NUR 631 | Advanced Physiology & Pathophysiology | Midterm Exam (2026/2027)
MIDTERM EXAM: NUR631 / NUR 631 (LATEST 2026 /
2027 UPDATE)
Advanced Physiology and Pathophysiology
Study Guide | Questions and Verified Answers | 100% Correct — GCU
Course: NUR 631 — Advanced Physiology and Pathophysiology
Institution: Grand Canyon University, College of Nursing and Health Care Professions
Term: Edition
Total Questions: 120 (8 sections) | Format: Multiple choice (4 options, single best answer)
Cognitive Distribution: 20% recall, 50% application, 30% analysis
Item Style: 75% scenario-based clinical reasoning; 25% direct knowledge
Alignment: GCU NUR 631 Syllabus, AACN Essentials of Master's Education, Advanced Physiology &
Pathophysiology Competencies (2026/2027)
Section 1: Cellular Physiology & Pathophysiology
Q1: A 68-year-old male with chronic heart failure develops increased urinary frequency, nocturia, and a
sensation of incomplete bladder emptying over the past six months. Digital rectal examination reveals a
diffusely enlarged, firm prostate gland. Which cellular adaptive mechanism best explains the prostate gland
enlargement in this patient?
A. Hyperplasia, an increase in the number of cells in an organ or tissue in response to hormonal stimulation
*[CORRECT]*
B. Hypertrophy, an increase in the size of existing cells due to increased workload or hormonal stimulation
C. Metaplasia, the reversible replacement of one differentiated cell type with another less differentiated type
D. Dysplasia, disordered growth and maturation of cells displaying atypical features without invasion
Correct Answer: A
Rationale: Benign prostatic hyperplasia (BPH) is the paradigmatic example of hormonal hyperplasia — an increase in the
absolute number of prostate stromal and epithelial cells driven by dihydrotestosterone (DHT) in aging men, consistent with
NUR 631 content on cellular adaptation. Hypertrophy involves enlargement of existing cells (e.g., myocardium in
hypertension), not proliferation. Metaplasia is replacement of one cell type with another (e.g., Barrett esophagus), while
dysplasia reflects disordered, atypical proliferation that is premalignant — neither describes BPH pathology.
Q2: A researcher is studying a cell line exposed to sustained hypoxia. Electron microscopy reveals
mitochondrial swelling, rupture of cristae, and release of cytochrome c into the cytosol. Which downstream
cellular process is most directly initiated by cytochrome c release?
A. Activation of caspase-9 within the apoptosome, executing the intrinsic (mitochondrial) apoptosis pathway
*[CORRECT]*
B. Activation of caspase-8 via the death receptor pathway, triggering extrinsic apoptosis
C. Massive calcium influx triggering necrotic cell death and inflammatory cascade
D. Upregulation of Bcl-2 anti-apoptotic proteins and initiation of autophagy
Correct Answer: A
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Rationale: Cytochrome c release from damaged mitochondria binds Apaf-1 and procaspase-9 to form the apoptosome,
activating caspase-9 and initiating the intrinsic (mitochondrial) apoptosis cascade — a central concept in NUR 631 cellular
injury content. Caspase-8 is the initiator of the extrinsic (death receptor) pathway activated by ligands such as FasL or TNF,
not by cytochrome c. Necrosis involves ATP depletion and membrane rupture with inflammation, not the regulated
apoptosome. Bcl-2 actually inhibits cytochrome c release; its upregulation would oppose apoptosis.
Q3: A 55-year-old patient receiving chemotherapy with doxorubicin develops progressive cardiomyopathy.
Cellular analysis of myocardial biopsy reveals increased reactive oxygen species (ROS), lipid peroxidation of
membranes, and DNA strand breaks. Which cellular mechanism is the primary source of the ROS generated
by doxorubicin?
