, SG 530 Exam 1,2,3,4 | Advanced Pathophysiology | Wilkes University
NSG 530 EXAM 1
Advanced Pathophysiology
Wilkes University
100-Question Practice Examination
2026/2027 Edition
1. A skeletal muscle cell exposed to sustained workload enlarges without increasing cell number. Which
adaptation best explains this response?
A) Hyperplasia
B) Metaplasia
C) Dysplasia
D) Hypertrophy
Correct Answer: Hypertrophy
Rationale: Hypertrophy is an increase in individual cell size caused by increased synthesis of structural proteins and
organelles. It is typical in tissues with limited proliferative capacity, such as skeletal and cardiac muscle. Hyperplasia
increases cell number, whereas metaplasia and dysplasia describe changes in cell phenotype or organization rather
than simple enlargement.
2. Endometrial tissue increases in cell number in response to estrogenic stimulation. This change is
classified as which cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Correct Answer: Hyperplasia
Rationale: Hyperplasia reflects an increase in the number of cells in a tissue and occurs when cells retain the
capacity to divide. Hormonal stimulation can produce physiologic or pathologic hyperplasia. Hypertrophy enlarges
existing cells, atrophy reduces cell size or number, and metaplasia substitutes one differentiated cell type for
another.
3. A smoker develops replacement of normal ciliated columnar bronchial epithelium by stratified squamous
epithelium. What process has occurred?
A) Dysplasia
B) Anaplasia
C) Metaplasia
D) Hyperplasia
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, Correct Answer: Metaplasia
Rationale: Metaplasia is a reversible adaptive substitution of one mature cell type by another better able to tolerate
chronic stress. In smokers, squamous cells resist irritation but sacrifice mucociliary function. Dysplasia involves
disordered growth, anaplasia denotes loss of differentiation, and hyperplasia increases the number of cells without
changing their mature lineage.
4. During prolonged immobilization, a limb muscle decreases in size and strength. Which mechanism
contributes most directly?
A) Persistent mitochondrial biogenesis
B) Increased DNA replication
C) Sustained cellular edema
D) Increased protein degradation with reduced protein synthesis
Correct Answer: Increased protein degradation with reduced protein synthesis
Rationale: Disuse atrophy develops when protein synthesis falls and proteolysis increases, often through ubiquitin-
proteasome and autophagic pathways. The result is smaller cells and reduced functional capacity. Mitochondrial
biogenesis and DNA replication would not explain shrinkage, while transient cellular edema causes swelling rather
than loss of mass.
5. Loss of ATP during ischemia most immediately impairs which membrane process?
A) Na+/K+-ATPase activity
B) Passive oxygen diffusion
C) Steroid hormone transport
D) Aquaporin expression
Correct Answer: Na+/K+-ATPase activity
Rationale: ATP depletion quickly disables energy-dependent ion pumps, especially the sodium-potassium ATPase.
Sodium and water then accumulate intracellularly, producing cellular swelling, while potassium leaks out. Passive
diffusion does not require ATP, and altered aquaporin expression or steroid transport is not the earliest mechanism
responsible for ischemic swelling.
6. A myocardial cell becomes swollen after brief hypoxia but recovers when oxygen is restored. This finding
is most consistent with what type of injury?
A) Reversible cellular injury
B) Coagulative necrosis
C) Apoptosis
D) Liquefactive necrosis
Correct Answer: Reversible cellular injury
Rationale: Early hypoxic injury can be reversible when ATP production and membrane ion gradients are restored
before irreversible membrane and mitochondrial damage occurs. Cellular swelling is a classic early manifestation.
Necrosis denotes irreversible injury with membrane disruption, whereas apoptosis is a regulated form of cell death
rather than transient hypoxic dysfunction.
7. Which intracellular change is most characteristic of irreversible cell injury?
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, A) Temporary ribosomal detachment
B) Inability to reverse mitochondrial dysfunction
C) Mild cellular swelling
D) Transient glycogen depletion
Correct Answer: Inability to reverse mitochondrial dysfunction
Rationale: Irreversible injury is marked by failure to restore mitochondrial function and severe membrane damage.
Once oxidative phosphorylation cannot recover, ATP depletion becomes critical and destructive pathways
accelerate. Ribosomal detachment, glycogen loss, and cellular swelling can occur during reversible injury and may
resolve if the stressor is removed promptly.
8. A patient with an acute myocardial infarction develops death of cardiac myocytes in the affected region.
Which pattern of necrosis is expected?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Fat necrosis
Correct Answer: Coagulative necrosis
Rationale: Ischemic infarction in most solid organs, including the heart, produces coagulative necrosis. Protein
denaturation temporarily preserves basic tissue architecture despite cell death. Liquefactive necrosis is typical of
brain infarcts and abscesses, caseous necrosis occurs in granulomatous infections such as tuberculosis, and fat
necrosis commonly follows pancreatic enzyme release or trauma.
9. A cerebral infarct evolves into a soft, cystic area. Which necrotic pattern best accounts for this change?
A) Liquefactive necrosis
B) Coagulative necrosis
C) Fibrinoid necrosis
D) Fat necrosis
Correct Answer: Liquefactive necrosis
Rationale: Brain infarction typically undergoes liquefactive necrosis because enzymatic digestion predominates over
structural protein preservation. Dead tissue is converted into a viscous liquid and eventually removed, often leaving a
cystic space. Coagulative necrosis is more typical of ischemia in other solid organs, whereas fibrinoid and fat
necrosis have different settings.
10. A pancreatic enzyme leak causes chalky white deposits in peripancreatic tissue. Which process is
occurring?
A) Caseous necrosis
B) Gangrenous necrosis
C) Enzymatic fat necrosis
D) Fibrinoid necrosis
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