MSN 570 Advanced Pathophysiology — Quiz 2 | USU Graduate Nursing Fall 2026/2027 Update | 100% Correct Verified
MSN 570 Advanced Pathophysiology — Quiz 2
USU Graduate Nursing | Fall 2026/2027 Update — 100% Correct Verified
Questions and Answers with Mechanism-Level Rationales
80 Questions · 7 Competency Sections · 70% Scenario-Based · Aligned to USU MSN 570 Quiz 2 Blueprint
Exam Overview: This quiz is organized into seven competency-aligned sections covering the second-quiz
material of MSN 570 Advanced Pathophysiology: (1) Cellular Injury, Adaptation, and Death; (2) Inflammation,
Immunity, and Infection; (3) Genetics and Genetic Disorders; (4) Neoplasia and Cancer Biology; (5) Fluid,
Electrolyte, and Acid-Base Disorders; (6) Cardiovascular Pathophysiology; and (7) Hematologic and
Immune-Mediated Disorders. Each question is multiple choice with four options (A-D) and exactly one correct
answer. Cognitive demand is distributed approximately 30% recall, 50% application, and 20% analysis.
Rationales double as a study guide: they identify the correct option, contrast common misconceptions
represented in distractors, and confirm alignment with USU course modules.
Section Map: Q1-11 Cellular Injury, Adaptation, and Death · Q12-24 Inflammation, Immunity, and Infection ·
Q25-35 Genetics and Genetic Disorders · Q36-47 Neoplasia and Cancer Biology · Q48-59 Fluid, Electrolyte, and
Acid-Base Disorders · Q60-70 Cardiovascular Pathophysiology · Q71-80 Hematologic and Immune-Mediated
Disorders.
100% Verification Note: Each rationale embeds confirmation against current USU MSN 570 course modules
and the Fall 2026/2027 Quiz 2 blueprint. Commonly confused concept pairs (necrosis vs. apoptosis; innate vs.
adaptive immunity; autosomal dominant vs. recessive; respiratory vs. metabolic acidosis; systolic vs. diastolic
heart failure; hemophilia A vs. vWD; ITP vs. TTP vs. DIC) are explicitly addressed in distractor explanations to
support graduate-level mastery.
Section 1: Cellular Injury, Adaptation, and Death (Cellular Stress, Necrosis,
Apoptosis, & Free Radical Injury)
Q1. [Application] A 68-year-old retired Service Member has had a fractured femur immobilized in a cast for 8
weeks. The quadriceps of the affected leg are visibly smaller than the contralateral side. Which cellular adaptive
mechanism explains this finding?
A. Hyperplasia, an increase in cell number due to hormonal stimulation.
B. Hypertrophy, an increase in cell size due to increased workload.
C. Metaplasia, the reversible replacement of one adult cell type with another.
D. Atrophy, a decrease in cell size and/or number in response to decreased workload, denervation, or
reduced trophic signals. [CORRECT]
Correct Answer: D
Rationale: Disuse atrophy follows prolonged immobilization and reduced mechanical loading; cells shrink
(decreased protein synthesis, increased proteolysis) and the organ visibly diminishes. Hypertrophy (A) is increased
cell size from workload; hyperplasia (B) is increased cell number; metaplasia (D) is cell-type replacement. USU
MSN 570 Module 4 frames atrophy as a reversible adaptive response to stress.
Page 1
,MSN 570 Advanced Pathophysiology — Quiz 2 | USU Graduate Nursing Fall 2026/2027 Update | 100% Correct Verified
Q2. [Analysis] Which pair correctly distinguishes hypertrophy from hyperplasia?
A. Hypertrophy = increased cell number; hyperplasia = increased cell size.
B. Both arise exclusively from chronic inflammation.
C. Hypertrophy = increased cell size (e.g., myocardium in hypertension); hyperplasia = increased cell
number (e.g., endometrium in unopposed estrogen). [CORRECT]
D. Both are irreversible malignant changes.
Correct Answer: C
Rationale: Hypertrophy is enlargement of individual cells (e.g., cardiac myocytes under pressure overload).
