NURS 231 Pathophysiology | Portage Learning | Final Exam
2026/2027 Complete Final Examination | Actual Questions &
Verified Answers | Comprehensive Pathophysiology
Assessment | Pass Guarantee
1. A 68-year-old man with a 40-pack-year history is admitted with acute
exacerbation of COPD. His ABG on 2 L O₂ shows pH 7.30, PaCO₂ 65 mm Hg,
HCO₃⁻ 35 mEq/L. Which cellular process is PRIMARILY disrupted that leads to
this acid–base picture?
A. Decreased respiratory rate lowers CO₂ elimination, increasing carbonic acid.
B. Lactic acid overproduction from hypoxia consumes bicarbonate.
C. Impaired renal ammoniagenesis prevents hydrogen secretion.
D. Excessive chloride reabsorption generates hyperchloremic acidosis.
Correct Answer: A
Rationale: COPD exacerbation causes alveolar hypoventilation → CO₂ retention
→ ↑PaCO₂ → ↑H₂CO₃ → respiratory acidosis; kidneys compensate by ↑HCO₃⁻
reabsorption (compensated resp. acidosis). B describes lactic acidosis (not
primary here). C is chronic kidney pathology. D is unrelated to COPD.
2. A patient with NYHA class III heart failure is started on an ACE inhibitor. Which
pathophysiologic sequence BEST explains how this drug slows disease
progression?
A. Arteriolar dilation → ↓ afterload → ↓ cardiac workload → ↓ myocardial oxygen
demand → ↓ ventricular remodeling.
B. Venous dilation → ↑ preload → ↑ stroke volume → ↑ renal perfusion → ↓ BNP.
C. Sodium retention → ↑ water excretion → ↓ edema → ↓ preload.
D. Chronotropic stimulation → ↑ cardiac output → ↑ coronary flow.
Correct Answer: A
Rationale: ACE-I blocks Angiot-II-mediated vasoconstriction & aldosterone → ↓
afterload/preload → ↓ wall stress & fibrotic remodeling. B incorrectly says
↑preload. C describes diuresis, not ACE-I. D is inotropic, not ACE-I effect.
,3. A type 2 diabetic with CKD stage 3 develops hyperkalemia (K⁺ 6.2 mEq/L). Which
intracellular-to-extracellular shift MOST contributed to this value?
A. Insulin excess moved K⁺ into cells.
B. Metabolic alkalosis shifted K⁺ out of cells.
C. Hyperosmolarity caused water exit dragging K⁺ with it.
D. β₂-agonist therapy drove K⁺ intracellularly.
Correct Answer: C
Rationale: Hyperglycemia → hyperosmolarity → water leaves cells → K⁺ follows
(“solvent drag”). A & D lower plasma K⁺. B is opposite: alkalosis shifts K⁺ IN.
4. A burn patient develops systemic inflammatory response. Which plasma protein
activation is the PRIMARY driver of capillary leak in the first 24 h?
A. Complement C3a → ↑ vascular permeability.
B. Immunoglobulin G → opsonization.
C. C-reactive protein → clot deposition.
D. Haptoglobin → hemoglobin binding.
Correct Answer: A
Rationale: C3a & C5a are anaphylatoxins → endothelial gap formation → leak.
B-IgG aids phagocytosis, not leak. C-CRP is marker. D-scavenges free Hb.
5. A patient with pulmonary embolism becomes hypotensive. Which
pathophysiologic step is MOST responsible for decreased cardiac output?
A. Bronchoconstriction → ↓ oxygenation → hypoxic myocardial depression.
B. Right-ventricular pressure overload → interventricular septum shifts left → ↓
LV preload.
C. Reflex systemic vasodilation → ↓ SVR.
D. Coronary artery spasm → global hypokinesis.
Correct Answer: B
Rationale: Acute RV afterload ↑ → RV dilatation → septal shift → ↓ LV filling → ↓
CO (McConnell’s physiology). A is minor. C occurs in sepsis, not PE. D is rare.
6. A patient with cirrhosis develops spontaneous bacterial peritonitis. Which
immune deficit is MOST implicated?
