, NURS 611 EXAM 3 PATHO ACTUAL EXAM COMPLETE
QUESTIONS AND CORRECT DETAILED ANSWERS WITH
RATIONALES|ALREADY GRADED A+ (MARYVILLE
UNIVERSITY) - 149 Questions
Section 1: Cellular Adaptation and Injury (Questions 1-13)
1 A researcher exposes cultured hepatocytes to a toxin that disrupts mitochondrial electron transport. Within
minutes, intracellular ATP levels plummet. Which of the following cellular changes is most likely to occur
FIRST, before irreversible injury sets in?
A) Swelling of mitochondria and loss of cristae
B) Formation of large amorphous densities in mitochondria
C) Fragmentation of nuclear DNA into 180-200 base pair fragments
D) Release of cytochrome c into the cytosol
Answer: A
Rationale: ATP depletion leads to failure of the Na+/K+ pump, causing cellular swelling and dilation of the ER.
Mitochondrial swelling occurs early in reversible injury. Amorphous densities (B) are a sign of irreversible injury.
DNA fragmentation (C) and cytochrome c release (D) are features of apoptosis, not the immediate consequence of
ATP loss.
2 In a patient with chronic gastroesophageal reflux disease (GERD), biopsy of the lower esophagus shows
columnar epithelium with goblet cells replacing the normal stratified squamous epithelium. This change is best
described as:
A) Hyperplasia
B) Metaplasia
C) Dysplasia
D) Anaplasia
Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another, often due to chronic
irritation. Here, squamous epithelium is replaced by columnar epithelium with goblet cells (Barrett esophagus).
Hyperplasia (A) involves increased cell number, not change in type. Dysplasia (C) shows disordered growth;
anaplasia (D) is loss of differentiation in malignancy.
3 A 45-year-old woman with a history of hypertension and diabetes presents with sudden-onset severe chest pain.
ECG shows ST-segment elevation. Cardiac troponin is elevated. Which of the following best describes the
predominant mechanism of cell injury in her myocardium?
A) Reperfusion injury due to oxygen free radical generation
B) Direct toxicity from hyperglycemia-induced osmotic stress
C) Pressure overload leading to myocyte hypertrophy
D) Apoptosis mediated by death receptors
Answer: A
Rationale: In acute myocardial infarction, ischemia followed by reperfusion (either spontaneous or therapeutic)
generates reactive oxygen species (ROS) that cause additional injury, including lipid peroxidation and protein
denaturation. While pressure overload (C) can cause hypertrophy, it is not the acute injury mechanism.
,Hyperglycemia (B) contributes to microvascular disease but not the acute event. Apoptosis (D) occurs later but
necrosis is predominant early.
4 A pathologist examines a tissue section stained with hematoxylin and eosin. The section shows cells with
pyknotic nuclei, deeply eosinophilic cytoplasm, and preservation of overall cell outline. The surrounding tissue
has no inflammatory infiltrate. Which type of cell death is most consistent with these findings?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Apoptosis
Answer: D
Rationale: Apoptosis is characterized by cell shrinkage, pyknosis (nuclear condensation), and eosinophilic
cytoplasm, with intact cell membranes and no inflammation. Coagulative necrosis (A) preserves tissue architecture
but elicits inflammation. Liquefactive necrosis (B) features digestion and inflammation. Caseous necrosis (C) has a
cheese-like appearance with granulomatous inflammation.
5 Which of the following intracellular events is most directly responsible for triggering the mitochondrial
permeability transition pore (MPTP) opening in irreversible ischemic injury?
A) Increased intracellular sodium concentration
B) Depletion of glycogen stores
C) Calcium overload in the mitochondrial matrix
D) Activation of caspase-8
Answer: C
Rationale: In ischemia, failure of calcium pumps leads to cytosolic and mitochondrial calcium overload. Calcium
binds to cyclophilin D, promoting MPTP opening, which dissipates the proton gradient and halts ATP synthesis,
leading to necrosis. Sodium increase (A) causes swelling but not MPTP opening. Glycogen depletion (B) is a
consequence, not trigger. Caspase-8 (D) is involved in extrinsic apoptosis, not MPTP.