A. Redox cycling within the mitochondrial electron transport chain generating superoxide anion *[CORRECT]*
B. Direct inhibition of catalase and superoxide dismutase within the cytoplasm
C. Activation of NADPH oxidase on the plasma membrane of cardiomyocytes
D. Disruption of lysosomal membranes releasing hydrolytic enzymes into the cytosol
Correct Answer: A
Rationale: Doxorubicin undergoes redox cycling at Complex I of the mitochondrial electron transport chain, accepting an
electron to form a semiquinone radical that reacts with oxygen to generate superoxide anion (O2–) — a key mechanism of
anthracycline cardiotoxicity taught in NUR 631. Doxorubicin does not directly inhibit catalase or SOD. While NADPH oxidase
produces ROS in phagocytes, doxorubicin cardiotoxicity is mitochondrial in origin. Lysosomal enzyme release characterizes
necrotic cell death, not the ROS-mediated apoptosis seen in doxorubicin injury.
Q4: A 72-year-old male with a 50 pack-year smoking history has chronic bronchitis. Biopsy of the bronchial
epithelium reveals replacement of normal ciliated columnar epithelium with stratified squamous epithelium.
Which cellular adaptive process is occurring, and what is its primary biological significance?
A. Metaplasia — a reversible, protective adaptation to chronic irritation that is potentially premalignant
*[CORRECT]*
B. Dysplasia — an irreversible, premalignant transformation indicating carcinoma in situ
C. Anaplasia — loss of cell differentiation representing frank malignancy
D. Hyperplasia — increased cell number without alteration in cell type
Correct Answer: A
Rationale: Replacement of ciliated pseudostratified columnar epithelium with stratified squamous epithelium in response
to chronic smoke irritation is squamous metaplasia — a reversible adaptive change that is potentially premalignant if the
irritant persists, consistent with NUR 631 cellular adaptation content. Dysplasia implies disordered, atypical cellular
architecture (loss of polarity, pleomorphism) and is not the same as a uniform cell-type switch. Anaplasia denotes loss of
differentiation seen in frank malignancy. Hyperplasia increases cell number without changing cell identity.
Q5: During a lecture on cellular metabolism, the instructor explains that glycolysis produces a net of two ATP
molecules per glucose molecule. Which enzymatic step in glycolysis is responsible for the substrate-level
phosphorylation that generates ATP directly?
A. Phosphoglycerate kinase and pyruvate kinase catalyze substrate-level phosphorylation transferring
phosphate to ADP *[CORRECT]*
B. Hexokinase phosphorylates glucose using ATP derived from oxidative phosphorylation
C. Phosphofructokinase-1 catalyzes the rate-limiting step using allosteric regulation by ATP
D. Aldolase cleaves fructose-1,6-bisphosphate into two three-carbon intermediates
Correct Answer: A
Rationale: In glycolysis, substrate-level phosphorylation occurs at two steps: phosphoglycerate kinase transfers a
phosphate from 1,3-bisphosphoglycerate to ADP, and pyruvate kinase transfers phosphate from phosphoenolpyruvate to
ADP — together yielding net 2 ATP per glucose, central to NUR 631 cellular metabolism content. Hexokinase and
Grand Canyon University | College of Nursing & Health Care Professions Page 2
,NUR 631 | Advanced Physiology & Pathophysiology | Midterm Exam (2026/2027)
phosphofructokinase-1 consume ATP (kinases that phosphorylate substrates) rather than generate it. Aldolase is a lyase
that cleaves fructose-1,6-bisphosphate and does not transfer phosphate to ADP.
Q6: A patient with severe ischemia-reperfusion injury following limb tourniquet release develops massive
skeletal muscle injury. Laboratory studies reveal elevated serum potassium, myoglobinuria, and tissue
acidosis. At the cellular level, which sequence of events best describes the mechanism of reperfusion injury in
this patient?
A. ATP depletion leads to failure of Na+/K+-ATPase, intracellular Na+ and Ca2+ accumulation, mitochondrial
dysfunction, and ROS burst upon oxygen return *[CORRECT]*
B. Direct oxidative damage to DNA triggers immediate p53-mediated apoptosis of cardiomyocytes
C. Complement activation directly lyses myocyte membranes independent of ion flux
D. Hyperoxia directly denatures intracellular proteins via oxidative carbonylation
Correct Answer: A
Rationale: Reperfusion injury follows a defined pathophysiology: ischemia depletes ATP, disabling Na+/K+-ATPase and the
Na+/Ca2+ exchanger, causing intracellular Na+ and Ca2+ accumulation that activates proteases and damages
mitochondria; restoration of oxygen then drives a ROS burst that overwhelms antioxidant defenses, as emphasized in NUR
631 cellular injury content. p53-mediated apoptosis is not the primary reperfusion mechanism. Complement plays a
secondary role and does not lyse membranes independent of ion dysregulation. Hyperoxia does not denature proteins in
this context.
