NSG 3280 Pathophysiology for Nurses -
Final Exam Review (2026/2027 Update)
Pathophysiology for Nurses I Review
Questions and Answers Grade A 100%
NSG 3280 Pathophysiology for Nurses - Final | Comprehensive
Examination
NSG 3280 Pathophysiology for Nurses - Final Exam Review
(2026/2027 Update) Pathophysiology for Nurses I Review
Questions and Answers Grade A 100% Correct (Verified
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 3280 Pathophysiology for Nurses - Final
Exam Review (2026/2027 Update) Pathophysiology for Nurses I
Review Questions and Answers Grade A 100% Correct
(Verified Solutions) Instant pdf - Galen. Every item uses a
focused exam stem, four response options, a keyed response,
and a clear rationale, making it easier to understand the
subject, spot distractors, and build real exam confidence.
Page 1
, Question 1
A cell undergoes reversible ischemic injury. Which cellular change is most
characteristic of this stage and distinguishes it from irreversible injury?
A. Rupture of lysosomal membranes with enzymatic digestion
B. Cellular swelling due to failure of ATP-dependent ion pumps
C. Nuclear chromatin clumping and DNA fragmentation
D. Mitochondrial permeability transition pore opening
Correct Answer: B - Cellular swelling due to failure of
ATP-dependent ion pumps
RATIONALE
Reversible ischemic injury causes ATP depletion, leading to failure of
Na+/K+-ATPase pumps and cellular swelling. Irreversible injury is
marked by lysosomal rupture, mitochondrial permeability transition,
and DNA fragmentation, which are not seen in reversible stages.
Question 2
In a patient with chronic inflammation, which cytokine profile most strongly
promotes tissue fibrosis and angiogenesis?
A. IL-4 and IL-13
B. TNF- and IL-1
C. IL-10 and TGF-
D. IFN- and IL-12
Correct Answer: C - IL-10 and TGF-
RATIONALE
TGF- and IL-10 are key mediators of chronic inflammation that drive
fibrosis and angiogenesis while suppressing excessive immune
responses. TNF- and IL-1 are acute-phase cytokines; IFN- and IL-12
promote Th1 responses; IL-4 and IL-13 drive Th2 and allergic
inflammation.
Page 2
, Question 3
A patient with severe diarrhea loses bicarbonate-rich fluid. Which acid-base
disturbance is expected, and what is the compensatory response?
A. Metabolic acidosis; hyperventilation to decrease PaCO2
B. Metabolic alkalosis; hypoventilation to increase PaCO2
C. Respiratory acidosis; renal excretion of HCO3-
D. Respiratory alkalosis; renal retention of HCO3-
Correct Answer: A - Metabolic acidosis; hyperventilation to
decrease PaCO2
RATIONALE
Loss of bicarbonate-rich fluid causes metabolic acidosis. The
respiratory system compensates by hyperventilating to blow off CO2,
lowering PaCO2. Renal compensation would also occur but is slower;
the other options describe opposite or inappropriate responses.
Question 4
Which statement best explains why a patient with a JAK2 V617F mutation
develops polycythemia vera?
A. The mutation enhances erythropoietin receptor sensitivity, leading to
constitutive activation of JAK-STAT signaling.
B. The mutation causes increased degradation of hypoxia-inducible
factor, reducing erythropoietin production.
C. The mutation leads to loss of function of the JAK2 kinase, impairing
erythroid differentiation.
D. The mutation induces autoimmune destruction of erythrocytes,
triggering compensatory erythropoiesis.
Correct Answer: A - The mutation enhances erythropoietin
receptor sensitivity, leading to constitutive activation of
JAK-STAT signaling.
Page 3
, RATIONALE
JAK2 V617F is a gain-of-function mutation that renders
hematopoietic cells hypersensitive to erythropoietin, causing
constitutive JAK-STAT activation and excessive erythrocyte
production. The other options describe mechanisms not associated
with polycythemia vera.
Question 5
Which hemodynamic change is most directly responsible for the development
of pulmonary edema in left-sided heart failure?
A. Increased pulmonary capillary hydrostatic pressure
B. Decreased pulmonary capillary oncotic pressure
C. Increased lymphatic drainage in the lungs
D. Decreased alveolar surface tension
Correct Answer: A - Increased pulmonary capillary hydrostatic
pressure
RATIONALE
Left-sided heart failure leads to increased pulmonary venous pressure,
which raises pulmonary capillary hydrostatic pressure, forcing fluid
into alveoli. Decreased oncotic pressure is more relevant in
hypoalbuminemia; increased lymphatic drainage would help clear
fluid; decreased surface tension would promote alveolar collapse, not
edema.
Question 6
In a patient with acute respiratory distress syndrome (ARDS), which
pathophysiologic mechanism primarily contributes to hypoxemia refractory to
oxygen therapy?
