NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
NSG 120 / NSG120 FINAL EXAM (LATEST UPDATE): NURSING
PATHOPHYSIOLOGY | EXAM REVIEW WITH QUESTIONS AND VERIFIED
ANSWERS | ALL UNITS COVERED | 100% CORRECT | GRADE A –
HERZING
Herzing University | NSG 120 Nursing Pathophysiology Course Examination | Aligned with NCLEX-RN Pathophysiology
Standards ( Edition)
Total Questions: 150 | Cognitive Levels: 20% Recall, 50% Application, 30% Analysis | Format: 75% Scenario-Based, 25%
Direct Knowledge
EXAM INSTRUCTIONS: This comprehensive final examination consists of 150 multiple-choice questions covering all
units of NSG 120 Nursing Pathophysiology. Each question has four options (A–D) with exactly ONE correct answer. The
correct answer is marked [CORRECT]. Rationales provide pathophysiological reasoning aligned with the NSG 120
curriculum and NCLEX-RN standards. Sections are organized by body system; recommended time: approximately 3 hours.
SECTION 1: Cellular Injury, Adaptation, & Death
Q1: A 68-year-old male with a long-standing history of hypertension presents with an echocardiogram
demonstrating increased ventricular wall thickness without an increase in cardiac chamber size. The
cardiologist documents this as an adaptive response to chronic pressure overload. Which cellular adaptation
best describes this finding?
A. Hyperplasia, an increase in the number of cardiac myocytes
B. Hypertrophy, an increase in the size of existing cardiac myocytes *[CORRECT]*
C. Metaplasia, a reversible change of one adult cell type to another
D. Dysplasia, disordered cellular growth and atypia
Correct Answer: B
Rationale: Hypertrophy is an increase in the SIZE of existing cells, exemplified by cardiac myocytes responding to chronic
pressure overload in hypertension or aortic stenosis. Cardiac myocytes are terminally differentiated and cannot divide, so
hyperplasia (A) is impossible. Metaplasia (C) is a reversible substitution of one adult cell type for another (e.g., Barrett
esophagus). Dysplasia (D) is disordered, atypical proliferation indicating pre-neoplastic change.
Q2: A 55-year-old woman with a 30-pack-year smoking history undergoes bronchoscopy with biopsy of the
bronchial epithelium. The pathologist reports stratified squamous epithelium replacing the normal
pseudostratified ciliated columnar epithelium. Which adaptive mechanism is described, and what is its
primary biological significance?
A. Atrophy, reversible decrease in cell size due to chronic irritation
B. Hypertrophy, increased cell size to compensate for injury
C. Metaplasia, a protective but premalignant adaptive substitution *[CORRECT]*
D. Apoptosis, programmed cell death of ciliated cells
Correct Answer: C
Rationale: The biopsy shows squamous metaplasia, a reversible adaptive substitution of stratified squamous epithelium for
columnar epithelium in response to chronic irritation (smoking). While protective initially by resisting irritation, persistent
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 1
,NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
injury can progress to dysplasia and squamous cell carcinoma. Atrophy (A) is decreased cell size/substance; hypertrophy
(B) is increased cell size; apoptosis (D) is programmed cell death.
Q3: A 45-year-old male is found unconscious in a closed garage with a running automobile. On arrival to the
ED, carboxyhemoglobin is 38%. The pathophysiological mechanism of cellular injury in this patient is best
described as:
A. Direct chemical injury to cellular membranes by carbon particles
B. Hypoxic injury due to impaired oxygen-carrying capacity of hemoglobin *[CORRECT]*
C. Free radical generation by lipid peroxidation of mitochondrial membranes
D. Ischemic injury due to decreased perfusion from carbon monoxide-induced vasoconstriction
Correct Answer: B
Rationale: Carbon monoxide has 240 times the affinity of oxygen for hemoglobin, forming carboxyhemoglobin and severely
reducing oxygen-carrying capacity, producing hypoxic cellular injury. While CO does impair mitochondrial cytochrome
oxidase (impacting oxidative phosphorylation), the dominant mechanism is functional anemia/hypoxia rather than direct
membrane chemical injury (A), free radical peroxidation (C), or vasoconstrictive ischemia (D). Treatment is 100% oxygen
or hyperbaric oxygen.