Q7: A cell biologist is studying a G-protein–coupled receptor (GPCR) signaling pathway. Ligand binding
activates a Gs alpha subunit, which then stimulates adenylyl cyclase. Which second messenger and
downstream kinase cascade is directly activated by this signaling event?
A. Cyclic AMP (cAMP) accumulation activates protein kinase A (PKA) *[CORRECT]*
B. Inositol triphosphate (IP3) release activates protein kinase C (PKC)
C. Cyclic GMP (cGMP) accumulation activates protein kinase G (PKG)
D. Diacylglycerol (DAG) accumulation activates protein kinase C (PKC)
Correct Answer: A
Rationale: Gs alpha subunit activation stimulates adenylyl cyclase to convert ATP to cyclic AMP (cAMP), which activates
protein kinase A (PKA) — the classic Gs-cAMP-PKA signaling cascade central to NUR 631 cell signaling content (e.g.,
beta-adrenergic receptor signaling). IP3 and DAG are generated by phospholipase C (activated by Gq), not adenylyl cyclase,
and IP3 releases calcium from the ER while DAG activates PKC. cGMP is generated by guanylyl cyclase and activates PKG
(e.g., nitric oxide signaling).
Q8: A pathologist examining a tissue specimen notes cells with shrunken, pyknotic nuclei, cytoplasmic
eosinophilia, and formation of apoptotic bodies without surrounding inflammation. Which cellular process is
most consistent with these findings?
A. Apoptosis, an energy-dependent, programmed cell death without inflammatory response *[CORRECT]*
B. Coagulative necrosis, an uncontrolled cell death with preserved tissue architecture and inflammation
C. Liquefactive necrosis, cell dissolution by enzymatic digestion typical of CNS infarcts
D. Caseous necrosis, cheese-like cell death characteristic of mycobacterial infection
Correct Answer: A
Rationale: Apoptosis is an energy-dependent (ATP-requiring), programmed process characterized by cell shrinkage, nuclear
pyknosis and karyorrhexis, cytoplasmic eosinophilia, and formation of membrane-bound apoptotic bodies phagocytosed
without inflammation — central to NUR 631 cell death content. Coagulative necrosis preserves tissue architecture (ghost
cells) but elicits an inflammatory response, unlike apoptosis. Liquefactive necrosis shows enzymatic dissolution and
neutrophil infiltration. Caseous necrosis is associated with granulomatous inflammation (e.g., tuberculosis).
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Q9: A 45-year-old male with a long-standing history of heavy alcohol use presents with hepatomegaly and
elevated liver enzymes. Liver biopsy reveals hepatocytes containing clear, lipid-laden vacuoles that displace
the nucleus to the periphery. Which form of cellular accumulation is depicted, and what is its underlying
mechanism?
A. Steatosis (fatty change) due to impaired beta-oxidation and increased triglyceride synthesis from ethanol
metabolism *[CORRECT]*
B. Glycogen storage disease due to defective lysosomal alpha-glucosidase
C. Hemosiderosis due to iron overload from chronic alcohol-induced mucosal damage
D. Hydropic degeneration from acute hypoxic injury and failure of the Na+/K+-ATPase
Correct Answer: A
Rationale: Alcohol metabolism generates excess NADH, which shifts the hepatocyte redox state, inhibits beta-oxidation of
fatty acids, and promotes triglyceride synthesis — leading to steatosis (fatty change) visible as lipid vacuoles displacing the
nucleus peripherally, a hallmark of NUR 631 cellular accumulation content. Glycogen storage disease reflects enzymatic
defects (e.g., acid alpha-glucosidase in Pompe disease). Hemosiderosis shows golden-brown hemosiderin granules.
Hydropic degeneration produces cloudy swelling from water influx, not lipid vacuoles.
Q10: A 28-year-old female presents with chronic atrophic gastritis from autoimmune destruction of parietal
cells. Endoscopic biopsy reveals decreased numbers of gastric glandular cells with smaller cell size and
reduced synthetic organelles. Which cellular adaptive mechanism is occurring in the remaining gastric
glandular cells?