A. Intrapulmonary shunting due to alveolar collapse and filling
B. Hypoventilation due to respiratory muscle fatigue
C. Diffusion limitation from thickened alveolar membrane
Page 4
Final Exam Review (2026/2027 Update)
Pathophysiology for Nurses I Review
Questions and Answers Grade A 100%
NSG 3280 Pathophysiology for Nurses - Final | Comprehensive
Examination
NSG 3280 Pathophysiology for Nurses - Final Exam Review
(2026/2027 Update) Pathophysiology for Nurses I Review
Questions and Answers Grade A 100% Correct (Verified
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 3280 Pathophysiology for Nurses - Final
Exam Review (2026/2027 Update) Pathophysiology for Nurses I
Review Questions and Answers Grade A 100% Correct
(Verified Solutions) Instant pdf - Galen. Every item uses a
focused exam stem, four response options, a keyed response,
and a clear rationale, making it easier to understand the
subject, spot distractors, and build real exam confidence.
Page 1
, Question 1
A cell undergoes reversible ischemic injury. Which cellular change is most
characteristic of this stage and distinguishes it from irreversible injury?
A. Rupture of lysosomal membranes with enzymatic digestion
B. Cellular swelling due to failure of ATP-dependent ion pumps
C. Nuclear chromatin clumping and DNA fragmentation
D. Mitochondrial permeability transition pore opening
Correct Answer: B - Cellular swelling due to failure of
ATP-dependent ion pumps
RATIONALE
Reversible ischemic injury causes ATP depletion, leading to failure of
Na+/K+-ATPase pumps and cellular swelling. Irreversible injury is
marked by lysosomal rupture, mitochondrial permeability transition,
and DNA fragmentation, which are not seen in reversible stages.
Question 2
In a patient with chronic inflammation, which cytokine profile most strongly
promotes tissue fibrosis and angiogenesis?
A. IL-4 and IL-13
B. TNF- and IL-1
C. IL-10 and TGF-
D. IFN- and IL-12
Correct Answer: C - IL-10 and TGF-
RATIONALE
TGF- and IL-10 are key mediators of chronic inflammation that drive
fibrosis and angiogenesis while suppressing excessive immune
responses. TNF- and IL-1 are acute-phase cytokines; IFN- and IL-12
promote Th1 responses; IL-4 and IL-13 drive Th2 and allergic
inflammation.
Page 2
, Question 3
A patient with severe diarrhea loses bicarbonate-rich fluid. Which acid-base
disturbance is expected, and what is the compensatory response?
A. Metabolic acidosis; hyperventilation to decrease PaCO2
B. Metabolic alkalosis; hypoventilation to increase PaCO2
C. Respiratory acidosis; renal excretion of HCO3-
D. Respiratory alkalosis; renal retention of HCO3-
Correct Answer: A - Metabolic acidosis; hyperventilation to
decrease PaCO2
RATIONALE
Loss of bicarbonate-rich fluid causes metabolic acidosis. The
respiratory system compensates by hyperventilating to blow off CO2,
lowering PaCO2. Renal compensation would also occur but is slower;
the other options describe opposite or inappropriate responses.
Question 4
Which statement best explains why a patient with a JAK2 V617F mutation
develops polycythemia vera?
A. The mutation enhances erythropoietin receptor sensitivity, leading to
constitutive activation of JAK-STAT signaling.
B. The mutation causes increased degradation of hypoxia-inducible
factor, reducing erythropoietin production.
C. The mutation leads to loss of function of the JAK2 kinase, impairing
erythroid differentiation.
D. The mutation induces autoimmune destruction of erythrocytes,
triggering compensatory erythropoiesis.
Correct Answer: A - The mutation enhances erythropoietin
receptor sensitivity, leading to constitutive activation of
JAK-STAT signaling.
Page 3
, RATIONALE
JAK2 V617F is a gain-of-function mutation that renders
hematopoietic cells hypersensitive to erythropoietin, causing
constitutive JAK-STAT activation and excessive erythrocyte
production. The other options describe mechanisms not associated
with polycythemia vera.
Question 5
Which hemodynamic change is most directly responsible for the development
of pulmonary edema in left-sided heart failure?
A. Increased pulmonary capillary hydrostatic pressure
B. Decreased pulmonary capillary oncotic pressure
C. Increased lymphatic drainage in the lungs
D. Decreased alveolar surface tension
Correct Answer: A - Increased pulmonary capillary hydrostatic
pressure
RATIONALE
Left-sided heart failure leads to increased pulmonary venous pressure,
which raises pulmonary capillary hydrostatic pressure, forcing fluid
into alveoli. Decreased oncotic pressure is more relevant in
hypoalbuminemia; increased lymphatic drainage would help clear
fluid; decreased surface tension would promote alveolar collapse, not
edema.
Question 6
In a patient with acute respiratory distress syndrome (ARDS), which
pathophysiologic mechanism primarily contributes to hypoxemia refractory to
oxygen therapy?
A. Intrapulmonary shunting due to alveolar collapse and filling
B. Hypoventilation due to respiratory muscle fatigue
C. Diffusion limitation from thickened alveolar membrane
Page 4
