MSN 570 Final Exam | Questions and Answers |
2026/2027 Updated | 100% Correct - USU.
SECTION I — Cellular Adaptation, Injury, Inflammation & Cell Death
1.
A patient with long-standing hypertension develops progressive thickening of the
left ventricular myocardium. Which cellular adaptation best explains this finding?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Atrophy
Correct answer: B. Hypertrophy
Rationale: Cardiac myocytes have limited ability to divide, so chronic pressure
overload primarily causes hypertrophy, an increase in cell size. Hypertension
increases afterload, requiring greater myocardial force generation. Although
initially compensatory, prolonged hypertrophy can eventually impair ventricular
relaxation, increase oxygen demand, and contribute to heart failure.
2.
A patient with chronic gastroesophageal reflux develops replacement of normal
esophageal squamous epithelium with columnar epithelium. This process is:
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Hypertrophy
Correct answer: C. Metaplasia
,Rationale: Metaplasia is a reversible adaptation in which one mature cell type is
replaced by another better suited to chronic environmental stress. Barrett
esophagus represents columnar metaplasia associated with chronic acid
exposure. Persistent injury can increase the risk of dysplasia and adenocarcinoma.
3.
Which cellular event occurs earliest when ATP depletion develops during ischemic
injury?
A. Increased protein synthesis
B. Failure of the sodium-potassium ATPase
C. Nuclear fragmentation
D. Mitochondrial DNA replication
Correct answer: B. Failure of the sodium-potassium ATPase
Rationale: ATP depletion impairs energy-dependent membrane pumps,
particularly the Na⁺/K⁺-ATPase. Intracellular sodium increases, water follows
osmotically, and cellular swelling develops. This is an early and potentially
reversible manifestation of cell injury.
4.
A patient experiences severe tissue hypoxia. Which consequence of mitochondrial
dysfunction contributes most directly to progressive cellular injury?
A. Increased ATP generation
B. Increased oxidative phosphorylation
C. Reduced ATP production
D. Increased protein folding
Correct answer: C. Reduced ATP production
Rationale: Mitochondria require oxygen for oxidative phosphorylation. Hypoxia
reduces ATP generation, impairing ion pumps, protein synthesis, membrane
,integrity, and cellular homeostasis. Prolonged mitochondrial injury can ultimately
result in irreversible cell damage and death.
5.
Which finding most strongly indicates irreversible cellular injury?
A. Cellular swelling
B. Fatty change
C. Ribosomal detachment
D. Severe mitochondrial dysfunction with membrane damage
Correct answer: D. Severe mitochondrial dysfunction with membrane damage
Rationale: Mild swelling and fatty change can be reversible. Severe mitochondrial
dysfunction with inability to restore ATP production, combined with extensive
membrane damage, indicates a transition to irreversible injury.
6.
Which form of cell death is characterized by programmed cellular destruction
without substantial inflammation?
A. Necrosis
B. Apoptosis
C. Gangrene
D. Infarction
Correct answer: B. Apoptosis
Rationale: Apoptosis is regulated cell death involving cellular shrinkage,
chromatin condensation, fragmentation, and phagocytosis of cellular remnants.
Because cellular contents generally remain contained, apoptosis produces little
inflammatory response.
, 7.
A patient suffers an ischemic infarction of the brain. Which type of necrosis is
expected?
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Correct answer: B. Liquefactive
Rationale: CNS ischemia characteristically produces liquefactive necrosis, in
which enzymatic digestion transforms dead tissue into a softened or liquefied
mass. Most ischemic infarctions in solid organs instead produce coagulative
necrosis.
8.
Which mechanism contributes most directly to tissue injury during reperfusion
following prolonged ischemia?
A. Decreased oxygen availability
B. Reactive oxygen species generation
C. Reduced calcium entry
D. Suppression of inflammatory signaling
Correct answer: B. Reactive oxygen species generation
Rationale: Reintroduction of oxygen can generate large amounts of reactive
oxygen species (ROS). ROS damage lipids, proteins, DNA, and cellular membranes.
Calcium overload and inflammatory activation can further worsen reperfusion
injury.
