1
NURS 611 EXAM 1 PATHO ACTUAL EXAM 2026/2027 | Test
Bank Newest Version | Complete Q&A with Rationales |
Already Graded A+ | Maryville University | Pass Guaranteed
ACTUAL EXAM - 60 QUESTIONS - CERTIFICATION LEVEL
A1: Cellular Adaptation, Injury, and Neoplasia (Questions 1-12)
Q1. A 65-year-old man with a history of hypertension presents with left ventricular
hypertrophy on echocardiogram. The increase in cardiac myocyte size represents
which cellular adaptation?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
B. Hypertrophy [CORRECT]
Rationale: Hypertrophy is an increase in cell size resulting in enlarged tissue mass
without an increase in cell number; cardiac myocytes are terminally differentiated
cells incapable of hyperplasia, so pressure overload causes hypertrophy via
mechanotransduction and protein synthesis upregulation. Hyperplasia involves
increased cell number, metaplasia is a reversible change in cell type, and dysplasia
represents disordered, pre-neoplastic growth.
Correct Answer: B
Q2. A 45-year-old woman with a history of prolonged bed rest demonstrates
decreased muscle mass in the lower extremities. This reduction in cell size and tissue
mass is best described as:
A. Apoptosis
B. Atrophy
C. Necrosis
D. Metaplasia
B. Atrophy [CORRECT]
Rationale: Atrophy is a decrease in cell size and tissue mass due to decreased protein
synthesis and increased protein degradation via the ubiquitin-proteasome pathway;
,2
disuse atrophy from immobilization results from diminished mechanical loading and
reduced growth factor signaling. Apoptosis is programmed cell death, necrosis is
unregulated cell death, and metaplasia involves cell type transformation.
Correct Answer: B
Q3. A 55-year-old man with chronic gastroesophageal reflux disease undergoes
endoscopy revealing columnar epithelium replacing squamous epithelium in the
distal esophagus. This cellular adaptation is termed:
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
C. Metaplasia [CORRECT]
Rationale: Metaplasia is a reversible change in which one differentiated cell type is
replaced by another cell type better suited to withstand an adverse environment;
Barrett's esophagus represents squamous-to-columnar metaplasia in response to
chronic acid exposure. Dysplasia implies disordered growth and pre-malignancy,
hyperplasia is increased cell number, and anaplasia indicates loss of differentiation in
malignancy.
Correct Answer: C
Q4. A 30-year-old woman with persistent human papillomavirus infection has a
cervical biopsy showing disordered epithelial maturation, nuclear hyperchromasia,
and loss of polarity extending through the full thickness of the epithelium. These
findings are consistent with:
A. Carcinoma in situ
B. Severe dysplasia
C. Hyperplasia
D. Metaplasia
B. Severe dysplasia [CORRECT]
Rationale: Dysplasia is characterized by disordered epithelial maturation, nuclear
pleomorphism, hyperchromasia, and loss of polarity; severe dysplasia (CIN 3) involves
full-thickness epithelial changes without basement membrane invasion, representing
a pre-neoplastic lesion. Carcinoma in situ is technically non-invasive but the term
,3
severe dysplasia best describes the pathological process described.
Correct Answer: B
Q5. A 70-year-old man with atherosclerosis experiences an acute myocardial
infarction. Histologic examination of the affected myocardium 3 days post-infarction
reveals preserved tissue architecture with loss of nuclei and eosinophilic cytoplasm.
This pattern of necrosis is classified as:
A. Liquefactive necrosis
B. Coagulative necrosis
C. Caseous necrosis
D. Fat necrosis
B. Coagulative necrosis [CORRECT]
Rationale: Coagulative necrosis results from ischemic injury denaturing structural
proteins and enzymes, preserving tissue architecture for days while nuclear detail is
lost; the infarcted myocardium appears firm and pale with ghost outlines of cells.
Liquefactive necrosis occurs in the brain and abscesses, caseous necrosis is
characteristic of tuberculosis, and fat necrosis involves saponification in pancreatic or
breast tissue.