Q4: A 28-year-old male sustains a gunshot wound to the femoral artery, losing approximately 1500 mL of
blood. He is hypotensive and tachycardic. At the cellular level, the mechanism of injury is best characterized
as:
A. Impaired oxygen delivery (hypoxic hypoxia) leading to depletion of ATP *[CORRECT]*
B. Direct physical trauma to tissue with membrane disruption
C. Chemical injury from released lysosomal enzymes
D. Free radical injury from reperfusion of ischemic tissue
Correct Answer: A
Rationale: Hemorrhage causes hypovolemic shock with decreased perfusion and oxygen delivery (ischemic/hypoxic hypoxia),
depleting intracellular ATP. Decreased ATP causes failure of Na+/K+-ATPase, cellular swelling, calcium influx, and
ultimately irreversible injury. Direct physical trauma (B) is localized to the wound; lysosomal enzyme release (C) is a
downstream consequence, not initial mechanism; reperfusion injury (D) occurs after restoration of blood flow, not during
ischemia.
Q5: A 62-year-old female with acute myocardial infarction has elevated cardiac enzymes. The pathologist
examining the infarcted myocardium 48 hours after the event would most likely identify which pattern of
necrosis?
A. Liquefactive necrosis with neutrophil infiltration and tissue liquefaction
B. Coagulative necrosis with preserved tissue architecture and eosinophilic cells *[CORRECT]*
C. Caseous necrosis with granulomatous inflammation and cheese-like appearance
D. Fat necrosis with saponification of triglycerides by lipase
Correct Answer: B
Rationale: Myocardial infarction produces coagulative necrosis, the most common pattern in solid organs (heart, kidney, liver,
spleen), characterized by preservation of tissue architecture for days after cell death, with cells becoming eosinophilic and
anucleate. Liquefactive necrosis (A) occurs in the brain or with bacterial infection. Caseous necrosis (C) is seen in
tuberculosis. Fat necrosis (D) occurs in pancreatic and breast tissue.
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 2
,NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
Q6: A 4-year-old child presents with progressively enlarging head circumference, vomiting, and ataxia. MRI
shows a posterior fossa tumor. The surgeon is concerned because brain tissue characteristically undergoes
which pattern of necrosis when ischemic or injured?
A. Coagulative necrosis with preserved tissue framework
B. Liquefactive necrosis from enzymatic digestion by microglia and neutrophils *[CORRECT]*
C. Caseous necrosis with granuloma formation
D. Fibrinoid necrosis of small blood vessels
Correct Answer: B
Rationale: Brain tissue undergoes liquefactive necrosis because it is rich in lipids and lacks substantial connective tissue
stroma, allowing enzymatic digestion by neutrophils and microglia to liquefy the tissue into a cystic cavity. Coagulative
necrosis (A) is characteristic of most solid organs but NOT the brain. Caseous necrosis (C) is granulomatous (TB).
Fibrinoid necrosis (D) affects vessel walls in malignant hypertension or immune complex disease.
Q7: A 35-year-old male with active pulmonary tuberculosis undergoes lung biopsy. The pathologist identifies
a central area of necrosis surrounded by epithelioid macrophages, multinucleated giant cells, and a rim of
lymphocytes. The necrotic center grossly resembles soft white cheese. This pattern is:
A. Coagulative necrosis with architectural preservation
B. Liquefactive necrosis from bacterial enzymatic digestion
C. Caseous necrosis, a variant of coagulative necrosis enclosed by granulomatous inflammation
*[CORRECT]*
D. Fat necrosis with saponification
Correct Answer: C
Rationale: Caseous necrosis (literally 'cheese-like') is a distinctive variant of coagulative necrosis encountered in tuberculosis
and certain fungal infections. The necrotic tissue is enclosed within a granuloma (epithelioid macrophages, Langhans giant
cells, lymphocytes). It differs from typical coagulative necrosis by loss of tissue architecture and amorphous granular
appearance. Liquefactive (B) and fat necrosis (D) describe different processes.