6 A 60-year-old man with a 40-pack-year smoking history undergoes a lung biopsy. Microscopic examination
reveals focal areas where the normal ciliated pseudostratified columnar epithelium is replaced by stratified
squamous epithelium. This change is classified as:
A) Squamous metaplasia
B) Squamous dysplasia
C) Squamous cell carcinoma in situ
D) Adenocarcinoma
Answer: A
Rationale: Squamous metaplasia is the replacement of columnar epithelium by squamous epithelium, often in
response to chronic irritation such as smoking. It is reversible if the irritant is removed. Dysplasia (B) shows
cytologic atypia; carcinoma in situ (C) is severe dysplasia involving full thickness; adenocarcinoma (D) is
gland-forming malignancy.
7 In a patient with prolonged hypotension, the kidneys show acute tubular necrosis affecting the proximal tubules.
Which of the following best describes the sequence of events leading to cell death in this scenario?
A) ATP depletion -> Na+/K+ pump failure -> cell swelling -> rupture of lysosomes -> autolysis
B) Free radical damage -> lipid peroxidation -> membrane blebbing -> apoptosis
C) Calcium influx -> activation of endonucleases -> DNA laddering -> cell shrinkage
D) Mitochondrial depolarization -> cytochrome c release -> caspase activation -> phagocytosis
, Answer: A
Rationale: In ischemic acute tubular necrosis, ATP depletion causes failure of ion pumps, leading to cellular
swelling. Continued ischemia results in lysosomal membrane breakdown, releasing hydrolytic enzymes that digest
the cell (autolysis). This is necrosis, not apoptosis. Options B, C, and D describe mechanisms more typical of
apoptosis or other forms of injury.
8 Which of the following cellular adaptations is most likely to occur in a skeletal muscle that is subjected to
continuous electrical stimulation over several weeks?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: Increased workload (e.g., continuous electrical stimulation) leads to hypertrophy of skeletal muscle
fibers, which increase in size due to increased synthesis of contractile proteins. Hyperplasia (A) does not occur in
skeletal muscle. Atrophy (C) would occur with disuse. Metaplasia (D) is a change in cell type, not seen in muscle
under these conditions.
9 A researcher is studying a toxin that causes cell injury by covalently binding to proteins, forming adducts.
Which of the following is the most likely consequence of this adduct formation?
A) Increased proteasomal degradation of the modified proteins
B) Loss of protein function and possible misfolding
C) Activation of the unfolded protein response (UPR) leading to autophagy
D) Direct activation of caspases
Answer: B
Rationale: Chemical adducts alter protein structure, leading to loss of function and potential misfolding. While the
UPR (C) may be activated, the most direct consequence is loss of function. Proteasomal degradation (A) may
increase but is a secondary response. Direct caspase activation (D) is not typical of adduct-forming toxins.
10 In a patient with chronic hypoxia due to severe anemia, which of the following adaptive responses is most
likely to be observed in the bone marrow?
A) Atrophy of erythroid precursors
B) Hyperplasia of erythroid precursors
C) Metaplasia to adipose tissue
D) Dysplasia with megaloblastic changes
Answer: B
Rationale: Chronic hypoxia stimulates erythropoietin production, leading to hyperplasia of erythroid precursors in
the bone marrow to increase red blood cell mass. Atrophy (A) would be maladaptive. Metaplasia (C) is not typical.
Dysplasia (D) is abnormal growth, not a physiologic adaptation to hypoxia.
11 A researcher is investigating the molecular mechanisms underlying cellular adaptation in cardiac myocytes
subjected to chronic pressure overload. Which of the following signaling pathways is most directly responsible
for the transition from adaptive hypertrophy to maladaptive remodeling and heart failure?
