1
NUR 2063 Pathophysiology Midterm Exam
Complete Review \ 75 Disease Process Questions
with Detailed Rationales
Section 1: Cellular Biology, Adaptation, and Injury (Questions 1-15)
1. A pathologist examines a tissue sample from a patient with chronic
hypertension and notes an increase in the size of the cardiac muscle cells
without an increase in the number of cells. This cellular adaptation is BEST
described as:
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Answer: B. Hypertrophy
RATIONALE: HYPERTROPHY is an increase in the SIZE of individual cells, resulting
in an increase in the size of the affected organ. It occurs in cells that are incapable
of division (such as cardiac myocytes and skeletal muscle cells) in response to
increased workload or pathologic stimuli. In chronic hypertension, the left
ventricle must pump against increased afterload (systemic vascular resistance),
causing the cardiac myocytes to enlarge. This pathologic hypertrophy initially
compensates but eventually leads to decreased compliance, impaired diastolic
filling, and heart failure. Hypertrophy is mediated by mechanical stretch, growth
factors (IGF-1, angiotensin II), and activation of signal transduction pathways.
• A: Hyperplasia - Incorrect. Hyperplasia is an increase in the NUMBER of
cells, not size. It occurs in tissues capable of cell division (e.g.,
endometrium, liver). Cardiac myocytes cannot undergo hyperplasia.
• C: Atrophy - Incorrect. Atrophy is a DECREASE in cell size and organ size due
to reduced workload, disuse, or inadequate nutrition.
pg. 1
,2
• D: Metaplasia - Incorrect. Metaplasia is the reversible replacement of one
mature cell type by another mature cell type (e.g., squamous metaplasia of
the bronchial epithelium in smokers).
2. A patient with chronic gastroesophageal reflux disease (GERD) undergoes
endoscopy with biopsy of the distal esophagus. The pathology report shows
columnar epithelium with goblet cells replacing the normal stratified squamous
epithelium. This adaptive change is known as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C. Metaplasia
RATIONALE: METAPLASIA is the reversible replacement of one differentiated cell
type by another differentiated cell type that is better able to withstand the
adverse environment. In GERD, chronic acid exposure damages the normal
stratified squamous epithelium of the distal esophagus. The stem cells reprogram
and differentiate into intestinal-type columnar epithelium with goblet cells
(Barrett's esophagus), which is more resistant to acid. While metaplasia is initially
adaptive, it can progress to DYSPLASIA (disordered growth) and eventually to
adenocarcinoma if the injurious stimulus persists.
• A: Hypertrophy - Incorrect. Hypertrophy is an increase in cell SIZE, not a
change in cell type.
• B: Hyperplasia - Incorrect. Hyperplasia is an increase in cell NUMBER, not a
change in cell type.
• D: Dysplasia - Incorrect. Dysplasia is disordered, atypical cellular growth
that is a precursor to malignancy. Barrett's esophagus without dysplasia is
metaplasia; Barrett's with dysplasia is a more advanced pre-malignant
change.
3. Which of the following is the FIRST and MOST REVERSIBLE change seen in
cellular injury?
pg. 2
,3
A. Karyolysis (nuclear dissolution)
B. Mitochondrial swelling and decreased ATP production
C. Plasma membrane rupture
D. Nuclear pyknosis (shrinkage)
Answer: B. Mitochondrial swelling and decreased ATP production
RATIONALE: The earliest and most reversible change in cellular injury is
MITOCHONDRIAL SWELLING and DECREASED ATP PRODUCTION. This occurs when
there is reduced oxygen delivery (hypoxia) or mitochondrial damage. The
decreased ATP leads to failure of the Na+/K+-ATPase pump, causing sodium and
water to enter the cell (cellular swelling—the earliest light microscopic change).
At this stage, if the injurious stimulus is removed and oxygen delivery is restored,
the cell can recover completely. If ATP depletion persists, irreversible injury and
cell death occur.
• A: Karyolysis - Incorrect. Karyolysis (nuclear dissolution due to DNA
digestion) is a LATE, irreversible change seen in necrosis.
• C: Membrane rupture - Incorrect. Plasma membrane rupture is an
irreversible change that leads to cell death (necrosis).
• D: Nuclear pyknosis - Incorrect. Pyknosis (nuclear shrinkage and chromatin
condensation) is an early sign of irreversible injury/apoptosis, not the
earliest cellular change.