Q8: A 47-year-old male with acute pancreatitis develops painful subcutaneous nodules on the lower
extremities. Biopsy demonstrates saponification of subcutaneous fat by pancreatic lipase. This type of necrosis
is best classified as:
A. Coagulative necrosis of adipocytes
B. Fat necrosis with calcium soap formation *[CORRECT]*
C. Caseous necrosis of subcutaneous tissue
D. Fibrinoid necrosis of small vessels
Correct Answer: B
Rationale: Fat necrosis occurs when pancreatic lipase is released into interstitial tissue, hydrolyzing triglycerides into free fatty
acids that combine with calcium to form calcium soaps (saponification). It is characteristic of acute pancreatitis and may
also occur in breast tissue. The gross appearance is chalky white. Coagulative (A), caseous (C), and fibrinoid necrosis (D)
describe different processes affecting different tissue types.
Q9: A 22-year-old female is diagnosed with acute promyelocytic leukemia (APL) and treated with all-trans
retinoic acid (ATRA). The mechanism by which ATRA induces leukemic blast cell death is best described as:
A. Necrosis via ATP depletion and membrane rupture
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 3
, NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
B. Apoptosis via activation of intrinsic (mitochondrial) caspase pathway *[CORRECT]*
C. Autophagy via lysosomal self-digestion
D. Pyroptosis via inflammasome activation
Correct Answer: B
Rationale: Apoptosis is programmed cell death characterized by caspase activation, cell shrinkage, chromatin condensation
(pyknosis), and apoptotic body formation without inflammation. ATRA induces differentiation and apoptosis of APL
blasts via the intrinsic (mitochondrial) pathway. Necrosis (A) involves ATP depletion, membrane rupture, and
inflammation. Autophagy (C) is lysosomal self-digestion for survival under stress. Pyroptosis (D) is inflammatory cell
death.
Q10: A 78-year-old female is found to have physiological changes of aging including decreased reserve
capacity, oxidative DNA damage accumulation, and cellular senescence. The leading proposed mechanism for
cellular aging involves:
A. Increased telomerase activity allowing indefinite cell division
B. Cumulative oxidative stress from free radical damage to DNA, lipids, and proteins *[CORRECT]*
C. Decreased apoptosis allowing accumulation of damaged cells
D. Increased mitochondrial biogenesis and ATP production
Correct Answer: B
Rationale: The free radical theory of aging proposes cumulative oxidative stress damage to DNA, lipids, and proteins
(including mitochondrial DNA) over time leads to cellular dysfunction, senescence, and aging. Telomeres shorten with
each cell division (telomerase is normally OFF in somatic cells), so (A) is opposite. Apoptosis generally declines with age
(C) but contributes to aging of dividing tissues. Mitochondrial function declines (D).
Q11: A 60-year-old male receives thrombolytic therapy for acute STEMI and within hours develops
reperfusion injury with arrhythmias. The mechanism most responsible for reperfusion injury after
restoration of blood flow is:
A. Continued ATP depletion despite restored oxygen supply
B. Generation of reactive oxygen species (ROS) and intracellular calcium overload *[CORRECT]*
C. Recurrent ischemia due to microvascular obstruction
D. Complement activation with secondary hemolysis
Correct Answer: B
Rationale: Reperfusion injury occurs when blood flow is restored to ischemic tissue. The sudden oxygen supply fuels
generation of reactive oxygen species (superoxide, hydrogen peroxide, hydroxyl radicals) via xanthine oxidase and
mitochondrial pathways. Concurrent mitochondrial calcium overload opens the permeability transition pore, accelerating
cell death. ATP levels actually recover (A). Microvascular obstruction (C) and complement activation (D) are minor
contributors.
