NUR 5240 Advanced Pathophysiology midterm exam
QUESTIONs, Verified Answers & Detailed Rationales |
2026/2027 Edition
QUESTION 1
Cellular adaptation is a reversible response to changes in environmental
stress. Which of the following adaptive cellular changes is characterized
by a decrease in the size of an organ or tissue resulting from a decrease
in cell size and number?
• A. Hypertrophy
• B. Metaplasia
• C. Atrophy
• D. Dysplasia
Correct Answer: C. Atrophy
Detailed Rationale: Atrophy represents a decrease in cell size and
functional capacity in response to disuse, diminished blood supply,
inadequate nutrition, or loss of endocrine stimulation. If enough cells
undergo this process, the entire tissue or organ becomes reduced in
size.
QUESTION 2
During severe myocardial ischemia, irreversible cell injury is heavily
mediated by intracellular calcium overload. What is the primary
pathological consequence of excessive cytosolic calcium accumulation?
, • A. Activation of intracellular enzymes (phospholipases, proteases,
endonucleases) that degrade cellular membranes and nuclear
DNA
• B. Accelerated synthesis of ATP via anaerobic glycolysis
• C. Stabilization of the mitochondrial outer membrane, preventing
cytochrome c leakage
• D. Enhanced transcription of protective heat shock proteins
Correct Answer: A. Activation of intracellular enzymes (phospholipases,
proteases, endonucleases) that degrade cellular membranes and
nuclear DNA
Detailed Rationale: Ischemia disrupts the plasma membrane and
sarcoplasmic reticulum calcium pumps, causing a massive influx of
calcium into the cytosol. This aberrant calcium surge hyperactivates
damaging catabolic enzymes including phospholipases (which destroy
membranes), proteases (which break down cytoskeletal and membrane
proteins), and endonucleases (which fragment chromatin).
QUESTION 3
Apoptosis and necrosis are two distinct mechanisms of cell death.
Which of the following features is uniquely characteristic of apoptosis
rather than necrosis?
• A. Random degradation of cellular DNA and cellular swelling
followed by plasma membrane rupture
• B. Intense local inflammatory response triggered by the leakage of
intracellular contents into adjacent tissues
, • C. Programmed, energy-dependent cell shrinkage, chromatin
condensation, and formation of apoptotic bodies that are
phagocytosed without triggering inflammation
• D. Primary failure of the sodium-potassium adenosine
triphosphatase pump driven by acute hypoxia
Correct Answer: C. Programmed, energy-dependent cell shrinkage,
chromatin condensation, and formation of apoptotic bodies that are
phagocytosed without triggering inflammation
Detailed Rationale: Apoptosis is a tightly regulated, energy-dependent
form of cell death designed to eliminate unwanted or damaged cells
cleanly. Unlike necrosis, which involves cell swelling, membrane lysis,
and significant inflammation, apoptosis features orderly nuclear
fragmentation and cellular budding into membrane-bound bodies
cleared by phagocytes without provoking an inflammatory reaction.
QUESTION 4
Acute inflammation involves vascular and cellular changes mediated by
chemical mediators. Which of the following plasma-derived protein
systems is activated by Hageman factor (Factor XII) and plays a central
role in producing vasodilation, vascular permeability, and pain?
• A. The complement cascade
• B. The kinin system (leading to bradykinin production)
• C. The coagulation cascade (exclusively forming fibrin clots
without inflammatory effects)
• D. The fibrinolytic system (which neutralizes all acute
inflammatory mediators)
, Correct Answer: B. The kinin system (leading to bradykinin production)
Detailed Rationale: Activation of Hageman factor (Factor XII) triggers
the kinin, coagulation, and complement systems. The kinin cascade
cleaves high-molecular-weight kininogen to produce bradykinin, which
causes potent vasodilation, increased vascular permeability, smooth
muscle contraction, and the induction of pain.
QUESTION 5
Goodpasture syndrome is a classic example of a Type II hypersensitivity
reaction. What is the primary immunological mechanism driving tissue
injury in this disorder?
• A. IgE antibodies cross-linking on the surface of mucosal mast cells
• B. Circulating immune complexes depositing within glomerular
capillary loops
• C. Autoantibodies directed against non-collagenous domains of
type IV collagen in glomerular and alveolar basement membranes,
leading to complement activation and neutrophil-mediated
damage
• D. Sensitized CD4+ T lymphocytes releasing cytokines 48 hours
post-exposure
Correct Answer: C. Autoantibodies directed against non-collagenous
domains of type IV collagen in glomerular and alveolar basement
membranes, leading to complement activation and neutrophil-
mediated damage
Detailed Rationale: Type II hypersensitivity involves antibody-mediated
destruction where circulating IgG autoantibodies bind directly to fixed
QUESTIONs, Verified Answers & Detailed Rationales |
2026/2027 Edition
QUESTION 1
Cellular adaptation is a reversible response to changes in environmental
stress. Which of the following adaptive cellular changes is characterized
by a decrease in the size of an organ or tissue resulting from a decrease
in cell size and number?
