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NR507 Advanced Pathophysiology Midterm Exam - Chamberlain University | Disease Processes & System Disorders

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Prepare for your NR507 Advanced Pathophysiology Midterm Exam at Chamberlain University with this comprehensive study guide. This essential resource covers disease mechanisms, system-specific disorders, cellular pathology, genetic influences, and clinical correlations for nursing students. Complete preparation for demonstrating pathophysiological knowledge in midterm assessment.

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Institution
NR507 Advanced Pathophysiology
Course
NR507 Advanced Pathophysiology

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NR507 Advanced Pathophysiology Midterm Exam -
Chamberlain University 2026-2027 | Disease
Processes & System Disorders

65 Items | Grade A

All items are applied clinical vignettes that require mechanism-level reasoning.



Domain 1 — Cellular Foundations & Adaptive Responses (16 Qs)

Q1

A 65-year-old male with 50-pack-year smoking history has chronic cough. Bronchoscopy
shows ciliated columnar epithelium replaced by stratified squamous epithelium. This
change is:

A. Hyperplasia

B. Metaplasia

C. Dysplasia

D. Anaplasia

Correct: B (Metaplasia)

Rationale: Reversible substitution of one differentiated cell type by another (columnar →
squamous) in response to chronic irritation. Protective but loses mucus-clearing
function. Hyperplasia = ↑ cell number; dysplasia = disordered growth; anaplasia = loss
of differentiation (malignant).

,Q2

A 30-year-old woman with BRCA1 mutation undergoes breast biopsy showing ductal
epithelium with loss of polarity, nuclear pleomorphism, and increased mitoses but intact
myoepithelial layer. This is:

A. Hyperplasia

B. Metaplasia

C. Dysplasia

D. Carcinoma in situ

Correct: C (Dysplasia)

Rationale: Disordered growth with cytologic atypia confined within basement
membrane. Represents pre-neoplastic change. Not invasive (D) or simple hyperplasia
(A).

Q3

A 55-year-old man with COPD has barrel chest and flattened diaphragm on CXR. These
changes result from:

A. Type I alveolar cell apoptosis

B. Centrilobular emphysema with loss of elastic recoil → air trapping

C. Bronchial smooth muscle hyperplasia

D. Mucus gland hypertrophy

Correct: B

,Rationale: Emphysema destroys alveolar walls → loss of elastic recoil → air trapping →
barrel chest/flat diaphragm. Other options describe different COPD pathologies
(bronchitis, asthma).

Q4

A 70-year-old man with CHF has bilateral pitting edema to knees. Which Starling force
change is primary?

A. ↑ plasma oncotic pressure

B. ↑ interstitial hydrostatic pressure

C. ↑ capillary hydrostatic pressure

D. ↓ capillary oncotic pressure

Correct: C

Rationale: Heart failure → ↑ venous pressure → ↑ capillary hydrostatic pressure → fluid
filtration > reabsorption → edema. Not ↓ oncotic (D) or ↑ interstitial pressure (B).

Q5

A 25-year-old man with acute appendicitis has RLQ pain, fever, and neutrophilia. Which
inflammatory mediator is most responsible for neutrophil margination?

A. IL-1

B. Histamine

C. C5a

D. Bradykinin

, Correct: C (C5a)

Rationale: Complement fragment C5a is potent chemoattractant and causes neutrophil
margination and chemotaxis. IL-1 (A) causes fever and acute phase response;
histamine (B) vasodilation; bradykinin (D) pain.

Q6

A 60-year-old woman with RA has pannus formation on hand X-ray. Pannus consists of:

A. Granulation tissue with fibroblasts and neovessels invading cartilage

B. Caseating necrosis with multinucleated giant cells

C. Fibrinoid necrosis of vessel walls

D. Amyloid deposition in synovium

Correct: A

Rationale: Pannus = inflammatory granulation tissue (fibroblasts, neovessels,
inflammatory cells) that erodes cartilage and bone. Not caseating (B) or amyloid (D).

Q7

A 45-year-old woman with SLE has photosensitive rash and anti-dsDNA antibodies.
Which type of hypersensitivity is primary in SLE?

A. Type I (IgE-mediated)

B. Type II (cytotoxic antibody)

C. Type III (immune complex)

D. Type IV (delayed T-cell)

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Institution
NR507 Advanced Pathophysiology
Course
NR507 Advanced Pathophysiology

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Uploaded on
January 15, 2026
Number of pages
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Written in
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Type
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