Q12: A 30-year-old male with a history of prolonged immobilization after fracture presents with significant
muscle wasting in the affected limb. The cellular adaptation occurring in this scenario is:
A. Hypertrophy of muscle fibers
B. Atrophy due to decreased workload and protein degradation exceeding synthesis *[CORRECT]*
C. Metaplasia of skeletal muscle to fibrous tissue
D. Apoptosis of muscle stem cells
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 4
Herzing University | Grade A | 100% Verified
NSG 120 / NSG120 FINAL EXAM (LATEST UPDATE): NURSING
PATHOPHYSIOLOGY | EXAM REVIEW WITH QUESTIONS AND VERIFIED
ANSWERS | ALL UNITS COVERED | 100% CORRECT | GRADE A –
HERZING
Herzing University | NSG 120 Nursing Pathophysiology Course Examination | Aligned with NCLEX-RN Pathophysiology
Standards ( Edition)
Total Questions: 150 | Cognitive Levels: 20% Recall, 50% Application, 30% Analysis | Format: 75% Scenario-Based, 25%
Direct Knowledge
EXAM INSTRUCTIONS: This comprehensive final examination consists of 150 multiple-choice questions covering all
units of NSG 120 Nursing Pathophysiology. Each question has four options (A–D) with exactly ONE correct answer. The
correct answer is marked [CORRECT]. Rationales provide pathophysiological reasoning aligned with the NSG 120
curriculum and NCLEX-RN standards. Sections are organized by body system; recommended time: approximately 3 hours.
SECTION 1: Cellular Injury, Adaptation, & Death
Q1: A 68-year-old male with a long-standing history of hypertension presents with an echocardiogram
demonstrating increased ventricular wall thickness without an increase in cardiac chamber size. The
cardiologist documents this as an adaptive response to chronic pressure overload. Which cellular adaptation
best describes this finding?
A. Hyperplasia, an increase in the number of cardiac myocytes
B. Hypertrophy, an increase in the size of existing cardiac myocytes *[CORRECT]*
C. Metaplasia, a reversible change of one adult cell type to another
D. Dysplasia, disordered cellular growth and atypia
Correct Answer: B
Rationale: Hypertrophy is an increase in the SIZE of existing cells, exemplified by cardiac myocytes responding to chronic
pressure overload in hypertension or aortic stenosis. Cardiac myocytes are terminally differentiated and cannot divide, so
hyperplasia (A) is impossible. Metaplasia (C) is a reversible substitution of one adult cell type for another (e.g., Barrett
esophagus). Dysplasia (D) is disordered, atypical proliferation indicating pre-neoplastic change.
Q2: A 55-year-old woman with a 30-pack-year smoking history undergoes bronchoscopy with biopsy of the
bronchial epithelium. The pathologist reports stratified squamous epithelium replacing the normal
pseudostratified ciliated columnar epithelium. Which adaptive mechanism is described, and what is its
primary biological significance?
A. Atrophy, reversible decrease in cell size due to chronic irritation
B. Hypertrophy, increased cell size to compensate for injury
C. Metaplasia, a protective but premalignant adaptive substitution *[CORRECT]*
D. Apoptosis, programmed cell death of ciliated cells
Correct Answer: C
Rationale: The biopsy shows squamous metaplasia, a reversible adaptive substitution of stratified squamous epithelium for
columnar epithelium in response to chronic irritation (smoking). While protective initially by resisting irritation, persistent
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 1
,NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
injury can progress to dysplasia and squamous cell carcinoma. Atrophy (A) is decreased cell size/substance; hypertrophy
(B) is increased cell size; apoptosis (D) is programmed cell death.
Q3: A 45-year-old male is found unconscious in a closed garage with a running automobile. On arrival to the
ED, carboxyhemoglobin is 38%. The pathophysiological mechanism of cellular injury in this patient is best
described as:
A. Direct chemical injury to cellular membranes by carbon particles
B. Hypoxic injury due to impaired oxygen-carrying capacity of hemoglobin *[CORRECT]*
C. Free radical generation by lipid peroxidation of mitochondrial membranes
D. Ischemic injury due to decreased perfusion from carbon monoxide-induced vasoconstriction
Correct Answer: B
Rationale: Carbon monoxide has 240 times the affinity of oxygen for hemoglobin, forming carboxyhemoglobin and severely
reducing oxygen-carrying capacity, producing hypoxic cellular injury. While CO does impair mitochondrial cytochrome
oxidase (impacting oxidative phosphorylation), the dominant mechanism is functional anemia/hypoxia rather than direct
membrane chemical injury (A), free radical peroxidation (C), or vasoconstrictive ischemia (D). Treatment is 100% oxygen
or hyperbaric oxygen.
