A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 54-year-old woman comes to the physician with abdominal distention and mild diffuse abdominal discomfort. She has not had nausea, vomiting, fever, or chills. She was diagnosed with alcoholic liver cirrhosis 2 years ago. Examination shows a protruding, distended abdomen that is dull to percussion with a positive fluid wave. Ultrasonography shows mild to moderate ascites. Appropriate treatment of the patient's condition is started. Four days later, the patient experiences palpitations and chest pain at home. She is brought to the emergency department, where her temperature is 37.3°C (99.1°F), pulse is 182/min, respirations are 18/min, and blood pressure is 82/50 mm Hg. An ECG shows ventricular tachycardia. Initial laboratory studies show:
Serum
Na+ 131 mEq/L
K+ 2.9 mEq/L
Cl- 92 mEq/L
Bicarbonate 34 mEq/L
Urea nitrogen 42 mg/dL
Creatinine 4.8 mg/dL
Glucose 90 mg/dL
Ca2+ 8.1 mg/dL
Mg2+ 1.5 mg/dL
Phosphate 4.7 mg/dL
Arterial Blood Gas
pH 7.52
pCO2 45 mm Hg
pO2 90.2 mm Hg
She is successfully cardioverted to normal sinus rhythm. Which of the following treatments is most likely responsible for this patient's presentation?"
-
A
HydrochlorothiazideIncorrect. HCTZ can cause similar electrolyte abnormalities but is not the standard first-line therapy for cirrhotic ascites; furosemide is.
-
B
FurosemideCorrect. Furosemide (a loop diuretic) is standard ascites treatment and produces the characteristic hypokalemic hypochloremic metabolic alkalosis with volume depletion and ventricular arrhythmias seen here.
-
C
LisinoprilIncorrect. Lisinopril causes HYPERkalemia and type 4 RTA (metabolic acidosis), the opposite electrolyte pattern.
-
D
MannitolIncorrect. Mannitol causes hypernatremia and hyperosmolar dehydration, not hypokalemic metabolic alkalosis.
-
E
SpironolactoneIncorrect. Spironolactone is the first-line diuretic for cirrhotic ascites but causes HYPERkalemia and metabolic acidosis - the opposite electrolyte pattern from this patient's hypokalemic metabolic alkalosis.
↑ Tap an answer to reveal the reasoning
Answer: B. A patient with cirrhosis and ascites who, 4 days after starting therapy for her ascites, develops electrolyte derangements and ventricular tachycardia. Decode the labs:
- Hyponatremia (Na 131): mild, common in cirrhosis.
- HYPOKALEMIA (K 2.9): significant.
- HYPOCHLOREMIA (Cl 92): low.
- HCO3 34: METABOLIC ALKALOSIS.
- BUN 42, Cr 4.8: pre-renal AKI from volume depletion.
- Glucose normal.
- Hypocalcemia/hypomagnesemia: borderline low Ca and Mg, contributing to the arrhythmia.
- ABG: pH 7.52 (alkalemia), pCO2 45 (slight compensatory hypoventilation), confirming METABOLIC ALKALOSIS.
The constellation of hypokalemia, hypochloremic metabolic alkalosis, hyponatremia, volume depletion (AKI), and torsades-prone hypomagnesemia is the classic presentation of LOOP DIURETIC TOXICITY - here, FUROSEMIDE used for ascites management.
Furosemide mechanism: inhibits Na-K-2Cl cotransporter in thick ascending limb, causing loss of Na+, K+, Cl-, H+, Ca2+, and Mg2+. Excessive diuresis causes volume contraction, hypokalemia, metabolic alkalosis (contraction alkalosis plus H+ loss in collecting duct from increased aldosterone), and dangerous electrolyte derangements predisposing to torsades and ventricular arrhythmias.
Distinguish from:
- Hydrochlorothiazide (HCTZ): also causes hypokalemia, hyponatremia, and metabolic alkalosis but is NOT first-line for cirrhotic ascites (typically furosemide + spironolactone is used at 40:100 ratio).
- Lisinopril (ACEI): causes HYPERkalemia and metabolic acidosis (type 4 RTA), opposite of this pattern.
- Mannitol: causes hypernatremia and hyperosmolar state, not this pattern.
In cirrhotic ascites management, furosemide is typically combined with spironolactone to prevent the hypokalemia that occurs with furosemide alone - failing to add spironolactone (as appears here) explains the severe hypokalemia.
**Why each option:**
**A.** HCTZ can cause similar electrolyte abnormalities but is not the standard first-line therapy for cirrhotic ascites; furosemide is.
**B.** Correct. Furosemide (a loop diuretic) is standard ascites treatment and produces the characteristic hypokalemic hypochloremic metabolic alkalosis with volume depletion and ventricular arrhythmias seen here.
**C.** Lisinopril causes HYPERkalemia and type 4 RTA (metabolic acidosis), the opposite electrolyte pattern.
**D.** Mannitol causes hypernatremia and hyperosmolar dehydration, not hypokalemic metabolic alkalosis.