N212 PATHOPHYSIOLOGY EXAM 2 (EASTWICK
COLLEGE) NEWEST 2026 ACTUAL EXAM| N212
PATHOPHYSIOLOGY EXAM 2 REVIEW WITH
COMPLETE REAL EXAM QUESTIONS AND CORRECT
VERIFIED ANSWERS/ ALREADY GRADED A+ (MOST
RECENT!!) — 200 Questions
Section 1: Cellular Injury and Adaptation (Questions 1-20)
1 In a patient with chronic gastroesophageal reflux disease, the squamous epithelium of the lower esophagus is
replaced by columnar epithelium. This adaptive response is best described as:
A) Metaplasia, which is a reversible change where one mature cell type is replaced by another, often due to
chronic irritation.
B) Dysplasia, characterized by disordered growth and cytologic atypia.
C) Hyperplasia, an increase in cell number without change in cell type.
D) Anaplasia, a loss of differentiation typical of malignant transformation.
Answer: A
Rationale: Barrett esophagus is a classic example of metaplasia, where chronic injury (acid reflux) induces
reprogramming of stem cells to a more resistant columnar phenotype. Dysplasia would show nuclear atypia;
hyperplasia involves increased cell number of the same type; anaplasia is a feature of cancer.
2 A laboratory experiment exposes cultured hepatocytes to a mitochondrial toxin that inhibits complex I of the
electron transport chain. Which of the following cellular consequences is most likely to occur FIRST?
A) Activation of caspase-9 via cytochrome c release.
B) Depletion of ATP and failure of the Na+/K+ ATPase pump.
C) Formation of reactive oxygen species (ROS) by the mitochondrial electron transport chain.
D) Swelling of the endoplasmic reticulum due to calcium influx.
Answer: B
Rationale: Inhibition of complex I rapidly reduces ATP production. ATP depletion impairs the Na+/K+ pump,
leading to cellular swelling. While ROS and calcium dysregulation occur, they are downstream events. Cytochrome
c release and caspase activation require mitochondrial outer membrane permeabilization, which is later.
3 Which of the following best explains why cardiac myocytes undergo hypertrophy rather than hyperplasia in
response to increased workload?
A) Cardiac myocytes are terminally differentiated and have exited the cell cycle, limiting their proliferative
capacity.
B) Hypertrophy provides a more efficient increase in contractile force compared to hyperplasia.
C) Hyperplasia would require angiogenesis, which is insufficient in the heart.
D) Cardiac myocytes lack growth factor receptors necessary for cell division.
Answer: A
Rationale: Cardiac myocytes are post-mitotic and cannot divide; thus, they respond to increased demand by
increasing cell size (hypertrophy). While efficiency and angiogenesis are considerations, the primary reason is the
lack of proliferative capacity. Growth factor receptors exist but do not trigger division.
,4 In a patient with a renal artery stenosis, the affected kidney shows a decrease in size and function. This adaptive
response is primarily mediated by:
A) Increased apoptosis due to chronic ischemia.
B) Atrophy resulting from reduced blood flow and decreased workload.
C) Necrosis of tubular epithelial cells from hypoxia.
D) Fibrosis replacing functional parenchyma.
Answer: B
Rationale: Reduced renal blood flow leads to decreased perfusion pressure and glomerular filtration, causing the
kidney to atrophy. Atrophy involves a decrease in cell size and number, often due to decreased workload, blood
supply, or trophic signals. Apoptosis contributes but is not the primary mechanism; necrosis would imply
irreversible injury.
5 A researcher treats cultured endothelial cells with a high dose of hydrogen peroxide. Within minutes, cells
exhibit swelling of mitochondria and loss of microvilli. However, upon removal of the oxidant, cells recover.
This stage of injury is best classified as:
A) Reversible cell injury, characterized by mitochondrial swelling and membrane blebbing that can be repaired.
B) Necrosis, because loss of microvilli indicates irreversible damage.
C) Apoptosis, as reactive oxygen species typically trigger programmed cell death.
D) Oncosis, a form of cell death with swelling and ATP depletion.
Answer: A
Rationale: The findings (mitochondrial swelling, loss of microvilli) are classic features of reversible injury. The key
is recovery after removal of the insult. Necrosis would involve irreversible changes like nuclear dissolution.
Apoptosis is characterized by cell shrinkage and nuclear fragmentation. Oncosis is a term for cell death with
swelling, but here recovery indicates reversibility.
