BIOD 331 PATHOPHYSIOLOGY EXAM 7 EXAM 2026–2027||quESTIOnS
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SECTION 1: RENAL PATHOPHYSIOLOGY (QUESTIONS 1-15)
Question 1
A patient with acute kidney injury (AKI) has a urine output of 20 mL/hour, blood pressure of 90/60
mmHg, and heart rate of 110 beats per minute. The patient has a history of severe diarrhea for 3
days. Which type of AKI is most likely?
A) Prerenal AKI (hypovolemia)
B) Intrinsic (intrarenal) AKI (acute tubular necrosis)
C) Postrenal AKI (obstruction)
D) Chronic kidney disease (CKD)
Answer: A) Prerenal AKI (hypovolemia)
Rationale: Prerenal AKI is caused by decreased renal perfusion due to hypovolemia (diarrhea,
vomiting, hemorrhage, burns), decreased cardiac output (heart failure), or decreased systemic
vascular resistance (sepsis). The patient has hypovolemia (severe diarrhea) with signs of
hypovolemic shock (hypotension, tachycardia, oliguria). Prerenal AKI is reversible with fluid
resuscitation. Intrinsic AKI (B) (acute tubular necrosis, ATN) occurs after prolonged prerenal state
or nephrotoxins. Postrenal AKI (C) is caused by obstruction (BPH, stones, tumor). CKD (D) is
chronic (>3 months).
Question 2
A patient with acute kidney injury (AKI) has a serum potassium level of 6.8 mEq/L (normal 3.5-5.0).
Which EKG finding is expected?
A) Tall, peaked T waves
B) Flat T waves
C) U waves
,D) Prolonged QT interval
Answer: A) Tall, peaked T waves
Rationale: Hyperkalemia (elevated potassium) causes tall, peaked (tented) T waves as an early
sign. As potassium rises (>6.5 mEq/L): widened QRS, prolonged PR interval, loss of P waves, sine
wave pattern, and asystole. Flat T waves (B) and U waves (C) are seen in hypokalemia. Prolonged
QT interval (D) is seen in hypocalcemia, hypomagnesemia, and certain medications. Treatment of
hyperkalemia includes IV calcium gluconate (stabilizes cardiac membrane), insulin with dextrose
(shifts potassium into cells), albuterol, sodium polystyrene sulfonate (Kayexalate), and
hemodialysis.
Question 3
A patient with chronic kidney disease (CKD) stage 5 (eGFR <15 mL/min/1.73 m2) has a serum
phosphate level of 7.5 mg/dL (normal 2.5-4.5). Which complication is directly related to
hyperphosphatemia?
A) Hypocalcemia and secondary hyperparathyroidism
B) Hypercalcemia
C) Hyponatremia
D) Hypokalemia
Answer: A) Hypocalcemia and secondary hyperparathyroidism
Rationale: In CKD, phosphate excretion is impaired, leading to hyperphosphatemia. Elevated
phosphate binds to calcium, forming calcium-phosphate complexes, which lowers ionized
calcium (hypocalcemia). Hypocalcemia stimulates parathyroid hormone (PTH) secretion
(secondary hyperparathyroidism), leading to renal osteodystrophy (bone disease). Treatment
includes dietary phosphate restriction, phosphate binders (calcium acetate, sevelamer, lanthanum
carbonate), and dialysis. Hypercalcemia (B) is not associated; calcitriol (active vitamin D)
deficiency also contributes to hypocalcemia.
Question 4
A patient with chronic kidney disease (CKD) has a hemoglobin level of 8.5 g/dL (normal 12-16).
The mechanism of anemia in CKD is:
A) Decreased erythropoietin (EPO) production by the kidneys
, B) Iron deficiency (from blood loss)
C) Vitamin B12 deficiency
D) Folate deficiency
Answer: A) Decreased erythropoietin (EPO) production by the kidneys
Rationale: The kidneys produce erythropoietin (EPO), which stimulates red blood cell production
in the bone marrow. In CKD, EPO production is decreased, leading to normocytic, normochromic
anemia. Treatment includes erythropoiesis-stimulating agents (ESAs) (epoetin alfa, darbepoetin
alfa) and iron supplementation. Iron deficiency (B) may also occur in CKD (due to blood loss from
dialysis or GI bleeding), but EPO deficiency is the primary mechanism. Vitamin B12 (C) and folate
(D) deficiencies are not specific to CKD.
Question 5
A patient with nephrotic syndrome has proteinuria >3.5 g/24 hours, hypoalbuminemia (albumin 2.0
g/dL), and edema. The mechanism of edema in nephrotic syndrome is:
A) Decreased plasma oncotic pressure due to hypoalbuminemia
B) Increased hydrostatic pressure due to heart failure
C) Lymphatic obstruction
D) Increased capillary permeability
Answer: A) Decreased plasma oncotic pressure due to hypoalbuminemia
Rationale: Nephrotic syndrome causes massive urinary protein loss, leading to
hypoalbuminemia (low albumin). Reduced plasma oncotic pressure decreases the force that
retains fluid within capillaries, causing fluid to shift into the interstitial space → edema.
Additionally, primary renal sodium retention (via ENaC activation) contributes to edema. Increased
hydrostatic pressure (B) is seen in heart failure. Lymphatic obstruction (C) causes lymphedema.
Increased capillary permeability (D) occurs in inflammation (e.g., ARDS, sepsis). Common causes
of nephrotic syndrome include minimal change disease (most common in children), membranous
nephropathy, FSGS, and diabetic nephropathy.
