NSG120 / NSG 120 Final Exam: Nursing Pathophysiology
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Cellular Adaptation, Injury & Inflammation
Q1: A 68-year-old male with long-standing hypertension is found to have left ventricular
wall thickening on echocardiogram. The nurse recognizes this cellular adaptation as
which of the following?
A. Hyperplasia due to increased cell number
B. Hypertrophy due to increased cell size [CORRECT]
C. Metaplasia due to replacement by a different cell type
D. Dysplasia due to abnormal cellular development
Correct Answer: B
Rationale: The best answer is B. In hypertension, the heart muscle has to pump against
elevated afterload, so the individual cardiac muscle cells get bigger — that's
hypertrophy, an increase in cell size, not cell number. This matches the pathophysiology
of chronic pressure overload on the left ventricle.
Q2: A patient who smoked heavily for 30 years develops a change in the lining of the
bronchi from pseudostratified ciliated columnar epithelium to stratified squamous
epithelium. This reversible cellular adaptation is best described as:
A. Atrophy from disuse
B. Hyperplasia from chronic irritation
C. Metaplasia from persistent stress [CORRECT]
D. Dysplasia from pre-malignant change
Correct Answer: C
Rationale: Here's what's happening at the cellular level — when one mature cell type is
replaced by another mature cell type better suited to handle chronic irritation, that's
metaplasia. The squamous epithelium can withstand the smoke better than the delicate
ciliated columnar cells, though it does come with increased cancer risk over time.
,Q3: During an ischemic event, which cellular change occurs first and is potentially
reversible if blood flow is restored promptly?
A. Karyolysis with nuclear dissolution
B. Coagulative necrosis with protein denaturation
C. Cellular swelling due to failure of the Na+/K+ pump [CORRECT]
D. Apoptosis with programmed cell death
Correct Answer: C
Rationale: The best answer is C. When oxygen drops, aerobic metabolism fails, ATP
production crashes, and the Na+/K+ pumps stop working — water rushes in and the cell
swells. This is still reversible if you restore perfusion quickly, which is why time is
muscle in an MI.
Q4: A 72-year-old patient presents with crushing chest pain. Lab work shows elevated
troponin. The nurse understands that in the zone of ischemia surrounding the infarcted
myocardium, which process is most likely occurring in the cells?
A. Coagulative necrosis with irreversible damage
B. Reversible cellular injury with potential for recovery [CORRECT]
C. Liquefactive necrosis with enzymatic digestion
D. Caseous necrosis with granuloma formation
Correct Answer: B
Rationale: This aligns with the disease process because in a myocardial infarction, you
have a central zone of coagulative necrosis where cells are dead, but surrounding that is
a zone of ischemia where cells are hypoxic, swollen, and stressed — yet still viable if
reperfused quickly. That's the whole goal of rapid PCI or thrombolytics.
Q5: Free radicals cause cellular injury primarily through which mechanism?
A. Disruption of the Golgi apparatus and protein packaging
B. Damage to cell membranes, proteins, and DNA through lipid peroxidation [CORRECT]
C. Activation of lysosomal enzymes causing autophagy
D. Inhibition of mitochondrial DNA replication only
Correct Answer: B
Rationale: Remember the difference — free radicals are unstable molecules with
unpaired electrons that steal electrons from lipids in cell membranes, setting off a chain
reaction called lipid peroxidation. This damages membranes, proteins, and DNA, which
is why antioxidants are so important.
, Q6: A post-operative patient develops a fever of 101.2°F on day 2. The nurse
understands that the primary endogenous pyrogen responsible for resetting the
hypothalamic set point is:
A. Histamine released from mast cells
B. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) [CORRECT]
C. Prostaglandin E2 acting directly on peripheral thermoreceptors
D. Complement protein C3a triggering vasodilation
Correct Answer: B
Rationale: The best answer is B. Macrophages and other immune cells release IL-1 and
TNF-α in response to infection or tissue injury, and these cytokines travel to the
hypothalamus to trigger prostaglandin release that raises the body's temperature set
point. That's the physiologic basis for giving antipyretics that block prostaglandin
synthesis.
Q7: During the acute inflammatory response, which vascular change occurs first after
tissue injury?
A. Increased vascular permeability with fluid leakage
B. Vasoconstriction followed by transient vasodilation
C. Vasodilation and increased blood flow causing redness and heat [CORRECT]
D. Leukocyte adhesion and transmigration through vessel walls
Correct Answer: C
Rationale: Here's what's happening at the cellular level — the very first thing after injury
is brief vasoconstriction, but then immediate vasodilation mediated by histamine and
other mediators. This increases blood flow to the area, which is why you see rubor
(redness) and calor (heat) as the classic first signs of acute inflammation.
Q8: A patient with chronic bronchitis has persistent productive cough and thickened
bronchial walls. Microscopically, the tissue shows an influx of macrophages,
lymphocytes, and fibroblasts with tissue scarring. This pattern best represents:
A. Acute inflammation with neutrophilic exudate
B. Chronic inflammation with mononuclear cell infiltration and fibrosis [CORRECT]
C. Abscess formation with localized pus collection
D. Serous inflammation with thin fluid accumulation
Correct Answer: B
– Herzing Actual Exam All Units Covered | Complete
Questions & Rationales | Pass Guaranteed - A+ Graded
Cellular Adaptation, Injury & Inflammation
Q1: A 68-year-old male with long-standing hypertension is found to have left ventricular
wall thickening on echocardiogram. The nurse recognizes this cellular adaptation as
which of the following?