A. Atrophy, a decrease in cell size and number due to decreased workload, nutrition, or hormonal stimulation
*[CORRECT]*
B. Apoptosis, programmed cell death mediated by caspase activation
C. Dysplasia, premalignant disordered cellular growth and maturation
D. Hyperplasia, an increase in cell number compensating for cell loss
Correct Answer: A
Rationale: Decreased cell size and number due to diminished hormonal or neural stimulation, reduced workload, or
inadequate nutrition defines atrophy — the cellular adaptation in autoimmune gastritis where loss of gastrin and intrinsic
factor signaling reduces parietal cell trophic support, consistent with NUR 631 cellular adaptation content. Apoptosis is
programmed cell death, not adaptive shrinkage. Dysplasia is premalignant cellular atypia. Hyperplasia is an increase in cell
number, the opposite of atrophy.
Q11: A cell membrane is selectively permeable and maintains concentration gradients of ions across its lipid
bilayer. Which transport mechanism is primarily responsible for maintaining the high intracellular potassium
and low intracellular sodium concentrations characteristic of resting cells?
A. Active transport via the Na+/K+-ATPase pump, moving 3 Na+ out and 2 K+ in per ATP hydrolyzed
*[CORRECT]*
B. Facilitated diffusion through voltage-gated potassium channels down the concentration gradient
C. Passive diffusion through leakage channels, equalizing ion concentrations over time
D. Secondary active transport coupled to the sodium gradient via the Na+/Ca2+ exchanger
Correct Answer: A
Rationale: The Na+/K+-ATPase is a P-type ATPase that hydrolyzes one ATP to export 3 Na+ and import 2 K+, maintaining
the electrochemical gradients essential for resting membrane potential and secondary active transport — a foundational
concept in NUR 631 membrane transport. Facilitated diffusion via K+ channels would equilibrate concentrations, not
maintain gradients. Passive diffusion similarly dissipates gradients. The Na+/Ca2+ exchanger depends on the Na+ gradient
established by the pump but does not directly set the K+ gradient.
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MIDTERM EXAM: NUR631 / NUR 631 (LATEST 2026 /
2027 UPDATE)
Advanced Physiology and Pathophysiology
Study Guide | Questions and Verified Answers | 100% Correct — GCU
Course: NUR 631 — Advanced Physiology and Pathophysiology
Institution: Grand Canyon University, College of Nursing and Health Care Professions
Term: Edition
Total Questions: 120 (8 sections) | Format: Multiple choice (4 options, single best answer)
Cognitive Distribution: 20% recall, 50% application, 30% analysis
Item Style: 75% scenario-based clinical reasoning; 25% direct knowledge
Alignment: GCU NUR 631 Syllabus, AACN Essentials of Master's Education, Advanced Physiology &
Pathophysiology Competencies (2026/2027)
Section 1: Cellular Physiology & Pathophysiology
Q1: A 68-year-old male with chronic heart failure develops increased urinary frequency, nocturia, and a
sensation of incomplete bladder emptying over the past six months. Digital rectal examination reveals a
diffusely enlarged, firm prostate gland. Which cellular adaptive mechanism best explains the prostate gland
enlargement in this patient?
A. Hyperplasia, an increase in the number of cells in an organ or tissue in response to hormonal stimulation
*[CORRECT]*
B. Hypertrophy, an increase in the size of existing cells due to increased workload or hormonal stimulation
C. Metaplasia, the reversible replacement of one differentiated cell type with another less differentiated type
D. Dysplasia, disordered growth and maturation of cells displaying atypical features without invasion
Correct Answer: A
Rationale: Benign prostatic hyperplasia (BPH) is the paradigmatic example of hormonal hyperplasia — an increase in the
absolute number of prostate stromal and epithelial cells driven by dihydrotestosterone (DHT) in aging men, consistent with
NUR 631 content on cellular adaptation. Hypertrophy involves enlargement of existing cells (e.g., myocardium in
hypertension), not proliferation. Metaplasia is replacement of one cell type with another (e.g., Barrett esophagus), while
dysplasia reflects disordered, atypical proliferation that is premalignant — neither describes BPH pathology.