Hyperplasia is an increase in cell number (e.g., glandular epithelium under estrogen). Hypertrophy and hyperplasia
can coexist (e.g., uterus in pregnancy). The distractors confuse the definitions or mischaracterize them as
malignant. USU MSN 570 Module 4 emphasizes the size-vs-number distinction.
Q3. [Application] A 56-year-old with chronic GERD undergoes endoscopy. Biopsy of the distal esophagus
reveals intestinal-type columnar epithelium replacing the normal stratified squamous epithelium. This is best
classified as:
A. Anaplasia, loss of cellular differentiation.
B. Dysplasia, disordered cellular maturation within the same tissue type.
C. Metaplasia, the reversible substitution of one differentiated adult cell type for another in response to
chronic injury—in this case, Barrett esophagus. [CORRECT]
D. Neoplasia, autonomous new growth.
Correct Answer: C
Rationale: Barrett esophagus is the classic example of intestinal metaplasia of the esophageal squamous epithelium
induced by chronic acid exposure; it is reversible upon injury removal but is a precursor lesion for adenocarcinoma.
Dysplasia (A) implies disordered maturation within the native cell type. USU MSN 570 Module 4 lists Barrett
esophagus as the canonical metaplasia example.
Q4. [Application] A cervical Pap smear shows cells with increased nuclear-to-cytoplasmic ratio, pleomorphism,
and disordered maturation, but the basement membrane is intact. This finding is best described as:
A. Metaplasia, normal replacement of one cell type by another.
B. Reversible hypertrophy.
C. Dysplasia, disordered cellular growth and maturation that may progress to carcinoma in situ if
untreated—but is not yet invasive. [CORRECT]
D. Carcinoma, invasive malignant cells breaching basement membrane.
Correct Answer: C
Rationale: Dysplasia (cervical intraepithelial neoplasia) features pleomorphism, increased N:C ratio, and loss of
polarity without basement membrane invasion. Without intervention it may progress to carcinoma in situ and
invasive carcinoma. USU MSN 570 Module 4 frames dysplasia as a pre-neoplastic adaptive-to-maladaptive
transition.
Q5. [Analysis] Which cellular event marks the transition from reversible to irreversible ischemic injury in a
cardiomyocyte after coronary occlusion?
A. ATP depletion below 70% of baseline.
B. Hyperkalemia confined to extracellular fluid.
C. Transient Na+/K+ pump failure alone.
D. Sustained rise in cytosolic Ca2+ producing mitochondrial permeability transition pore opening, marked
ROS generation, and membrane damage—manifest biochemically as massive ATP depletion and
structurally as irreversible injury. [CORRECT]
Correct Answer: D
Page 2
, MSN 570 Advanced Pathophysiology — Quiz 2 | USU Graduate Nursing Fall 2026/2027 Update | 100% Correct Verified
Rationale: The transition from reversible to irreversible ischemic injury occurs when Ca2+ overload, ATP
depletion, ROS, and membrane phospholipid degradation cross a threshold that opens the mitochondrial
permeability transition pore and dissipates the inner mitochondrial membrane potential—cell death follows. USU
MSN 570 Module 5 emphasizes calcium-mediated mitochondrial injury as the biochemical point of no return.
Q6. [Recall] Which statement most accurately distinguishes necrosis from apoptosis?
A. Both terms are synonyms and indistinguishable histologically.
B. Apoptosis elicits inflammation; necrosis does not.
C. Necrosis is unregulated cell swelling, membrane rupture, and intense inflammation; apoptosis is a
regulated, ATP-dependent, caspase-mediated program producing apoptotic bodies phagocytosed without
inflammation. [CORRECT]
D. Necrosis is a regulated, ATP-dependent caspase cascade producing minimal inflammation; apoptosis is
unregulated cell swelling and membrane rupture with intense inflammation.
Correct Answer: C
Rationale: Necrosis is pathologic, unregulated cell swelling with membrane rupture, enzymatic digestion, and
inflammation. Apoptosis is regulated (intrinsic or extrinsic caspase cascades), energy-dependent, produces
apoptotic bodies, and elicits no inflammation. USU MSN 570 Module 5 emphasizes this commonly confused pair.
Q7. [Application] A researcher induces apoptosis in a transformed cell line by adding Fas ligand to the culture.
