NURS 5315 EXAM 1 (UTA) NEWEST 2026 ACTUAL EXAM
TEST BANK| NURS5315 ADVANCED PATHOPHYSIOLOGY
EXAM 1 REVIEW WITH COMPLETE 300 REAL EXAM
QUESTIONS AND CORRECT VERIFIED ANSWERS/
ALREADY GRADED A+ (MOST RECENT!!) — 300 Questions
Section 1: Cellular Adaptation, Injury, and Death (Questions 1-30)
1 A patient with chronic obstructive pulmonary disease (COPD) has long-term hypoxemia. Which cellular
adaptation is most likely to occur in the skeletal muscle of this patient, and what is the primary molecular
mechanism?
A) Hypertrophy due to increased IGF-1 signaling
B) Hyperplasia due to activation of satellite cells
C) Atrophy due to upregulated ubiquitin-proteasome pathway
D) Metaplasia due to reprogramming of myogenic transcription factors
Answer: C
Rationale: Chronic hypoxemia leads to disuse and decreased oxygen delivery, activating the ubiquitin-proteasome
pathway and causing muscle atrophy (correct). Hypertrophy (A) requires increased workload and IGF-1;
hyperplasia (B) is not typical in skeletal muscle; metaplasia (D) is a change in cell type, not seen here.
2 A researcher treats hepatocytes with a low dose of a chemical that inhibits mitochondrial ATP synthase. After 2
hours, the cells show swelling of the endoplasmic reticulum and loss of microvilli, but no nuclear changes.
Which statement best describes the cellular state?
A) Irreversible injury: the cells will undergo necrosis within minutes
B) Reversible injury: the cells can recover if the inhibitor is removed
C) Apoptosis: the cells are in early stage of programmed cell death
D) Necroptosis: a regulated form of necrosis is initiated
Answer: B
Rationale: Cellular swelling and ER dilation without nuclear changes (pyknosis, karyorrhexis, karyolysis) indicate
reversible injury (B). Irreversible injury (A) would show nuclear changes; apoptosis (C) would show cell shrinkage
and chromatin condensation; necroptosis (D) would involve RIP kinases and plasma membrane rupture.
3 In a model of myocardial ischemia-reperfusion injury, which molecular event is most directly responsible for
the transition from reversible to irreversible injury in cardiac myocytes?
A) Formation of the mitochondrial permeability transition pore (mPTP)
B) Depletion of ATP to below 50% of normal levels
C) Accumulation of intracellular sodium and calcium
D) Activation of caspase-9 via cytochrome c release
Answer: A
Rationale: Opening of the mPTP causes loss of mitochondrial membrane potential, ATP depletion, and release of
pro-apoptotic factors, marking the point of no return (A). ATP depletion (B) and ion imbalances (C) occur in
reversible injury; caspase activation (D) is downstream of mPTP opening and can be part of apoptosis, but mPTP
opening itself is the critical event for irreversible injury in ischemia-reperfusion.
,4 A pathologist examines a biopsy from a patient with chronic gastritis. The gastric epithelium shows
intestinal-type goblet cells and absorptive cells. This change is best described as:
A) Dysplasia with loss of differentiation
B) Hyperplasia due to chronic inflammation
C) Metaplasia, which may be reversible if the irritant is removed
D) Anaplasia, indicating malignant transformation
Answer: C
Rationale: Replacement of gastric epithelium with intestinal-type cells is intestinal metaplasia (C), a common
adaptive response to chronic irritation. Dysplasia (A) involves abnormal growth and maturation; hyperplasia (B) is
increased cell number without change in type; anaplasia (D) is severe loss of differentiation seen in cancer.
5 A researcher treats cultured neurons with a high concentration of glutamate, leading to excitotoxicity. Which of
the following sequences of events most accurately describes the early steps in this form of cell injury?
