PATHO 370 Pathophysiology Midterm Exam
Actual Exam 2026/2027 – Complete
Comprehensive Assessment with Detailed
Rationales | 100% Verified | Pass Guaranteed –
A+ Graded
Section A: Cellular Pathophysiology & Adaptation (10 Questions)
Q1: A 68-year-old male with a 40-year history of alcohol use disorder presents with
hepatomegaly. Liver biopsy reveals vacuolated hepatocytes with clear cytoplasmic
inclusions that do not displace the nucleus. The nurse recognizes this as intracellular
accumulation of which substance?
A. Hemosiderin
B. Lipofuscin
C. Triglycerides [CORRECT]
D. Glycogen
Correct Answer: C
Rationale: Steatosis (fatty change) in hepatocytes is characterized by triglyceride
accumulation appearing as clear cytoplasmic vacuoles that do not displace the nucleus,
commonly seen in alcohol use disorder. Hemosiderin appears as golden-brown
granules, lipofuscin is "wear-and-tear" pigment in aging cells, and glycogen accumulates
in conditions like von Gierke disease.
Q2: A patient who underwent coronary artery bypass grafting 6 hours ago develops
ventricular arrhythmias and myocardial stunning. The nurse understands this
phenomenon is best described as:
A. Apoptosis-mediated myocardial remodeling
B. Ischemia-reperfusion injury [CORRECT]
C. Coagulative necrosis progression
D. Cellular hypertrophy from increased workload
Correct Answer: B
,Rationale: Ischemia-reperfusion injury causes paradoxical tissue damage upon
restoration of blood flow due to ROS production, calcium overload, and inflammation,
manifesting as arrhythmias and myocardial stunning. Apoptosis is programmed cell
death, coagulative necrosis occurs during ischemia (not reperfusion), and hypertrophy
is an adaptive response unrelated to reperfusion.
Q3: A 55-year-old woman with emphysema has type II pneumocyte hyperplasia. The
pathophysiology instructor explains that hyperplasia differs from hypertrophy because
hyperplasia involves:
A. Decrease in cell size due to disuse
B. Increase in cell number [CORRECT]
C. Replacement of one cell type with another
D. Abnormal maturation of cells
Correct Answer: B
Rationale: Hyperplasia is defined as an increase in cell number, whereas hypertrophy is
an increase in cell size. Atrophy is decreased cell size, metaplasia is replacement of one
cell type with another, and dysplasia represents abnormal cell growth and maturation.
Q4: During a laboratory session, students observe liver tissue from a patient who died of
hypovolemic shock. The hepatocytes show eosinophilic cytoplasm with preserved
cellular outlines but loss of nuclei. This pattern of cell death is characteristic of:
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis [CORRECT]
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis, typically caused by ischemia, preserves cellular
outlines while denaturing cytoplasmic proteins and destroying nuclei, resulting in "ghost
cells." Liquefactive necrosis involves enzymatic digestion (brain abscesses), caseous
necrosis has cheese-like appearance (TB), and fat necrosis occurs in adipose tissue
(pancreatitis).
, Q5: A patient receiving high-dose acetaminophen develops hepatic failure. The nurse
understands that the primary mechanism of acetaminophen-induced hepatocyte injury
is:
A. Direct mitochondrial DNA replication inhibition
B. Free radical formation and glutathione depletion [CORRECT]
C. Excessive intracellular calcium efflux
D. Accelerated telomere shortening
Correct Answer: B
Rationale: Acetaminophen metabolism produces NAPQI, a toxic metabolite that causes
free radical formation and depletes glutathione, leading to oxidative stress and
hepatocyte necrosis. It does not primarily affect mitochondrial DNA replication, cause
calcium efflux, or accelerate telomere shortening.
Q6: A 42-year-old woman with chronic gastroesophageal reflux disease has Barrett
esophagus. The cellular adaptation demonstrated in this condition is:
A. Dysplasia with potential for malignant transformation
B. Metaplasia of squamous to columnar epithelium [CORRECT]
C. Hypertrophy of esophageal smooth muscle
D. Hyperplasia of submucosal glands
Correct Answer: B
Rationale: Barrett esophagus is metaplasia—replacement of normal squamous
epithelium with intestinal-type columnar epithelium due to chronic acid exposure. While
dysplasia may develop later, the initial adaptation is metaplasia, not hypertrophy or
hyperplasia.
Q7: A nurse is caring for a patient with acute tubular necrosis following prolonged
hypotension. The patient asks why the kidneys were damaged. The nurse's best
response explains that hypoxia causes cell injury primarily through:
A. Activation of lysosomal enzymes only
B. ATP depletion and subsequent cellular swelling [CORRECT]
C. Immediate nuclear dissolution without preceding changes
D. Accelerated protein synthesis exceeding cellular capacity
Correct Answer: B
Rationale: Hypoxia causes cell injury primarily through ATP depletion, leading to failure
of the Na+/K+-ATPase pump, cellular swelling, and subsequent membrane damage.