Which pathway is engaged?
A. Necroptosis via receptor-interacting protein kinases (RIPK1/RIPK3) and MLKL.
B. Pyroptosis via inflammasome and gasdermin D.
C. Intrinsic (mitochondrial) pathway, mediated by Bcl-2 family proteins, cytochrome c release,
apoptosome formation, and caspase-9.
D. Extrinsic (death receptor) pathway, mediated by Fas (CD95) receptor activation, FADD recruitment,
and initiator caspase-8 cleavage, then executioner caspases-3/6/7. [CORRECT]
Correct Answer: D
Rationale: Fas ligand binds Fas (CD95), recruiting FADD and activating caspase-8, the initiator of the extrinsic
apoptotic pathway. The intrinsic pathway (A) involves mitochondrial cytochrome c and caspase-9. Necroptosis (C)
is a regulated necrosis pathway. USU MSN 570 Module 5 distinguishes the two apoptotic arms.
Q8. [Recall] Necroptosis is best characterized as:
A. ATP-dependent apoptosis producing apoptotic bodies.
B. A caspase-independent, regulated form of necrosis mediated by RIPK1/RIPK3 and the effector MLKL,
producing cell swelling and membrane rupture—often activated when caspase-8 is inhibited. [CORRECT]
C. An accidental, unregulated cell death from ischemia.
D. Iron-dependent lipid peroxidation driven cell death (ferroptosis).
Correct Answer: B
Rationale: Necroptosis is a genetically regulated, caspase-independent form of necrosis executed by the
RIPK1/RIPK3/MLKL axis; it produces inflammatory morphology and is engaged when caspase-8 is blocked. USU
MSN 570 Module 5 includes necroptosis as a regulated death modality distinct from apoptosis and accidental
necrosis.
Q9. [Analysis] In reperfusion injury following thrombolytic therapy for STEMI, much of the irreversible injury
paradoxically worsens upon restoration of blood flow. The dominant molecular mechanism is:
A. Re-established ATP synthesis immediately repairs all membranes.
B. Reperfusion suppresses inflammation.
C. Restored flow removes intracellular Ca2+ from cells.
Page 3
MSN 570 Advanced Pathophysiology — Quiz 2
USU Graduate Nursing | Fall 2026/2027 Update — 100% Correct Verified
Questions and Answers with Mechanism-Level Rationales
80 Questions · 7 Competency Sections · 70% Scenario-Based · Aligned to USU MSN 570 Quiz 2 Blueprint
Exam Overview: This quiz is organized into seven competency-aligned sections covering the second-quiz
material of MSN 570 Advanced Pathophysiology: (1) Cellular Injury, Adaptation, and Death; (2) Inflammation,
Immunity, and Infection; (3) Genetics and Genetic Disorders; (4) Neoplasia and Cancer Biology; (5) Fluid,
Electrolyte, and Acid-Base Disorders; (6) Cardiovascular Pathophysiology; and (7) Hematologic and
Immune-Mediated Disorders. Each question is multiple choice with four options (A-D) and exactly one correct
answer. Cognitive demand is distributed approximately 30% recall, 50% application, and 20% analysis.
Rationales double as a study guide: they identify the correct option, contrast common misconceptions
represented in distractors, and confirm alignment with USU course modules.
Section Map: Q1-11 Cellular Injury, Adaptation, and Death · Q12-24 Inflammation, Immunity, and Infection ·
Q25-35 Genetics and Genetic Disorders · Q36-47 Neoplasia and Cancer Biology · Q48-59 Fluid, Electrolyte, and
Acid-Base Disorders · Q60-70 Cardiovascular Pathophysiology · Q71-80 Hematologic and Immune-Mediated
Disorders.
100% Verification Note: Each rationale embeds confirmation against current USU MSN 570 course modules
and the Fall 2026/2027 Quiz 2 blueprint. Commonly confused concept pairs (necrosis vs. apoptosis; innate vs.
adaptive immunity; autosomal dominant vs. recessive; respiratory vs. metabolic acidosis; systolic vs. diastolic
heart failure; hemophilia A vs. vWD; ITP vs. TTP vs. DIC) are explicitly addressed in distractor explanations to
support graduate-level mastery.