A. Decreased Kupffer-cell function → impaired pathogen clearance.
B. Hypoalbuminemia → low complement binding.
C. Portosystemic shunting → bypass of hepatic macrophages.
, D. All of the above.
Correct Answer: D
Rationale: All listed factors reduce opsonic activity & complement in ascitic fluid,
predisposing to SBP.
7. A patient in septic shock has ScvO₂ 45 % (normal ≥ 70 %). Which cellular event is
the PRIMARY cause of this value?
A. Mitochondrial dysfunction → impaired O₂ utilization.
B. Increased O₂ extraction → tissues extract more O₂.
C. Adrenergic shunting → blood bypasses capillary beds.
D. Pyruvate dehydrogenase inhibition → anaerobic glycolysis.
Correct Answer: B
Rationale: Early sepsis ↑flow but ↓Hgb or ↓DO₂ → tissues extract MORE O₂ →
↓ScvO₂. A occurs later (cytopathic hypoxia). C is late shunting. D is metabolic, not
O₂ saturation.
8. A patient with Cushing syndrome develops glucose intolerance. Which step BEST
explains the hyperglycemia?
A. Cortisol inhibits insulin receptor substrate phosphorylation → insulin
resistance.
B. Cortisol stimulates pancreatic α-cells → ↑ glucagon.
C. Cortisol blocks GLUT-4 translocation in muscle.
D. Both A & C.
Correct Answer: D
Rationale: Cortisol is counter-regulatory: ↓IRS signaling & ↓GLUT-4 → peripheral
insulin resistance; ↑hepatic gluconeogenesis.
9. A patient with left-sided stroke shows neglect syndrome. Which anatomic region
is MOST likely infarcted?
A. Right parietal lobe.
B. Left frontal lobe.
C. Right occipital lobe.
D. Brainstem.
Correct Answer: A
Rationale: Non-dominant (usually right) parietal cortex integrates spatial
awareness; damage causes neglect. B causes Broca’s. C causes visual deficits. D
causes crossed findings.
2026/2027 Complete Final Examination | Actual Questions &
Verified Answers | Comprehensive Pathophysiology
Assessment | Pass Guarantee
1. A 68-year-old man with a 40-pack-year history is admitted with acute
exacerbation of COPD. His ABG on 2 L O₂ shows pH 7.30, PaCO₂ 65 mm Hg,
HCO₃⁻ 35 mEq/L. Which cellular process is PRIMARILY disrupted that leads to
this acid–base picture?
A. Decreased respiratory rate lowers CO₂ elimination, increasing carbonic acid.
B. Lactic acid overproduction from hypoxia consumes bicarbonate.
C. Impaired renal ammoniagenesis prevents hydrogen secretion.
D. Excessive chloride reabsorption generates hyperchloremic acidosis.
Correct Answer: A
Rationale: COPD exacerbation causes alveolar hypoventilation → CO₂ retention
→ ↑PaCO₂ → ↑H₂CO₃ → respiratory acidosis; kidneys compensate by ↑HCO₃⁻
reabsorption (compensated resp. acidosis). B describes lactic acidosis (not
primary here). C is chronic kidney pathology. D is unrelated to COPD.
2. A patient with NYHA class III heart failure is started on an ACE inhibitor. Which
pathophysiologic sequence BEST explains how this drug slows disease
progression?
A. Arteriolar dilation → ↓ afterload → ↓ cardiac workload → ↓ myocardial oxygen
demand → ↓ ventricular remodeling.
B. Venous dilation → ↑ preload → ↑ stroke volume → ↑ renal perfusion → ↓ BNP.
C. Sodium retention → ↑ water excretion → ↓ edema → ↓ preload.
D. Chronotropic stimulation → ↑ cardiac output → ↑ coronary flow.
Correct Answer: A
Rationale: ACE-I blocks Angiot-II-mediated vasoconstriction & aldosterone → ↓
afterload/preload → ↓ wall stress & fibrotic remodeling. B incorrectly says
↑preload. C describes diuresis, not ACE-I. D is inotropic, not ACE-I effect.
