Paradoxical Aciduria in Patients of GOO( Gastric Outlet Obstuction) due to CDU ( Chronic Duodenal Ulcer)
Patients with gastric outlet obstruction represent the classic clinical scenario for metabolic alkalosis in which a deficiency of chloride and potassium in ECF is also present. Parietal cells in the stomach mucosa produce gastric fluid that has a high hydrochloric acid concentration. For each proton pumped into gastric fluid, bicarbonate is added to ECF by the parietal cell. Patients who lose large amounts of gastric fluid deplete their ECF of protons and chloride, as well as potassium. Renal function plays a key role in hypochloremic, hypokalemic metabolic alkalosis. In these alkalemic patients urine pH can be lower than 7. Such patients paradoxically produce an acid urine despite having alkalemia because of three phenomena.
1.These patients have lost large amounts of ECF, and consequently the renin-angiotensin-aldosterone hormonal axis is activated. As aldosterone levels increase, patients have an accelerated exchange of tubule sodium for potassium and protons in the DCT of the nephron.
2.A second phenomenon contributing to the paradoxical production of an acidic urine in a patient with alkalemia is depletion of chloride, which has the renal consequence that with less chloride available in the proximal segments of the nephron, there is less capacity to reabsorb sodium with chloride and consequently delivery of sodium ions to the DCT is increased.
3.Finally, loss of potassium in gastric fluid contributes to the paradoxical production of acidic urine in these patients because with less potassium available in the tubule cells of the DCT, the capacity to exchange potassium for a sodium molecule in the tubule fluid is impaired. In the circumstance of hypokalemia, the tubule cells are driven by aldosterone to make greater use of protons as the exchange cation for the sodium transported out of the tubule fluid.