Hypokalemia metabolic alkalosis with

Aldosterone and other steroids with mineralocorticoid properties promote the reabsorption of sodium from the distal part of the distal convoluted tubule and from the cortical collecting renal tubules, loosely coupled to the excretion of potassium and hydrogen ion. Sodium reabsorption in the sweat and salivary glands, gastrointestinal mucosa, and across cell membranes in general is also increased. Excessive levels of aldosterone produced by tumors or overdosage with synthetic mineralocorticoids lead to hypokalemia, metabolic alkalosis, increased plasma volume, and hypertension. 

Use with caution in Bartter s syndrome, hypocalcemia, hypokalemia, metabolic alkalosis (powder for oral snspension contains 1,680 mg (20 mEq of sodium bicarbonate). 

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 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. 

Patients with metabolic alkalosis rarely have symptoms attributable to alkalemia. Rather, complaints are usually related to volume depletion (muscle cramps, positional dizziness, and weakness) or to hypokalemia (muscle weakness, polyuria, and polydipsia). 

No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

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. 

Mineralocorticoid excess also plays a significant role in the maintenance of metabolic alkalosis. In patients with volume-responsive metabolic alkalosis, intravascular volume depletion stimulates aldosterone secretion. As discussed earlier, excess mineralocorticoid activity may also underlie the generation of metabolic alkalosis. In either situation, the increased mineralocorticoid effect stimulates collecting duct H+ secretion. Metabolic alkalosis may also be maintained by persistent hypokalemia. Hypokalemia has a multitude of effects on renal acid-base homeostasis, enhancing proximal tubular bicarbonate reabsorption, stimulating ammoniagenesis and increasing distal tubular H secretion. ... 

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. 

The side effects of diuretics are discussed in Chapter 28. With regard to diuretic use in heart failure, the most important adverse sequelae of diuretics are electrolyte abnormalities, including hyponatremia, hypokalemia, and hypochloremic metabolic alkalosis. Both hypokalemia and renal wasting can be limited by administration of oral KCl supplements or a K -sparing diuretic. 

Most clinical cases of secondary aldosteronism are associated with hypertension or edema. Of course, in hypertension. Starling s law still applies in edema, it does not apply. In either case, persistent hyperaldosteronemia results in sodium retention, which expands the volume of the body fluid by promoting water retention. In hypertension, the expansion concerns mainly the blood volume, and hypertension is aggravated. In edema, the expansion mainly affects the extracellular fluid, and edema is exacerbated. Persistent hyperaldosteronemia in both hypertension and edema leads to hypokalemia with muscle weakness and even paralysis, polyuria, and metabolic alkalosis [33] (see Fig. 9-13). 

Auestad et al., 2003). In 1978 and 1979, two soy-based formulas were released that contained markedly decreased chloride content. The result was a large number of cases of what was termed the chloride deficiency syndrome diagnosed between 1 and 6 months of age (Roy, 1984). These infants presented with failure to thrive, lethargy, muscular weakness, and loss of appetite. Laboratory analysis revealed metabolic alkalosis, hypochloremia, hypokalemia, and hyponatremia. Nine- and 10-year follow-up of some of these infants showed no measurable deficits in cognitive development (Willoughby et al., 1990). 

A 39-year-old man with suspected urinary tract infection received amikacin and after 4 days he developed severe renal tubular dysfunction resulting in refractory hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and polyuria. This constellation of biochemical abnormalities mimic Type 5 Bart-ter s syndrome (activating mutation of the calcium sensing receptor in the thick ascending loop of Henle and the distal tubule). Laboratory values returned to normal 15 days after discontinuation of amikacin... 

Acid-base and electrolyte balance High therapeutic dose especially when used in rheumatic fever, stimulates respiration and causes respiratory alkalosis. Reduction in bicarbonate and potassium level reduces the buffering capacity of the extracellular and intracellular fluid. Hypokalemia may lead to dehydration and hypernatremia. They also interfere with carbohydrate metabolism resulting in accumulation of pyruvic acid and lactic acid. 

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