NSG 6020 3P —South University Exam
NSG 6020 3P
Exam
Questions and Answers| Latest Update| Guaranteed Pass| South University
Page 1 of 33
, NSG 6020 3P —South University Exam
Question 1. A patient presents with cellular swelling and loss of ATP production after a
period of ischemia. Which of the following best describes the initial mechanism of injury?
A. Failure of the sodium-potassium ATPase pump
B. Activation of complement cascade
C. Increased mitochondrial biogenesis
D. Decreased intracellular calcium
Answer: A
Rationale: Ischemia halts oxidative phosphorylation, depleting ATP needed to run the
Na+/K+ ATPase pump. Sodium and water accumulate intracellularly, causing hydropic
(cellular) swelling, the earliest reversible sign of cell injury.
Question 2. Which mediator is primarily responsible for the vasodilation and increased
vascular permeability seen in the early stages of acute inflammation?
A. Interleukin-10
B. Histamine
C. Interferon-gamma
D. Erythropoietin
Answer: B
Rationale: Histamine, released from mast cells and basophils, is the primary early
mediator causing arteriolar vasodilation and increased venular permeability, producing
the redness and edema of acute inflammation.
Question 3. A patient with chronic hypoxia develops secondary polycythemia. What is
the underlying physiologic trigger?
A. Increased renal erythropoietin secretion
B. Decreased iron absorption
C. Bone marrow suppression
D. Increased plasma volume
Answer: A
Rationale: Chronic hypoxemia stimulates peritubular cells in the kidney to release
erythropoietin, which stimulates bone marrow erythropoiesis to increase oxygen-
carrying capacity, resulting in secondary polycythemia.
Question 4. In left-sided heart failure, pulmonary congestion occurs primarily due to
which mechanism?
A. Decreased pulmonary capillary hydrostatic pressure
B. Increased left atrial and pulmonary venous pressure
Page 2 of 33
, NSG 6020 3P —South University Exam
C. Increased plasma oncotic pressure
D. Decreased pulmonary vascular resistance
Answer: B
Rationale: Failure of the left ventricle raises left atrial pressure, which backs up into the
pulmonary veins and capillaries, raising hydrostatic pressure and forcing fluid into the
alveolar interstitium, producing pulmonary edema.
Question 5. Which pathophysiologic process characterizes Type 1 diabetes mellitus?
A. Peripheral insulin resistance with compensatory hyperinsulinemia
B. Autoimmune destruction of pancreatic beta cells
C. Excess glucagon suppression
D. Increased incretin hormone activity
Answer: B
Rationale: Type 1 diabetes results from T-cell mediated autoimmune destruction of
pancreatic beta cells, leading to absolute insulin deficiency, in contrast to Type 2
diabetes which involves insulin resistance.
Question 6. A patient in septic shock develops a lactate level of 6 mmol/L. This finding
best reflects which process?
A. Enhanced aerobic metabolism
B. Anaerobic metabolism from tissue hypoperfusion
C. Increased hepatic lactate clearance
D. Respiratory alkalosis compensation
Answer: B
Rationale: Sepsis-induced hypoperfusion and mitochondrial dysfunction force cells to
shift to anaerobic glycolysis, generating excess lactate; elevated lactate is a marker of
tissue hypoxia and severity of shock.
Question 7. Which acid-base disturbance would be expected in a patient with prolonged
vomiting?
A. Metabolic acidosis
B. Respiratory acidosis
C. Metabolic alkalosis
D. Respiratory alkalosis
Answer: C
Rationale: Loss of hydrochloric acid from gastric contents causes a net loss of hydrogen
ions and chloride, resulting in metabolic alkalosis with compensatory hypoventilation.
Page 3 of 33
, NSG 6020 3P —South University Exam
Question 8. A patient with chronic kidney disease develops secondary
hyperparathyroidism. What is the primary trigger for this response?
A. Hypercalcemia
B. Hyperphosphatemia and decreased activated vitamin D
C. Hypophosphatemia
D. Excess calcitonin secretion
Answer: B
Rationale: Failing kidneys cannot excrete phosphate or activate vitamin D, leading to
hyperphosphatemia and hypocalcemia, both of which stimulate the parathyroid glands
to secrete more PTH, causing bone resorption.
Question 9. Which type of hypersensitivity reaction is responsible for anaphylaxis?
A. Type I, IgE-mediated
B. Type II, cytotoxic
C. Type III, immune complex
D. Type IV, delayed cell-mediated
Answer: A
Rationale: Anaphylaxis is a Type I hypersensitivity reaction in which allergen cross-links
IgE on mast cells and basophils, triggering rapid degranulation and release of histamine
and other mediators.
Question 10. A patient with COPD develops chronic CO2 retention. What compensatory
renal response is expected?
A. Excretion of bicarbonate
B. Retention of bicarbonate
C. Excretion of hydrogen ions decreases
D. Retention of chloride increases beyond bicarbonate
Answer: B
Rationale: In chronic respiratory acidosis, the kidneys compensate over days by
increasing reabsorption and generation of bicarbonate to buffer the excess carbonic acid,
normalizing pH toward baseline.
Question 11. Which mechanism explains the formation of atherosclerotic plaque?
