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Chamberlain NR507 Final Exam Prep 2 2026 | Advanced Pathophysiology Questions & Answers | PDF

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INSTANT PDF DOWNLOAD. This Chamberlain NR507 Advanced Pathophysiology Final Exam Prep 2 study resource provides focused review of key pathophysiology concepts relevant to graduate nursing coursework and exam preparation. It includes practice questions and answers designed to reinforce understanding of disease mechanisms, cellular responses, inflammation, immune function, and major physiological disorders. This resource supports focused revision, knowledge reinforcement, and final exam preparation.

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Chamberlain NR507 Final Exam Prep 2(2026) Adv
Patho Questions & Answers (PDF)
300 QUESTIONS




TABLE OF CONTENTS

# TOPIC

1 Chamberlain NR507 Final Exam Prep 2(2026) Adv Patho Questions & Answers (PDF)

,Q1
Which mechanism best explains reperfusion injury following ischemic myocardial tissue
restoration?

A) Decreased mitochondrial ATP production

B) Excessive reactive oxygen species and calcium overload CORRECT

C) Activation of anaerobic glycolysis

D) Reduced inflammatory cytokine release


Rationale
Reperfusion injury is driven by a burst of reactive oxygen species and intracellular calcium overload that
trigger mitochondrial permeability transition and cell death.



Q2
A pathologist notes cells with abnormal size, shape, and organization, but the basement
membrane remains intact. This finding is most consistent with:

A) Metaplasia

B) Hyperplasia

C) Dysplasia CORRECT

D) Anaplasia


Rationale
Dysplasia refers to disorganized growth with abnormal cell morphology and loss of polarity, yet the
basement membrane remains intact, distinguishing it from invasive carcinoma.



Q3
Cell swelling is caused by:

A) ATP depletion CORRECT

B) Hyperplasia

C) Atrophy

D) Fibrosis



2

,Rationale
Hypoxic injury depletes ATP, impairing the Na⁺/K⁺ pump, causing sodium and water influx and cellular
swelling (hydropic change).



Q4
Which type of cell death is energy-dependent, non-inflammatory, and characterized by cell
shrinkage and nuclear fragmentation?

A) Necrosis

B) Apoptosis CORRECT

C) Autophagy

D) Pyroptosis


Rationale
Apoptosis is an active, programmed process of cell death that does not incite inflammation and features
cell shrinkage and nuclear condensation.



Q5
A 68-year-old male with long-standing hypertension has increased left ventricular wall thickness
without chamber dilation. Which cellular adaptation is primarily responsible?

A) Hyperplasia of cardiac myocytes

B) Hypertrophy of cardiac myocytes CORRECT

C) Metaplasia of cardiac tissue

D) Atrophy of ventricular myocardium


Rationale
Chronic pressure overload stimulates an increase in individual myocyte size (hypertrophy), because
cardiac cells are terminally differentiated and cannot undergo hyperplasia.



Q6
Which of the following is a hallmark of irreversible cellular injury?

A) Cellular swelling


3

, B) Fatty change

C) Membrane rupture and mitochondrial dysfunction CORRECT

D) Ribosomal detachment


Rationale
Irreversible injury is characterized by severe membrane damage, mitochondrial dysfunction with ATP
loss, and lysosomal enzyme release.



Q7
A cell that has lost specialized features and resembles a primitive cell is described as:

A) Dysplastic

B) Metaplastic

C) Anaplastic CORRECT

D) Hyperplastic


Rationale
Anaplasia is the lack of differentiation, often seen in malignant tumors.



Q8
Which pigment accumulates in cells after free radical injury and is associated with aging?

A) Bilirubin

B) Lipofuscin CORRECT

C) Melanin

D) Hemosiderin


Rationale
Lipofuscin is a “wear-and-tear” pigment resulting from free radical–mediated lipid peroxidation.




4

Información del documento

Subido en
19 de octubre de 2026
Número de páginas
110
Escrito en
2026/2027
Tipo
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