emphysema. Histology shows alveolar wall
apoptosis and decreased elastin. Which enzyme imbalance is most central?

A. Neutrophil elastase ↑ and α1-antitrypsin ↓ (A)

B. Collagenase ↑ and TIMP ↓

C. Xanthine oxidase ↑ and catalase ↓

D. Pancreatic lipase ↑ and lipoprotein lipase ↓

Correct Answer: A

Rationale: Smoking oxidizes α1-AT → uninhibited elastase → elastin degradation →
emphysema. Other choices relate to fibrosis, reperfusion, or fat metabolism.

Q5. A renal allograft biopsy 3 months post-transplant shows endothelialitis and
interstitial lymphocytic infiltrate. Which process is primarily responsible?

A. Hyperacute rejection

B. Acute cellular rejection (P)

C. Chronic rejection

D. Calcineurin inhibitor toxicity

Correct Answer: B

Rationale: Endothelialitis + T-cell infiltrate defines acute cellular rejection. Hyperacute is
minutes (pre-formed Ab), chronic is months-years fibrosis, CNI toxicity causes striped
fibrosis.

, Q6. A 30-year-old HIV-positive patient starts ART. Two weeks later CD4 count rises from
80 to 250 cells/µL but he develops fever, pulmonary infiltrates, and pleuritic pain. Which
immunopathologic mechanism explains these findings?

A. IRIS – immune reconstitution inflammatory syndrome (P)

B. Drug-induced hypersensitivity pneumonitis

C. Cytokine storm from ART

D. Latent HIV replication in alveoli

Correct Answer: A

Rationale: Rapid CD4 recovery → exuberant Th1 response to subclinical pathogens →
IRIS. Not direct drug toxicity or viral replication.

Q7. A 50-year-old woman has hereditary non-polyposis colon cancer (HNPCC). DNA
analysis reveals microsatellite instability. Which DNA repair pathway is defective?

A. Base-excision repair

B. Nucleotide-excision repair

C. Mismatch repair (R)

D. Homologous recombination

Correct Answer: C

Rationale: HNPCC involves germline mutation in MSH2/MLH1 → mismatch repair
failure → microsatellite instability.
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