A 32-year-old woman is brought to the emergency department due to weakness, tingling, and numbness in her extremities. She takes no medications. Blood pressure is 110/70 mm Hg, pulse is 90/min, and respirations are 14/min. Physical examination is unremarkable. Laboratory results are as follows: Which of the following is the most likely cause of this patient's condition?

Question

A 32-year-old woman is brought to the emergency department due to weakness, tingling, and numbness in her extremities.  She takes no medications.  Blood pressure is 110/70 mm Hg, pulse is 90/min, and respirations are 14/min.  Physical examination is unremarkable.  Laboratory results are as follows:  Which of the following is the most likely cause of this patient's condition?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d4ed_9742_bc81_cd09bcb2465c_MD0003_00 This patient's pH >7.45 and serum HCO₃^- >24 mEq/L is consistent with primary metabolic alkalosis. Measurement of urine chloride can be helpful in the differential diagnosis of metabolic alkalosis because adequate Cl^- delivery to the distal renal tubules is necessary for excretion of HCO₃^-, which means that total body chloride depletion often plays an important role in the initiation and maintenance of metabolic alkalosis. ₃ ^- ^- excretion of HCO₃^- ₃ ^- Etiologies of metabolic alkalosis that involve total body chloride depletion are characterized by hypovolemia and will demonstrate low urine chloride (<20 mEq/L). These types of metabolic alkalosis are considered saline responsive because repletion of Cl^- with normal saline will normalize renal HCO₃^- excretion and correct the alkalosis. Such etiologies include: ^- ₃ ^- Nasogastric suctioning or severe vomiting, which involves loss of H⁺ and Cl^- (ie, hydrochloric acid) from the stomach. Loop or thiazide diuretic overuse, which involves loss of Cl^- and retention of HCO₃^- by the kidneys, eventually leading to total body chloride depletion (as well as hypovolemia). Of note, although these patients are overall chloride depleted, urine chloride may be high in the setting of recent diuretic ingestion (eg, within several hours of measurement). Etiologies of metabolic alkalosis in the absence of chloride depletion include conditions of mineralocorticoid excess, such as primary hyperaldosteronism (Choice C). These patients are typically hypervolemic, and the metabolic alkalosis is primarily driven by aldosterone-mediated H⁺ loss from the kidneys. High urine chloride (>20 mEq/L) is present, and the metabolic alkalosis does not correct with Cl^- repletion (saline unresponsive). ⁺ ^- Autosomal recessive renal tubular channelopathies represent a special case. Bartter syndrome mimics loop diuretic overuse and Gitelman syndrome mimics thiazide diuretic overuse. Although affected patients are chloride depleted, high urine chloride is present because the defect persistently impairs renal Cl^- reabsorption. The metabolic alkalosis is saline unresponsive, and kidney transplantation is the only definitive treatment. ^- (Choice A) Chronic hypoventilation (eg, obesity hypoventilation syndrome) causes a chronic respiratory acidosis. Low pH <7.35 is expected with high PaCO₂ and a compensatory elevation in HCO₃^-. ₂ ₃ ^- (Choices B and E) Persistent diarrhea and renal tubular acidosis are typical causes of nonanion gap metabolic acidosis. Low pH is expected with low HCO₃^- and a compensatory decrease in PaCO₂. ₃ ^- ₂ Educational objective: Chloride is essential for renal excretion of HCO₃^- and total body chloride depletion often plays an important role in metabolic alkalosis. Etiologies of metabolic alkalosis characterized by chloride depletion include severe vomiting and diuretic overuse. These etiologies demonstrate low urine chloride (<20 mEq/L), and the alkalosis corrects with Cl^- repletion (saline responsive). ₃ ^- ^- References: Metabolic alkalosis. (http://www.ncbi.nlm.nih.gov/pubmed/9294840) Approach to metabolic alkalosis. (http://www.ncbi.nlm.nih.gov/pubmed/24766943)

A 32-Year-Old Woman Is Brought to the Emergency Department Due