NSG 5140 Advanced Pathophysiology Midterm Exam
Review 2 | South College EXAM with Questions and
Answers/Plus a Rationale Updated 2026 A+/Instant
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EXAM COVERAGE - 1. Cellular Biology and Adaptation - 2. Fluid,
Electrolyte, and Acid-Base Imbalances - 3. Inflammation, Immunity,
and Hypersensitivity - 4. Genetic Disorders and Epigenetics - 5.
Neurological Pathophysiology - 6. Cardiovascular Pathophysiology -
7. Pulmonary Pathophysiology - 8. Renal and Urological
Pathophysiology
1. A 56-year-old chronic smoker presents with a persistent cough and hemoptysis. A bronchoscopy
reveals that the normal pseudostratified ciliated columnar epithelium of the bronchi has been
replaced by stratified squamous epithelium. Which cellular adaptation mechanism best explains
this finding?
A. Hypertrophy
B. Metaplasia
C. Dysplasia
D. Atrophy
CORRECT ANSWER : B
Rationale: Metaplasia is the reversible replacement of one mature cell type by another, often
less differentiated cell type, as an adaptive response to chronic irritation or injury, such as
cigarette smoke in the bronchial mucosa. Hypertrophy involves an increase in the size of cells,
atrophy involves a decrease in cell size, and dysplasia refers to deranged cellular growth that is
not a true adaptive substitution. Therefore, B is correct because the squamous replacement is a
classic case of metaplasia.
2. A patient with severe peripheral artery disease experiences intermittent claudication. During
periods of ischemia, cellular injury occurs primarily due to a depletion of intracellular ATP.
Which downstream consequence directly contributes to acute cell swelling (oncosis)?
A. Upregulation of protein synthesis
B. Efflux of extracellular potassium
, C. Inhibition of the Na+/K+-ATPase membrane pump
D. Increased mitochondrial oxidative phosphorylation
CORRECT ANSWER : C
Rationale: ATP depletion halts the energy-dependent Na+/K+-ATPase pump, leading to an
intracellular accumulation of sodium and water alongside an efflux of potassium, resulting in
acute cellular swelling and vacuolation. Upregulation of protein synthesis and increased
oxidative phosphorylation do not occur under ischemic ATP depletion, while potassium efflux
alone does not drive the osmotic influx causing swelling. Therefore, C is the correct mechanism
underlying hypoxic cell swelling.
3. During an acute myocardial infarction, reperfusion of ischemic cardiac tissue can sometimes
exacerbate cellular injury rather than salvaging it. Which molecular species is the primary driver
of this reperfusion injury?
A. Carbon monoxide radicals
B. Reactive oxygen species (ROS)
C. Nitric oxide scavengers
D. Unconjugated bilirubin
CORRECT ANSWER : B
Rationale: Reperfusion introduces a sudden influx of oxygen to ischemic cells whose antioxidant
defenses are compromised, leading to a massive generation of reactive oxygen species (ROS)
such as superoxide and hydroxyl radicals that damage cellular membranes and DNA. Carbon
monoxide radicals, nitric oxide scavengers, and unconjugated bilirubin are not the primary
mediators driving reperfusion tissue damage. Therefore, B correctly identifies the reactive
oxygen species responsible for this secondary injury cascade.
4. A 45-year-old male presents with acute severe flank pain and hematuria. Laboratory workup
reveals hyperuricemia, and a renal ultrasound demonstrates uric acid nephrolithiasis. Which
underlying pathophysiological process is primarily responsible for his elevated serum uric acid
levels?
A. Decreased synthesis of lysosomal enzymes
B. Overproduction or underexcretion of purine catabolism end-products
C. Accelerated degradation of membrane phospholipids
D. Excessive hepatic synthesis of low-density lipoproteins
, CORRECT ANSWER : B
Rationale: Uric acid is the end-product of purine catabolism; hyperuricemia results from either
overproduction or impaired renal excretion of purines, leading to crystal precipitation in joints
or renal tubules. Decreased lysosomal enzymes, membrane phospholipid degradation, and
hepatic LDL synthesis are associated with lysosomal storage diseases, cellular membrane injury,
and dyslipidemia respectively. Therefore, B correctly describes the metabolic pathway driving
hyperuricemia and stone formation.
5. A patient with long-standing poorly controlled hypertension develops left ventricular
hypertrophy. Which intracellular signaling pathway is primarily activated to drive the
enlargement of individual myocardial fibers?
A. Caspase-8 mediated apoptosis
B. Mechanical stretch and growth factor signaling activating protein synthesis
C. Lysosomal degradation of contractile proteins
D. Decreased transcription of structural genes
CORRECT ANSWER : B
Rationale: Myocardial hypertrophy in response to pressure overload is driven by mechanical
stretch, neurohormonal activation, and growth factor signaling that upregulate protein synthesis
and structural gene transcription. Caspase-8 mediates apoptosis rather than growth, lysosomal
degradation leads to atrophy, and decreased transcription would prevent hypertrophy.
Therefore, B is correct because mechanical and trophic stimuli stimulate protein accretion and
cellular enlargement.