6 In a histology section of a liver biopsy from a patient with viral hepatitis, some hepatocytes appear shrunken
with intensely eosinophilic cytoplasm and pyknotic nuclei. These cells are most likely undergoing:
A) Apoptosis, as evidenced by cell shrinkage and chromatin condensation.
B) Coagulative necrosis, with preservation of cell outlines.
C) Liquefactive necrosis, typical of viral infections.
D) Caseous necrosis, characterized by granular debris.
Answer: A
Rationale: Apoptotic cells (Councilman bodies in hepatitis) show shrinkage, eosinophilic cytoplasm, and pyknosis.
Coagulative necrosis retains cell outlines but with loss of nuclei. Liquefactive necrosis forms cysts; caseous
necrosis is crumbly and associated with granulomas.
7 Which of the following molecular events is most directly responsible for the transition from reversible to
irreversible cell injury during ischemia?
A) Depletion of ATP to less than 5% of normal levels.
B) Massive influx of calcium into the cytosol, activating phospholipases and proteases.
C) Formation of oxygen free radicals upon reperfusion.
D) Swelling of the endoplasmic reticulum due to failure of the SERCA pump.
Answer: B
Rationale: Irreversible injury is marked by severe mitochondrial dysfunction and loss of membrane integrity.
Calcium influx activates enzymes that degrade membranes and proteins, leading to cell death. ATP depletion is
critical but reversible if brief; reperfusion injury can exacerbate but is not the direct transition point.
,8 A patient with a genetic deficiency in superoxide dismutase (SOD) is expected to have increased susceptibility
to cell injury from:
A) Hypoxic injury, because SOD is required for mitochondrial respiration.
B) Reperfusion injury, as SOD normally scavenges superoxide radicals.
C) Chemical injury from heavy metals, which are detoxified by SOD.
D) Apoptosis triggered by DNA damage, as SOD repairs oxidative lesions.
Answer: B
Rationale: SOD converts superoxide (O2•") to hydrogen peroxide. Deficiency leads to accumulation of superoxide,
especially during reperfusion when oxygen is reintroduced, causing oxidative damage. SOD does not participate in
respiration, heavy metal detoxification, or direct DNA repair.
9 In a patient with chronic iron overload (hemochromatosis), hepatocytes show increased deposition of
hemosiderin. This is an example of:
A) Intracellular accumulation of an endogenous pigment due to excess substrate.
B) Dystrophic calcification resulting from cell injury.
C) Metaplastic change in response to iron toxicity.
D) Hyaline change, representing protein accumulation.
Answer: A
Rationale: Hemosiderin is a pigment derived from iron, accumulating when iron exceeds cellular storage capacity.
This is a form of intracellular accumulation, not calcification, metaplasia, or hyaline change. Dystrophic
calcification occurs in dead tissue; hyaline change is homogeneous eosinophilic material.
10 A researcher studies a novel drug that inhibits the unfolded protein response (UPR) in cells. Under conditions
of ER stress, cells treated with this drug would be more likely to:
A) Undergo autophagy to degrade misfolded proteins.
B) Activate the intrinsic apoptotic pathway via CHOP induction.
C) Fail to reduce misfolded protein load, leading to increased apoptosis.
D) Enhance proteasomal degradation of ER proteins.
Answer: C
Rationale: The UPR is a protective response that reduces misfolded proteins. Inhibiting it prevents adaptation, so
cells accumulate toxic proteins and undergo apoptosis. Autophagy is a separate process; CHOP is part of UPR but
its induction would be blocked; proteasomal degradation is not directly UPR-mediated.
11 In a cell exposed to chronic hypoxia, which molecular adaptation is most likely to be observed within the first
24 hours?
A) Upregulation of hypoxia-inducible factor 1± (HIF-1±) leading to increased erythropoietin transcription
B) Increased expression of pro-apoptotic BAX protein in the mitochondria
C) Activation of the unfolded protein response (UPR) due to ER stress
D) Stabilization of p53 and subsequent cell cycle arrest at G1/S checkpoint
Answer: A
Rationale: HIF-1± is rapidly stabilized under hypoxia and drives adaptive responses like erythropoietin production.
BAX upregulation promotes apoptosis, not adaptation. UPR is triggered by ER stress, not directly by hypoxia. p53
stabilization typically follows DNA damage, not isolated hypoxia.
12 A researcher treats cultured hepatocytes with a chemical that inhibits the proteasome. Which cellular adaptation
is most likely to be impaired?