A) NMDA receptor activation !’ calcium influx !’ calpain activation !’ cytoskeletal breakdown
B) AMPA receptor activation !’ sodium influx !’ cell swelling !’ lysis
C) Metabotropic receptor activation !’ G-protein signaling !’ caspase activation !’ apoptosis
D) Glutamate transporter reversal !’ ATP depletion !’ necrosis
Answer: A
Rationale: Excitotoxicity primarily involves excessive NMDA receptor activation, leading to calcium overload (A).
Calpain activation then degrades cytoskeletal proteins. While sodium influx (B) contributes to swelling, the key
injury mechanism is calcium-mediated; metabotropic receptors (C) are less directly involved; transporter reversal
(D) occurs but is not the earliest step.
6 Which of the following best distinguishes apoptosis from necrosis at the molecular level?
A) Apoptosis requires ATP, while necrosis is ATP-independent
B) Necrosis always involves inflammation, while apoptosis never does
C) Apoptosis is initiated by extrinsic or intrinsic pathways, while necrosis is always accidental
D) Caspase activation is unique to apoptosis, while necrosis involves calpains and cathepsins
Answer: A
Rationale: Apoptosis is an energy-dependent process requiring ATP for caspase activation and DNA fragmentation
(A). While necrosis is often ATP-independent, some forms (necroptosis) require ATP; inflammation is typical in
necrosis but can occur in late apoptosis; caspase activation is a hallmark of apoptosis, but some forms of regulated
necrosis also involve caspases indirectly.
7 A patient with a genetic deficiency in the enzyme superoxide dismutase (SOD) is expected to have increased
susceptibility to cell injury under which condition?
A) Hypoxic injury due to reduced ATP production
B) Reperfusion injury due to accumulation of superoxide anions
C) Chemical injury due to impaired cytochrome P450 activity
D) Apoptosis due to defective Fas signaling
Answer: B
Rationale: SOD converts superoxide radical (O2•") to hydrogen peroxide. Deficiency leads to superoxide
accumulation, particularly during reperfusion when oxygen is reintroduced (B). Hypoxic injury (A) is more related
to ATP depletion; cytochrome P450 (C) is involved in metabolism; Fas signaling (D) is part of extrinsic apoptosis.
8 In a patient with chronic anemia, the bone marrow shows increased erythroid precursors. This represents which
type of cellular adaptation, and what is the primary stimulus?
,A) Hypertrophy: increased erythropoietin causing enlargement of erythroblasts
B) Hyperplasia: increased erythropoietin causing proliferation of erythroid progenitors
C) Metaplasia: erythropoietin causing conversion of myeloid cells to erythroid cells
D) Dysplasia: erythropoietin causing abnormal maturation of erythroblasts
Answer: B
Rationale: Chronic anemia leads to increased erythropoietin, which stimulates proliferation of erythroid progenitor
cells, resulting in hyperplasia (B). Hypertrophy (A) is an increase in cell size, not number; metaplasia (C) is a
change in cell type; dysplasia (D) involves abnormal growth and is not a typical adaptive response.
9 A researcher induces autophagy in cultured fibroblasts by nutrient deprivation. Which of the following
molecular markers would confirm activation of autophagy?
A) Increased expression of Bcl-2 and decreased Bax
B) Conversion of LC3-I to LC3-II and formation of autophagosomes
C) Activation of caspase-3 and cleavage of PARP
D) Release of cytochrome c from mitochondria into cytosol
Answer: B
Rationale: Autophagy is characterized by the formation of autophagosomes, which involves lipidation of LC3-I to
LC3-II (B). Bcl-2/Bax changes (A) are associated with apoptosis; caspase-3 activation (C) and cytochrome c
release (D) are hallmarks of apoptosis, not autophagy.
10 A researcher treats cells with a drug that inhibits the proteasome. Which of the following is the most likely
consequence?
