PATHOPHYSIOLOGY FOR NURSING PRACTICE 2026/2027 | CHAMBERLAIN | 50
QUESTIONS | DETAILED RATIONALES | MULTIPLE-CHOICE – GRADED A+
INSTRUCTIONS
Select the single best answer for each question.
Each question has one correct answer and three plausible distractors.
Questions focus on renal, gastrointestinal, and neurological pathophysiology.
Assume standard adult physiology unless otherwise specified.
SECTION I: RENAL PATHOPHYSIOLOGY (Questions 1–10)
Q1 (NR283-Ex3-01). A patient with chronic kidney disease (CKD) develops anemia. The primary cause of
anemia in CKD is:
A) Decreased production of erythropoietin by the kidneys
B) Iron deficiency
C) Vitamin B12 deficiency
D) Hemolysis
Answer: A
Rationale: The kidneys produce erythropoietin (EPO), which stimulates red blood cell production in the bone
marrow. In CKD, EPO production decreases, leading to normocytic, normochromic anemia. Iron deficiency
(B) and B12 deficiency (C) may coexist but are not the primary causes. Hemolysis (D) is not characteristic.
Reference: Norris TL. Porth's Pathophysiology: Concepts of Altered Health States. 11th ed. Wolters Kluwer;
2019.
Bloom Level: Comprehension
, NR 283 PATHOPHYSIOLOGY EXAM 3: MECHANISMS OF DISEASE:
PATHOPHYSIOLOGY FOR NURSING PRACTICE 2026/2027 | CHAMBERLAIN | 50
QUESTIONS | DETAILED RATIONALES | MULTIPLE-CHOICE – GRADED A+
Q2 (NR283-Ex3-02). A patient with acute glomerulonephritis presents with hematuria, proteinuria, and
hypertension. The pathophysiology of acute glomerulonephritis involves:
A) Immune complex deposition in the glomeruli triggering inflammation
B) Ischemia of the renal tubules
C) Obstruction of the ureters
D) Decreased renal blood flow
Answer: A
Rationale: Acute glomerulonephritis is caused by immune complex deposition in the glomeruli, triggering
inflammation and damage to the glomerular basement membrane. This leads to hematuria, proteinuria, and
decreased GFR (causing hypertension and edema). Tubular ischemia (B) is seen in acute tubular necrosis.
Ureteral obstruction (C) causes hydronephrosis. Decreased renal blood flow (D) causes prerenal azotemia.
Reference: Norris TL. Porth's Pathophysiology: Concepts of Altered Health States. 11th ed. Wolters Kluwer;
2019.
Bloom Level: Analysis
Q3 (NR283-Ex3-03). A patient with chronic kidney disease (CKD) develops metabolic acidosis. The
mechanism of metabolic acidosis in CKD involves:
A) Decreased excretion of hydrogen ions (H+) and decreased production of bicarbonate (HCO3-)
B) Increased excretion of hydrogen ions
C) Increased production of bicarbonate
D) Respiratory compensation only
, NR 283 PATHOPHYSIOLOGY EXAM 3: MECHANISMS OF DISEASE:
PATHOPHYSIOLOGY FOR NURSING PRACTICE 2026/2027 | CHAMBERLAIN | 50
QUESTIONS | DETAILED RATIONALES | MULTIPLE-CHOICE – GRADED A+
Answer: A
Rationale: The kidneys are responsible for excreting hydrogen ions (H+) and regenerating bicarbonate
(HCO3-). In CKD, these functions are impaired, leading to metabolic acidosis (low HCO3-, low pH).
Increased H+ excretion (B) would correct acidosis. Increased bicarbonate production (C) would correct
acidosis. Respiratory compensation (D) occurs but is not the mechanism.
Reference: Norris TL. Porth's Pathophysiology: Concepts of Altered Health States. 11th ed. Wolters Kluwer;
2019.
Bloom Level: Comprehension
Q4 (NR283-Ex3-04). A patient with nephrotic syndrome presents with massive proteinuria,
hypoalbuminemia, and edema. The pathophysiology of nephrotic syndrome involves:
A) Increased permeability of the glomerular basement membrane to proteins
B) Decreased permeability of the glomerular basement membrane
C) Increased tubular reabsorption of protein
D) Decreased glomerular filtration rate
Answer: A
Rationale: Nephrotic syndrome is caused by increased permeability of the glomerular basement membrane,
allowing proteins (especially albumin) to pass into the urine. This leads to massive proteinuria,
hypoalbuminemia, and edema (due to decreased plasma oncotic pressure). Decreased permeability (B) would
prevent proteinuria. Increased tubular reabsorption (C) would not cause proteinuria. Decreased GFR (D)
would cause azotemia, not proteinuria.
Reference: Norris TL. Porth's Pathophysiology: Concepts of Altered Health States. 11th ed. Wolters Kluwer;
2019.
, NR 283 PATHOPHYSIOLOGY EXAM 3: MECHANISMS OF DISEASE:
PATHOPHYSIOLOGY FOR NURSING PRACTICE 2026/2027 | CHAMBERLAIN | 50
QUESTIONS | DETAILED RATIONALES | MULTIPLE-CHOICE – GRADED A+
Bloom Level: Comprehension
Q5 (NR283-Ex3-05). A patient with acute kidney injury (AKI) following sepsis develops oliguria (urine
output <400 mL/day). The most likely phase of AKI this patient is experiencing is:
A) Oliguric phase
B) Diuretic phase
C) Recovery phase
D) Pre-renal phase
Answer: A
Rationale: AKI typically has three phases: oliguric (low urine output, often 1-2 weeks), diuretic (increased
urine output, as tubules recover), and recovery (gradual return of function). This patient has oliguria,
consistent with the oliguric phase. Pre-renal (D) is a cause, not a phase.
Reference: Norris TL. Porth's Pathophysiology: Concepts of Altered Health States. 11th ed. Wolters Kluwer;
2019.
Bloom Level: Comprehension
Q6 (NR283-Ex3-06). A patient with diabetes mellitus develops nephrotic syndrome, characterized by massive
proteinuria (>3.5 g/day). The pathophysiology of proteinuria in diabetic nephropathy involves:
A) Damage to the glomerular basement membrane (thickening) and loss of negative charge
B) Damage to the renal tubules
C) Obstruction of the ureters
D) Decreased renal blood flow