Q2: A researcher is studying a cell line exposed to sustained hypoxia. Electron microscopy reveals
mitochondrial swelling, rupture of cristae, and release of cytochrome c into the cytosol. Which downstream
cellular process is most directly initiated by cytochrome c release?
A. Activation of caspase-9 within the apoptosome, executing the intrinsic (mitochondrial) apoptosis pathway
*[CORRECT]*
B. Activation of caspase-8 via the death receptor pathway, triggering extrinsic apoptosis
C. Massive calcium influx triggering necrotic cell death and inflammatory cascade
D. Upregulation of Bcl-2 anti-apoptotic proteins and initiation of autophagy
Correct Answer: A
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Rationale: Cytochrome c release from damaged mitochondria binds Apaf-1 and procaspase-9 to form the apoptosome,
activating caspase-9 and initiating the intrinsic (mitochondrial) apoptosis cascade — a central concept in NUR 631 cellular
injury content. Caspase-8 is the initiator of the extrinsic (death receptor) pathway activated by ligands such as FasL or TNF,
not by cytochrome c. Necrosis involves ATP depletion and membrane rupture with inflammation, not the regulated
apoptosome. Bcl-2 actually inhibits cytochrome c release; its upregulation would oppose apoptosis.
Q3: A 55-year-old patient receiving chemotherapy with doxorubicin develops progressive cardiomyopathy.
Cellular analysis of myocardial biopsy reveals increased reactive oxygen species (ROS), lipid peroxidation of
membranes, and DNA strand breaks. Which cellular mechanism is the primary source of the ROS generated
by doxorubicin?
A. Redox cycling within the mitochondrial electron transport chain generating superoxide anion *[CORRECT]*
B. Direct inhibition of catalase and superoxide dismutase within the cytoplasm
C. Activation of NADPH oxidase on the plasma membrane of cardiomyocytes
D. Disruption of lysosomal membranes releasing hydrolytic enzymes into the cytosol
Correct Answer: A
Rationale: Doxorubicin undergoes redox cycling at Complex I of the mitochondrial electron transport chain, accepting an
electron to form a semiquinone radical that reacts with oxygen to generate superoxide anion (O2–) — a key mechanism of
anthracycline cardiotoxicity taught in NUR 631. Doxorubicin does not directly inhibit catalase or SOD. While NADPH oxidase
produces ROS in phagocytes, doxorubicin cardiotoxicity is mitochondrial in origin. Lysosomal enzyme release characterizes
necrotic cell death, not the ROS-mediated apoptosis seen in doxorubicin injury.
Q4: A 72-year-old male with a 50 pack-year smoking history has chronic bronchitis. Biopsy of the bronchial
epithelium reveals replacement of normal ciliated columnar epithelium with stratified squamous epithelium.
Which cellular adaptive process is occurring, and what is its primary biological significance?
A. Metaplasia — a reversible, protective adaptation to chronic irritation that is potentially premalignant
*[CORRECT]*
B. Dysplasia — an irreversible, premalignant transformation indicating carcinoma in situ
C. Anaplasia — loss of cell differentiation representing frank malignancy
D. Hyperplasia — increased cell number without alteration in cell type
Correct Answer: A
Rationale: Replacement of ciliated pseudostratified columnar epithelium with stratified squamous epithelium in response
to chronic smoke irritation is squamous metaplasia — a reversible adaptive change that is potentially premalignant if the
irritant persists, consistent with NUR 631 cellular adaptation content. Dysplasia implies disordered, atypical cellular
architecture (loss of polarity, pleomorphism) and is not the same as a uniform cell-type switch. Anaplasia denotes loss of
differentiation seen in frank malignancy. Hyperplasia increases cell number without changing cell identity.
Q5: During a lecture on cellular metabolism, the instructor explains that glycolysis produces a net of two ATP
molecules per glucose molecule. Which enzymatic step in glycolysis is responsible for the substrate-level
phosphorylation that generates ATP directly?
