Vomiting is the most likely cause of this patient's hypokalemia. She presents with hypokalemic metabolic alkalosis with extracellular volume depletion. Hypokalemia, defined as a serum potassium concentration <3.5 mEq/L (3.5 mmol/L), can be life-threatening when severe. Patients usually have minimal symptoms unless serum potassium levels are <3.0 mEq/L (3.0 mmol/L); symptoms correlate with the rapidity of the decrease, ranging from generalized weakness and malaise to paralysis, depending on the serum potassium level. This patient's history (generalized weakness and lightheadedness), physical examination findings (volume contraction and dental caries), and urine electrolyte levels are most consistent with vomiting from bulimia nervosa. Vomiting results in loss of hydrogen chloride and fluid from gastric secretions, and, if persistent, results in volume contraction. Hypovolemia activates the renin-angiotensin system with an increase in sodium-hydrogen exchange and increased bicarbonate reabsorption in the proximal tubule due to increased luminal hydrogen ion, and exacerbated by decreased chloride available for reabsorption with sodium. Increased aldosterone secretion stimulates sodium-potassium exchange in the distal tubule. The urine electrolytes in this patient reflect these physiologic changes. With volume depletion, the urine sodium concentration is generally low (<20 mEq/L [20 mmol/L]) due to the kidney's conservation of sodium. However, in this case, excess filtered bicarbonate associated with the alkalosis is excreted through the renal tubule, and sodium is lost in the urine as an obligatory cation with bicarbonate necessary to maintain electroneutrality; this results in increased urine sodium excretion. Because of this, the urine chloride is a more accurate determination of volume status than the urine sodium in metabolic alkalosis. The urine chloride concentration is low (<20 mEq/L [20 mmol/L]), reflecting gastrointestinal losses and prolonged volume contraction that leads to avid reabsorption of chloride with sodium. The urine potassium concentration in this patient is elevated (>40 mEq/L [40 mmol/L]) due to increased aldosterone production and distal nephron bicarbonate delivery that promote potassium loss through the kidney. Treatment of these abnormalities is to treat the vomiting and provide volume expansion with normal saline and potassium replacement, which will reverse these changes and correct the acid-base and electrolyte abnormalities.

Bartter syndrome mimics the effect of a loop diuretic and is accompanied by increased urine sodium (>40 mEq/L [40 mmol/L]), urine potassium (>40 mEq/L [40 mmol/L]), and chloride excretion (>40 mEq/L [40 mmol/L]).

Hypokalemic periodic paralysis is due to a shift of potassium into cells and is not associated with a metabolic alkalosis; furthermore, urine potassium would be low (<20 mEq/L [20 mmol/L]) and not increased.

Hypokalemia from Sjögren syndrome occurs in the setting of renal tubular acidosis, and a hyperchloremic metabolic acidosis would occur, which is not seen in this patient.