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NR 507 / NR507 Advanced Pathophysiology Midterm Exam V1 | Verified Answers | Latest Update 2026 / 2027 | Chamberlain University | Exam Review & Practice Questions

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NR 507 / NR507 Advanced Pathophysiology Midterm Exam V1 | Verified Answers | Latest Update 2026 / 2027 | Chamberlain University | Exam Review & Practice Questions

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NR 507 / NR507 Advanced Pathophysiology
Midterm Exam V1 | Verified Answers | Latest
Update | Chamberlain University
| Exam Review & Practice Questions

Question 1

A 55-year-old male construction worker develops increased muscle mass in his
dominant arm after years of heavy manual labor. A biopsy would MOST likely
reveal which cellular change?

A. Increased number of muscle cells (hyperplasia)
B. Increased size of individual muscle cells with more myofibrils and mitochondria
(hypertrophy)
C. Replacement of muscle cells with fibrous tissue (fibrosis)
D. Abnormal muscle cell morphology with nuclear pleomorphism (dysplasia)

Correct Answer: B. Increased size of individual muscle cells with more myofibrils and
mitochondria

Rationale: Skeletal muscle cells are terminally differentiated and cannot divide. They
respond to increased workload through hypertrophy (increased cell size) by adding
more myofibrils, mitochondria, and sarcoplasmic reticulum .



Question 2

A 48-year-old female with chronic gastroesophageal reflux disease (GERD)
undergoes endoscopy revealing replacement of normal squamous esophageal
epithelium with columnar epithelium (Barrett's esophagus). This cellular change
BEST represents:

A. Dysplasia
B. Hyperplasia

,C. Metaplasia
D. Coagulative necrosis

Correct Answer: C. Metaplasia

Rationale: Barrett's esophagus is squamous-to-columnar metaplasia caused by chronic
acid exposure. The new epithelium is more resistant to acid but carries risk of
adenocarcinoma. Metaplasia is reversible if the stimulus is removed .



Question 3

During myocardial ischemia, which of the following FIRST occurs at the cellular
level?

A. Nuclear chromatin margination and karyorrhexis
B. Lysosomal membrane rupture releasing digestive enzymes
C. Failure of Na+/K+ ATPase causing cellular swelling and calcium influx
D. Mitochondrial membrane rupture releasing cytochrome c

Correct Answer: C. Failure of Na+/K+ ATPase causing cellular swelling and calcium
influx

Rationale: ATP depletion during ischemia first causes Na+/K+ ATPase pump failure →
intracellular sodium accumulation → osmotic water entry → cellular swelling (earliest
reversible change). Calcium influx activates destructive enzymes .



Question 4

A pathologist examining tissue from a patient who died of a stroke finds liquefied
brain tissue with a fluid-filled cavity. This type of necrosis occurred because:

A. The brain has high protein content that denatures during ischemia
B. The brain has high lipid content and abundant hydrolytic enzymes that completely
digest necrotic tissue
C. Bacterial infection caused enzymatic dissolution of brain tissue
D. Caseous material accumulated due to granulomatous inflammation

,Correct Answer: B. The brain has high lipid content and abundant hydrolytic enzymes
that completely digest necrotic tissue

Rationale: Liquefactive necrosis in the brain results from high fat content and abundant
hydrolytic enzymes. Unlike other organs where coagulative necrosis preserves cell
outlines, brain tissue is completely digested forming a fluid-filled cyst .



Question 5

A 60-year-old female with chronic hypertension and hyperlipidemia experiences
sudden severe chest pain. Cardiac enzymes confirm a myocardial infarction (MI).
Which process is MOST likely responsible for her MI?

A. Apoptosis of myocardial cells
B. Coagulative necrosis
C. Caseous necrosis
D. Liquefactive necrosis

Correct Answer: B. Coagulative necrosis

Rationale: Myocardial infarction results from ischemia, which causes coagulative
necrosis. This type of necrosis preserves cell outlines for days while the cells die, leading
to an inflammatory response and eventual scar formation .



Question 6

Why is reperfusion injury a concern after restoring blood flow to ischemic tissue?

A. The tissue has already died and cannot be salvaged
B. Restoration of oxygen leads to free radical generation, neutrophil activation, and
calcium overload
C. Blood flow causes the tissue to swell and rupture
D. The tissue is no longer viable

Correct Answer: B. Restoration of oxygen leads to free radical generation, neutrophil
activation, and calcium overload

, Rationale: Reperfusion injury occurs paradoxically when oxygen is restored to ischemic
tissue. Xanthine oxidase generates massive free radicals, neutrophils are activated
releasing proteases and ROS, and calcium overload worsens mitochondrial dysfunction.
Reperfusion injury can exceed the original ischemic damage .



Question 7

A 40-year-old female undergoes surgical resection of a mesenteric artery
thrombus restoring blood flow to ischemic bowel. Despite successful reperfusion,
the patient develops worsening bowel injury. This paradox is BEST explained by:

A. Continued ischemic injury despite restored blood flow
B. Reperfusion injury from massive free radical generation, neutrophil activation, and
calcium overload upon oxygen restoration
C. Bacterial translocation from the bowel causing systemic infection
D. Surgical trauma causing additional ischemic injury

Correct Answer: B. Reperfusion injury from massive free radical generation, neutrophil
activation, and calcium overload upon oxygen restoration

Rationale: Reperfusion injury occurs paradoxically when oxygen is restored to ischemic
tissue. Xanthine oxidase generates massive free radicals, neutrophils are activated
releasing proteases and ROS, and calcium overload worsens mitochondrial dysfunction .



Question 8

During apoptosis, which of the following nuclear changes is considered the
HALLMARK morphological feature?

A. Nuclear swelling and membrane rupture
B. Chromatin condensation and DNA fragmentation into nucleosomal ladder pattern
C. Nuclear dissolution without membrane changes
D. Nuclear enlargement with prominent nucleoli

Correct Answer: B. Chromatin condensation and DNA fragmentation into nucleosomal
ladder pattern

Información del documento

Subido en
30 de julio de 2026
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116
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2025/2026
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