HESI PatHoPHySIology Exam: mEd Surg
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1. A patient with chronic anemia is found to have small, pale red blood cells. This is an
example of which cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: Hypertrophy is an increase in cell size leading to an increase in organ size. In chronic
anemia, the bone marrow produces more red blood cells (hyperplasia), but the small, pale cells
(microcytic, hypochromic) are a result of iron deficiency, not hypertrophy. This question is
tricky—actually, small, pale RBCs are characteristic of iron deficiency anemia, which is a result of
impaired hemoglobin synthesis, not hypertrophy. The correct cellular adaptation here
is metaplasia (if considering cellular change) or dysplasia (abnormal cell growth). However, in
the context of this question, the best answer is Metaplasia—the bone marrow may undergo
metaplastic changes in response to chronic anemia. Correction: The question may be testing
that the small, pale cells are a result of dysplasia. Let's adjust: In iron deficiency anemia, the
cells are microcytic and hypochromic due to impaired hemoglobin synthesis, not a cellular
adaptation per se. The best answer from the options is Metaplasia—but actually, the correct
answer is Hypertrophy if referring to the bone marrow's compensatory response, or Dysplasia if
referring to abnormal cell morphology. Given the options, the best answer is Metaplasia.
2. A patient with chronic obstructive pulmonary disease (COPD) has a barrel-shaped chest.
This is an example of which cellular adaptation?
1
, A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: The barrel-shaped chest in COPD is due to air trapping and hyperinflation of the
lungs, leading to hypertrophy of the diaphragm and accessory muscles of respiration.
Hyperplasia would be an increase in cell number; atrophy is a decrease in cell size; metaplasia is
a change from one cell type to another. Hypertrophy is an increase in cell size, which occurs in
the muscles of respiration in COPD .
3. A patient who has smoked for 30 years has squamous cell metaplasia of the bronchial
epithelium. This is an example of:
A) An irreversible change
B) A protective mechanism
C) A genetic mutation
D) A precancerous lesion
Answer: B
Rationale: Squamous cell metaplasia is a change from ciliated columnar epithelium to stratified
squamous epithelium in response to chronic irritation from smoking. This is considered a
protective mechanism because squamous epithelium is more resistant to irritation, but it also
results in loss of ciliary function and mucus production, increasing infection risk. Metaplasia is
potentially reversible if the irritant is removed .
4. A patient experiences ischemia-reperfusion injury to the heart muscle. Which mechanism is
responsible for the cellular damage during reperfusion?
A) Lactic acidosis
B) Free radical formation (oxidative stress)
C) ATP depletion
D) Cellular swelling
Answer: B
Rationale: Ischemia-reperfusion injury occurs when blood supply returns to tissue after a period
of ischemia. The reintroduction of oxygen leads to the production of reactive oxygen species
(free radicals), which cause cellular damage. This is known as oxidative stress. ATP depletion (C)
2
, occurs during ischemia, not reperfusion; lactic acidosis (A) occurs during anaerobic metabolism;
cellular swelling (D) is a sign of cellular injury .
5. A patient with a myocardial infarction has necrosis of heart muscle cells. Which type of
necrosis is most likely to occur in the heart?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Fat necrosis
Answer: A
Rationale: Coagulative necrosis is characteristic of ischemic injury in solid organs, including the
heart and kidneys. The cell structure is preserved for several days, but the cells are dead.
Liquefactive necrosis occurs in the brain; caseous necrosis occurs in tuberculosis; fat necrosis
occurs in the breast and pancreas. Coagulative necrosis is the hallmark of myocardial infarction .
6. A patient with a brain injury has liquefactive necrosis of the brain tissue. Which mechanism
is responsible for this type of necrosis?
A) Enzymatic digestion of dead tissue
B) Ischemia
C) Inflammation
D) Infection
Answer: A
Rationale: Liquefactive necrosis occurs when dead tissue is digested by enzymes, forming a
liquid, viscous mass. This is characteristic of brain tissue because of its high lipid content and
because it is rich in hydrolytic enzymes. The dead tissue becomes liquefied, forming a cavity.
The other options are incorrect .
7. Which cellular adaptation occurs as a result of decreased workload or decreased blood
supply?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
3
, Answer: C
Rationale: Atrophy is a decrease in cell size and organ size that occurs in response to decreased
workload, decreased blood supply, denervation, or aging. It is a reversible adaptation.
Hyperplasia and hypertrophy occur in response to increased workload or stimulation;
metaplasia is a change from one cell type to another .
8. A patient with chronic gastroesophageal reflux disease (GERD) develops Barrett's
esophagus. This is an example of which cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: D
Rationale: Barrett's esophagus is a type of metaplasia in which the normal squamous
epithelium of the esophagus is replaced by columnar epithelium that resembles gastric or
intestinal lining. This occurs in response to chronic acid exposure from GERD. Barrett's
esophagus is a precancerous condition, increasing the risk of esophageal adenocarcinoma.
Metaplasia is potentially reversible if the irritant is removed .
9. A patient with chronic hepatitis develops cirrhosis. The liver cells undergo which type of
cell death?
A) Necrosis
B) Apoptosis
C) Autophagy
D) Pyroptosis
Answer: A
Rationale: Cirrhosis is the end-stage of liver disease characterized by fibrosis and nodule
formation. Hepatocyte death occurs through necrosis and apoptosis, but necrosis is the
predominant mechanism in chronic hepatitis. Apoptosis is programmed cell death, which is
more controlled and does not cause inflammation; necrosis causes inflammation and tissue
damage .
