Match each patient's presenting laboratory profile with the most likely underlying pathoph… — USMLE Step 3

Match each patient's presenting laboratory profile with the most likely underlying pathophysiological diagnosis. All patients present with a primary hypokalemic metabolic alkalosis and a normal serum creatinine level.

Serum $K^+$ 2.4 mEq/L, Serum $HCO_3^-$ 35 mEq/L, Urine $Cl^-$ 8 mEq/L, Blood pressure 102/64 mmHgCovert emesis (Extrarenal chloride loss)
Serum $K^+$ 2.7 mEq/L, Serum $HCO_3^-$ 32 mEq/L, Urine $Cl^-$ 65 mEq/L, Urine $Ca^{2+}/Cr$ ratio 0.02, Blood pressure 112/72 mmHgGitelman syndrome (Distal convoluted tubule defect)
Serum $K^+$ 2.6 mEq/L, Serum $HCO_3^-$ 33 mEq/L, Urine $Cl^-$ 72 mEq/L, Urine $Ca^{2+}/Cr$ ratio 0.28, Blood pressure 108/68 mmHgBartter syndrome (Thick ascending limb defect)
Serum $K^+$ 3.0 mEq/L, Serum $HCO_3^-$ 31 mEq/L, Urine $Cl^-$ 58 mEq/L, Plasma Aldosterone/Renin ratio 45, Blood pressure 168/102 mmHgPrimary hyperaldosteronism (Autonomous mineralocorticoid excess)

Answer

The normotensive patient with low urine chloride matches Covert emesis. The hypertensive patient matches Primary hyperaldosteronism. Between the two normotensive salt-wasters, the patient with hypocalciuria matches Gitelman syndrome, and the patient with hypercalciuria matches Bartter syndrome.

The correct matches require a systematic, multi-step interpretation of the laboratory panels. First, blood pressure divides the etiologies: hypertension suggests mineralocorticoid excess, isolating primary hyperaldosteronism. Next, urine chloride separates volume-contracted states attempting to intensely conserve chloride (covert emesis,

< 20

mEq/L) from renal salt-wasting states (

> 20

mEq/L). Finally, urine calcium effectively differentiates the remaining tubulopathies: Bartter syndrome causes hypercalciuria (like loop diuretics), whereas Gitelman syndrome causes hypocalciuria (like thiazide diuretics).

Step-by-Step Solution

Analyze blood pressure to categorize the etiologies of hypokalemic metabolic alkalosis.

Three patients are normotensive/hypotensive; one patient is severely hypertensive.

Hypertension isolated mineralocorticoid excess states (like primary hyperaldosteronism) from volume-contracted states or tubulopathies.

Evaluate urine chloride in the normotensive patients.

One patient has a urine

Cl^-

of 8 mEq/L; the other two have urine

Cl^-

> 60 mEq/L.

Urine chloride differentiates extrarenal chloride loss/volume depletion (saline-responsive,

< 20

mEq/L) from intrinsic renal salt-wasting defects (saline-resistant,

> 20

mEq/L).

Differentiate the two saline-resistant normotensive tubulopathies using the urine calcium-to-creatinine ratio.

One patient has profound hypocalciuria (ratio 0.02); the other has hypercalciuria (ratio 0.28).

Gitelman syndrome (DCT defect) mimics thiazides by increasing calcium reabsorption. Bartter syndrome (TAL defect) mimics loop diuretics by wasting calcium.

Key Concept

Algorithm for evaluating hypokalemic metabolic alkalosis using blood pressure, urine chloride, and urine calcium.

Estimated Time:2m 30s

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