NSG 120 Nursing Pathophysiology
Herzing University Academic Year
2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and
NSG 120 Nursing Pathophysiology Herzing University Academic |
Comprehensive Examination
NSG 120 Nursing Pathophysiology Herzing University
Academic Year 2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and Correct Answer
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 120 Nursing Pathophysiology Herzing
University Academic Year 2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and Correct Answer
Rationales. 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 patient with chronic kidney disease has an arterial blood gas showing pH
7.28, PaCO2 32 mmHg, HCO3- 16 mEq/L. Which primary acid-base
disturbance and compensatory mechanism is occurring?
A. Metabolic acidosis with respiratory compensation
B. Respiratory acidosis with renal compensation
C. Metabolic alkalosis with respiratory compensation
D. Respiratory alkalosis with renal compensation
Correct Answer: A - Metabolic acidosis with respiratory
compensation
RATIONALE
Low pH and low HCO3- indicate metabolic acidosis; the low PaCO2
reflects respiratory compensation via hyperventilation. In CKD,
impaired acid excretion causes metabolic acidosis. The other options
do not match the primary bicarbonate deficit.
Question 2
Which statement best explains why a patient with a mutation in the CFTR gene
develops pancreatic insufficiency?
A. Defective chloride transport leads to dehydrated, viscous secretions
that obstruct pancreatic ducts.
B. Autoimmune destruction of pancreatic beta cells causes insulin
deficiency.
C. Excessive sodium reabsorption causes hypernatremia and pancreatic
edema.
D. Premature activation of trypsinogen within the pancreas leads to
autodigestion.
Correct Answer: A - Defective chloride transport leads to
dehydrated, viscous secretions that obstruct pancreatic ducts.
Page 2
, RATIONALE
CFTR mutations impair chloride and water transport, producing thick
mucus that blocks pancreatic ducts, preventing enzyme release. This
leads to malabsorption. The other options describe unrelated
mechanisms such as autoimmune diabetes or acute pancreatitis.
Question 3
A patient presents with fever, hypotension, and widespread vasodilation.
Which pathophysiologic mechanism is most consistent with septic shock?
A. Cytokine-mediated endothelial injury and nitric oxide overproduction
B. IgE-mediated mast cell degranulation and histamine release
C. Direct myocardial depression from viral myocarditis
D. Increased systemic vascular resistance from sympathetic overdrive
Correct Answer: A - Cytokine-mediated endothelial injury and
nitric oxide overproduction
RATIONALE
Septic shock involves systemic inflammation, endothelial dysfunction,
and excess nitric oxide causing vasodilation and hypotension.
Anaphylaxis (B) also causes vasodilation but is IgE-mediated.
Cardiogenic shock (C) and neurogenic shock (D) have different
hemodynamics.
Question 4
Which laboratory finding best differentiates iron deficiency anemia from
anemia of chronic disease?
A. Low serum ferritin in iron deficiency versus normal or high ferritin in
anemia of chronic disease
B. Elevated TIBC in anemia of chronic disease versus low TIBC in iron
deficiency
C. High reticulocyte count in iron deficiency versus low in anemia of
chronic disease
Page 3
, D. Macrocytosis in iron deficiency versus microcytosis in anemia of
chronic disease
Correct Answer: A - Low serum ferritin in iron deficiency versus
normal or high ferritin in anemia of chronic disease
RATIONALE
Ferritin reflects iron stores; it is low in iron deficiency and
normal/high in anemia of chronic disease due to inflammation. TIBC
is high in iron deficiency and low in chronic disease. Both are
typically microcytic, and reticulocytes are low in both.
Question 5
In a patient with acute respiratory distress syndrome (ARDS), which
pathophysiologic change primarily causes refractory hypoxemia?
A. Intrapulmonary shunt due to alveolar flooding and collapse
B. Increased airway resistance from bronchospasm
C. Decreased pulmonary capillary permeability
D. Hyperventilation-induced respiratory alkalosis
Correct Answer: A - Intrapulmonary shunt due to alveolar
flooding and collapse
RATIONALE
ARDS involves increased capillary permeability, alveolar edema, and
collapse, leading to intrapulmonary shunting and hypoxemia
unresponsive to oxygen. Bronchospasm (B) is more characteristic of
asthma. Capillary permeability is increased, not decreased (C).
Question 6
Which mechanism explains the hyperkalemia observed in metabolic acidosis?