A) Accumulation of misfolded proteins and ER stress leading to apoptosis
B) Increased degradation of cyclins and cell cycle arrest
C) Enhanced autophagy and cell survival
D) Activation of NF-ºB and increased inflammation
Answer: A
Rationale: Proteasome inhibition prevents degradation of ubiquitinated proteins, leading to accumulation of
misfolded proteins, ER stress, and eventually apoptosis (A). It would decrease degradation of cyclins (B) not
increase; autophagy may be induced but is not the primary consequence; NF-ºB activation is typically reduced
because IºB is not degraded.
11 A research study examines the response of hepatocytes to chronic ethanol exposure. The cells exhibit an
increase in smooth endoplasmic reticulum (SER) and upregulation of cytochrome P450 enzymes. This adaptive
response is best classified as which type of cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Metaplasia
D) Dysplasia
Answer: B
Rationale: Hypertrophy refers to an increase in cell size due to increased functional demand or specific hormonal
stimulation. The proliferation of SER and CYP enzymes represents an increase in cellular machinery, not cell
number (hyperplasia), nor a change in cell type (metaplasia) or abnormal growth (dysplasia).
12 In myocardial ischemia, which sequence of events most accurately describes the progression from reversible to
irreversible cell injury?
A) ATP depletion !’ mitochondrial swelling !’ plasma membrane blebbing !’ nuclear pyknosis
, B) ATP depletion !’ loss of ion gradients !’ cellular swelling !’ lysosomal enzyme leakage
C) Calcium influx !’ activation of phospholipases !’ mitochondrial permeability transition !’ ATP depletion
D) Reactive oxygen species generation !’ lipid peroxidation !’ DNA fragmentation !’ protein denaturation
Answer: C
Rationale: Irreversible injury is marked by mitochondrial dysfunction and massive calcium influx, which triggers
phospholipase activation and the mitochondrial permeability transition, leading to ATP depletion. While options A
and B describe aspects of reversible injury, option C captures the critical step of irreversible injury. Option D
describes oxidative stress but not the typical sequence in ischemia.
13 A pathologist examines a tissue section showing cells with abundant eosinophilic cytoplasm, pyknotic nuclei,
and fragmentation into membrane-bound apoptotic bodies. Immunohistochemistry is positive for caspase-3.
Which of the following best explains the absence of inflammation in this tissue?
A) Apoptotic cells are phagocytosed before releasing cellular contents
B) Necrosis induces a rapid anti-inflammatory response
C) Caspase-3 degrades pro-inflammatory cytokines
D) The cells are undergoing autophagic cell death, not apoptosis
Answer: A
Rationale: Apoptosis is a programmed, non-inflammatory cell death because apoptotic bodies are quickly engulfed
by phagocytes before they can release pro-inflammatory contents. Necrosis (option B) typically triggers
inflammation. Caspase-3 executes apoptosis but does not degrade cytokines (option C). Autophagy (option D) is a
different process.
14 In the setting of chronic gastric reflux, the squamous epithelium of the lower esophagus is replaced by
columnar epithelium resembling that of the intestine. This change is an example of:
A) Dysplasia
B) Anaplasia
C) Metaplasia
D) Hyperplasia
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another, often in response to
chronic irritation. Barrett esophagus is a classic example. Dysplasia (A) is abnormal growth, anaplasia (B) is loss of
differentiation, and hyperplasia (D) is increased cell number.
15 A cell exposed to a sublethal dose of a toxin shows swelling of the endoplasmic reticulum and dissociation of
ribosomes from the rough ER. This finding is most consistent with which type of cellular injury?
A) Hypoxic injury
B) Chemical injury
C) Radiation injury
D) Immune-mediated injury
Answer: B
Rationale: Chemical toxins often target the ER and ribosomes, leading to dissociation of ribosomes and ER
swelling. Hypoxic injury (A) primarily affects mitochondria. Radiation (C) causes DNA damage, and immune
injury (D) involves complement or cytotoxic T cells.
16 Which of the following laboratory findings is most indicative of irreversible cell injury in a patient with acute
myocardial infarction?