• A. Hypertrophy
• B. Metaplasia
• C. Atrophy
• D. Dysplasia
Correct Answer: C. Atrophy
Detailed Rationale: Atrophy represents a decrease in cell size and
functional capacity in response to disuse, diminished blood supply,
inadequate nutrition, or loss of endocrine stimulation. If enough cells
undergo this process, the entire tissue or organ becomes reduced in
size.
QUESTION 2
During severe myocardial ischemia, irreversible cell injury is heavily
mediated by intracellular calcium overload. What is the primary
pathological consequence of excessive cytosolic calcium accumulation?
, • A. Activation of intracellular enzymes (phospholipases, proteases,
endonucleases) that degrade cellular membranes and nuclear
DNA
• B. Accelerated synthesis of ATP via anaerobic glycolysis
• C. Stabilization of the mitochondrial outer membrane, preventing
cytochrome c leakage
• D. Enhanced transcription of protective heat shock proteins
Correct Answer: A. Activation of intracellular enzymes (phospholipases,
proteases, endonucleases) that degrade cellular membranes and
nuclear DNA
Detailed Rationale: Ischemia disrupts the plasma membrane and
sarcoplasmic reticulum calcium pumps, causing a massive influx of
calcium into the cytosol. This aberrant calcium surge hyperactivates
damaging catabolic enzymes including phospholipases (which destroy
membranes), proteases (which break down cytoskeletal and membrane
proteins), and endonucleases (which fragment chromatin).
QUESTION 3
Apoptosis and necrosis are two distinct mechanisms of cell death.
Which of the following features is uniquely characteristic of apoptosis
rather than necrosis?
• A. Random degradation of cellular DNA and cellular swelling
followed by plasma membrane rupture
• B. Intense local inflammatory response triggered by the leakage of
intracellular contents into adjacent tissues
, • C. Programmed, energy-dependent cell shrinkage, chromatin
condensation, and formation of apoptotic bodies that are
phagocytosed without triggering inflammation
• D. Primary failure of the sodium-potassium adenosine
triphosphatase pump driven by acute hypoxia
Correct Answer: C. Programmed, energy-dependent cell shrinkage,
chromatin condensation, and formation of apoptotic bodies that are
phagocytosed without triggering inflammation
Detailed Rationale: Apoptosis is a tightly regulated, energy-dependent
form of cell death designed to eliminate unwanted or damaged cells
cleanly. Unlike necrosis, which involves cell swelling, membrane lysis,
and significant inflammation, apoptosis features orderly nuclear
fragmentation and cellular budding into membrane-bound bodies
cleared by phagocytes without provoking an inflammatory reaction.
QUESTION 4
Acute inflammation involves vascular and cellular changes mediated by
chemical mediators. Which of the following plasma-derived protein
systems is activated by Hageman factor (Factor XII) and plays a central
role in producing vasodilation, vascular permeability, and pain?
• A. The complement cascade
• B. The kinin system (leading to bradykinin production)
• C. The coagulation cascade (exclusively forming fibrin clots
without inflammatory effects)
• D. The fibrinolytic system (which neutralizes all acute
inflammatory mediators)
, Correct Answer: B. The kinin system (leading to bradykinin production)
Detailed Rationale: Activation of Hageman factor (Factor XII) triggers
the kinin, coagulation, and complement systems. The kinin cascade
cleaves high-molecular-weight kininogen to produce bradykinin, which
causes potent vasodilation, increased vascular permeability, smooth
muscle contraction, and the induction of pain.
QUESTION 5
Goodpasture syndrome is a classic example of a Type II hypersensitivity
reaction. What is the primary immunological mechanism driving tissue
injury in this disorder?
• A. IgE antibodies cross-linking on the surface of mucosal mast cells
• B. Circulating immune complexes depositing within glomerular
capillary loops
• C. Autoantibodies directed against non-collagenous domains of
type IV collagen in glomerular and alveolar basement membranes,
leading to complement activation and neutrophil-mediated
damage
• D. Sensitized CD4+ T lymphocytes releasing cytokines 48 hours
post-exposure
Correct Answer: C. Autoantibodies directed against non-collagenous
domains of type IV collagen in glomerular and alveolar basement
membranes, leading to complement activation and neutrophil-
mediated damage
Detailed Rationale: Type II hypersensitivity involves antibody-mediated
destruction where circulating IgG autoantibodies bind directly to fixed
