A 68-year-old man comes to the emergency department due to a 1-week history of increasing leg and abdominal swelling. The patient has a history of pulmonary hypertension and cor pulmonale from advanced chronic obstructive pulmonary disease. Other medical conditions include hypertension and gout. Physical examination shows scattered rhonchi, prolonged expiratory phase of expiration, mild ascites, and extensive edema of the abdominal wall and lower extremities. The patient is hospitalized and intravenous loop diuretic therapy is begun. Two days later, acetazolamide is added to his treatment regimen. Which of the following most likely prompted the additional therapy in this patient?

Question

A 68-year-old man comes to the emergency department due to a 1-week history of increasing leg and abdominal swelling.  The patient has a history of pulmonary hypertension and cor pulmonale from advanced chronic obstructive pulmonary disease.  Other medical conditions include hypertension and gout.  Physical examination shows scattered rhonchi, prolonged expiratory phase of expiration, mild ascites, and extensive edema of the abdominal wall and lower extremities.  The patient is hospitalized and intravenous loop diuretic therapy is begun.  Two days later, acetazolamide is added to his treatment regimen.  Which of the following most likely prompted the additional therapy in this patient?

Quizplus · Accepted Answer

11ec160b_3c67_7ff0_9249_5915114c53ab_MD0001_00 Loop diuretics (eg, furosemide) inhibit the Na⁺-K⁺-2Cl⁻ transporter in the ascending loop of Henle to stimulate potent excretion of Na⁺ and water and reduce total body fluid volume. Electrolyte abnormalities are common with the use of loop diuretics; metabolic alkalosis occurs due to the following mechanisms: This metabolic alkalosis can have important implications because it stimulates compensatory hypoventilation that may hinder weaning from mechanical ventilation in critically ill patients. Carbonic anhydrase inhibitors (eg, acetazolamide) help offset the metabolic alkalosis; these drugs inhibit the reabsorption of sodium bicarbonate (NaHCO₃) in the proximal tubule, leading to increased HCO₃⁻ excretion. The metabolic acidosis that is generated reduces blood alkalinity to help normalize pH. (Choice A) Loop diuretics increase renal uric acid reabsorption and are associated with hyperuricemia (increased blood uric acid level) and increased risk of gout. Probenecid blocks proximal tubule uric acid reabsorption and may reduce loop diuretic-associated hyperuricemia. (Choice B) Hypokalemia is a common adverse effect of loop diuretics. The addition of a potassium-sparing diuretic (eg, spironolactone) can help offset the hypokalemia by reducing K⁺ secretion in the collecting tubules. Potassium-sparing diuretics also encourage a mild metabolic acidosis, but less so than carbonic anhydrase inhibitors. (Choice C) Carbonic anhydrase inhibitors have only a weak diuretic effect because most of the Na⁺ blocked from reabsorption in the proximal tubules is reabsorbed more distally. Thiazide diuretics (eg, metolazone) act distally in the nephron and potentiate the diuretic effect of loop diuretics by blocking the reabsorption of increased Na⁺ delivered to the distal convoluted tubules, producing a profound synergistic diuresis. (Choice E) Loop diuretics can cause significant intravascular volume depletion with reduced renal perfusion and consequent renal retention of urea (evidenced by blood urea nitrogen/creatinine ratio >20). This prerenal azotemia is improved by temporary cessation of diuretics to allow intravascular volume to reaccumulate, but it is not improved by carbonic anhydrase inhibitor therapy. Educational objective: Carbonic anhydrase inhibitors (eg, acetazolamide) block the reabsorption of sodium bicarbonate in the proximal tubule to cause metabolic acidosis. These drugs can be used to help offset the metabolic alkalosis caused by loop diuretics.

A 68-Year-Old Man Comes to the Emergency Department Due to a 1-Week