NR 507 Final Exam
Advanced Pathophysiology
Questions with Answers | Latest update
,Question 1
A patient's GFR is estimated at 45 mL/min/1.73m2 and has remained
stable for over three months. According to KDIGO staging, this
represents which category?
A. CKD Stage 2 (60-89 mL/min)
B. CKD Stage 3a (45-59 mL/min)
C. CKD Stage 4 (15-29 mL/min)
D. CKD Stage 5 (<15 mL/min)
Answer: B. CKD Stage 3a (45-59 mL/min)
Rationale: KDIGO staging classifies CKD by sustained GFR reduction: Stage
3a spans 45-59 mL/min/1.73m2, representing a mild-to-moderate decrease
in kidney function. A GFR of 45 mL/min/1.73m2, persisting over three
months, falls at the upper boundary of Stage 3a.
Question 2
Which mechanism best explains the development of anemia in chronic
kidney disease?
A. Increased erythropoietin production by damaged nephrons
B. Decreased erythropoietin production by peritubular fibroblasts
C. Excessive iron absorption in the duodenum
D. Hemolysis due to uremic toxin accumulation on red cell membranes
Answer: B. Decreased erythropoietin production by peritubular
fibroblasts
Rationale: Peritubular fibroblast-like cells in the kidney normally sense
hypoxia and produce erythropoietin. As nephrons are destroyed in CKD,
these cells are lost or replaced by fibrotic tissue, so erythropoietin synthesis
falls, producing a normocytic, normochromic anemia.
Question 3
,A patient with acute tubular necrosis (ATN) is in the maintenance
phase. What is the priority physiologic concern during this phase?
A. Hypovolemia from massive diuresis
B. Hyperkalemia and fluid overload from oliguria
C. Metabolic alkalosis from bicarbonate retention
D. Hypercalcemia from bone breakdown
Answer: B. Hyperkalemia and fluid overload from oliguria
Rationale: During the maintenance (oliguric) phase of ATN, urine output is
markedly reduced, so potassium, fluid, and metabolic acids accumulate,
creating risk for life-threatening hyperkalemia, volume overload, and
metabolic acidosis.
Question 4
Prerenal azotemia is best distinguished from intrinsic renal failure by
which finding?
A. Elevated BUN:creatinine ratio above 20:1 with a low fractional excretion
of sodium
B. Low BUN:creatinine ratio with muddy brown casts
C. Elevated fractional excretion of sodium above 2%
D. Presence of red blood cell casts
Answer: A. Elevated BUN:creatinine ratio above 20:1 with a low
fractional excretion of sodium
Rationale: In prerenal azotemia the kidney tubules are structurally intact and
avidly reabsorb sodium and water in response to decreased perfusion,
producing a high BUN:creatinine ratio and a low fractional excretion of
sodium (<1%). Muddy brown casts and elevated FeNa are characteristic of
intrinsic (tubular) injury.
Question 5
A patient with nephrotic syndrome would be expected to show which
laboratory pattern?
A. Hematuria, hypertension, and red cell casts
B. Massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia
, C. Low urine protein with elevated serum albumin
D. Oliguria with a normal serum lipid profile
Answer: B. Massive proteinuria, hypoalbuminemia, edema, and
hyperlipidemia
Rationale: Nephrotic syndrome results from increased glomerular capillary
permeability to protein, producing heavy proteinuria (>3.5 g/day), which
causes hypoalbuminemia, decreased oncotic pressure and edema, and
compensatory hepatic lipoprotein synthesis leading to hyperlipidemia.
Question 6
Which finding is most characteristic of nephritic syndrome rather than
nephrotic syndrome?
A. Hyperlipidemia
B. Hematuria with red blood cell casts and hypertension
C. Massive proteinuria exceeding 3.5 g/day
D. Lipiduria with fatty casts
Answer: B. Hematuria with red blood cell casts and hypertension
Rationale: Nephritic syndrome reflects glomerular inflammation with
disruption of the capillary wall, allowing red blood cells to enter the urine,
often forming casts, along with hypertension from sodium and water
retention. Heavy proteinuria and hyperlipidemia are hallmarks of nephrotic
syndrome instead.
Question 7
In chronic kidney disease, secondary hyperparathyroidism develops
primarily because of which sequence of events?
A. Decreased phosphate excretion and decreased activation of vitamin D
lead to hypocalcemia, stimulating PTH release
B. Increased vitamin D activation leads to hypercalcemia and PTH
suppression
C. Damaged nephrons overproduce calcitriol, raising serum calcium
D. Decreased PTH receptor sensitivity in bone leads to osteopetrosis
Advanced Pathophysiology
Questions with Answers | Latest update
,Question 1
A patient's GFR is estimated at 45 mL/min/1.73m2 and has remained
stable for over three months. According to KDIGO staging, this
represents which category?
