MSN 570 Pathophysiology Midterm Study Guide 2 United
States University Actual Exam 2026/2027 – Complete 75
Questions with Detailed Rationales | 100% Verified | Pass
Guaranteed – A+ Graded
SECTION A: Cellular Biology, Adaptation, Injury & Death (Q1–Q12)
Q1: A 34-year-old athlete's leg is placed in a cast for six weeks; on removal, the calf
muscles are visibly smaller and weaker. Histologic examination shows individual
muscle cells of reduced size with intact architecture. This cellular adaptation is:
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Atrophy — a decrease in cell size and functional capacity from disuse [CORRECT]
Correct Answer: D
Rationale: Disuse atrophy involves shrinkage of existing cells due to decreased
workload and stimulation, as with immobilization. Hyperplasia increases cell number,
metaplasia changes cell type, and dysplasia is disordered growth.
Q2: A patient with long-standing, uncontrolled hypertension develops marked thickening
of the left ventricular wall on echocardiogram. The underlying cellular mechanism is:
A. Hypertrophy — enlargement of individual cardiac myocytes, the only adaptive
response available to cardiac muscle [CORRECT]
B. Hyperplasia — increased myocyte numbers
C. Dysplasia — disordered myocyte architecture
D. Metaplasia — conversion to a different tissue type
Correct Answer: A
Rationale: Adult cardiac muscle cannot divide mitotically, so chronic pressure overload
produces enlargement of individual myocytes (hypertrophy). Hyperplasia does not
occur in terminally differentiated cardiac muscle.
Q3: A 52-year-old man with 20 years of gastroesophageal reflux undergoes endoscopy;
biopsy of the distal esophagus shows replacement of normal stratified squamous
epithelium with intestinal-type columnar epithelium. This change is:
A. Reversible hypertrophy of esophageal squamous cells
,B. Physiologic hyperplasia
C. Metaplasia (Barrett esophagus) — a reversible change conferring increased
adenocarcinoma risk [CORRECT]
D. Anaplasia of squamous origin
Correct Answer: C
Rationale: Chronic acid exposure drives squamous-to-columnar metaplasia (Barrett
esophagus), a protective but premalignant adaptation. Hypertrophy and hyperplasia do
not change cell type, and anaplasia describes overt malignant change.
Q4: A cervical Pap smear shows disordered cellular maturation, increased
nuclear-to-cytoplasmic ratio, and architectural disturbance without full-thickness atypia.
This finding is best described as:
A. Metaplasia
B. Dysplasia — a premalignant disordered growth pattern [CORRECT]
C. Apoptosis
D. Atrophy
Correct Answer: B
Rationale: Dysplasia exhibits loss of uniformity, nuclear atypia, and disordered
maturation that may progress to carcinoma in situ. Metaplasia changes cell type
without atypia, and apoptosis and atrophy are degenerative processes without
premalignant significance.
Q5: A myocardial cell subjected to prolonged ischemia (>20 minutes) develops plasma
membrane rupture, massive cytosolic calcium influx, and mitochondrial vacuolization.
These features distinguish which state?
A. Reversible injury with membrane blebbing
B. Physiologic adaptation
C. Irreversible injury — the point of no return defined by membrane damage and calcium
influx [CORRECT]
D. Sublethal metabolic adaptation
Correct Answer: C
Rationale: Membrane rupture, calcium influx, and mitochondrial vacuolization mark
irreversible injury leading to cell death. Reversible injury shows only swelling and
blebbing with intact membranes.
Q6: A patient sustains a global cerebral hypoxic event; autopsy demonstrates a
softened, liquefied area of brain parenchyma with microglial digestion of dead tissue.
This type of necrosis is:
A. Liquefactive necrosis — characteristic of CNS ischemia and abscesses [CORRECT]
B. Coagulative necrosis
, C. Caseous necrosis
D. Fat necrosis
Correct Answer: A
Rationale: The brain's lipid-rich tissue and sparse connective tissue framework allow
complete enzymatic liquefaction. Coagulative necrosis (heart, kidney) preserves
architecture, caseous necrosis occurs in TB, and fat necrosis involves adipose tissue.
Q7: Which set of features correctly characterizes apoptosis?
A. Cell swelling, membrane rupture, and intense neutrophilic inflammation
B. Cell shrinkage, chromatin condensation, caspase activation, and absence of
inflammation [CORRECT]
C. Random DNA destruction from external trauma
D. Coagulative necrosis of an entire organ region
Correct Answer: B
Rationale: Apoptosis is energy-dependent programmed single-cell death with shrinkage,
nuclear fragmentation, and tidy clearance without inflammation. Swelling, rupture, and
inflammation define necrosis.
Q8: Why does necrosis — but not apoptosis — typically elicit a significant inflammatory
response?
A. Necrosis is always triggered by immune cells
B. Apoptosis occurs only in immune-privileged organs
C. Necrotic cells do not activate complement
D. Necrotic cell membrane rupture releases intracellular contents, including
damage-associated molecular patterns, into the extracellular space [CORRECT]
Correct Answer: D
Rationale: Ruptured necrotic cells spill contents (DAMPs) that recruit neutrophils and
macrophages, whereas apoptotic bodies remain membrane-bound and are silently
phagocytosed. The other options misstate basic mechanisms.