A) Autophagy of damaged organelles
, B) Ubiquitin-mediated degradation of misfolded proteins
C) Heat shock protein (HSP) chaperone activity
D) Lysosomal acidification during heterophagy
Answer: B
Rationale: Proteasomes degrade ubiquitin-tagged proteins. Inhibition blocks this pathway. Autophagy involves
lysosomes, not proteasomes. HSP activity is independent of proteasomes. Lysosomal acidification is separate from
proteasomal degradation.
13 In a cell undergoing reversible cell injury, which ultrastructural change is typically the earliest detectable
event?
A) Nuclear pyknosis
B) Swelling of mitochondria and endoplasmic reticulum
C) Formation of amorphous densities in mitochondrial matrix
D) Fragmentation of the plasma membrane
Answer: B
Rationale: Cellular swelling due to failure of ion pumps is the earliest change. Pyknosis is a feature of irreversible
injury (necrosis). Amorphous densities indicate irreversible mitochondrial damage. Plasma membrane
fragmentation occurs late in necrosis.
14 A cell accumulates excessive iron due to a genetic defect. Which form of cell injury is most likely to result
from this accumulation?
A) Chemical injury via free radical generation
B) Hypoxic injury due to impaired oxygen diffusion
C) Immunologic injury from complement activation
D) Apoptotic injury via death receptor ligation
Answer: A
Rationale: Free iron catalyzes Fenton reactions producing hydroxyl radicals, causing oxidative stress. Iron overload
does not directly cause hypoxia or complement activation. Apoptosis from death receptors is triggered by specific
ligands, not iron.
15 Which of the following cellular adaptations is characterized by an increase in the number of cells in a tissue?
A) Atrophy
B) Hypertrophy
C) Hyperplasia
D) Metaplasia
Answer: C
Rationale: Hyperplasia is an increase in cell number. Atrophy is a decrease in cell size/number. Hypertrophy is
increase in cell size. Metaplasia is a change in cell type.
16 In a cell with defective autophagy, which cellular component is most likely to accumulate?
A) Polyubiquitinated proteins
B) Lipofuscin granules
C) Glycogen particles
D) Lipid droplets
Answer: B
Rationale: Autophagy removes damaged organelles and protein aggregates; lipofuscin is an indigestible pigment
that accumulates when autophagy is impaired. Polyubiquitinated proteins are cleared by proteasomes, not
COLLEGE) NEWEST 2026 ACTUAL EXAM| N212
PATHOPHYSIOLOGY EXAM 2 REVIEW WITH
COMPLETE REAL EXAM QUESTIONS AND CORRECT
VERIFIED ANSWERS/ ALREADY GRADED A+ (MOST
RECENT!!) — 200 Questions
Section 1: Cellular Injury and Adaptation (Questions 1-20)
1 In a patient with chronic gastroesophageal reflux disease, the squamous epithelium of the lower esophagus is
replaced by columnar epithelium. This adaptive response is best described as:
A) Metaplasia, which is a reversible change where one mature cell type is replaced by another, often due to
chronic irritation.
B) Dysplasia, characterized by disordered growth and cytologic atypia.
C) Hyperplasia, an increase in cell number without change in cell type.
D) Anaplasia, a loss of differentiation typical of malignant transformation.
Answer: A
Rationale: Barrett esophagus is a classic example of metaplasia, where chronic injury (acid reflux) induces
reprogramming of stem cells to a more resistant columnar phenotype. Dysplasia would show nuclear atypia;
hyperplasia involves increased cell number of the same type; anaplasia is a feature of cancer.
2 A laboratory experiment exposes cultured hepatocytes to a mitochondrial toxin that inhibits complex I of the
electron transport chain. Which of the following cellular consequences is most likely to occur FIRST?
A) Activation of caspase-9 via cytochrome c release.
B) Depletion of ATP and failure of the Na+/K+ ATPase pump.
C) Formation of reactive oxygen species (ROS) by the mitochondrial electron transport chain.
D) Swelling of the endoplasmic reticulum due to calcium influx.
Answer: B
Rationale: Inhibition of complex I rapidly reduces ATP production. ATP depletion impairs the Na+/K+ pump,
leading to cellular swelling. While ROS and calcium dysregulation occur, they are downstream events. Cytochrome
c release and caspase activation require mitochondrial outer membrane permeabilization, which is later.
3 Which of the following best explains why cardiac myocytes undergo hypertrophy rather than hyperplasia in
response to increased workload?
A) Cardiac myocytes are terminally differentiated and have exited the cell cycle, limiting their proliferative
capacity.