6. A researcher is studying cellular aging and notes progressive telomere shortening in somatic
cells after multiple divisions. Which specialized enzyme is typically inactive in these somatic
cells, preventing them from maintaining telomere length?
A. DNA polymerase delta
B. RNA polymerase II
C. Telomerase
D. Topoisomerase II
CORRECT ANSWER : C
Rationale: Telomerase is a ribonucleoprotein enzyme that maintains telomere length by adding
repetitive nucleotide sequences to the ends of chromosomes; it is active in germ cells and stem
, cells but largely inactive in normal somatic cells, leading to replicative senescence. DNA
polymerase delta, RNA polymerase II, and topoisomerase II are housekeeping enzymes involved
in replication and transcription rather than telomere maintenance. Therefore, C is correct as
telomerase inactivity limits the replicative lifespan of somatic cells.
7. A forensic pathologist examines a body and notes rigor mortis 12 hours post-mortem. At the
cellular level, what specific biochemical state accounts for the development of post-mortem
muscle rigidity?
A. Uncontrolled high intracellular ATP generation
B. Depletion of ATP preventing actin-myosin cross-bridge dissociation
C. Massive active transport of calcium into the sarcoplasmic reticulum
D. Upregulation of sliding filament contraction via glycolysis
CORRECT ANSWER : B
Rationale: Rigor mortis occurs after death because cellular respiration ceases, resulting in a
total depletion of ATP; without ATP, the cross-bridges between actin and myosin filaments
cannot detach, locking the muscles in a contracted state. ATP generation and active calcium
transport cease post-mortem, and anaerobic glycolysis quickly exhausts its substrates.
Therefore, B correctly identifies the lack of ATP-driven detachment as the cause of post-mortem
rigidity.
8. An individual experiences severe frostbite during a winter mountaineering expedition. Which of
the following mechanisms contributes most significantly to the localized tissue necrosis seen in
frostbite?
A. Ice crystal formation leading to osmotic shifts and microvascular thrombosis
B. Hyper-proliferation of dermal fibroblasts via unregulated mitosis
C. Activation of primary active transport systems pumping water out of cells
D. Enhanced production of protective heat-shock proteins
CORRECT ANSWER : A
Rationale: Frostbite causes tissue injury through intracellular and extracellular ice crystal
formation, which creates hyperosmotic gradients leading to cellular dehydration, coupled with
microvascular stasis, endothelial injury, and subsequent thrombosis. Unregulated mitosis, active
water pumping out of cells, and heat-shock proteins do not drive frostbite necrosis. Therefore, A
is correct because physical ice formation and vascular occlusion cause direct tissue infarction.
Review 2 | South College EXAM with Questions and
Answers/Plus a Rationale Updated 2026 A+/Instant
Download PDF
EXAM COVERAGE - 1. Cellular Biology and Adaptation - 2. Fluid,
Electrolyte, and Acid-Base Imbalances - 3. Inflammation, Immunity,
and Hypersensitivity - 4. Genetic Disorders and Epigenetics - 5.
Neurological Pathophysiology - 6. Cardiovascular Pathophysiology -
7. Pulmonary Pathophysiology - 8. Renal and Urological
Pathophysiology
1. A 56-year-old chronic smoker presents with a persistent cough and hemoptysis. A bronchoscopy
reveals that the normal pseudostratified ciliated columnar epithelium of the bronchi has been
replaced by stratified squamous epithelium. Which cellular adaptation mechanism best explains
this finding?
A. Hypertrophy
B. Metaplasia
C. Dysplasia
D. Atrophy
CORRECT ANSWER : B
Rationale: Metaplasia is the reversible replacement of one mature cell type by another, often
less differentiated cell type, as an adaptive response to chronic irritation or injury, such as
cigarette smoke in the bronchial mucosa. Hypertrophy involves an increase in the size of cells,
atrophy involves a decrease in cell size, and dysplasia refers to deranged cellular growth that is
not a true adaptive substitution. Therefore, B is correct because the squamous replacement is a
classic case of metaplasia.
2. A patient with severe peripheral artery disease experiences intermittent claudication. During
periods of ischemia, cellular injury occurs primarily due to a depletion of intracellular ATP.
Which downstream consequence directly contributes to acute cell swelling (oncosis)?
A. Upregulation of protein synthesis
B. Efflux of extracellular potassium
, C. Inhibition of the Na+/K+-ATPase membrane pump
D. Increased mitochondrial oxidative phosphorylation
CORRECT ANSWER : C
Rationale: ATP depletion halts the energy-dependent Na+/K+-ATPase pump, leading to an
intracellular accumulation of sodium and water alongside an efflux of potassium, resulting in
acute cellular swelling and vacuolation. Upregulation of protein synthesis and increased
oxidative phosphorylation do not occur under ischemic ATP depletion, while potassium efflux
alone does not drive the osmotic influx causing swelling. Therefore, C is the correct mechanism
underlying hypoxic cell swelling.
3. During an acute myocardial infarction, reperfusion of ischemic cardiac tissue can sometimes
exacerbate cellular injury rather than salvaging it. Which molecular species is the primary driver
of this reperfusion injury?