4. A patient who suffered a myocardial infarction 48 hours ago has an elevated
serum troponin I level. The pathophysiologic mechanism of troponin release
into the bloodstream involves:
A. Apoptosis with intact cell membrane
B. Necrosis with loss of cell membrane integrity
C. Atrophy of cardiac myocytes
D. Metaplasia of cardiac tissue
Answer: B. Necrosis with loss of cell membrane integrity
RATIONALE: In myocardial infarction, prolonged ischemia (> 20-40 minutes)
causes IRREVERSIBLE cellular injury and NECROSIS (coagulative necrosis in the
heart). Necrosis is characterized by loss of cell membrane integrity, allowing
pg. 3
, 4
intracellular contents—including cardiac enzymes and structural proteins
(troponin I, troponin T, CK-MB)—to leak into the bloodstream. Troponin is the
most sensitive and specific biomarker for myocardial necrosis because it is not
normally present in the blood. The magnitude of troponin elevation correlates
with the extent of myocardial injury.
• A: Apoptosis - Incorrect. Apoptosis is programmed cell death with an
INTACT cell membrane that does not release intracellular contents into the
circulation. Apoptosis does not cause an inflammatory response.
• C: Atrophy - Incorrect. Atrophy is a decrease in cell size, not cell death.
• D: Metaplasia - Incorrect. Metaplasia is a change in cell type, not cell death.
5. A patient with a large, deep pressure ulcer has extensive tissue destruction.
The wound bed contains liquefied, creamy yellow material. The FNP recognizes
this as which type of necrosis?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Answer: B. Liquefactive necrosis
RATIONALE: LIQUEFACTIVE NECROSIS is characterized by the enzymatic digestion
of dead cells, resulting in a liquid, viscous mass (pus). It is typically seen in: (1)
Bacterial and fungal infections (because neutrophils release hydrolytic enzymes
that liquefy the tissue), and (2) Ischemic injury to the brain (because brain tissue
is rich in hydrolytic enzymes and lipids, and lacks a substantial fibrous stroma).
The creamy yellow material is pus composed of dead neutrophils, cellular debris,
and liquefied tissue.
• A: Coagulative necrosis - Incorrect. Coagulative necrosis preserves the
basic tissue architecture (ghost cells) and is typical of ischemic injury in
solid organs (heart, kidney, spleen). The tissue is firm, not liquefied.
• C: Caseous necrosis - Incorrect. Caseous necrosis ("cheese-like") is
characteristic of tuberculosis. It has a friable, granular appearance and is a
combination of coagulative and liquefactive necrosis.
pg. 4
NUR 2063 Pathophysiology Midterm Exam
Complete Review \ 75 Disease Process Questions
with Detailed Rationales
Section 1: Cellular Biology, Adaptation, and Injury (Questions 1-15)
1. A pathologist examines a tissue sample from a patient with chronic
hypertension and notes an increase in the size of the cardiac muscle cells
without an increase in the number of cells. This cellular adaptation is BEST
described as:
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Answer: B. Hypertrophy
RATIONALE: HYPERTROPHY is an increase in the SIZE of individual cells, resulting
in an increase in the size of the affected organ. It occurs in cells that are incapable
of division (such as cardiac myocytes and skeletal muscle cells) in response to
increased workload or pathologic stimuli. In chronic hypertension, the left
ventricle must pump against increased afterload (systemic vascular resistance),
causing the cardiac myocytes to enlarge. This pathologic hypertrophy initially
compensates but eventually leads to decreased compliance, impaired diastolic
filling, and heart failure. Hypertrophy is mediated by mechanical stretch, growth
factors (IGF-1, angiotensin II), and activation of signal transduction pathways.
• A: Hyperplasia - Incorrect. Hyperplasia is an increase in the NUMBER of
cells, not size. It occurs in tissues capable of cell division (e.g.,
endometrium, liver). Cardiac myocytes cannot undergo hyperplasia.
• C: Atrophy - Incorrect. Atrophy is a DECREASE in cell size and organ size due
to reduced workload, disuse, or inadequate nutrition.
pg. 1
,2
• D: Metaplasia - Incorrect. Metaplasia is the reversible replacement of one
mature cell type by another mature cell type (e.g., squamous metaplasia of
the bronchial epithelium in smokers).
2. A patient with chronic gastroesophageal reflux disease (GERD) undergoes
endoscopy with biopsy of the distal esophagus. The pathology report shows
columnar epithelium with goblet cells replacing the normal stratified squamous
epithelium. This adaptive change is known as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C. Metaplasia
RATIONALE: METAPLASIA is the reversible replacement of one differentiated cell
type by another differentiated cell type that is better able to withstand the
adverse environment. In GERD, chronic acid exposure damages the normal
stratified squamous epithelium of the distal esophagus. The stem cells reprogram
and differentiate into intestinal-type columnar epithelium with goblet cells
(Barrett's esophagus), which is more resistant to acid. While metaplasia is initially
adaptive, it can progress to DYSPLASIA (disordered growth) and eventually to
adenocarcinoma if the injurious stimulus persists.