A. Phosphoglycerate kinase and pyruvate kinase catalyze substrate-level phosphorylation transferring
phosphate to ADP *[CORRECT]*
B. Hexokinase phosphorylates glucose using ATP derived from oxidative phosphorylation
C. Phosphofructokinase-1 catalyzes the rate-limiting step using allosteric regulation by ATP
D. Aldolase cleaves fructose-1,6-bisphosphate into two three-carbon intermediates
Correct Answer: A
Rationale: In glycolysis, substrate-level phosphorylation occurs at two steps: phosphoglycerate kinase transfers a
phosphate from 1,3-bisphosphoglycerate to ADP, and pyruvate kinase transfers phosphate from phosphoenolpyruvate to
ADP — together yielding net 2 ATP per glucose, central to NUR 631 cellular metabolism content. Hexokinase and
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,NUR 631 | Advanced Physiology & Pathophysiology | Midterm Exam (2026/2027)
phosphofructokinase-1 consume ATP (kinases that phosphorylate substrates) rather than generate it. Aldolase is a lyase
that cleaves fructose-1,6-bisphosphate and does not transfer phosphate to ADP.
Q6: A patient with severe ischemia-reperfusion injury following limb tourniquet release develops massive
skeletal muscle injury. Laboratory studies reveal elevated serum potassium, myoglobinuria, and tissue
acidosis. At the cellular level, which sequence of events best describes the mechanism of reperfusion injury in
this patient?
A. ATP depletion leads to failure of Na+/K+-ATPase, intracellular Na+ and Ca2+ accumulation, mitochondrial
dysfunction, and ROS burst upon oxygen return *[CORRECT]*
B. Direct oxidative damage to DNA triggers immediate p53-mediated apoptosis of cardiomyocytes
C. Complement activation directly lyses myocyte membranes independent of ion flux
D. Hyperoxia directly denatures intracellular proteins via oxidative carbonylation
Correct Answer: A
Rationale: Reperfusion injury follows a defined pathophysiology: ischemia depletes ATP, disabling Na+/K+-ATPase and the
Na+/Ca2+ exchanger, causing intracellular Na+ and Ca2+ accumulation that activates proteases and damages
mitochondria; restoration of oxygen then drives a ROS burst that overwhelms antioxidant defenses, as emphasized in NUR
631 cellular injury content. p53-mediated apoptosis is not the primary reperfusion mechanism. Complement plays a
secondary role and does not lyse membranes independent of ion dysregulation. Hyperoxia does not denature proteins in
this context.
Q7: A cell biologist is studying a G-protein–coupled receptor (GPCR) signaling pathway. Ligand binding
activates a Gs alpha subunit, which then stimulates adenylyl cyclase. Which second messenger and
downstream kinase cascade is directly activated by this signaling event?
A. Cyclic AMP (cAMP) accumulation activates protein kinase A (PKA) *[CORRECT]*
B. Inositol triphosphate (IP3) release activates protein kinase C (PKC)
C. Cyclic GMP (cGMP) accumulation activates protein kinase G (PKG)
D. Diacylglycerol (DAG) accumulation activates protein kinase C (PKC)
Correct Answer: A
Rationale: Gs alpha subunit activation stimulates adenylyl cyclase to convert ATP to cyclic AMP (cAMP), which activates
protein kinase A (PKA) — the classic Gs-cAMP-PKA signaling cascade central to NUR 631 cell signaling content (e.g.,
beta-adrenergic receptor signaling). IP3 and DAG are generated by phospholipase C (activated by Gq), not adenylyl cyclase,
and IP3 releases calcium from the ER while DAG activates PKC. cGMP is generated by guanylyl cyclase and activates PKG
(e.g., nitric oxide signaling).
Q8: A pathologist examining a tissue specimen notes cells with shrunken, pyknotic nuclei, cytoplasmic
eosinophilia, and formation of apoptotic bodies without surrounding inflammation. Which cellular process is
most consistent with these findings?
A. Apoptosis, an energy-dependent, programmed cell death without inflammatory response *[CORRECT]*
B. Coagulative necrosis, an uncontrolled cell death with preserved tissue architecture and inflammation
C. Liquefactive necrosis, cell dissolution by enzymatic digestion typical of CNS infarcts
D. Caseous necrosis, cheese-like cell death characteristic of mycobacterial infection
Correct Answer: A
Rationale: Apoptosis is an energy-dependent (ATP-requiring), programmed process characterized by cell shrinkage, nuclear
pyknosis and karyorrhexis, cytoplasmic eosinophilia, and formation of membrane-bound apoptotic bodies phagocytosed
without inflammation — central to NUR 631 cell death content. Coagulative necrosis preserves tissue architecture (ghost
cells) but elicits an inflammatory response, unlike apoptosis. Liquefactive necrosis shows enzymatic dissolution and
neutrophil infiltration. Caseous necrosis is associated with granulomatous inflammation (e.g., tuberculosis).