B) Hypertrophy provides a more efficient increase in contractile force compared to hyperplasia.
C) Hyperplasia would require angiogenesis, which is insufficient in the heart.
D) Cardiac myocytes lack growth factor receptors necessary for cell division.
Answer: A
Rationale: Cardiac myocytes are post-mitotic and cannot divide; thus, they respond to increased demand by
increasing cell size (hypertrophy). While efficiency and angiogenesis are considerations, the primary reason is the
lack of proliferative capacity. Growth factor receptors exist but do not trigger division.
,4 In a patient with a renal artery stenosis, the affected kidney shows a decrease in size and function. This adaptive
response is primarily mediated by:
A) Increased apoptosis due to chronic ischemia.
B) Atrophy resulting from reduced blood flow and decreased workload.
C) Necrosis of tubular epithelial cells from hypoxia.
D) Fibrosis replacing functional parenchyma.
Answer: B
Rationale: Reduced renal blood flow leads to decreased perfusion pressure and glomerular filtration, causing the
kidney to atrophy. Atrophy involves a decrease in cell size and number, often due to decreased workload, blood
supply, or trophic signals. Apoptosis contributes but is not the primary mechanism; necrosis would imply
irreversible injury.
5 A researcher treats cultured endothelial cells with a high dose of hydrogen peroxide. Within minutes, cells
exhibit swelling of mitochondria and loss of microvilli. However, upon removal of the oxidant, cells recover.
This stage of injury is best classified as:
A) Reversible cell injury, characterized by mitochondrial swelling and membrane blebbing that can be repaired.
B) Necrosis, because loss of microvilli indicates irreversible damage.
C) Apoptosis, as reactive oxygen species typically trigger programmed cell death.
D) Oncosis, a form of cell death with swelling and ATP depletion.
Answer: A
Rationale: The findings (mitochondrial swelling, loss of microvilli) are classic features of reversible injury. The key
is recovery after removal of the insult. Necrosis would involve irreversible changes like nuclear dissolution.
Apoptosis is characterized by cell shrinkage and nuclear fragmentation. Oncosis is a term for cell death with
swelling, but here recovery indicates reversibility.
6 In a histology section of a liver biopsy from a patient with viral hepatitis, some hepatocytes appear shrunken
with intensely eosinophilic cytoplasm and pyknotic nuclei. These cells are most likely undergoing:
A) Apoptosis, as evidenced by cell shrinkage and chromatin condensation.
B) Coagulative necrosis, with preservation of cell outlines.
C) Liquefactive necrosis, typical of viral infections.
D) Caseous necrosis, characterized by granular debris.
Answer: A
Rationale: Apoptotic cells (Councilman bodies in hepatitis) show shrinkage, eosinophilic cytoplasm, and pyknosis.
Coagulative necrosis retains cell outlines but with loss of nuclei. Liquefactive necrosis forms cysts; caseous
necrosis is crumbly and associated with granulomas.
7 Which of the following molecular events is most directly responsible for the transition from reversible to
irreversible cell injury during ischemia?
A) Depletion of ATP to less than 5% of normal levels.
B) Massive influx of calcium into the cytosol, activating phospholipases and proteases.
C) Formation of oxygen free radicals upon reperfusion.
D) Swelling of the endoplasmic reticulum due to failure of the SERCA pump.
Answer: B
Rationale: Irreversible injury is marked by severe mitochondrial dysfunction and loss of membrane integrity.
Calcium influx activates enzymes that degrade membranes and proteins, leading to cell death. ATP depletion is
critical but reversible if brief; reperfusion injury can exacerbate but is not the direct transition point.
,8 A patient with a genetic deficiency in superoxide dismutase (SOD) is expected to have increased susceptibility
to cell injury from:
A) Hypoxic injury, because SOD is required for mitochondrial respiration.
B) Reperfusion injury, as SOD normally scavenges superoxide radicals.
C) Chemical injury from heavy metals, which are detoxified by SOD.
D) Apoptosis triggered by DNA damage, as SOD repairs oxidative lesions.
Answer: B
Rationale: SOD converts superoxide (O2•") to hydrogen peroxide. Deficiency leads to accumulation of superoxide,
especially during reperfusion when oxygen is reintroduced, causing oxidative damage. SOD does not participate in
respiration, heavy metal detoxification, or direct DNA repair.
9 In a patient with chronic iron overload (hemochromatosis), hepatocytes show increased deposition of
hemosiderin. This is an example of:
A) Intracellular accumulation of an endogenous pigment due to excess substrate.