9.
2026/2027 Updated | 100% Correct - USU.
SECTION I — Cellular Adaptation, Injury, Inflammation & Cell Death
1.
A patient with long-standing hypertension develops progressive thickening of the
left ventricular myocardium. Which cellular adaptation best explains this finding?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Atrophy
Correct answer: B. Hypertrophy
Rationale: Cardiac myocytes have limited ability to divide, so chronic pressure
overload primarily causes hypertrophy, an increase in cell size. Hypertension
increases afterload, requiring greater myocardial force generation. Although
initially compensatory, prolonged hypertrophy can eventually impair ventricular
relaxation, increase oxygen demand, and contribute to heart failure.
2.
A patient with chronic gastroesophageal reflux develops replacement of normal
esophageal squamous epithelium with columnar epithelium. This process is:
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Hypertrophy
Correct answer: C. Metaplasia
,Rationale: Metaplasia is a reversible adaptation in which one mature cell type is
replaced by another better suited to chronic environmental stress. Barrett
esophagus represents columnar metaplasia associated with chronic acid
exposure. Persistent injury can increase the risk of dysplasia and adenocarcinoma.
3.
Which cellular event occurs earliest when ATP depletion develops during ischemic
injury?
A. Increased protein synthesis
B. Failure of the sodium-potassium ATPase
C. Nuclear fragmentation
D. Mitochondrial DNA replication
Correct answer: B. Failure of the sodium-potassium ATPase
Rationale: ATP depletion impairs energy-dependent membrane pumps,
particularly the Na⁺/K⁺-ATPase. Intracellular sodium increases, water follows
osmotically, and cellular swelling develops. This is an early and potentially
reversible manifestation of cell injury.
4.
A patient experiences severe tissue hypoxia. Which consequence of mitochondrial
dysfunction contributes most directly to progressive cellular injury?
A. Increased ATP generation
B. Increased oxidative phosphorylation
C. Reduced ATP production
D. Increased protein folding
Correct answer: C. Reduced ATP production
Rationale: Mitochondria require oxygen for oxidative phosphorylation. Hypoxia
reduces ATP generation, impairing ion pumps, protein synthesis, membrane
,integrity, and cellular homeostasis. Prolonged mitochondrial injury can ultimately
result in irreversible cell damage and death.
5.
Which finding most strongly indicates irreversible cellular injury?
A. Cellular swelling
B. Fatty change
C. Ribosomal detachment
D. Severe mitochondrial dysfunction with membrane damage
Correct answer: D. Severe mitochondrial dysfunction with membrane damage
Rationale: Mild swelling and fatty change can be reversible. Severe mitochondrial
dysfunction with inability to restore ATP production, combined with extensive
membrane damage, indicates a transition to irreversible injury.
6.
Which form of cell death is characterized by programmed cellular destruction
without substantial inflammation?
A. Necrosis
B. Apoptosis
C. Gangrene
D. Infarction
Correct answer: B. Apoptosis
Rationale: Apoptosis is regulated cell death involving cellular shrinkage,
chromatin condensation, fragmentation, and phagocytosis of cellular remnants.
Because cellular contents generally remain contained, apoptosis produces little
inflammatory response.
, 7.
A patient suffers an ischemic infarction of the brain. Which type of necrosis is
expected?
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Correct answer: B. Liquefactive
Rationale: CNS ischemia characteristically produces liquefactive necrosis, in
which enzymatic digestion transforms dead tissue into a softened or liquefied
mass. Most ischemic infarctions in solid organs instead produce coagulative
necrosis.
8.
Which mechanism contributes most directly to tissue injury during reperfusion
following prolonged ischemia?
A. Decreased oxygen availability
B. Reactive oxygen species generation
C. Reduced calcium entry
D. Suppression of inflammatory signaling
Correct answer: B. Reactive oxygen species generation
Rationale: Reintroduction of oxygen can generate large amounts of reactive
oxygen species (ROS). ROS damage lipids, proteins, DNA, and cellular membranes.
Calcium overload and inflammatory activation can further worsen reperfusion
injury.
9.