Section 1: Cellular Injury, Adaptation, and Death (Cellular Stress, Necrosis,
Apoptosis, & Free Radical Injury)
Q1. [Application] A 68-year-old retired Service Member has had a fractured femur immobilized in a cast for 8
weeks. The quadriceps of the affected leg are visibly smaller than the contralateral side. Which cellular adaptive
mechanism explains this finding?
A. Hyperplasia, an increase in cell number due to hormonal stimulation.
B. Hypertrophy, an increase in cell size due to increased workload.
C. Metaplasia, the reversible replacement of one adult cell type with another.
D. Atrophy, a decrease in cell size and/or number in response to decreased workload, denervation, or
reduced trophic signals. [CORRECT]
Correct Answer: D
Rationale: Disuse atrophy follows prolonged immobilization and reduced mechanical loading; cells shrink
(decreased protein synthesis, increased proteolysis) and the organ visibly diminishes. Hypertrophy (A) is increased
cell size from workload; hyperplasia (B) is increased cell number; metaplasia (D) is cell-type replacement. USU
MSN 570 Module 4 frames atrophy as a reversible adaptive response to stress.
Page 1
,MSN 570 Advanced Pathophysiology — Quiz 2 | USU Graduate Nursing Fall 2026/2027 Update | 100% Correct Verified
Q2. [Analysis] Which pair correctly distinguishes hypertrophy from hyperplasia?
A. Hypertrophy = increased cell number; hyperplasia = increased cell size.
B. Both arise exclusively from chronic inflammation.
C. Hypertrophy = increased cell size (e.g., myocardium in hypertension); hyperplasia = increased cell
number (e.g., endometrium in unopposed estrogen). [CORRECT]
D. Both are irreversible malignant changes.
Correct Answer: C
Rationale: Hypertrophy is enlargement of individual cells (e.g., cardiac myocytes under pressure overload).
Hyperplasia is an increase in cell number (e.g., glandular epithelium under estrogen). Hypertrophy and hyperplasia
can coexist (e.g., uterus in pregnancy). The distractors confuse the definitions or mischaracterize them as
malignant. USU MSN 570 Module 4 emphasizes the size-vs-number distinction.
Q3. [Application] A 56-year-old with chronic GERD undergoes endoscopy. Biopsy of the distal esophagus
reveals intestinal-type columnar epithelium replacing the normal stratified squamous epithelium. This is best
classified as:
A. Anaplasia, loss of cellular differentiation.
B. Dysplasia, disordered cellular maturation within the same tissue type.
C. Metaplasia, the reversible substitution of one differentiated adult cell type for another in response to
chronic injury—in this case, Barrett esophagus. [CORRECT]
D. Neoplasia, autonomous new growth.
Correct Answer: C
Rationale: Barrett esophagus is the classic example of intestinal metaplasia of the esophageal squamous epithelium
induced by chronic acid exposure; it is reversible upon injury removal but is a precursor lesion for adenocarcinoma.
Dysplasia (A) implies disordered maturation within the native cell type. USU MSN 570 Module 4 lists Barrett
esophagus as the canonical metaplasia example.
Q4. [Application] A cervical Pap smear shows cells with increased nuclear-to-cytoplasmic ratio, pleomorphism,
and disordered maturation, but the basement membrane is intact. This finding is best described as:
A. Metaplasia, normal replacement of one cell type by another.
B. Reversible hypertrophy.
C. Dysplasia, disordered cellular growth and maturation that may progress to carcinoma in situ if
untreated—but is not yet invasive. [CORRECT]
D. Carcinoma, invasive malignant cells breaching basement membrane.
Correct Answer: C
Rationale: Dysplasia (cervical intraepithelial neoplasia) features pleomorphism, increased N:C ratio, and loss of
polarity without basement membrane invasion. Without intervention it may progress to carcinoma in situ and
invasive carcinoma. USU MSN 570 Module 4 frames dysplasia as a pre-neoplastic adaptive-to-maladaptive
transition.
Q5. [Analysis] Which cellular event marks the transition from reversible to irreversible ischemic injury in a
cardiomyocyte after coronary occlusion?
