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NURS 5315 Advanced Pathophysiology
UTA Exam 1 2026/2027 | Real Verified
Questions, Detailed Rationales, Graded
A+ Complete Study Guide
Section 1: Cellular Adaptation, Injury, and Death (Questions 1-40)
1. A 58-year-old male with long-standing uncontrolled hypertension develops increased left
ventricular wall thickness while individual cardiac muscle cells become larger rather than
increasing in number. Which cellular adaptation best explains this pathophysiologic response?
A. Metaplasia
B. Hyperplasia
C. Hypertrophy
D. Atrophy
ANS: C
Rationale: Cardiac myocytes are permanent cells that cannot divide. Chronic pressure overload
from hypertension stimulates hypertrophy—an increase in cell size via accelerated protein
synthesis and sarcomere replication—to compensate for increased workload. Hyperplasia
(increased cell number) cannot occur in terminally differentiated cardiac muscle .
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2. A patient with chronic gastroesophageal reflux disease develops replacement of normal
distal esophageal squamous epithelium with specialized columnar epithelium containing
goblet cells. Which cellular adaptation is occurring?
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
ANS: C
Rationale: Metaplasia is a reversible change in which one differentiated cell type is replaced by
another mature cell type better suited to withstand chronic irritation. Barrett esophagus is
intestinal metaplasia, where squamous epithelium changes to columnar epithelium with goblet
cells in response to chronic acid reflux .
3. A patient experiences prolonged tissue hypoxia with depleted ATP, impaired sodium-
potassium pump activity, cellular swelling, and progressive membrane dysfunction. Which
initial cellular consequence of hypoxia most directly explains the intracellular fluid
accumulation?
A. Failure of oxidative phosphorylation with ATP depletion
B. Increased mitochondrial protein synthesis
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C. Increased intracellular calcium sequestration
D. Accelerated DNA replication
ANS: A
Rationale: Hypoxia impairs mitochondrial oxidative phosphorylation, depleting ATP. Without
ATP, the Na⁺/K⁺-ATPase pump fails, allowing sodium to accumulate intracellularly. Water follows
sodium osmotically, causing cellular swelling (oncosis). This is the earliest reversible
consequence of hypoxic injury .
4. A patient with severe ischemic injury to the myocardium develops irreversible cellular
damage followed by preservation of the general tissue architecture during early stages of cell
death. Which type of necrosis is most characteristic?
A. Fat necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Coagulative necrosis
ANS: D
Rationale: Coagulative necrosis is characteristic of ischemic injury in organs except the brain.
Protein denaturation predominates over enzymatic digestion, preserving tissue architecture for
days. The brain undergoes liquefactive necrosis instead .
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5. A patient with a cerebral infarction develops enzymatic digestion of damaged brain tissue,
resulting in softening and eventual formation of a fluid-filled cavity. Which type of necrosis
best describes this process?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fibrinoid necrosis
D. Fat necrosis
ANS: B
Rationale: Liquefactive necrosis occurs in the brain and in bacterial abscesses. Brain tissue is
rich in lipids and hydrolytic enzymes and lacks a resilient structural framework, so enzymatic
digestion predominates, causing tissue to liquefy into a fluid-filled cavity .
6. A patient with acute pancreatitis develops destruction of adipose tissue surrounding the
pancreas. Released pancreatic lipase breaks down triglycerides, and fatty acids combine with
calcium to form insoluble deposits. Which type of necrosis is occurring?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Fibrinoid necrosis
ANS: C
NURS 5315 Advanced Pathophysiology
UTA Exam 1 2026/2027 | Real Verified
Questions, Detailed Rationales, Graded
A+ Complete Study Guide
Section 1: Cellular Adaptation, Injury, and Death (Questions 1-40)
1. A 58-year-old male with long-standing uncontrolled hypertension develops increased left
ventricular wall thickness while individual cardiac muscle cells become larger rather than
increasing in number. Which cellular adaptation best explains this pathophysiologic response?
A. Metaplasia
B. Hyperplasia
C. Hypertrophy
D. Atrophy
ANS: C
Rationale: Cardiac myocytes are permanent cells that cannot divide. Chronic pressure overload
from hypertension stimulates hypertrophy—an increase in cell size via accelerated protein
synthesis and sarcomere replication—to compensate for increased workload. Hyperplasia
(increased cell number) cannot occur in terminally differentiated cardiac muscle .
, 2
2. A patient with chronic gastroesophageal reflux disease develops replacement of normal
distal esophageal squamous epithelium with specialized columnar epithelium containing
goblet cells. Which cellular adaptation is occurring?
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
ANS: C
Rationale: Metaplasia is a reversible change in which one differentiated cell type is replaced by
another mature cell type better suited to withstand chronic irritation. Barrett esophagus is
intestinal metaplasia, where squamous epithelium changes to columnar epithelium with goblet
cells in response to chronic acid reflux .
3. A patient experiences prolonged tissue hypoxia with depleted ATP, impaired sodium-
potassium pump activity, cellular swelling, and progressive membrane dysfunction. Which
initial cellular consequence of hypoxia most directly explains the intracellular fluid
accumulation?
A. Failure of oxidative phosphorylation with ATP depletion
B. Increased mitochondrial protein synthesis
, 3
C. Increased intracellular calcium sequestration
D. Accelerated DNA replication
ANS: A
Rationale: Hypoxia impairs mitochondrial oxidative phosphorylation, depleting ATP. Without
ATP, the Na⁺/K⁺-ATPase pump fails, allowing sodium to accumulate intracellularly. Water follows
sodium osmotically, causing cellular swelling (oncosis). This is the earliest reversible
consequence of hypoxic injury .
4. A patient with severe ischemic injury to the myocardium develops irreversible cellular
damage followed by preservation of the general tissue architecture during early stages of cell
death. Which type of necrosis is most characteristic?
A. Fat necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Coagulative necrosis
ANS: D
Rationale: Coagulative necrosis is characteristic of ischemic injury in organs except the brain.
Protein denaturation predominates over enzymatic digestion, preserving tissue architecture for
days. The brain undergoes liquefactive necrosis instead .
, 4
5. A patient with a cerebral infarction develops enzymatic digestion of damaged brain tissue,
resulting in softening and eventual formation of a fluid-filled cavity. Which type of necrosis
best describes this process?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fibrinoid necrosis
D. Fat necrosis
ANS: B
Rationale: Liquefactive necrosis occurs in the brain and in bacterial abscesses. Brain tissue is
rich in lipids and hydrolytic enzymes and lacks a resilient structural framework, so enzymatic
digestion predominates, causing tissue to liquefy into a fluid-filled cavity .
6. A patient with acute pancreatitis develops destruction of adipose tissue surrounding the
pancreas. Released pancreatic lipase breaks down triglycerides, and fatty acids combine with
calcium to form insoluble deposits. Which type of necrosis is occurring?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Fibrinoid necrosis
ANS: C