A. Endothelial injury with lipid accumulation and inflammatory response
B. Excess nitric oxide production
C. Decreased LDL oxidation
D. Increased vessel elasticity
Page 4 of 33
NSG 6020 3P
Exam
Questions and Answers| Latest Update| Guaranteed Pass| South University
Page 1 of 33
, NSG 6020 3P —South University Exam
Question 1. A patient presents with cellular swelling and loss of ATP production after a
period of ischemia. Which of the following best describes the initial mechanism of injury?
A. Failure of the sodium-potassium ATPase pump
B. Activation of complement cascade
C. Increased mitochondrial biogenesis
D. Decreased intracellular calcium
Answer: A
Rationale: Ischemia halts oxidative phosphorylation, depleting ATP needed to run the
Na+/K+ ATPase pump. Sodium and water accumulate intracellularly, causing hydropic
(cellular) swelling, the earliest reversible sign of cell injury.
Question 2. Which mediator is primarily responsible for the vasodilation and increased
vascular permeability seen in the early stages of acute inflammation?
A. Interleukin-10
B. Histamine
C. Interferon-gamma
D. Erythropoietin
Answer: B
Rationale: Histamine, released from mast cells and basophils, is the primary early
mediator causing arteriolar vasodilation and increased venular permeability, producing
the redness and edema of acute inflammation.
Question 3. A patient with chronic hypoxia develops secondary polycythemia. What is
the underlying physiologic trigger?
A. Increased renal erythropoietin secretion
B. Decreased iron absorption
C. Bone marrow suppression
D. Increased plasma volume
Answer: A
Rationale: Chronic hypoxemia stimulates peritubular cells in the kidney to release
erythropoietin, which stimulates bone marrow erythropoiesis to increase oxygen-
carrying capacity, resulting in secondary polycythemia.
Question 4. In left-sided heart failure, pulmonary congestion occurs primarily due to
which mechanism?
A. Decreased pulmonary capillary hydrostatic pressure
B. Increased left atrial and pulmonary venous pressure
Page 2 of 33
, NSG 6020 3P —South University Exam
C. Increased plasma oncotic pressure
D. Decreased pulmonary vascular resistance
Answer: B
Rationale: Failure of the left ventricle raises left atrial pressure, which backs up into the
pulmonary veins and capillaries, raising hydrostatic pressure and forcing fluid into the
alveolar interstitium, producing pulmonary edema.
Question 5. Which pathophysiologic process characterizes Type 1 diabetes mellitus?
A. Peripheral insulin resistance with compensatory hyperinsulinemia
B. Autoimmune destruction of pancreatic beta cells
C. Excess glucagon suppression
D. Increased incretin hormone activity
Answer: B
Rationale: Type 1 diabetes results from T-cell mediated autoimmune destruction of
pancreatic beta cells, leading to absolute insulin deficiency, in contrast to Type 2
diabetes which involves insulin resistance.
Question 6. A patient in septic shock develops a lactate level of 6 mmol/L. This finding
best reflects which process?
A. Enhanced aerobic metabolism
B. Anaerobic metabolism from tissue hypoperfusion
C. Increased hepatic lactate clearance
D. Respiratory alkalosis compensation
Answer: B
Rationale: Sepsis-induced hypoperfusion and mitochondrial dysfunction force cells to
shift to anaerobic glycolysis, generating excess lactate; elevated lactate is a marker of
tissue hypoxia and severity of shock.
Question 7. Which acid-base disturbance would be expected in a patient with prolonged
vomiting?
A. Metabolic acidosis
B. Respiratory acidosis
C. Metabolic alkalosis
D. Respiratory alkalosis
Answer: C
Rationale: Loss of hydrochloric acid from gastric contents causes a net loss of hydrogen
ions and chloride, resulting in metabolic alkalosis with compensatory hypoventilation.
Page 3 of 33
, NSG 6020 3P —South University Exam
Question 8. A patient with chronic kidney disease develops secondary
hyperparathyroidism. What is the primary trigger for this response?
A. Hypercalcemia
B. Hyperphosphatemia and decreased activated vitamin D
C. Hypophosphatemia
D. Excess calcitonin secretion
Answer: B
Rationale: Failing kidneys cannot excrete phosphate or activate vitamin D, leading to
hyperphosphatemia and hypocalcemia, both of which stimulate the parathyroid glands
to secrete more PTH, causing bone resorption.
Question 9. Which type of hypersensitivity reaction is responsible for anaphylaxis?
A. Type I, IgE-mediated
B. Type II, cytotoxic
C. Type III, immune complex
D. Type IV, delayed cell-mediated
Answer: A
Rationale: Anaphylaxis is a Type I hypersensitivity reaction in which allergen cross-links
IgE on mast cells and basophils, triggering rapid degranulation and release of histamine
and other mediators.
Question 10. A patient with COPD develops chronic CO2 retention. What compensatory
renal response is expected?
A. Excretion of bicarbonate
B. Retention of bicarbonate
C. Excretion of hydrogen ions decreases
D. Retention of chloride increases beyond bicarbonate
Answer: B
Rationale: In chronic respiratory acidosis, the kidneys compensate over days by
increasing reabsorption and generation of bicarbonate to buffer the excess carbonic acid,
normalizing pH toward baseline.
Question 11. Which mechanism explains the formation of atherosclerotic plaque?
A. Endothelial injury with lipid accumulation and inflammatory response
B. Excess nitric oxide production
C. Decreased LDL oxidation
D. Increased vessel elasticity
Page 4 of 33
