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Exam (elaborations)

NR 507 – Advanced Pathophysiology (Chamberlain University, 2025/2026) – Midterm Exam Review with Verified Questions & Answers (Grade A)

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This document provides the complete NR 507 midterm exam review for Chamberlain University, fully updated for the 2025/2026 academic year. It contains 100% verified questions and correct answers that cover essential pathophysiological concepts and disease mechanisms across body systems. Topics include cellular injury, inflammation, genetics, endocrine and cardiovascular disorders, neurological pathologies, and immune system dysfunctions. An excellent study resource for mastering advanced pathophysiology and preparing for the NR 507 midterm exam.

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NR 507
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Uploaded on
November 7, 2025
Number of pages
16
Written in
2025/2026
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NR507 / NR 507 Midterm Exam (New
2025/2026 Update) Advanced
Pathophysiology | Questions and
Verified Answers | 100% Correct | A
Grade – Chamberlain
Section 1: Cellular Injury (Questions 1-10)
Question 1: In reversible cellular injury, which mechanism primarily
leads to cellular swelling due to impaired ATP production?

• A. Nuclear pyknosis
• B. Mitochondrial dysfunction
• C. Plasma membrane rupture
• D. Lysosomal enzyme leakage

B Rationale: Mitochondrial dysfunction impairs ATP synthesis, leading
to failure of the Na+/K+ ATPase pump, causing sodium influx and
cellular swelling (hydropic change), which is reversible if restored early.
A is a feature of irreversible injury; C and D indicate necrosis.

Question 2: Which type of cellular adaptation occurs when hepatocytes
enlarge in response to chronic alcohol exposure?
• A. Atrophy
• B. Hypertrophy
• C. Hyperplasia
• D. Metaplasia

B Rationale: Hypertrophy involves increased cell size due to synthetic
demands, as in alcoholic liver disease where hepatocytes accumulate fat

, 2



and proteins. A is size reduction; C is cell number increase; D is cell
type change.
Question 3: Free radical injury in ischemia-reperfusion damage
primarily targets which cellular component?

• A. Nucleus
• B. Lipids in membranes
• C. Cytoskeleton
• D. Ribosomes

B Rationale: Free radicals cause lipid peroxidation in polyunsaturated
fatty acids of cell membranes, leading to membrane instability and
leakage. A, C, and D are secondary targets with less direct impact.

Question 4: The transition from reversible to irreversible cellular injury
is marked by?

• A. Glycogen depletion
• B. Mitochondrial permeability transition
• C. Endoplasmic reticulum dilation
• D. Cytoplasmic vacuolation

B Rationale: Mitochondrial permeability transition releases cytochrome
c, initiating apoptosis or necrosis, a key irreversible event. A, C, and D
are reversible changes.

Question 5: In hypoxic injury, the earliest ultrastructural change
observed is?

• A. Blebbing of the plasma membrane
• B. Swelling of the endoplasmic reticulum
• C. Chromatin clumping
• D. Karyorrhexis

, 3



B Rationale: ER swelling occurs first due to impaired protein folding
from ATP loss in hypoxia. A and C are later; D is irreversible nuclear
fragmentation.

Question 6: Which enzyme system detoxifies reactive oxygen species in
cellular injury?

• A. Cytochrome P450
• B. Superoxide dismutase
• C. Caspase-3
• D. DNA polymerase
B Rationale: Superoxide dismutase converts superoxide to hydrogen
peroxide, a primary antioxidant defense. A metabolizes xenobiotics; C
executes apoptosis; D repairs DNA.

Question 7: Calcific deposits in damaged cells (dystrophic calcification)
result from?
• A. Hypercalcemia
• B. Mitochondrial calcium overload
• C. Lysosomal phosphate release
• D. Extracellular matrix degradation

B Rationale: Damaged mitochondria sequester calcium, leading to
phosphate precipitation as calcium phosphate crystals. A is systemic; C
and D are unrelated.
Question 8: Apoptosis in cellular injury is triggered by which intrinsic
pathway activator?

• A. TNF-alpha
• B. Bax/Bak oligomerization
• C. Fas ligand
• D. Granzyme B

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