A) Elevated serum troponin I
TEST BANK| NURS5315 ADVANCED PATHOPHYSIOLOGY
EXAM 1 REVIEW WITH COMPLETE 300 REAL EXAM
QUESTIONS AND CORRECT VERIFIED ANSWERS/
ALREADY GRADED A+ (MOST RECENT!!) — 300 Questions
Section 1: Cellular Adaptation, Injury, and Death (Questions 1-30)
1 A patient with chronic obstructive pulmonary disease (COPD) has long-term hypoxemia. Which cellular
adaptation is most likely to occur in the skeletal muscle of this patient, and what is the primary molecular
mechanism?
A) Hypertrophy due to increased IGF-1 signaling
B) Hyperplasia due to activation of satellite cells
C) Atrophy due to upregulated ubiquitin-proteasome pathway
D) Metaplasia due to reprogramming of myogenic transcription factors
Answer: C
Rationale: Chronic hypoxemia leads to disuse and decreased oxygen delivery, activating the ubiquitin-proteasome
pathway and causing muscle atrophy (correct). Hypertrophy (A) requires increased workload and IGF-1;
hyperplasia (B) is not typical in skeletal muscle; metaplasia (D) is a change in cell type, not seen here.
2 A researcher treats hepatocytes with a low dose of a chemical that inhibits mitochondrial ATP synthase. After 2
hours, the cells show swelling of the endoplasmic reticulum and loss of microvilli, but no nuclear changes.
Which statement best describes the cellular state?
A) Irreversible injury: the cells will undergo necrosis within minutes
B) Reversible injury: the cells can recover if the inhibitor is removed
C) Apoptosis: the cells are in early stage of programmed cell death
D) Necroptosis: a regulated form of necrosis is initiated
Answer: B
Rationale: Cellular swelling and ER dilation without nuclear changes (pyknosis, karyorrhexis, karyolysis) indicate
reversible injury (B). Irreversible injury (A) would show nuclear changes; apoptosis (C) would show cell shrinkage
and chromatin condensation; necroptosis (D) would involve RIP kinases and plasma membrane rupture.
3 In a model of myocardial ischemia-reperfusion injury, which molecular event is most directly responsible for
the transition from reversible to irreversible injury in cardiac myocytes?
A) Formation of the mitochondrial permeability transition pore (mPTP)
B) Depletion of ATP to below 50% of normal levels
C) Accumulation of intracellular sodium and calcium
D) Activation of caspase-9 via cytochrome c release
Answer: A
Rationale: Opening of the mPTP causes loss of mitochondrial membrane potential, ATP depletion, and release of
pro-apoptotic factors, marking the point of no return (A). ATP depletion (B) and ion imbalances (C) occur in
reversible injury; caspase activation (D) is downstream of mPTP opening and can be part of apoptosis, but mPTP
opening itself is the critical event for irreversible injury in ischemia-reperfusion.
,4 A pathologist examines a biopsy from a patient with chronic gastritis. The gastric epithelium shows
intestinal-type goblet cells and absorptive cells. This change is best described as:
A) Dysplasia with loss of differentiation
B) Hyperplasia due to chronic inflammation
C) Metaplasia, which may be reversible if the irritant is removed
D) Anaplasia, indicating malignant transformation
Answer: C
Rationale: Replacement of gastric epithelium with intestinal-type cells is intestinal metaplasia (C), a common
adaptive response to chronic irritation. Dysplasia (A) involves abnormal growth and maturation; hyperplasia (B) is
increased cell number without change in type; anaplasia (D) is severe loss of differentiation seen in cancer.
5 A researcher treats cultured neurons with a high concentration of glutamate, leading to excitotoxicity. Which of
the following sequences of events most accurately describes the early steps in this form of cell injury?