A. CKD Stage 2 (60-89 mL/min)
B. CKD Stage 3a (45-59 mL/min)
C. CKD Stage 4 (15-29 mL/min)
D. CKD Stage 5 (<15 mL/min)
Answer: B. CKD Stage 3a (45-59 mL/min)
Rationale: KDIGO staging classifies CKD by sustained GFR reduction: Stage
3a spans 45-59 mL/min/1.73m2, representing a mild-to-moderate decrease
in kidney function. A GFR of 45 mL/min/1.73m2, persisting over three
months, falls at the upper boundary of Stage 3a.
Question 2
Which mechanism best explains the development of anemia in chronic
kidney disease?
A. Increased erythropoietin production by damaged nephrons
B. Decreased erythropoietin production by peritubular fibroblasts
C. Excessive iron absorption in the duodenum
D. Hemolysis due to uremic toxin accumulation on red cell membranes
Answer: B. Decreased erythropoietin production by peritubular
fibroblasts
Rationale: Peritubular fibroblast-like cells in the kidney normally sense
hypoxia and produce erythropoietin. As nephrons are destroyed in CKD,
these cells are lost or replaced by fibrotic tissue, so erythropoietin synthesis
falls, producing a normocytic, normochromic anemia.
Question 3
,A patient with acute tubular necrosis (ATN) is in the maintenance
phase. What is the priority physiologic concern during this phase?
A. Hypovolemia from massive diuresis
B. Hyperkalemia and fluid overload from oliguria
C. Metabolic alkalosis from bicarbonate retention
D. Hypercalcemia from bone breakdown
Answer: B. Hyperkalemia and fluid overload from oliguria
Rationale: During the maintenance (oliguric) phase of ATN, urine output is
markedly reduced, so potassium, fluid, and metabolic acids accumulate,
creating risk for life-threatening hyperkalemia, volume overload, and
metabolic acidosis.
Question 4
Prerenal azotemia is best distinguished from intrinsic renal failure by
which finding?
A. Elevated BUN:creatinine ratio above 20:1 with a low fractional excretion
of sodium
B. Low BUN:creatinine ratio with muddy brown casts
C. Elevated fractional excretion of sodium above 2%
D. Presence of red blood cell casts
Answer: A. Elevated BUN:creatinine ratio above 20:1 with a low
fractional excretion of sodium
Rationale: In prerenal azotemia the kidney tubules are structurally intact and
avidly reabsorb sodium and water in response to decreased perfusion,
producing a high BUN:creatinine ratio and a low fractional excretion of
sodium (<1%). Muddy brown casts and elevated FeNa are characteristic of
intrinsic (tubular) injury.
Question 5
A patient with nephrotic syndrome would be expected to show which
laboratory pattern?
A. Hematuria, hypertension, and red cell casts
B. Massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia
, C. Low urine protein with elevated serum albumin
D. Oliguria with a normal serum lipid profile
Answer: B. Massive proteinuria, hypoalbuminemia, edema, and
hyperlipidemia
Rationale: Nephrotic syndrome results from increased glomerular capillary
permeability to protein, producing heavy proteinuria (>3.5 g/day), which
causes hypoalbuminemia, decreased oncotic pressure and edema, and
compensatory hepatic lipoprotein synthesis leading to hyperlipidemia.
Question 6
Which finding is most characteristic of nephritic syndrome rather than
nephrotic syndrome?
A. Hyperlipidemia
B. Hematuria with red blood cell casts and hypertension
C. Massive proteinuria exceeding 3.5 g/day
D. Lipiduria with fatty casts
Answer: B. Hematuria with red blood cell casts and hypertension
Rationale: Nephritic syndrome reflects glomerular inflammation with
disruption of the capillary wall, allowing red blood cells to enter the urine,
often forming casts, along with hypertension from sodium and water
retention. Heavy proteinuria and hyperlipidemia are hallmarks of nephrotic
syndrome instead.
Question 7
In chronic kidney disease, secondary hyperparathyroidism develops
primarily because of which sequence of events?
A. Decreased phosphate excretion and decreased activation of vitamin D
lead to hypocalcemia, stimulating PTH release
B. Increased vitamin D activation leads to hypercalcemia and PTH
suppression
C. Damaged nephrons overproduce calcitriol, raising serum calcium
D. Decreased PTH receptor sensitivity in bone leads to osteopetrosis