Q4: A 28-year-old male sustains a gunshot wound to the femoral artery, losing approximately 1500 mL of
blood. He is hypotensive and tachycardic. At the cellular level, the mechanism of injury is best characterized
as:
A. Impaired oxygen delivery (hypoxic hypoxia) leading to depletion of ATP *[CORRECT]*
B. Direct physical trauma to tissue with membrane disruption
C. Chemical injury from released lysosomal enzymes
D. Free radical injury from reperfusion of ischemic tissue
Correct Answer: A
Rationale: Hemorrhage causes hypovolemic shock with decreased perfusion and oxygen delivery (ischemic/hypoxic hypoxia),
depleting intracellular ATP. Decreased ATP causes failure of Na+/K+-ATPase, cellular swelling, calcium influx, and
ultimately irreversible injury. Direct physical trauma (B) is localized to the wound; lysosomal enzyme release (C) is a
downstream consequence, not initial mechanism; reperfusion injury (D) occurs after restoration of blood flow, not during
ischemia.
Q5: A 62-year-old female with acute myocardial infarction has elevated cardiac enzymes. The pathologist
examining the infarcted myocardium 48 hours after the event would most likely identify which pattern of
necrosis?
A. Liquefactive necrosis with neutrophil infiltration and tissue liquefaction
B. Coagulative necrosis with preserved tissue architecture and eosinophilic cells *[CORRECT]*
C. Caseous necrosis with granulomatous inflammation and cheese-like appearance
D. Fat necrosis with saponification of triglycerides by lipase
Correct Answer: B
Rationale: Myocardial infarction produces coagulative necrosis, the most common pattern in solid organs (heart, kidney, liver,
spleen), characterized by preservation of tissue architecture for days after cell death, with cells becoming eosinophilic and
anucleate. Liquefactive necrosis (A) occurs in the brain or with bacterial infection. Caseous necrosis (C) is seen in
tuberculosis. Fat necrosis (D) occurs in pancreatic and breast tissue.
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 2
,NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
Q6: A 4-year-old child presents with progressively enlarging head circumference, vomiting, and ataxia. MRI
shows a posterior fossa tumor. The surgeon is concerned because brain tissue characteristically undergoes
which pattern of necrosis when ischemic or injured?
A. Coagulative necrosis with preserved tissue framework
B. Liquefactive necrosis from enzymatic digestion by microglia and neutrophils *[CORRECT]*
C. Caseous necrosis with granuloma formation
D. Fibrinoid necrosis of small blood vessels
Correct Answer: B
Rationale: Brain tissue undergoes liquefactive necrosis because it is rich in lipids and lacks substantial connective tissue
stroma, allowing enzymatic digestion by neutrophils and microglia to liquefy the tissue into a cystic cavity. Coagulative
necrosis (A) is characteristic of most solid organs but NOT the brain. Caseous necrosis (C) is granulomatous (TB).
Fibrinoid necrosis (D) affects vessel walls in malignant hypertension or immune complex disease.
Q7: A 35-year-old male with active pulmonary tuberculosis undergoes lung biopsy. The pathologist identifies
a central area of necrosis surrounded by epithelioid macrophages, multinucleated giant cells, and a rim of
lymphocytes. The necrotic center grossly resembles soft white cheese. This pattern is:
A. Coagulative necrosis with architectural preservation
B. Liquefactive necrosis from bacterial enzymatic digestion
C. Caseous necrosis, a variant of coagulative necrosis enclosed by granulomatous inflammation
*[CORRECT]*
D. Fat necrosis with saponification
Correct Answer: C
Rationale: Caseous necrosis (literally 'cheese-like') is a distinctive variant of coagulative necrosis encountered in tuberculosis
and certain fungal infections. The necrotic tissue is enclosed within a granuloma (epithelioid macrophages, Langhans giant
cells, lymphocytes). It differs from typical coagulative necrosis by loss of tissue architecture and amorphous granular
appearance. Liquefactive (B) and fat necrosis (D) describe different processes.