A) NMDA receptor activation !’ calcium influx !’ calpain activation !’ cytoskeletal breakdown
B) AMPA receptor activation !’ sodium influx !’ cell swelling !’ lysis
C) Metabotropic receptor activation !’ G-protein signaling !’ caspase activation !’ apoptosis
D) Glutamate transporter reversal !’ ATP depletion !’ necrosis
Answer: A
Rationale: Excitotoxicity primarily involves excessive NMDA receptor activation, leading to calcium overload (A).
Calpain activation then degrades cytoskeletal proteins. While sodium influx (B) contributes to swelling, the key
injury mechanism is calcium-mediated; metabotropic receptors (C) are less directly involved; transporter reversal
(D) occurs but is not the earliest step.
6 Which of the following best distinguishes apoptosis from necrosis at the molecular level?
A) Apoptosis requires ATP, while necrosis is ATP-independent
B) Necrosis always involves inflammation, while apoptosis never does
C) Apoptosis is initiated by extrinsic or intrinsic pathways, while necrosis is always accidental
D) Caspase activation is unique to apoptosis, while necrosis involves calpains and cathepsins
Answer: A
Rationale: Apoptosis is an energy-dependent process requiring ATP for caspase activation and DNA fragmentation
(A). While necrosis is often ATP-independent, some forms (necroptosis) require ATP; inflammation is typical in
necrosis but can occur in late apoptosis; caspase activation is a hallmark of apoptosis, but some forms of regulated
necrosis also involve caspases indirectly.
7 A patient with a genetic deficiency in the enzyme superoxide dismutase (SOD) is expected to have increased
susceptibility to cell injury under which condition?
A) Hypoxic injury due to reduced ATP production
B) Reperfusion injury due to accumulation of superoxide anions
C) Chemical injury due to impaired cytochrome P450 activity
D) Apoptosis due to defective Fas signaling
Answer: B
Rationale: SOD converts superoxide radical (O2•") to hydrogen peroxide. Deficiency leads to superoxide
accumulation, particularly during reperfusion when oxygen is reintroduced (B). Hypoxic injury (A) is more related
to ATP depletion; cytochrome P450 (C) is involved in metabolism; Fas signaling (D) is part of extrinsic apoptosis.
8 In a patient with chronic anemia, the bone marrow shows increased erythroid precursors. This represents which
type of cellular adaptation, and what is the primary stimulus?
,A) Hypertrophy: increased erythropoietin causing enlargement of erythroblasts
B) Hyperplasia: increased erythropoietin causing proliferation of erythroid progenitors
C) Metaplasia: erythropoietin causing conversion of myeloid cells to erythroid cells
D) Dysplasia: erythropoietin causing abnormal maturation of erythroblasts
Answer: B
Rationale: Chronic anemia leads to increased erythropoietin, which stimulates proliferation of erythroid progenitor
cells, resulting in hyperplasia (B). Hypertrophy (A) is an increase in cell size, not number; metaplasia (C) is a
change in cell type; dysplasia (D) involves abnormal growth and is not a typical adaptive response.
9 A researcher induces autophagy in cultured fibroblasts by nutrient deprivation. Which of the following
molecular markers would confirm activation of autophagy?
A) Increased expression of Bcl-2 and decreased Bax
B) Conversion of LC3-I to LC3-II and formation of autophagosomes
C) Activation of caspase-3 and cleavage of PARP
D) Release of cytochrome c from mitochondria into cytosol
Answer: B
Rationale: Autophagy is characterized by the formation of autophagosomes, which involves lipidation of LC3-I to
LC3-II (B). Bcl-2/Bax changes (A) are associated with apoptosis; caspase-3 activation (C) and cytochrome c
release (D) are hallmarks of apoptosis, not autophagy.
10 A researcher treats cells with a drug that inhibits the proteasome. Which of the following is the most likely
consequence?