Question 6
A patient with acute post-streptococcal glomerulonephritis presents with tea-colored urine,
hypertension, periorbital edema, and oliguria. The underlying pathophysiology is:
AnD AnSwErS wITH rATIOnALES/GrADED A+/2026 uPDATE/100%
cOrrEcT /InSTAnT DOwnLOAD
SECTION 1: RENAL PATHOPHYSIOLOGY (QUESTIONS 1-15)
Question 1
A patient with acute kidney injury (AKI) has a urine output of 20 mL/hour, blood pressure of 90/60
mmHg, and heart rate of 110 beats per minute. The patient has a history of severe diarrhea for 3
days. Which type of AKI is most likely?
A) Prerenal AKI (hypovolemia)
B) Intrinsic (intrarenal) AKI (acute tubular necrosis)
C) Postrenal AKI (obstruction)
D) Chronic kidney disease (CKD)
Answer: A) Prerenal AKI (hypovolemia)
Rationale: Prerenal AKI is caused by decreased renal perfusion due to hypovolemia (diarrhea,
vomiting, hemorrhage, burns), decreased cardiac output (heart failure), or decreased systemic
vascular resistance (sepsis). The patient has hypovolemia (severe diarrhea) with signs of
hypovolemic shock (hypotension, tachycardia, oliguria). Prerenal AKI is reversible with fluid
resuscitation. Intrinsic AKI (B) (acute tubular necrosis, ATN) occurs after prolonged prerenal state
or nephrotoxins. Postrenal AKI (C) is caused by obstruction (BPH, stones, tumor). CKD (D) is
chronic (>3 months).
Question 2
A patient with acute kidney injury (AKI) has a serum potassium level of 6.8 mEq/L (normal 3.5-5.0).
Which EKG finding is expected?
A) Tall, peaked T waves
B) Flat T waves
C) U waves
,D) Prolonged QT interval
Answer: A) Tall, peaked T waves
Rationale: Hyperkalemia (elevated potassium) causes tall, peaked (tented) T waves as an early
sign. As potassium rises (>6.5 mEq/L): widened QRS, prolonged PR interval, loss of P waves, sine
wave pattern, and asystole. Flat T waves (B) and U waves (C) are seen in hypokalemia. Prolonged
QT interval (D) is seen in hypocalcemia, hypomagnesemia, and certain medications. Treatment of
hyperkalemia includes IV calcium gluconate (stabilizes cardiac membrane), insulin with dextrose
(shifts potassium into cells), albuterol, sodium polystyrene sulfonate (Kayexalate), and
hemodialysis.
Question 3
A patient with chronic kidney disease (CKD) stage 5 (eGFR <15 mL/min/1.73 m2) has a serum
phosphate level of 7.5 mg/dL (normal 2.5-4.5). Which complication is directly related to
hyperphosphatemia?
A) Hypocalcemia and secondary hyperparathyroidism
B) Hypercalcemia
C) Hyponatremia
D) Hypokalemia
Answer: A) Hypocalcemia and secondary hyperparathyroidism
Rationale: In CKD, phosphate excretion is impaired, leading to hyperphosphatemia. Elevated
phosphate binds to calcium, forming calcium-phosphate complexes, which lowers ionized
calcium (hypocalcemia). Hypocalcemia stimulates parathyroid hormone (PTH) secretion
(secondary hyperparathyroidism), leading to renal osteodystrophy (bone disease). Treatment
includes dietary phosphate restriction, phosphate binders (calcium acetate, sevelamer, lanthanum
carbonate), and dialysis. Hypercalcemia (B) is not associated; calcitriol (active vitamin D)
deficiency also contributes to hypocalcemia.
Question 4
A patient with chronic kidney disease (CKD) has a hemoglobin level of 8.5 g/dL (normal 12-16).
The mechanism of anemia in CKD is:
A) Decreased erythropoietin (EPO) production by the kidneys
, B) Iron deficiency (from blood loss)
C) Vitamin B12 deficiency
D) Folate deficiency
Answer: A) Decreased erythropoietin (EPO) production by the kidneys
Rationale: The kidneys produce erythropoietin (EPO), which stimulates red blood cell production
in the bone marrow. In CKD, EPO production is decreased, leading to normocytic, normochromic
anemia. Treatment includes erythropoiesis-stimulating agents (ESAs) (epoetin alfa, darbepoetin
alfa) and iron supplementation. Iron deficiency (B) may also occur in CKD (due to blood loss from
dialysis or GI bleeding), but EPO deficiency is the primary mechanism. Vitamin B12 (C) and folate
(D) deficiencies are not specific to CKD.
Question 5
A patient with nephrotic syndrome has proteinuria >3.5 g/24 hours, hypoalbuminemia (albumin 2.0
g/dL), and edema. The mechanism of edema in nephrotic syndrome is:
A) Decreased plasma oncotic pressure due to hypoalbuminemia
B) Increased hydrostatic pressure due to heart failure
C) Lymphatic obstruction
D) Increased capillary permeability
Answer: A) Decreased plasma oncotic pressure due to hypoalbuminemia
Rationale: Nephrotic syndrome causes massive urinary protein loss, leading to
hypoalbuminemia (low albumin). Reduced plasma oncotic pressure decreases the force that
retains fluid within capillaries, causing fluid to shift into the interstitial space → edema.
Additionally, primary renal sodium retention (via ENaC activation) contributes to edema. Increased
hydrostatic pressure (B) is seen in heart failure. Lymphatic obstruction (C) causes lymphedema.
Increased capillary permeability (D) occurs in inflammation (e.g., ARDS, sepsis). Common causes
of nephrotic syndrome include minimal change disease (most common in children), membranous
nephropathy, FSGS, and diabetic nephropathy.
Question 6
A patient with acute post-streptococcal glomerulonephritis presents with tea-colored urine,
hypertension, periorbital edema, and oliguria. The underlying pathophysiology is:
