Hypokalemia metabolic alkalosis

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. 

Caution in hypocalcemia, hypokalemia, metabolic alkalosis, respiratory alkalosis, Bartter s syndrome (powder for oral suspension contains 1,680 mg or 20 mEq of sodium bicarbonate)... 

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

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. 

Liddle s syndrome is an autosomal dominant disorder that is caused by persistent hyperactivity of the epithelial Na channel. Its symptoms mimic aldosterone excess, but plasma aldosterone levels are actually reduced (pseudoaldosteronism). The disease is characterized by early onset arterial hypertension, hypokalemia, and metabolic alkalosis. 

The findings of hypomagnesemia include muscle weakness, cramps, agitation, confusion, tremor, seizures, ECG changes (increased PR interval, prolonged QRS complex, and increased QT interval), findings of hypocalcemia (see above), refractory hypokalemia (see above), metabolic alkalosis, and digoxin toxicity.42,47,48... 

Metabolic alkalosis is characterized by an increased arterial pH, a primary increase in the HCOf concentration, and a compensatory increase in the PaC02. Patients will always hypoventilate to compensate for metabolic alkalosis—even if it results in profound hypoxemia. For a metabolic alkalosis to persist there must concurrently be a process that elevates serum HC03 concentration (gastric or renal loss of acids) and another that impairs renal HC03 excretion (hypovolemia, hypokalemia, or mineralocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 25-5. 

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. 

It is important to note that, even more than in heart failure, overly aggressive use of diuretics in this setting can be disastrous. Vigorous diuretic therapy can cause marked depletion of intravascular volume, hypokalemia, and metabolic alkalosis. Hepatorenal syndrome and hepatic encephalopathy are the unfortunate consequences of excessive diuretic use in the cirrhotic patient. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Lactic acidosis, respiratory dysfunction, uncompensated metabolic alkalosis, hypocalcemia, hypokalemia, hypercapnia... 

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). 

Conversely, metabolic alkalosis results in hypokalemia as a result of a net loss of hydrogen ion in the serum. In response, the body releases intracellular hydrogen ion into the serum to increase the acidity of the blood in exchange for extracellular potassium ions. This creates a relative deficiency of serum potassium. Serum potassium falls approximately 0.6 mEq/L for each 0.1 unit rise in blood pH. Similarly, this is frequently termed false hypokalemia because there isn t a true deficiency in total body potassium. 

Aggressive diuretic therapy may produce a metabolic alkalosis, and the accompanying hypokalemia may be serious. 

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. 

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