A. ATP depletion below 70% of baseline.
B. Hyperkalemia confined to extracellular fluid.
C. Transient Na+/K+ pump failure alone.
D. Sustained rise in cytosolic Ca2+ producing mitochondrial permeability transition pore opening, marked
ROS generation, and membrane damage—manifest biochemically as massive ATP depletion and
structurally as irreversible injury. [CORRECT]
Correct Answer: D
Page 2
, MSN 570 Advanced Pathophysiology — Quiz 2 | USU Graduate Nursing Fall 2026/2027 Update | 100% Correct Verified
Rationale: The transition from reversible to irreversible ischemic injury occurs when Ca2+ overload, ATP
depletion, ROS, and membrane phospholipid degradation cross a threshold that opens the mitochondrial
permeability transition pore and dissipates the inner mitochondrial membrane potential—cell death follows. USU
MSN 570 Module 5 emphasizes calcium-mediated mitochondrial injury as the biochemical point of no return.
Q6. [Recall] Which statement most accurately distinguishes necrosis from apoptosis?
A. Both terms are synonyms and indistinguishable histologically.
B. Apoptosis elicits inflammation; necrosis does not.
C. Necrosis is unregulated cell swelling, membrane rupture, and intense inflammation; apoptosis is a
regulated, ATP-dependent, caspase-mediated program producing apoptotic bodies phagocytosed without
inflammation. [CORRECT]
D. Necrosis is a regulated, ATP-dependent caspase cascade producing minimal inflammation; apoptosis is
unregulated cell swelling and membrane rupture with intense inflammation.
Correct Answer: C
Rationale: Necrosis is pathologic, unregulated cell swelling with membrane rupture, enzymatic digestion, and
inflammation. Apoptosis is regulated (intrinsic or extrinsic caspase cascades), energy-dependent, produces
apoptotic bodies, and elicits no inflammation. USU MSN 570 Module 5 emphasizes this commonly confused pair.
Q7. [Application] A researcher induces apoptosis in a transformed cell line by adding Fas ligand to the culture.
Which pathway is engaged?
A. Necroptosis via receptor-interacting protein kinases (RIPK1/RIPK3) and MLKL.
B. Pyroptosis via inflammasome and gasdermin D.
C. Intrinsic (mitochondrial) pathway, mediated by Bcl-2 family proteins, cytochrome c release,
apoptosome formation, and caspase-9.
D. Extrinsic (death receptor) pathway, mediated by Fas (CD95) receptor activation, FADD recruitment,
and initiator caspase-8 cleavage, then executioner caspases-3/6/7. [CORRECT]
Correct Answer: D
Rationale: Fas ligand binds Fas (CD95), recruiting FADD and activating caspase-8, the initiator of the extrinsic
apoptotic pathway. The intrinsic pathway (A) involves mitochondrial cytochrome c and caspase-9. Necroptosis (C)
is a regulated necrosis pathway. USU MSN 570 Module 5 distinguishes the two apoptotic arms.
Q8. [Recall] Necroptosis is best characterized as:
A. ATP-dependent apoptosis producing apoptotic bodies.
B. A caspase-independent, regulated form of necrosis mediated by RIPK1/RIPK3 and the effector MLKL,
producing cell swelling and membrane rupture—often activated when caspase-8 is inhibited. [CORRECT]
C. An accidental, unregulated cell death from ischemia.
D. Iron-dependent lipid peroxidation driven cell death (ferroptosis).
Correct Answer: B
Rationale: Necroptosis is a genetically regulated, caspase-independent form of necrosis executed by the
RIPK1/RIPK3/MLKL axis; it produces inflammatory morphology and is engaged when caspase-8 is blocked. USU
MSN 570 Module 5 includes necroptosis as a regulated death modality distinct from apoptosis and accidental
necrosis.
Q9. [Analysis] In reperfusion injury following thrombolytic therapy for STEMI, much of the irreversible injury
paradoxically worsens upon restoration of blood flow. The dominant molecular mechanism is:
A. Re-established ATP synthesis immediately repairs all membranes.
B. Reperfusion suppresses inflammation.
C. Restored flow removes intracellular Ca2+ from cells.
Page 3