,3. A type 2 diabetic with CKD stage 3 develops hyperkalemia (K⁺ 6.2 mEq/L). Which
intracellular-to-extracellular shift MOST contributed to this value?
A. Insulin excess moved K⁺ into cells.
B. Metabolic alkalosis shifted K⁺ out of cells.
C. Hyperosmolarity caused water exit dragging K⁺ with it.
D. β₂-agonist therapy drove K⁺ intracellularly.
Correct Answer: C
Rationale: Hyperglycemia → hyperosmolarity → water leaves cells → K⁺ follows
(“solvent drag”). A & D lower plasma K⁺. B is opposite: alkalosis shifts K⁺ IN.
4. A burn patient develops systemic inflammatory response. Which plasma protein
activation is the PRIMARY driver of capillary leak in the first 24 h?
A. Complement C3a → ↑ vascular permeability.
B. Immunoglobulin G → opsonization.
C. C-reactive protein → clot deposition.
D. Haptoglobin → hemoglobin binding.
Correct Answer: A
Rationale: C3a & C5a are anaphylatoxins → endothelial gap formation → leak.
B-IgG aids phagocytosis, not leak. C-CRP is marker. D-scavenges free Hb.
5. A patient with pulmonary embolism becomes hypotensive. Which
pathophysiologic step is MOST responsible for decreased cardiac output?
A. Bronchoconstriction → ↓ oxygenation → hypoxic myocardial depression.
B. Right-ventricular pressure overload → interventricular septum shifts left → ↓
LV preload.
C. Reflex systemic vasodilation → ↓ SVR.
D. Coronary artery spasm → global hypokinesis.
Correct Answer: B
Rationale: Acute RV afterload ↑ → RV dilatation → septal shift → ↓ LV filling → ↓
CO (McConnell’s physiology). A is minor. C occurs in sepsis, not PE. D is rare.
6. A patient with cirrhosis develops spontaneous bacterial peritonitis. Which
immune deficit is MOST implicated?
A. Decreased Kupffer-cell function → impaired pathogen clearance.
B. Hypoalbuminemia → low complement binding.
C. Portosystemic shunting → bypass of hepatic macrophages.
, D. All of the above.
Correct Answer: D
Rationale: All listed factors reduce opsonic activity & complement in ascitic fluid,
predisposing to SBP.
7. A patient in septic shock has ScvO₂ 45 % (normal ≥ 70 %). Which cellular event is
the PRIMARY cause of this value?
A. Mitochondrial dysfunction → impaired O₂ utilization.
B. Increased O₂ extraction → tissues extract more O₂.
C. Adrenergic shunting → blood bypasses capillary beds.
D. Pyruvate dehydrogenase inhibition → anaerobic glycolysis.
Correct Answer: B
Rationale: Early sepsis ↑flow but ↓Hgb or ↓DO₂ → tissues extract MORE O₂ →
↓ScvO₂. A occurs later (cytopathic hypoxia). C is late shunting. D is metabolic, not
O₂ saturation.
8. A patient with Cushing syndrome develops glucose intolerance. Which step BEST
explains the hyperglycemia?
A. Cortisol inhibits insulin receptor substrate phosphorylation → insulin
resistance.
B. Cortisol stimulates pancreatic α-cells → ↑ glucagon.
C. Cortisol blocks GLUT-4 translocation in muscle.
D. Both A & C.
Correct Answer: D
Rationale: Cortisol is counter-regulatory: ↓IRS signaling & ↓GLUT-4 → peripheral
insulin resistance; ↑hepatic gluconeogenesis.
9. A patient with left-sided stroke shows neglect syndrome. Which anatomic region
is MOST likely infarcted?
A. Right parietal lobe.
B. Left frontal lobe.
C. Right occipital lobe.
D. Brainstem.
Correct Answer: A
Rationale: Non-dominant (usually right) parietal cortex integrates spatial
awareness; damage causes neglect. B causes Broca’s. C causes visual deficits. D
causes crossed findings.