Correct Answer: B
Q6. A 60-year-old man with a history of alcohol abuse presents with severe epigastric
pain. CT shows pancreatic inflammation with peripancreatic fat stranding. Histology
reveals chalky white deposits within adipose tissue surrounding the pancreas. This
represents:
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Gangrenous necrosis
C. Fat necrosis [CORRECT]
Rationale: Fat necrosis occurs when lipases from the pancreas or trauma hydrolyze
triglycerides into fatty acids, which combine with calcium to form insoluble calcium
soaps (saponification), appearing as chalky white deposits; this is characteristic of
acute pancreatitis and traumatic breast injury. Coagulative necrosis preserves
architecture, liquefactive involves enzymatic liquefaction, and gangrenous necrosis
, 4
refers to ischemic tissue death with bacterial infection.
Correct Answer: C
Q7. A 40-year-old woman undergoes reperfusion therapy after a thrombotic stroke.
Within hours, she develops cerebral edema. The cellular injury mechanism primarily
responsible for reperfusion-induced damage is:
A. ATP depletion
B. Free radical formation
C. Lysosomal enzyme release
D. Protein misfolding
B. Free radical formation [CORRECT]
Rationale: Reperfusion injury generates reactive oxygen species (ROS) including
superoxide anion, hydroxyl radical, and hydrogen peroxide via xanthine oxidase
activation and mitochondrial electron transport chain leakage; these free radicals
damage lipids, proteins, and DNA, causing membrane lipid peroxidation and blood-
brain barrier disruption. ATP depletion occurs during ischemia, while lysosomal
release and protein misfolding are secondary consequences.
Correct Answer: B
Q8. A 25-year-old man presents with progressive neurodegeneration and choreiform
movements. Genetic testing reveals a CAG trinucleotide repeat expansion in the HTT
gene. The neuronal death observed in this condition primarily occurs through which
mechanism?
A. Necrosis
B. Apoptosis
C. Autophagy
D. Pyroptosis
B. Apoptosis [CORRECT]
Rationale: Huntington's disease involves mutant huntingtin protein accumulation
causing mitochondrial dysfunction, impaired energy metabolism, and activation of
intrinsic apoptotic pathways via cytochrome c release and caspase activation; this
represents pathologic apoptosis triggered by genetic mutation. Necrosis is
unregulated, autophagy is a catabolic recycling process, and pyroptosis is an
inflammatory caspase-dependent cell death.
Correct Answer: B
NURS 611 EXAM 1 PATHO ACTUAL EXAM 2026/2027 | Test
Bank Newest Version | Complete Q&A with Rationales |
Already Graded A+ | Maryville University | Pass Guaranteed
ACTUAL EXAM - 60 QUESTIONS - CERTIFICATION LEVEL
A1: Cellular Adaptation, Injury, and Neoplasia (Questions 1-12)
Q1. A 65-year-old man with a history of hypertension presents with left ventricular
hypertrophy on echocardiogram. The increase in cardiac myocyte size represents
which cellular adaptation?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
B. Hypertrophy [CORRECT]
Rationale: Hypertrophy is an increase in cell size resulting in enlarged tissue mass
without an increase in cell number; cardiac myocytes are terminally differentiated
cells incapable of hyperplasia, so pressure overload causes hypertrophy via
mechanotransduction and protein synthesis upregulation. Hyperplasia involves
increased cell number, metaplasia is a reversible change in cell type, and dysplasia
represents disordered, pre-neoplastic growth.
Correct Answer: B
Q2. A 45-year-old woman with a history of prolonged bed rest demonstrates
decreased muscle mass in the lower extremities. This reduction in cell size and tissue
mass is best described as:
A. Apoptosis
B. Atrophy
C. Necrosis
D. Metaplasia
B. Atrophy [CORRECT]
Rationale: Atrophy is a decrease in cell size and tissue mass due to decreased protein
synthesis and increased protein degradation via the ubiquitin-proteasome pathway;
,2
disuse atrophy from immobilization results from diminished mechanical loading and
reduced growth factor signaling. Apoptosis is programmed cell death, necrosis is
unregulated cell death, and metaplasia involves cell type transformation.
Correct Answer: B
Q3. A 55-year-old man with chronic gastroesophageal reflux disease undergoes
endoscopy revealing columnar epithelium replacing squamous epithelium in the
distal esophagus. This cellular adaptation is termed:
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
C. Metaplasia [CORRECT]
Rationale: Metaplasia is a reversible change in which one differentiated cell type is
replaced by another cell type better suited to withstand an adverse environment;
Barrett's esophagus represents squamous-to-columnar metaplasia in response to
chronic acid exposure. Dysplasia implies disordered growth and pre-malignancy,
hyperplasia is increased cell number, and anaplasia indicates loss of differentiation in
malignancy.