• A: Hypertrophy - Incorrect. Hypertrophy is an increase in cell SIZE, not a
change in cell type.
• B: Hyperplasia - Incorrect. Hyperplasia is an increase in cell NUMBER, not a
change in cell type.
• D: Dysplasia - Incorrect. Dysplasia is disordered, atypical cellular growth
that is a precursor to malignancy. Barrett's esophagus without dysplasia is
metaplasia; Barrett's with dysplasia is a more advanced pre-malignant
change.
3. Which of the following is the FIRST and MOST REVERSIBLE change seen in
cellular injury?
pg. 2
,3
A. Karyolysis (nuclear dissolution)
B. Mitochondrial swelling and decreased ATP production
C. Plasma membrane rupture
D. Nuclear pyknosis (shrinkage)
Answer: B. Mitochondrial swelling and decreased ATP production
RATIONALE: The earliest and most reversible change in cellular injury is
MITOCHONDRIAL SWELLING and DECREASED ATP PRODUCTION. This occurs when
there is reduced oxygen delivery (hypoxia) or mitochondrial damage. The
decreased ATP leads to failure of the Na+/K+-ATPase pump, causing sodium and
water to enter the cell (cellular swelling—the earliest light microscopic change).
At this stage, if the injurious stimulus is removed and oxygen delivery is restored,
the cell can recover completely. If ATP depletion persists, irreversible injury and
cell death occur.
• A: Karyolysis - Incorrect. Karyolysis (nuclear dissolution due to DNA
digestion) is a LATE, irreversible change seen in necrosis.
• C: Membrane rupture - Incorrect. Plasma membrane rupture is an
irreversible change that leads to cell death (necrosis).
• D: Nuclear pyknosis - Incorrect. Pyknosis (nuclear shrinkage and chromatin
condensation) is an early sign of irreversible injury/apoptosis, not the
earliest cellular change.
4. A patient who suffered a myocardial infarction 48 hours ago has an elevated
serum troponin I level. The pathophysiologic mechanism of troponin release
into the bloodstream involves:
A. Apoptosis with intact cell membrane
B. Necrosis with loss of cell membrane integrity
C. Atrophy of cardiac myocytes
D. Metaplasia of cardiac tissue
Answer: B. Necrosis with loss of cell membrane integrity
RATIONALE: In myocardial infarction, prolonged ischemia (> 20-40 minutes)
causes IRREVERSIBLE cellular injury and NECROSIS (coagulative necrosis in the
heart). Necrosis is characterized by loss of cell membrane integrity, allowing
pg. 3
, 4
intracellular contents—including cardiac enzymes and structural proteins
(troponin I, troponin T, CK-MB)—to leak into the bloodstream. Troponin is the
most sensitive and specific biomarker for myocardial necrosis because it is not
normally present in the blood. The magnitude of troponin elevation correlates
with the extent of myocardial injury.
• A: Apoptosis - Incorrect. Apoptosis is programmed cell death with an
INTACT cell membrane that does not release intracellular contents into the
circulation. Apoptosis does not cause an inflammatory response.
• C: Atrophy - Incorrect. Atrophy is a decrease in cell size, not cell death.
• D: Metaplasia - Incorrect. Metaplasia is a change in cell type, not cell death.
5. A patient with a large, deep pressure ulcer has extensive tissue destruction.
The wound bed contains liquefied, creamy yellow material. The FNP recognizes
this as which type of necrosis?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Answer: B. Liquefactive necrosis
RATIONALE: LIQUEFACTIVE NECROSIS is characterized by the enzymatic digestion
of dead cells, resulting in a liquid, viscous mass (pus). It is typically seen in: (1)
Bacterial and fungal infections (because neutrophils release hydrolytic enzymes
that liquefy the tissue), and (2) Ischemic injury to the brain (because brain tissue
is rich in hydrolytic enzymes and lipids, and lacks a substantial fibrous stroma).
The creamy yellow material is pus composed of dead neutrophils, cellular debris,
and liquefied tissue.
• A: Coagulative necrosis - Incorrect. Coagulative necrosis preserves the
basic tissue architecture (ghost cells) and is typical of ischemic injury in
solid organs (heart, kidney, spleen). The tissue is firm, not liquefied.
• C: Caseous necrosis - Incorrect. Caseous necrosis ("cheese-like") is
characteristic of tuberculosis. It has a friable, granular appearance and is a
combination of coagulative and liquefactive necrosis.
pg. 4