A. Carbon monoxide radicals
B. Reactive oxygen species (ROS)
C. Nitric oxide scavengers
D. Unconjugated bilirubin
CORRECT ANSWER : B
Rationale: Reperfusion introduces a sudden influx of oxygen to ischemic cells whose antioxidant
defenses are compromised, leading to a massive generation of reactive oxygen species (ROS)
such as superoxide and hydroxyl radicals that damage cellular membranes and DNA. Carbon
monoxide radicals, nitric oxide scavengers, and unconjugated bilirubin are not the primary
mediators driving reperfusion tissue damage. Therefore, B correctly identifies the reactive
oxygen species responsible for this secondary injury cascade.
4. A 45-year-old male presents with acute severe flank pain and hematuria. Laboratory workup
reveals hyperuricemia, and a renal ultrasound demonstrates uric acid nephrolithiasis. Which
underlying pathophysiological process is primarily responsible for his elevated serum uric acid
levels?
A. Decreased synthesis of lysosomal enzymes
B. Overproduction or underexcretion of purine catabolism end-products
C. Accelerated degradation of membrane phospholipids
D. Excessive hepatic synthesis of low-density lipoproteins
, CORRECT ANSWER : B
Rationale: Uric acid is the end-product of purine catabolism; hyperuricemia results from either
overproduction or impaired renal excretion of purines, leading to crystal precipitation in joints
or renal tubules. Decreased lysosomal enzymes, membrane phospholipid degradation, and
hepatic LDL synthesis are associated with lysosomal storage diseases, cellular membrane injury,
and dyslipidemia respectively. Therefore, B correctly describes the metabolic pathway driving
hyperuricemia and stone formation.
5. A patient with long-standing poorly controlled hypertension develops left ventricular
hypertrophy. Which intracellular signaling pathway is primarily activated to drive the
enlargement of individual myocardial fibers?
A. Caspase-8 mediated apoptosis
B. Mechanical stretch and growth factor signaling activating protein synthesis
C. Lysosomal degradation of contractile proteins
D. Decreased transcription of structural genes
CORRECT ANSWER : B
Rationale: Myocardial hypertrophy in response to pressure overload is driven by mechanical
stretch, neurohormonal activation, and growth factor signaling that upregulate protein synthesis
and structural gene transcription. Caspase-8 mediates apoptosis rather than growth, lysosomal
degradation leads to atrophy, and decreased transcription would prevent hypertrophy.
Therefore, B is correct because mechanical and trophic stimuli stimulate protein accretion and
cellular enlargement.
6. A researcher is studying cellular aging and notes progressive telomere shortening in somatic
cells after multiple divisions. Which specialized enzyme is typically inactive in these somatic
cells, preventing them from maintaining telomere length?
A. DNA polymerase delta
B. RNA polymerase II
C. Telomerase
D. Topoisomerase II
CORRECT ANSWER : C
Rationale: Telomerase is a ribonucleoprotein enzyme that maintains telomere length by adding
repetitive nucleotide sequences to the ends of chromosomes; it is active in germ cells and stem
, cells but largely inactive in normal somatic cells, leading to replicative senescence. DNA
polymerase delta, RNA polymerase II, and topoisomerase II are housekeeping enzymes involved
in replication and transcription rather than telomere maintenance. Therefore, C is correct as
telomerase inactivity limits the replicative lifespan of somatic cells.
7. A forensic pathologist examines a body and notes rigor mortis 12 hours post-mortem. At the
cellular level, what specific biochemical state accounts for the development of post-mortem
muscle rigidity?
A. Uncontrolled high intracellular ATP generation
B. Depletion of ATP preventing actin-myosin cross-bridge dissociation
C. Massive active transport of calcium into the sarcoplasmic reticulum
D. Upregulation of sliding filament contraction via glycolysis
CORRECT ANSWER : B
Rationale: Rigor mortis occurs after death because cellular respiration ceases, resulting in a
total depletion of ATP; without ATP, the cross-bridges between actin and myosin filaments
cannot detach, locking the muscles in a contracted state. ATP generation and active calcium
transport cease post-mortem, and anaerobic glycolysis quickly exhausts its substrates.
Therefore, B correctly identifies the lack of ATP-driven detachment as the cause of post-mortem
rigidity.
8. An individual experiences severe frostbite during a winter mountaineering expedition. Which of
the following mechanisms contributes most significantly to the localized tissue necrosis seen in
frostbite?
A. Ice crystal formation leading to osmotic shifts and microvascular thrombosis
B. Hyper-proliferation of dermal fibroblasts via unregulated mitosis
C. Activation of primary active transport systems pumping water out of cells
D. Enhanced production of protective heat-shock proteins
CORRECT ANSWER : A
Rationale: Frostbite causes tissue injury through intracellular and extracellular ice crystal
formation, which creates hyperosmotic gradients leading to cellular dehydration, coupled with
microvascular stasis, endothelial injury, and subsequent thrombosis. Unregulated mitosis, active
water pumping out of cells, and heat-shock proteins do not drive frostbite necrosis. Therefore, A
is correct because physical ice formation and vascular occlusion cause direct tissue infarction.