Correct Answer: C
Q4. A 30-year-old woman with persistent human papillomavirus infection has a
cervical biopsy showing disordered epithelial maturation, nuclear hyperchromasia,
and loss of polarity extending through the full thickness of the epithelium. These
findings are consistent with:
A. Carcinoma in situ
B. Severe dysplasia
C. Hyperplasia
D. Metaplasia
B. Severe dysplasia [CORRECT]
Rationale: Dysplasia is characterized by disordered epithelial maturation, nuclear
pleomorphism, hyperchromasia, and loss of polarity; severe dysplasia (CIN 3) involves
full-thickness epithelial changes without basement membrane invasion, representing
a pre-neoplastic lesion. Carcinoma in situ is technically non-invasive but the term
,3
severe dysplasia best describes the pathological process described.
Correct Answer: B
Q5. A 70-year-old man with atherosclerosis experiences an acute myocardial
infarction. Histologic examination of the affected myocardium 3 days post-infarction
reveals preserved tissue architecture with loss of nuclei and eosinophilic cytoplasm.
This pattern of necrosis is classified as:
A. Liquefactive necrosis
B. Coagulative necrosis
C. Caseous necrosis
D. Fat necrosis
B. Coagulative necrosis [CORRECT]
Rationale: Coagulative necrosis results from ischemic injury denaturing structural
proteins and enzymes, preserving tissue architecture for days while nuclear detail is
lost; the infarcted myocardium appears firm and pale with ghost outlines of cells.
Liquefactive necrosis occurs in the brain and abscesses, caseous necrosis is
characteristic of tuberculosis, and fat necrosis involves saponification in pancreatic or
breast tissue.
Correct Answer: B
Q6. A 60-year-old man with a history of alcohol abuse presents with severe epigastric
pain. CT shows pancreatic inflammation with peripancreatic fat stranding. Histology
reveals chalky white deposits within adipose tissue surrounding the pancreas. This
represents:
A. Coagulative necrosis
B. Liquefactive necrosis
C. Fat necrosis
D. Gangrenous necrosis
C. Fat necrosis [CORRECT]
Rationale: Fat necrosis occurs when lipases from the pancreas or trauma hydrolyze
triglycerides into fatty acids, which combine with calcium to form insoluble calcium
soaps (saponification), appearing as chalky white deposits; this is characteristic of
acute pancreatitis and traumatic breast injury. Coagulative necrosis preserves
architecture, liquefactive involves enzymatic liquefaction, and gangrenous necrosis
, 4
refers to ischemic tissue death with bacterial infection.
Correct Answer: C
Q7. A 40-year-old woman undergoes reperfusion therapy after a thrombotic stroke.
Within hours, she develops cerebral edema. The cellular injury mechanism primarily
responsible for reperfusion-induced damage is:
A. ATP depletion
B. Free radical formation
C. Lysosomal enzyme release
D. Protein misfolding
B. Free radical formation [CORRECT]
Rationale: Reperfusion injury generates reactive oxygen species (ROS) including
superoxide anion, hydroxyl radical, and hydrogen peroxide via xanthine oxidase
activation and mitochondrial electron transport chain leakage; these free radicals
damage lipids, proteins, and DNA, causing membrane lipid peroxidation and blood-
brain barrier disruption. ATP depletion occurs during ischemia, while lysosomal
release and protein misfolding are secondary consequences.
Correct Answer: B
Q8. A 25-year-old man presents with progressive neurodegeneration and choreiform
movements. Genetic testing reveals a CAG trinucleotide repeat expansion in the HTT
gene. The neuronal death observed in this condition primarily occurs through which
mechanism?
A. Necrosis
B. Apoptosis
C. Autophagy
D. Pyroptosis
B. Apoptosis [CORRECT]
Rationale: Huntington's disease involves mutant huntingtin protein accumulation
causing mitochondrial dysfunction, impaired energy metabolism, and activation of
intrinsic apoptotic pathways via cytochrome c release and caspase activation; this
represents pathologic apoptosis triggered by genetic mutation. Necrosis is
unregulated, autophagy is a catabolic recycling process, and pyroptosis is an
inflammatory caspase-dependent cell death.
Correct Answer: B