A) Activation of PI3K/Akt pathway leading to increased protein synthesis and cell size
B) Sust activation of Gq-coupled receptors and downstream calcineurin-NFAT signaling
C) Upregulation of IGF-1 receptor signaling and subsequent mTOR activation
D) Increased expression of antioxidant enzymes such as superoxide dismutase
QUESTIONS AND CORRECT DETAILED ANSWERS WITH
RATIONALES|ALREADY GRADED A+ (MARYVILLE
UNIVERSITY) - 149 Questions
Section 1: Cellular Adaptation and Injury (Questions 1-13)
1 A researcher exposes cultured hepatocytes to a toxin that disrupts mitochondrial electron transport. Within
minutes, intracellular ATP levels plummet. Which of the following cellular changes is most likely to occur
FIRST, before irreversible injury sets in?
A) Swelling of mitochondria and loss of cristae
B) Formation of large amorphous densities in mitochondria
C) Fragmentation of nuclear DNA into 180-200 base pair fragments
D) Release of cytochrome c into the cytosol
Answer: A
Rationale: ATP depletion leads to failure of the Na+/K+ pump, causing cellular swelling and dilation of the ER.
Mitochondrial swelling occurs early in reversible injury. Amorphous densities (B) are a sign of irreversible injury.
DNA fragmentation (C) and cytochrome c release (D) are features of apoptosis, not the immediate consequence of
ATP loss.
2 In a patient with chronic gastroesophageal reflux disease (GERD), biopsy of the lower esophagus shows
columnar epithelium with goblet cells replacing the normal stratified squamous epithelium. This change is best
described as:
A) Hyperplasia
B) Metaplasia
C) Dysplasia
D) Anaplasia
Answer: B
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another, often due to chronic
irritation. Here, squamous epithelium is replaced by columnar epithelium with goblet cells (Barrett esophagus).
Hyperplasia (A) involves increased cell number, not change in type. Dysplasia (C) shows disordered growth;
anaplasia (D) is loss of differentiation in malignancy.
3 A 45-year-old woman with a history of hypertension and diabetes presents with sudden-onset severe chest pain.
ECG shows ST-segment elevation. Cardiac troponin is elevated. Which of the following best describes the
predominant mechanism of cell injury in her myocardium?
A) Reperfusion injury due to oxygen free radical generation
B) Direct toxicity from hyperglycemia-induced osmotic stress
C) Pressure overload leading to myocyte hypertrophy
D) Apoptosis mediated by death receptors
Answer: A
Rationale: In acute myocardial infarction, ischemia followed by reperfusion (either spontaneous or therapeutic)
generates reactive oxygen species (ROS) that cause additional injury, including lipid peroxidation and protein
denaturation. While pressure overload (C) can cause hypertrophy, it is not the acute injury mechanism.
,Hyperglycemia (B) contributes to microvascular disease but not the acute event. Apoptosis (D) occurs later but
necrosis is predominant early.
4 A pathologist examines a tissue section stained with hematoxylin and eosin. The section shows cells with
pyknotic nuclei, deeply eosinophilic cytoplasm, and preservation of overall cell outline. The surrounding tissue
has no inflammatory infiltrate. Which type of cell death is most consistent with these findings?
A) Coagulative necrosis
B) Liquefactive necrosis
C) Caseous necrosis
D) Apoptosis
Answer: D
Rationale: Apoptosis is characterized by cell shrinkage, pyknosis (nuclear condensation), and eosinophilic
cytoplasm, with intact cell membranes and no inflammation. Coagulative necrosis (A) preserves tissue architecture
but elicits inflammation. Liquefactive necrosis (B) features digestion and inflammation. Caseous necrosis (C) has a
cheese-like appearance with granulomatous inflammation.
5 Which of the following intracellular events is most directly responsible for triggering the mitochondrial
permeability transition pore (MPTP) opening in irreversible ischemic injury?
A) Increased intracellular sodium concentration
B) Depletion of glycogen stores
C) Calcium overload in the mitochondrial matrix
D) Activation of caspase-8
Answer: C
Rationale: In ischemia, failure of calcium pumps leads to cytosolic and mitochondrial calcium overload. Calcium
binds to cyclophilin D, promoting MPTP opening, which dissipates the proton gradient and halts ATP synthesis,
leading to necrosis. Sodium increase (A) causes swelling but not MPTP opening. Glycogen depletion (B) is a
consequence, not trigger. Caspase-8 (D) is involved in extrinsic apoptosis, not MPTP.