Q8: A 47-year-old male with acute pancreatitis develops painful subcutaneous nodules on the lower
extremities. Biopsy demonstrates saponification of subcutaneous fat by pancreatic lipase. This type of necrosis
is best classified as:
A. Coagulative necrosis of adipocytes
B. Fat necrosis with calcium soap formation *[CORRECT]*
C. Caseous necrosis of subcutaneous tissue
D. Fibrinoid necrosis of small vessels
Correct Answer: B
Rationale: Fat necrosis occurs when pancreatic lipase is released into interstitial tissue, hydrolyzing triglycerides into free fatty
acids that combine with calcium to form calcium soaps (saponification). It is characteristic of acute pancreatitis and may
also occur in breast tissue. The gross appearance is chalky white. Coagulative (A), caseous (C), and fibrinoid necrosis (D)
describe different processes affecting different tissue types.
Q9: A 22-year-old female is diagnosed with acute promyelocytic leukemia (APL) and treated with all-trans
retinoic acid (ATRA). The mechanism by which ATRA induces leukemic blast cell death is best described as:
A. Necrosis via ATP depletion and membrane rupture
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 3
, NSG 120 / NSG120 FINAL EXAM — NURSING PATHOPHYSIOLOGY (LATEST UPDATE)
Herzing University | Grade A | 100% Verified
B. Apoptosis via activation of intrinsic (mitochondrial) caspase pathway *[CORRECT]*
C. Autophagy via lysosomal self-digestion
D. Pyroptosis via inflammasome activation
Correct Answer: B
Rationale: Apoptosis is programmed cell death characterized by caspase activation, cell shrinkage, chromatin condensation
(pyknosis), and apoptotic body formation without inflammation. ATRA induces differentiation and apoptosis of APL
blasts via the intrinsic (mitochondrial) pathway. Necrosis (A) involves ATP depletion, membrane rupture, and
inflammation. Autophagy (C) is lysosomal self-digestion for survival under stress. Pyroptosis (D) is inflammatory cell
death.
Q10: A 78-year-old female is found to have physiological changes of aging including decreased reserve
capacity, oxidative DNA damage accumulation, and cellular senescence. The leading proposed mechanism for
cellular aging involves:
A. Increased telomerase activity allowing indefinite cell division
B. Cumulative oxidative stress from free radical damage to DNA, lipids, and proteins *[CORRECT]*
C. Decreased apoptosis allowing accumulation of damaged cells
D. Increased mitochondrial biogenesis and ATP production
Correct Answer: B
Rationale: The free radical theory of aging proposes cumulative oxidative stress damage to DNA, lipids, and proteins
(including mitochondrial DNA) over time leads to cellular dysfunction, senescence, and aging. Telomeres shorten with
each cell division (telomerase is normally OFF in somatic cells), so (A) is opposite. Apoptosis generally declines with age
(C) but contributes to aging of dividing tissues. Mitochondrial function declines (D).
Q11: A 60-year-old male receives thrombolytic therapy for acute STEMI and within hours develops
reperfusion injury with arrhythmias. The mechanism most responsible for reperfusion injury after
restoration of blood flow is:
A. Continued ATP depletion despite restored oxygen supply
B. Generation of reactive oxygen species (ROS) and intracellular calcium overload *[CORRECT]*
C. Recurrent ischemia due to microvascular obstruction
D. Complement activation with secondary hemolysis
Correct Answer: B
Rationale: Reperfusion injury occurs when blood flow is restored to ischemic tissue. The sudden oxygen supply fuels
generation of reactive oxygen species (superoxide, hydrogen peroxide, hydroxyl radicals) via xanthine oxidase and
mitochondrial pathways. Concurrent mitochondrial calcium overload opens the permeability transition pore, accelerating
cell death. ATP levels actually recover (A). Microvascular obstruction (C) and complement activation (D) are minor
contributors.
Q12: A 30-year-old male with a history of prolonged immobilization after fracture presents with significant
muscle wasting in the affected limb. The cellular adaptation occurring in this scenario is:
A. Hypertrophy of muscle fibers
B. Atrophy due to decreased workload and protein degradation exceeding synthesis *[CORRECT]*
C. Metaplasia of skeletal muscle to fibrous tissue
D. Apoptosis of muscle stem cells
NSG 120 Nursing Pathophysiology | Exam Review with Verified Answers | All Units Covered Page 4