A. Hyperplasia due to increased cell number
B. Hypertrophy due to increased cell size [CORRECT]
C. Metaplasia due to replacement by a different cell type
D. Dysplasia due to abnormal cellular development
Correct Answer: B
Rationale: The best answer is B. In hypertension, the heart muscle has to pump against
elevated afterload, so the individual cardiac muscle cells get bigger — that's
hypertrophy, an increase in cell size, not cell number. This matches the pathophysiology
of chronic pressure overload on the left ventricle.
Q2: A patient who smoked heavily for 30 years develops a change in the lining of the
bronchi from pseudostratified ciliated columnar epithelium to stratified squamous
epithelium. This reversible cellular adaptation is best described as:
A. Atrophy from disuse
B. Hyperplasia from chronic irritation
C. Metaplasia from persistent stress [CORRECT]
D. Dysplasia from pre-malignant change
Correct Answer: C
Rationale: Here's what's happening at the cellular level — when one mature cell type is
replaced by another mature cell type better suited to handle chronic irritation, that's
metaplasia. The squamous epithelium can withstand the smoke better than the delicate
ciliated columnar cells, though it does come with increased cancer risk over time.
,Q3: During an ischemic event, which cellular change occurs first and is potentially
reversible if blood flow is restored promptly?
A. Karyolysis with nuclear dissolution
B. Coagulative necrosis with protein denaturation
C. Cellular swelling due to failure of the Na+/K+ pump [CORRECT]
D. Apoptosis with programmed cell death
Correct Answer: C
Rationale: The best answer is C. When oxygen drops, aerobic metabolism fails, ATP
production crashes, and the Na+/K+ pumps stop working — water rushes in and the cell
swells. This is still reversible if you restore perfusion quickly, which is why time is
muscle in an MI.
Q4: A 72-year-old patient presents with crushing chest pain. Lab work shows elevated
troponin. The nurse understands that in the zone of ischemia surrounding the infarcted
myocardium, which process is most likely occurring in the cells?
A. Coagulative necrosis with irreversible damage
B. Reversible cellular injury with potential for recovery [CORRECT]
C. Liquefactive necrosis with enzymatic digestion
D. Caseous necrosis with granuloma formation
Correct Answer: B
Rationale: This aligns with the disease process because in a myocardial infarction, you
have a central zone of coagulative necrosis where cells are dead, but surrounding that is
a zone of ischemia where cells are hypoxic, swollen, and stressed — yet still viable if
reperfused quickly. That's the whole goal of rapid PCI or thrombolytics.
Q5: Free radicals cause cellular injury primarily through which mechanism?
A. Disruption of the Golgi apparatus and protein packaging
B. Damage to cell membranes, proteins, and DNA through lipid peroxidation [CORRECT]
C. Activation of lysosomal enzymes causing autophagy
D. Inhibition of mitochondrial DNA replication only
Correct Answer: B
Rationale: Remember the difference — free radicals are unstable molecules with
unpaired electrons that steal electrons from lipids in cell membranes, setting off a chain
reaction called lipid peroxidation. This damages membranes, proteins, and DNA, which
is why antioxidants are so important.
, Q6: A post-operative patient develops a fever of 101.2°F on day 2. The nurse
understands that the primary endogenous pyrogen responsible for resetting the
hypothalamic set point is:
A. Histamine released from mast cells
B. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) [CORRECT]
C. Prostaglandin E2 acting directly on peripheral thermoreceptors
D. Complement protein C3a triggering vasodilation
Correct Answer: B
Rationale: The best answer is B. Macrophages and other immune cells release IL-1 and
TNF-α in response to infection or tissue injury, and these cytokines travel to the
hypothalamus to trigger prostaglandin release that raises the body's temperature set
point. That's the physiologic basis for giving antipyretics that block prostaglandin
synthesis.
Q7: During the acute inflammatory response, which vascular change occurs first after
tissue injury?
A. Increased vascular permeability with fluid leakage
B. Vasoconstriction followed by transient vasodilation
C. Vasodilation and increased blood flow causing redness and heat [CORRECT]
D. Leukocyte adhesion and transmigration through vessel walls
Correct Answer: C
Rationale: Here's what's happening at the cellular level — the very first thing after injury
is brief vasoconstriction, but then immediate vasodilation mediated by histamine and
other mediators. This increases blood flow to the area, which is why you see rubor
(redness) and calor (heat) as the classic first signs of acute inflammation.
Q8: A patient with chronic bronchitis has persistent productive cough and thickened
bronchial walls. Microscopically, the tissue shows an influx of macrophages,
lymphocytes, and fibroblasts with tissue scarring. This pattern best represents:
A. Acute inflammation with neutrophilic exudate
B. Chronic inflammation with mononuclear cell infiltration and fibrosis [CORRECT]
C. Abscess formation with localized pus collection
D. Serous inflammation with thin fluid accumulation
Correct Answer: B