6 A 60-year-old man with a 40-pack-year smoking history undergoes a lung biopsy. Microscopic examination
reveals focal areas where the normal ciliated pseudostratified columnar epithelium is replaced by stratified
squamous epithelium. This change is classified as:
A) Squamous metaplasia
B) Squamous dysplasia
C) Squamous cell carcinoma in situ
D) Adenocarcinoma
Answer: A
Rationale: Squamous metaplasia is the replacement of columnar epithelium by squamous epithelium, often in
response to chronic irritation such as smoking. It is reversible if the irritant is removed. Dysplasia (B) shows
cytologic atypia; carcinoma in situ (C) is severe dysplasia involving full thickness; adenocarcinoma (D) is
gland-forming malignancy.
7 In a patient with prolonged hypotension, the kidneys show acute tubular necrosis affecting the proximal tubules.
Which of the following best describes the sequence of events leading to cell death in this scenario?
A) ATP depletion -> Na+/K+ pump failure -> cell swelling -> rupture of lysosomes -> autolysis
B) Free radical damage -> lipid peroxidation -> membrane blebbing -> apoptosis
C) Calcium influx -> activation of endonucleases -> DNA laddering -> cell shrinkage
D) Mitochondrial depolarization -> cytochrome c release -> caspase activation -> phagocytosis
, Answer: A
Rationale: In ischemic acute tubular necrosis, ATP depletion causes failure of ion pumps, leading to cellular
swelling. Continued ischemia results in lysosomal membrane breakdown, releasing hydrolytic enzymes that digest
the cell (autolysis). This is necrosis, not apoptosis. Options B, C, and D describe mechanisms more typical of
apoptosis or other forms of injury.
8 Which of the following cellular adaptations is most likely to occur in a skeletal muscle that is subjected to
continuous electrical stimulation over several weeks?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: B
Rationale: Increased workload (e.g., continuous electrical stimulation) leads to hypertrophy of skeletal muscle
fibers, which increase in size due to increased synthesis of contractile proteins. Hyperplasia (A) does not occur in
skeletal muscle. Atrophy (C) would occur with disuse. Metaplasia (D) is a change in cell type, not seen in muscle
under these conditions.
9 A researcher is studying a toxin that causes cell injury by covalently binding to proteins, forming adducts.
Which of the following is the most likely consequence of this adduct formation?
A) Increased proteasomal degradation of the modified proteins
B) Loss of protein function and possible misfolding
C) Activation of the unfolded protein response (UPR) leading to autophagy
D) Direct activation of caspases
Answer: B
Rationale: Chemical adducts alter protein structure, leading to loss of function and potential misfolding. While the
UPR (C) may be activated, the most direct consequence is loss of function. Proteasomal degradation (A) may
increase but is a secondary response. Direct caspase activation (D) is not typical of adduct-forming toxins.
10 In a patient with chronic hypoxia due to severe anemia, which of the following adaptive responses is most
likely to be observed in the bone marrow?
A) Atrophy of erythroid precursors
B) Hyperplasia of erythroid precursors
C) Metaplasia to adipose tissue
D) Dysplasia with megaloblastic changes
Answer: B
Rationale: Chronic hypoxia stimulates erythropoietin production, leading to hyperplasia of erythroid precursors in
the bone marrow to increase red blood cell mass. Atrophy (A) would be maladaptive. Metaplasia (C) is not typical.
Dysplasia (D) is abnormal growth, not a physiologic adaptation to hypoxia.
11 A researcher is investigating the molecular mechanisms underlying cellular adaptation in cardiac myocytes
subjected to chronic pressure overload. Which of the following signaling pathways is most directly responsible
for the transition from adaptive hypertrophy to maladaptive remodeling and heart failure?
A) Activation of PI3K/Akt pathway leading to increased protein synthesis and cell size
B) Sust activation of Gq-coupled receptors and downstream calcineurin-NFAT signaling
C) Upregulation of IGF-1 receptor signaling and subsequent mTOR activation
D) Increased expression of antioxidant enzymes such as superoxide dismutase