Q9: Following successful thrombolytic restoration of coronary blood flow, a patient's
infarcted myocardium paradoxically sustains additional cell death. The mechanism is:
A. Reperfusion injury mediated by reactive oxygen species, calcium overload, and
inflammatory cell influx [CORRECT]
B. Further ATP restoration toxicity
C. Loss of the cell's sodium-potassium pump activation
D. Decreased neutrophil infiltration at the injury site
Correct Answer: A
States University Actual Exam 2026/2027 – Complete 75
Questions with Detailed Rationales | 100% Verified | Pass
Guaranteed – A+ Graded
SECTION A: Cellular Biology, Adaptation, Injury & Death (Q1–Q12)
Q1: A 34-year-old athlete's leg is placed in a cast for six weeks; on removal, the calf
muscles are visibly smaller and weaker. Histologic examination shows individual
muscle cells of reduced size with intact architecture. This cellular adaptation is:
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Atrophy — a decrease in cell size and functional capacity from disuse [CORRECT]
Correct Answer: D
Rationale: Disuse atrophy involves shrinkage of existing cells due to decreased
workload and stimulation, as with immobilization. Hyperplasia increases cell number,
metaplasia changes cell type, and dysplasia is disordered growth.
Q2: A patient with long-standing, uncontrolled hypertension develops marked thickening
of the left ventricular wall on echocardiogram. The underlying cellular mechanism is:
A. Hypertrophy — enlargement of individual cardiac myocytes, the only adaptive
response available to cardiac muscle [CORRECT]
B. Hyperplasia — increased myocyte numbers
C. Dysplasia — disordered myocyte architecture
D. Metaplasia — conversion to a different tissue type
Correct Answer: A
Rationale: Adult cardiac muscle cannot divide mitotically, so chronic pressure overload
produces enlargement of individual myocytes (hypertrophy). Hyperplasia does not
occur in terminally differentiated cardiac muscle.
Q3: A 52-year-old man with 20 years of gastroesophageal reflux undergoes endoscopy;
biopsy of the distal esophagus shows replacement of normal stratified squamous
epithelium with intestinal-type columnar epithelium. This change is:
A. Reversible hypertrophy of esophageal squamous cells
,B. Physiologic hyperplasia
C. Metaplasia (Barrett esophagus) — a reversible change conferring increased
adenocarcinoma risk [CORRECT]
D. Anaplasia of squamous origin
Correct Answer: C
Rationale: Chronic acid exposure drives squamous-to-columnar metaplasia (Barrett
esophagus), a protective but premalignant adaptation. Hypertrophy and hyperplasia do
not change cell type, and anaplasia describes overt malignant change.
Q4: A cervical Pap smear shows disordered cellular maturation, increased
nuclear-to-cytoplasmic ratio, and architectural disturbance without full-thickness atypia.
This finding is best described as:
A. Metaplasia
B. Dysplasia — a premalignant disordered growth pattern [CORRECT]
C. Apoptosis
D. Atrophy
Correct Answer: B
Rationale: Dysplasia exhibits loss of uniformity, nuclear atypia, and disordered
maturation that may progress to carcinoma in situ. Metaplasia changes cell type
without atypia, and apoptosis and atrophy are degenerative processes without
premalignant significance.
Q5: A myocardial cell subjected to prolonged ischemia (>20 minutes) develops plasma
membrane rupture, massive cytosolic calcium influx, and mitochondrial vacuolization.
These features distinguish which state?
A. Reversible injury with membrane blebbing
B. Physiologic adaptation
C. Irreversible injury — the point of no return defined by membrane damage and calcium
influx [CORRECT]
D. Sublethal metabolic adaptation
Correct Answer: C
Rationale: Membrane rupture, calcium influx, and mitochondrial vacuolization mark
irreversible injury leading to cell death. Reversible injury shows only swelling and
blebbing with intact membranes.
Q6: A patient sustains a global cerebral hypoxic event; autopsy demonstrates a
softened, liquefied area of brain parenchyma with microglial digestion of dead tissue.
This type of necrosis is:
A. Liquefactive necrosis — characteristic of CNS ischemia and abscesses [CORRECT]
B. Coagulative necrosis
, C. Caseous necrosis
D. Fat necrosis
Correct Answer: A
Rationale: The brain's lipid-rich tissue and sparse connective tissue framework allow
complete enzymatic liquefaction. Coagulative necrosis (heart, kidney) preserves
architecture, caseous necrosis occurs in TB, and fat necrosis involves adipose tissue.
Q7: Which set of features correctly characterizes apoptosis?
A. Cell swelling, membrane rupture, and intense neutrophilic inflammation
B. Cell shrinkage, chromatin condensation, caspase activation, and absence of
inflammation [CORRECT]
C. Random DNA destruction from external trauma
D. Coagulative necrosis of an entire organ region
Correct Answer: B
Rationale: Apoptosis is energy-dependent programmed single-cell death with shrinkage,
nuclear fragmentation, and tidy clearance without inflammation. Swelling, rupture, and
inflammation define necrosis.
Q8: Why does necrosis — but not apoptosis — typically elicit a significant inflammatory
response?
A. Necrosis is always triggered by immune cells
B. Apoptosis occurs only in immune-privileged organs
C. Necrotic cells do not activate complement
D. Necrotic cell membrane rupture releases intracellular contents, including
damage-associated molecular patterns, into the extracellular space [CORRECT]
Correct Answer: D
Rationale: Ruptured necrotic cells spill contents (DAMPs) that recruit neutrophils and
macrophages, whereas apoptotic bodies remain membrane-bound and are silently
phagocytosed. The other options misstate basic mechanisms.
Q9: Following successful thrombolytic restoration of coronary blood flow, a patient's
infarcted myocardium paradoxically sustains additional cell death. The mechanism is:
A. Reperfusion injury mediated by reactive oxygen species, calcium overload, and
inflammatory cell influx [CORRECT]
B. Further ATP restoration toxicity
C. Loss of the cell's sodium-potassium pump activation
D. Decreased neutrophil infiltration at the injury site
Correct Answer: A