4
[2026/2027] uPdatEd VErSIon | VErIfIEd
QuEStIonS & dEtaIlEd ratIonalES
alrEady graEdEd a+
1. A patient with chronic anemia is found to have small, pale red blood cells. This is an
example of which cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: Hypertrophy is an increase in cell size leading to an increase in organ size. In chronic
anemia, the bone marrow produces more red blood cells (hyperplasia), but the small, pale cells
(microcytic, hypochromic) are a result of iron deficiency, not hypertrophy. This question is
tricky—actually, small, pale RBCs are characteristic of iron deficiency anemia, which is a result of
impaired hemoglobin synthesis, not hypertrophy. The correct cellular adaptation here
is metaplasia (if considering cellular change) or dysplasia (abnormal cell growth). However, in
the context of this question, the best answer is Metaplasia—the bone marrow may undergo
metaplastic changes in response to chronic anemia. Correction: The question may be testing
that the small, pale cells are a result of dysplasia. Let's adjust: In iron deficiency anemia, the
cells are microcytic and hypochromic due to impaired hemoglobin synthesis, not a cellular
adaptation per se. The best answer from the options is Metaplasia—but actually, the correct
answer is Hypertrophy if referring to the bone marrow's compensatory response, or Dysplasia if
referring to abnormal cell morphology. Given the options, the best answer is Metaplasia.
2. A patient with chronic obstructive pulmonary disease (COPD) has a barrel-shaped chest.
This is an example of which cellular adaptation?
1
, A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: The barrel-shaped chest in COPD is due to air trapping and hyperinflation of the
lungs, leading to hypertrophy of the diaphragm and accessory muscles of respiration.
Hyperplasia would be an increase in cell number; atrophy is a decrease in cell size; metaplasia is
a change from one cell type to another. Hypertrophy is an increase in cell size, which occurs in
the muscles of respiration in COPD .
3. A patient who has smoked for 30 years has squamous cell metaplasia of the bronchial
epithelium. This is an example of:
A) An irreversible change
B) A protective mechanism
C) A genetic mutation
D) A precancerous lesion
Answer: B
Rationale: Squamous cell metaplasia is a change from ciliated columnar epithelium to stratified
squamous epithelium in response to chronic irritation from smoking. This is considered a
protective mechanism because squamous epithelium is more resistant to irritation, but it also
results in loss of ciliary function and mucus production, increasing infection risk. Metaplasia is
potentially reversible if the irritant is removed .
4. A patient experiences ischemia-reperfusion injury to the heart muscle. Which mechanism is
responsible for the cellular damage during reperfusion?
A) Lactic acidosis
B) Free radical formation (oxidative stress)
C) ATP depletion
D) Cellular swelling
Answer: B
Rationale: Ischemia-reperfusion injury occurs when blood supply returns to tissue after a period
of ischemia. The reintroduction of oxygen leads to the production of reactive oxygen species
(free radicals), which cause cellular damage. This is known as oxidative stress. ATP depletion (C)
2
, occurs during ischemia, not reperfusion; lactic acidosis (A) occurs during anaerobic metabolism;
cellular swelling (D) is a sign of cellular injury .
5. A patient with a myocardial infarction has necrosis of heart muscle cells. Which type of
necrosis is most likely to occur in the heart?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Fat necrosis
Answer: A
Rationale: Coagulative necrosis is characteristic of ischemic injury in solid organs, including the
heart and kidneys. The cell structure is preserved for several days, but the cells are dead.
Liquefactive necrosis occurs in the brain; caseous necrosis occurs in tuberculosis; fat necrosis
occurs in the breast and pancreas. Coagulative necrosis is the hallmark of myocardial infarction .
6. A patient with a brain injury has liquefactive necrosis of the brain tissue. Which mechanism
is responsible for this type of necrosis?
A) Enzymatic digestion of dead tissue
B) Ischemia
C) Inflammation
D) Infection
Answer: A
Rationale: Liquefactive necrosis occurs when dead tissue is digested by enzymes, forming a
liquid, viscous mass. This is characteristic of brain tissue because of its high lipid content and
because it is rich in hydrolytic enzymes. The dead tissue becomes liquefied, forming a cavity.
The other options are incorrect .
7. Which cellular adaptation occurs as a result of decreased workload or decreased blood
supply?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
3
, Answer: C
Rationale: Atrophy is a decrease in cell size and organ size that occurs in response to decreased
workload, decreased blood supply, denervation, or aging. It is a reversible adaptation.
Hyperplasia and hypertrophy occur in response to increased workload or stimulation;
metaplasia is a change from one cell type to another .
8. A patient with chronic gastroesophageal reflux disease (GERD) develops Barrett's
esophagus. This is an example of which cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: D
Rationale: Barrett's esophagus is a type of metaplasia in which the normal squamous
epithelium of the esophagus is replaced by columnar epithelium that resembles gastric or
intestinal lining. This occurs in response to chronic acid exposure from GERD. Barrett's
esophagus is a precancerous condition, increasing the risk of esophageal adenocarcinoma.
Metaplasia is potentially reversible if the irritant is removed .
9. A patient with chronic hepatitis develops cirrhosis. The liver cells undergo which type of
cell death?
A) Necrosis
B) Apoptosis
C) Autophagy
D) Pyroptosis
Answer: A
Rationale: Cirrhosis is the end-stage of liver disease characterized by fibrosis and nodule
formation. Hepatocyte death occurs through necrosis and apoptosis, but necrosis is the
predominant mechanism in chronic hepatitis. Apoptosis is programmed cell death, which is
more controlled and does not cause inflammation; necrosis causes inflammation and tissue
damage .
4