B) Dystrophic calcification resulting from cell injury.
C) Metaplastic change in response to iron toxicity.
D) Hyaline change, representing protein accumulation.
Answer: A
Rationale: Hemosiderin is a pigment derived from iron, accumulating when iron exceeds cellular storage capacity.
This is a form of intracellular accumulation, not calcification, metaplasia, or hyaline change. Dystrophic
calcification occurs in dead tissue; hyaline change is homogeneous eosinophilic material.
10 A researcher studies a novel drug that inhibits the unfolded protein response (UPR) in cells. Under conditions
of ER stress, cells treated with this drug would be more likely to:
A) Undergo autophagy to degrade misfolded proteins.
B) Activate the intrinsic apoptotic pathway via CHOP induction.
C) Fail to reduce misfolded protein load, leading to increased apoptosis.
D) Enhance proteasomal degradation of ER proteins.
Answer: C
Rationale: The UPR is a protective response that reduces misfolded proteins. Inhibiting it prevents adaptation, so
cells accumulate toxic proteins and undergo apoptosis. Autophagy is a separate process; CHOP is part of UPR but
its induction would be blocked; proteasomal degradation is not directly UPR-mediated.
11 In a cell exposed to chronic hypoxia, which molecular adaptation is most likely to be observed within the first
24 hours?
A) Upregulation of hypoxia-inducible factor 1± (HIF-1±) leading to increased erythropoietin transcription
B) Increased expression of pro-apoptotic BAX protein in the mitochondria
C) Activation of the unfolded protein response (UPR) due to ER stress
D) Stabilization of p53 and subsequent cell cycle arrest at G1/S checkpoint
Answer: A
Rationale: HIF-1± is rapidly stabilized under hypoxia and drives adaptive responses like erythropoietin production.
BAX upregulation promotes apoptosis, not adaptation. UPR is triggered by ER stress, not directly by hypoxia. p53
stabilization typically follows DNA damage, not isolated hypoxia.
12 A researcher treats cultured hepatocytes with a chemical that inhibits the proteasome. Which cellular adaptation
is most likely to be impaired?
A) Autophagy of damaged organelles
, B) Ubiquitin-mediated degradation of misfolded proteins
C) Heat shock protein (HSP) chaperone activity
D) Lysosomal acidification during heterophagy
Answer: B
Rationale: Proteasomes degrade ubiquitin-tagged proteins. Inhibition blocks this pathway. Autophagy involves
lysosomes, not proteasomes. HSP activity is independent of proteasomes. Lysosomal acidification is separate from
proteasomal degradation.
13 In a cell undergoing reversible cell injury, which ultrastructural change is typically the earliest detectable
event?
A) Nuclear pyknosis
B) Swelling of mitochondria and endoplasmic reticulum
C) Formation of amorphous densities in mitochondrial matrix
D) Fragmentation of the plasma membrane
Answer: B
Rationale: Cellular swelling due to failure of ion pumps is the earliest change. Pyknosis is a feature of irreversible
injury (necrosis). Amorphous densities indicate irreversible mitochondrial damage. Plasma membrane
fragmentation occurs late in necrosis.
14 A cell accumulates excessive iron due to a genetic defect. Which form of cell injury is most likely to result
from this accumulation?
A) Chemical injury via free radical generation
B) Hypoxic injury due to impaired oxygen diffusion
C) Immunologic injury from complement activation
D) Apoptotic injury via death receptor ligation
Answer: A
Rationale: Free iron catalyzes Fenton reactions producing hydroxyl radicals, causing oxidative stress. Iron overload
does not directly cause hypoxia or complement activation. Apoptosis from death receptors is triggered by specific
ligands, not iron.
15 Which of the following cellular adaptations is characterized by an increase in the number of cells in a tissue?
A) Atrophy
B) Hypertrophy
C) Hyperplasia
D) Metaplasia
Answer: C
Rationale: Hyperplasia is an increase in cell number. Atrophy is a decrease in cell size/number. Hypertrophy is
increase in cell size. Metaplasia is a change in cell type.
16 In a cell with defective autophagy, which cellular component is most likely to accumulate?
A) Polyubiquitinated proteins
B) Lipofuscin granules
C) Glycogen particles
D) Lipid droplets
Answer: B
Rationale: Autophagy removes damaged organelles and protein aggregates; lipofuscin is an indigestible pigment
that accumulates when autophagy is impaired. Polyubiquitinated proteins are cleared by proteasomes, not