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, NUR 631 | Advanced Physiology & Pathophysiology | Midterm Exam (2026/2027)
Q9: A 45-year-old male with a long-standing history of heavy alcohol use presents with hepatomegaly and
elevated liver enzymes. Liver biopsy reveals hepatocytes containing clear, lipid-laden vacuoles that displace
the nucleus to the periphery. Which form of cellular accumulation is depicted, and what is its underlying
mechanism?
A. Steatosis (fatty change) due to impaired beta-oxidation and increased triglyceride synthesis from ethanol
metabolism *[CORRECT]*
B. Glycogen storage disease due to defective lysosomal alpha-glucosidase
C. Hemosiderosis due to iron overload from chronic alcohol-induced mucosal damage
D. Hydropic degeneration from acute hypoxic injury and failure of the Na+/K+-ATPase
Correct Answer: A
Rationale: Alcohol metabolism generates excess NADH, which shifts the hepatocyte redox state, inhibits beta-oxidation of
fatty acids, and promotes triglyceride synthesis — leading to steatosis (fatty change) visible as lipid vacuoles displacing the
nucleus peripherally, a hallmark of NUR 631 cellular accumulation content. Glycogen storage disease reflects enzymatic
defects (e.g., acid alpha-glucosidase in Pompe disease). Hemosiderosis shows golden-brown hemosiderin granules.
Hydropic degeneration produces cloudy swelling from water influx, not lipid vacuoles.
Q10: A 28-year-old female presents with chronic atrophic gastritis from autoimmune destruction of parietal
cells. Endoscopic biopsy reveals decreased numbers of gastric glandular cells with smaller cell size and
reduced synthetic organelles. Which cellular adaptive mechanism is occurring in the remaining gastric
glandular cells?
A. Atrophy, a decrease in cell size and number due to decreased workload, nutrition, or hormonal stimulation
*[CORRECT]*
B. Apoptosis, programmed cell death mediated by caspase activation
C. Dysplasia, premalignant disordered cellular growth and maturation
D. Hyperplasia, an increase in cell number compensating for cell loss
Correct Answer: A
Rationale: Decreased cell size and number due to diminished hormonal or neural stimulation, reduced workload, or
inadequate nutrition defines atrophy — the cellular adaptation in autoimmune gastritis where loss of gastrin and intrinsic
factor signaling reduces parietal cell trophic support, consistent with NUR 631 cellular adaptation content. Apoptosis is
programmed cell death, not adaptive shrinkage. Dysplasia is premalignant cellular atypia. Hyperplasia is an increase in cell
number, the opposite of atrophy.
Q11: A cell membrane is selectively permeable and maintains concentration gradients of ions across its lipid
bilayer. Which transport mechanism is primarily responsible for maintaining the high intracellular potassium
and low intracellular sodium concentrations characteristic of resting cells?
A. Active transport via the Na+/K+-ATPase pump, moving 3 Na+ out and 2 K+ in per ATP hydrolyzed
*[CORRECT]*
B. Facilitated diffusion through voltage-gated potassium channels down the concentration gradient
C. Passive diffusion through leakage channels, equalizing ion concentrations over time
D. Secondary active transport coupled to the sodium gradient via the Na+/Ca2+ exchanger
Correct Answer: A
Rationale: The Na+/K+-ATPase is a P-type ATPase that hydrolyzes one ATP to export 3 Na+ and import 2 K+, maintaining
the electrochemical gradients essential for resting membrane potential and secondary active transport — a foundational
concept in NUR 631 membrane transport. Facilitated diffusion via K+ channels would equilibrate concentrations, not
maintain gradients. Passive diffusion similarly dissipates gradients. The Na+/Ca2+ exchanger depends on the Na+ gradient
established by the pump but does not directly set the K+ gradient.
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