Hyperaldosteronism metabolic alkalosis

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

This condition is far less common than chloride responsive metabolic alkalosis and is almost always associated with either an underlying disease (primary hyperaldosteronism, Cushing s syndrome, or Bartter s syndrome) or with excess addition of exogenous base. In these conditions, urine CL will usually be >20 mmol/L. 

Henle (e.g., furosemide, bumetanide, and torsemide) and distal convoluted tubule (thiazides), have most commonly been associated with the generation of metabolic alkalosis. These agents promote the excretion of sodium and potassium almost exclusively in association with chloride, without a proportionate increase in bicarbonate excretion. Collecting duct hydrogen ion secretion is stimulated directly by the increased luminal flow rate and sodium delivery, and indirectly by intravascular volume contraction, which results in secondary hyperaldosteronism. Renal ammoniagenesis may also be stimulated by concomitant hypokalemia, further augmenting net acid excretion. 

Hypokalemia is common in the patient with liver failure who has normal renal function. Poor nutritional intake and vomiting may initiate this disorder. Severe vomiting may lead to volume contraction metabolic alkalosis, with increased renal excretion of potassium. Secondary hyperaldosteronism, seen in the liver failure patient with intravascular depletion, also increases renal excretion of potassium. Loop diuretic therapy causes increased renal excretion of potassium, whereas diarrhea from lactulose therapy increases fecal excretion of potassium. All these conditions can lead to profound hypokalemia. Therefore, potassium requirements in the liver failure patient receiving specialized nutritional support often are increased substantially. 

The urine results are typical of a patient with dehydration and metabolic alkalosis due to vomiting. Aldosterone is being secreted in an attempt to expand his ECF and the patient is conserving sodium despite his hypematraemia. The hyperaldosteronism is promoting potassium loss despite his hypokalaemia and the patient has the classical paradoxical acid urine. 

Primary Hyperaldosteronism Caused by adrenal adenoma which secretes aldosterone. Results in hypertension, hypokalemia, metabolic alkalosis, suppressed renin. 

Conn s disease is primary hyperaldosteronism caused by a rare aldosterone-secreting tumour. Consequently, excessive amounts of potassium and hydrogen ions are lost in the urine resulting in hypoka-laemia and metabolic alkalosis. Secondary hyperaldosteronism due to kidney or liver disease is more common. 

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