A) Accumulation of misfolded proteins and ER stress leading to apoptosis
B) Increased degradation of cyclins and cell cycle arrest
C) Enhanced autophagy and cell survival
D) Activation of NF-ºB and increased inflammation
Answer: A
Rationale: Proteasome inhibition prevents degradation of ubiquitinated proteins, leading to accumulation of
misfolded proteins, ER stress, and eventually apoptosis (A). It would decrease degradation of cyclins (B) not
increase; autophagy may be induced but is not the primary consequence; NF-ºB activation is typically reduced
because IºB is not degraded.
11 A research study examines the response of hepatocytes to chronic ethanol exposure. The cells exhibit an
increase in smooth endoplasmic reticulum (SER) and upregulation of cytochrome P450 enzymes. This adaptive
response is best classified as which type of cellular adaptation?
A) Hyperplasia
B) Hypertrophy
C) Metaplasia
D) Dysplasia
Answer: B
Rationale: Hypertrophy refers to an increase in cell size due to increased functional demand or specific hormonal
stimulation. The proliferation of SER and CYP enzymes represents an increase in cellular machinery, not cell
number (hyperplasia), nor a change in cell type (metaplasia) or abnormal growth (dysplasia).
12 In myocardial ischemia, which sequence of events most accurately describes the progression from reversible to
irreversible cell injury?
A) ATP depletion !’ mitochondrial swelling !’ plasma membrane blebbing !’ nuclear pyknosis
, B) ATP depletion !’ loss of ion gradients !’ cellular swelling !’ lysosomal enzyme leakage
C) Calcium influx !’ activation of phospholipases !’ mitochondrial permeability transition !’ ATP depletion
D) Reactive oxygen species generation !’ lipid peroxidation !’ DNA fragmentation !’ protein denaturation
Answer: C
Rationale: Irreversible injury is marked by mitochondrial dysfunction and massive calcium influx, which triggers
phospholipase activation and the mitochondrial permeability transition, leading to ATP depletion. While options A
and B describe aspects of reversible injury, option C captures the critical step of irreversible injury. Option D
describes oxidative stress but not the typical sequence in ischemia.
13 A pathologist examines a tissue section showing cells with abundant eosinophilic cytoplasm, pyknotic nuclei,
and fragmentation into membrane-bound apoptotic bodies. Immunohistochemistry is positive for caspase-3.
Which of the following best explains the absence of inflammation in this tissue?
A) Apoptotic cells are phagocytosed before releasing cellular contents
B) Necrosis induces a rapid anti-inflammatory response
C) Caspase-3 degrades pro-inflammatory cytokines
D) The cells are undergoing autophagic cell death, not apoptosis
Answer: A
Rationale: Apoptosis is a programmed, non-inflammatory cell death because apoptotic bodies are quickly engulfed
by phagocytes before they can release pro-inflammatory contents. Necrosis (option B) typically triggers
inflammation. Caspase-3 executes apoptosis but does not degrade cytokines (option C). Autophagy (option D) is a
different process.
14 In the setting of chronic gastric reflux, the squamous epithelium of the lower esophagus is replaced by
columnar epithelium resembling that of the intestine. This change is an example of:
A) Dysplasia
B) Anaplasia
C) Metaplasia
D) Hyperplasia
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another, often in response to
chronic irritation. Barrett esophagus is a classic example. Dysplasia (A) is abnormal growth, anaplasia (B) is loss of
differentiation, and hyperplasia (D) is increased cell number.
15 A cell exposed to a sublethal dose of a toxin shows swelling of the endoplasmic reticulum and dissociation of
ribosomes from the rough ER. This finding is most consistent with which type of cellular injury?
A) Hypoxic injury
B) Chemical injury
C) Radiation injury
D) Immune-mediated injury
Answer: B
Rationale: Chemical toxins often target the ER and ribosomes, leading to dissociation of ribosomes and ER
swelling. Hypoxic injury (A) primarily affects mitochondria. Radiation (C) causes DNA damage, and immune
injury (D) involves complement or cytotoxic T cells.
16 Which of the following laboratory findings is most indicative of irreversible cell injury in a patient with acute
myocardial infarction?
A) Elevated serum troponin I
