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insulin deficiency

Potassium, the chief intracellular cation, plays a key role in a variety of mammalian biochemical processes. Total body potassium content averages 50 mEq/kg of body weight or approximately 3500 mEq in total body stores. Hypokalemia may arise from redistribution of extracellular potassium into intracellular sites, such as occurs with high-dose insulin and alkalosis, or as a result of losses to total body potassium, such as occurs with villous adenomas of the rectum, mannitol administration, and aldosteronism. Hypokalemia may be particularly dangerous if respiratory alkalosis is present. In this situation, cardiac muscle sensitivity is increased, especially in the presence of digitalis, and skeletal muscle and nervous tissue excitability are decreased. In an adult, a serum potassium level of 3.0 mEq/L in the absence of acid/base disturbance usually represents a total body deficit of 100 to 200 mEq of potassium. Each additional 1.0 mEq/L decrease of plasma potassium concentration reflects an additional deficit of 200 to 400 mEq. EKG changes associated with hypokalemia include depression of ST segments, flattening of T waves, and prominent U waves. EKG changes may be evident when the plasma concentration falls below 3 mEq/L and usually indicate a potassium deficit of at least 500 mEq. The presence of hypokalemic myocardial irritability, especially when manifest as identifiable EKG alterations, is associated with significantly increased anesthetic and operative risk. Preoperative correction of the potassium deficit is necessary in virtually all circumstances, regardless of the operative imperatives. Serum sodium irregularities frequently accompany potassium concentration disorders, particularly when the effects of the primary pathology are systemic, such as is the case with hyperaldosteronism. Although mild hyponatremia may on occasion be associated with villous adenoma of the rectum, potassium is the primary electrolyte constituent of the mucus secreted by the tumor and hypokalemia is usually the sole electrolyte derangement.
Primary aldosteronism (hyperaldosteronism) is caused by spontaneous increased production of aldosterone by the adrenal glomerulosa cells. It is characterized by hypertension and hypokalemia with suppression of plasma renin activity. Increased aldosterone leads to sodium retention and expansion of the extracellular fluid volume, causing renal juxtaglomerular cells and the macula densa to stop renin production and results in hypertension. Both potassium and hydrogen ion are excreted in the urine in exchange for sodium, resulting in hypokalemia and alkalosis. Glucose intolerance may accompany significant potassium depletion. The symptoms and signs of primary aldosteronism are nonspecific and include fatigue, weakness, and nocturia. With severe potassium depletion, patients may develop increased thirst, polyuria, and paresthesias. Hypertension is moderate to severe and may be refractory to standard medical management. The principal causes of primary aldosteronism are aldosterone-producing adenomas (60%) and idiopathic hyperaldosteronism (40%) from bilateral adrenal cortical hyperplasia. In contrast, secondary hyperaldosteronism is a physiologic response of the renin-angiotensin system to decreased renal perfusion. The adrenal cortex functions normally and secretes aldosterone in response to the elevated plasma renin and angiotensin caused by conditions such as renal artery stenosis, cirrhosis, congestive heart failure, and pregnancy. Secondary hyperaldosteronism responds to treatment of the underlying cause.