FINAL EXAM NSG 527 QUESTIONS AND
ANSWERS STUDY GUIDE UPDATED A PLUS
GUIDE SOLUTION
SECTION ONE: CELLULAR ADAPTATION AND INJURY
Question 1
A patient with a history of chronic alcohol abuse presents with severe epigastric pain.
Lab tests show elevated serum lipase. The pathologist notes the pancreatic cells
have been destroyed by digestive enzymes. What is the primary intracellular
mechanism that allows digestive enzymes to destroy the pancreas from the inside?
A. The enzymes mutate and become resistant to normal inhibitors.
B. Lysosomal membranes rupture, releasing acid hydrolases that activate the
digestive proenzymes within the acinar cells.
C. The endoplasmic reticulum synthesizes active trypsin instead of trypsinogen.
D. Apoptosis is triggered, causing programmed release of toxins.
,Answer: B
RATIONALE: In acute pancreatitis, such as that caused by alcohol or gallstones, the
primary cellular injury begins with the premature activation of digestive enzymes.
Trypsinogen and other proenzymes are normally safely packaged in zymogen
granules. However, injury causes lysosomal membranes to fuse with these zymogen
granules. The lysosomal acid hydrolases activate the trypsinogen into trypsin inside
the cell. This active trypsin then activates all other pancreatic enzymes (like lipase
and amylase) directly within the acinar cell, causing massive autodigestion, cellular
swelling, and necrosis.
Question 2
A biopsy of a smoker's airway shows stratified squamous epithelium replacing the
normal ciliated columnar epithelium. The cells are fully mature and there is no
nuclear atypia. How is this process best described pathophysiologically?
A. Dysplasia
B. Anaplasia
C. Metaplasia
D. Hyperplasia
Answer: C
RATIONALE: Metaplasia is the reversible replacement of one fully differentiated adult
cell type with another adult cell type. In the respiratory tract, chronic tobacco
exposure destroys the fragile ciliated columnar cells. To protect the underlying tissue
from the chronic irritant, basal stem cells differentiate into tougher, more resistant
stratified squamous epithelium. Dysplasia would involve atypical, disorganized cells
with nuclear changes, which is a precursor to cancer. Anaplasia refers to
, undifferentiated, primitive-looking cells typical of malignancy. Hyperplasia is simply
an increase in the number of normal cells.
Question 3
A patient suffers a massive ischemic stroke. The neurologist explains that the core
infarct is surrounded by a penumbra. Why is the tissue in the penumbra salvageable,
unlike the core?
A. The penumbra has an alternative blood supply from collateral circulation, while the
core does not.
B. Cells in the penumbra have shifted to anaerobic glycolysis to maintain their
membrane integrity, whereas cells in the core have lost ATP completely, causing
membrane failure and uncontrolled calcium influx.
C. The penumbra is located in the white matter, which is resistant to ischemia.
D. Glutamate excitotoxicity only affects the core and spares the penumbra.
Answer: B
RATIONALE: In an ischemic stroke, blood flow drops in a gradient. The core receives
almost no blood flow (below 10 mL/100g/min). Without oxygen, the electron transport
chain stops, ATP is depleted, and the sodium-potassium pump fails. This allows
uncontrolled sodium and calcium influx into the cells, causing acute cellular swelling
(oncosis) and rapid death by necrosis. The penumbra has reduced blood flow (around
10 to 20 mL/100g/min). This is not enough to generate action potentials (causing
clinical symptoms like paralysis), but it is just enough ATP to keep the cell
membranes intact. If perfusion is restored (e.g., with tPA), the penumbra cells can
recover.
SECTION TWO: IMMUNOLOGY AND INFLAMMATION
ANSWERS STUDY GUIDE UPDATED A PLUS
GUIDE SOLUTION
SECTION ONE: CELLULAR ADAPTATION AND INJURY
Question 1
A patient with a history of chronic alcohol abuse presents with severe epigastric pain.
Lab tests show elevated serum lipase. The pathologist notes the pancreatic cells
have been destroyed by digestive enzymes. What is the primary intracellular
mechanism that allows digestive enzymes to destroy the pancreas from the inside?
A. The enzymes mutate and become resistant to normal inhibitors.
B. Lysosomal membranes rupture, releasing acid hydrolases that activate the
digestive proenzymes within the acinar cells.
C. The endoplasmic reticulum synthesizes active trypsin instead of trypsinogen.
D. Apoptosis is triggered, causing programmed release of toxins.
,Answer: B
RATIONALE: In acute pancreatitis, such as that caused by alcohol or gallstones, the
primary cellular injury begins with the premature activation of digestive enzymes.
Trypsinogen and other proenzymes are normally safely packaged in zymogen
granules. However, injury causes lysosomal membranes to fuse with these zymogen
granules. The lysosomal acid hydrolases activate the trypsinogen into trypsin inside
the cell. This active trypsin then activates all other pancreatic enzymes (like lipase
and amylase) directly within the acinar cell, causing massive autodigestion, cellular
swelling, and necrosis.
Question 2
A biopsy of a smoker's airway shows stratified squamous epithelium replacing the
normal ciliated columnar epithelium. The cells are fully mature and there is no
nuclear atypia. How is this process best described pathophysiologically?
A. Dysplasia
B. Anaplasia
C. Metaplasia
D. Hyperplasia
Answer: C
RATIONALE: Metaplasia is the reversible replacement of one fully differentiated adult
cell type with another adult cell type. In the respiratory tract, chronic tobacco
exposure destroys the fragile ciliated columnar cells. To protect the underlying tissue
from the chronic irritant, basal stem cells differentiate into tougher, more resistant
stratified squamous epithelium. Dysplasia would involve atypical, disorganized cells
with nuclear changes, which is a precursor to cancer. Anaplasia refers to
, undifferentiated, primitive-looking cells typical of malignancy. Hyperplasia is simply
an increase in the number of normal cells.
Question 3
A patient suffers a massive ischemic stroke. The neurologist explains that the core
infarct is surrounded by a penumbra. Why is the tissue in the penumbra salvageable,
unlike the core?
A. The penumbra has an alternative blood supply from collateral circulation, while the
core does not.
B. Cells in the penumbra have shifted to anaerobic glycolysis to maintain their
membrane integrity, whereas cells in the core have lost ATP completely, causing
membrane failure and uncontrolled calcium influx.
C. The penumbra is located in the white matter, which is resistant to ischemia.
D. Glutamate excitotoxicity only affects the core and spares the penumbra.
Answer: B
RATIONALE: In an ischemic stroke, blood flow drops in a gradient. The core receives
almost no blood flow (below 10 mL/100g/min). Without oxygen, the electron transport
chain stops, ATP is depleted, and the sodium-potassium pump fails. This allows
uncontrolled sodium and calcium influx into the cells, causing acute cellular swelling
(oncosis) and rapid death by necrosis. The penumbra has reduced blood flow (around
10 to 20 mL/100g/min). This is not enough to generate action potentials (causing
clinical symptoms like paralysis), but it is just enough ATP to keep the cell
membranes intact. If perfusion is restored (e.g., with tPA), the penumbra cells can
recover.
SECTION TWO: IMMUNOLOGY AND INFLAMMATION