Actual Exam 2026/2027 – Complete
Comprehensive Assessment with Detailed
Rationales | 100% Verified | Pass Guaranteed –
A+ Graded
Section A: Cellular Pathophysiology & Adaptation (10 Questions)
Q1: A 68-year-old male with a 40-year history of alcohol use disorder presents with
hepatomegaly. Liver biopsy reveals vacuolated hepatocytes with clear cytoplasmic
inclusions that do not displace the nucleus. The nurse recognizes this as intracellular
accumulation of which substance?
A. Hemosiderin
B. Lipofuscin
C. Triglycerides [CORRECT]
D. Glycogen
Correct Answer: C
Rationale: Steatosis (fatty change) in hepatocytes is characterized by triglyceride
accumulation appearing as clear cytoplasmic vacuoles that do not displace the nucleus,
commonly seen in alcohol use disorder. Hemosiderin appears as golden-brown
granules, lipofuscin is "wear-and-tear" pigment in aging cells, and glycogen accumulates
in conditions like von Gierke disease.
Q2: A patient who underwent coronary artery bypass grafting 6 hours ago develops
ventricular arrhythmias and myocardial stunning. The nurse understands this
phenomenon is best described as:
A. Apoptosis-mediated myocardial remodeling
B. Ischemia-reperfusion injury [CORRECT]
C. Coagulative necrosis progression
D. Cellular hypertrophy from increased workload
Correct Answer: B
,Rationale: Ischemia-reperfusion injury causes paradoxical tissue damage upon
restoration of blood flow due to ROS production, calcium overload, and inflammation,
manifesting as arrhythmias and myocardial stunning. Apoptosis is programmed cell
death, coagulative necrosis occurs during ischemia (not reperfusion), and hypertrophy
is an adaptive response unrelated to reperfusion.
Q3: A 55-year-old woman with emphysema has type II pneumocyte hyperplasia. The
pathophysiology instructor explains that hyperplasia differs from hypertrophy because
hyperplasia involves:
A. Decrease in cell size due to disuse
B. Increase in cell number [CORRECT]
C. Replacement of one cell type with another
D. Abnormal maturation of cells
Correct Answer: B
Rationale: Hyperplasia is defined as an increase in cell number, whereas hypertrophy is
an increase in cell size. Atrophy is decreased cell size, metaplasia is replacement of one
cell type with another, and dysplasia represents abnormal cell growth and maturation.
Q4: During a laboratory session, students observe liver tissue from a patient who died of
hypovolemic shock. The hepatocytes show eosinophilic cytoplasm with preserved
cellular outlines but loss of nuclei. This pattern of cell death is characteristic of:
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis [CORRECT]
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis, typically caused by ischemia, preserves cellular
outlines while denaturing cytoplasmic proteins and destroying nuclei, resulting in "ghost
cells." Liquefactive necrosis involves enzymatic digestion (brain abscesses), caseous
necrosis has cheese-like appearance (TB), and fat necrosis occurs in adipose tissue
(pancreatitis).
, Q5: A patient receiving high-dose acetaminophen develops hepatic failure. The nurse
understands that the primary mechanism of acetaminophen-induced hepatocyte injury
is:
A. Direct mitochondrial DNA replication inhibition
B. Free radical formation and glutathione depletion [CORRECT]
C. Excessive intracellular calcium efflux
D. Accelerated telomere shortening
Correct Answer: B
Rationale: Acetaminophen metabolism produces NAPQI, a toxic metabolite that causes
free radical formation and depletes glutathione, leading to oxidative stress and
hepatocyte necrosis. It does not primarily affect mitochondrial DNA replication, cause
calcium efflux, or accelerate telomere shortening.
Q6: A 42-year-old woman with chronic gastroesophageal reflux disease has Barrett
esophagus. The cellular adaptation demonstrated in this condition is:
A. Dysplasia with potential for malignant transformation
B. Metaplasia of squamous to columnar epithelium [CORRECT]
C. Hypertrophy of esophageal smooth muscle
D. Hyperplasia of submucosal glands
Correct Answer: B
Rationale: Barrett esophagus is metaplasia—replacement of normal squamous
epithelium with intestinal-type columnar epithelium due to chronic acid exposure. While
dysplasia may develop later, the initial adaptation is metaplasia, not hypertrophy or
hyperplasia.
Q7: A nurse is caring for a patient with acute tubular necrosis following prolonged
hypotension. The patient asks why the kidneys were damaged. The nurse's best
response explains that hypoxia causes cell injury primarily through:
A. Activation of lysosomal enzymes only
B. ATP depletion and subsequent cellular swelling [CORRECT]
C. Immediate nuclear dissolution without preceding changes
D. Accelerated protein synthesis exceeding cellular capacity
Correct Answer: B
Rationale: Hypoxia causes cell injury primarily through ATP depletion, leading to failure
of the Na+/K+-ATPase pump, cellular swelling, and subsequent membrane damage.