A. Hydrogen ions move into cells in exchange for potassium moving out
B. Increased renal potassium excretion due to aldosterone excess
C. Cellular uptake of potassium stimulated by insulin release
Page 4
Herzing University Academic Year
2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and
NSG 120 Nursing Pathophysiology Herzing University Academic |
Comprehensive Examination
NSG 120 Nursing Pathophysiology Herzing University
Academic Year 2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and Correct Answer
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 120 Nursing Pathophysiology Herzing
University Academic Year 2026/2027 Midterm Comprehensive
Examination 50 Verified Questions and Correct Answer
Rationales. 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 patient with chronic kidney disease has an arterial blood gas showing pH
7.28, PaCO2 32 mmHg, HCO3- 16 mEq/L. Which primary acid-base
disturbance and compensatory mechanism is occurring?
A. Metabolic acidosis with respiratory compensation
B. Respiratory acidosis with renal compensation
C. Metabolic alkalosis with respiratory compensation
D. Respiratory alkalosis with renal compensation
Correct Answer: A - Metabolic acidosis with respiratory
compensation
RATIONALE
Low pH and low HCO3- indicate metabolic acidosis; the low PaCO2
reflects respiratory compensation via hyperventilation. In CKD,
impaired acid excretion causes metabolic acidosis. The other options
do not match the primary bicarbonate deficit.
Question 2
Which statement best explains why a patient with a mutation in the CFTR gene
develops pancreatic insufficiency?
A. Defective chloride transport leads to dehydrated, viscous secretions
that obstruct pancreatic ducts.
B. Autoimmune destruction of pancreatic beta cells causes insulin
deficiency.
C. Excessive sodium reabsorption causes hypernatremia and pancreatic
edema.
D. Premature activation of trypsinogen within the pancreas leads to
autodigestion.
Correct Answer: A - Defective chloride transport leads to
dehydrated, viscous secretions that obstruct pancreatic ducts.
Page 2
, RATIONALE
CFTR mutations impair chloride and water transport, producing thick
mucus that blocks pancreatic ducts, preventing enzyme release. This
leads to malabsorption. The other options describe unrelated
mechanisms such as autoimmune diabetes or acute pancreatitis.
Question 3
A patient presents with fever, hypotension, and widespread vasodilation.
Which pathophysiologic mechanism is most consistent with septic shock?
A. Cytokine-mediated endothelial injury and nitric oxide overproduction
B. IgE-mediated mast cell degranulation and histamine release
C. Direct myocardial depression from viral myocarditis
D. Increased systemic vascular resistance from sympathetic overdrive
Correct Answer: A - Cytokine-mediated endothelial injury and
nitric oxide overproduction
RATIONALE
Septic shock involves systemic inflammation, endothelial dysfunction,
and excess nitric oxide causing vasodilation and hypotension.
Anaphylaxis (B) also causes vasodilation but is IgE-mediated.
Cardiogenic shock (C) and neurogenic shock (D) have different
hemodynamics.
Question 4
Which laboratory finding best differentiates iron deficiency anemia from
anemia of chronic disease?
A. Low serum ferritin in iron deficiency versus normal or high ferritin in
anemia of chronic disease
B. Elevated TIBC in anemia of chronic disease versus low TIBC in iron
deficiency
C. High reticulocyte count in iron deficiency versus low in anemia of
chronic disease
Page 3
, D. Macrocytosis in iron deficiency versus microcytosis in anemia of
chronic disease
Correct Answer: A - Low serum ferritin in iron deficiency versus
normal or high ferritin in anemia of chronic disease
RATIONALE
Ferritin reflects iron stores; it is low in iron deficiency and
normal/high in anemia of chronic disease due to inflammation. TIBC
is high in iron deficiency and low in chronic disease. Both are
typically microcytic, and reticulocytes are low in both.
Question 5
In a patient with acute respiratory distress syndrome (ARDS), which
pathophysiologic change primarily causes refractory hypoxemia?
A. Intrapulmonary shunt due to alveolar flooding and collapse
B. Increased airway resistance from bronchospasm
C. Decreased pulmonary capillary permeability
D. Hyperventilation-induced respiratory alkalosis
Correct Answer: A - Intrapulmonary shunt due to alveolar
flooding and collapse
RATIONALE
ARDS involves increased capillary permeability, alveolar edema, and
collapse, leading to intrapulmonary shunting and hypoxemia
unresponsive to oxygen. Bronchospasm (B) is more characteristic of
asthma. Capillary permeability is increased, not decreased (C).
Question 6
Which mechanism explains the hyperkalemia observed in metabolic acidosis?
A. Hydrogen ions move into cells in exchange for potassium moving out
B. Increased renal potassium excretion due to aldosterone excess
C. Cellular uptake of potassium stimulated by insulin release
Page 4
