Potassium loss with vomiting

Potassium loss occurs with diarrhoea, vomiting or small bowel fistula, and may be aggravated by diuretic therapy. 

Potassium-rich foods often cannot completely replace potassium associated with chloride losses (vomiting, diuretics, or nasogastric suction) because it is almost entirely coupled to phosphate. Furthermore, increasing dietary intake of these foods may lead to unwanted weight gain. 

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. 

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. 

The glucagon/insulin ratio can rise under certain pathological conditions (i.e., insulin-dependent diabetes). A small percentage of diabetics develop ketoacidosis, a condition that results from the overproduction and underuhlization of ketone bodies. Increased concentrations of p hydmxybutyrate and acetoacetate, which are acids, can cause a drop in the pH of the blood. This acidification, known as acidosis, can impair the ablLity of the heart to contract and result in a loss of consciousness and coma, which, in rare cases, may be fatal. Diabetic ketoacidosis may manifest as abdominal pain, nausea, and vomiting. A subject may hyperventilate (breathe quickly and deeply) to correct acidosis, as described under Sodium, Potassium, and Water in Chapter 10. It is the responsibility of the clinician, when confronted with a subject whose breath smells of acetone or who is hyperventilating, to facilitate prompt treatment. 

Normal faeces contain 60-85% water, and the body loses between 70 and 200 ml of water per day through defecation. In diarrhoea, water loss of up to four times this volume per loose stool occurs, and sodium and potassium alkaline salts are excreted along with it, leading to a fall in plasma pH (acidosis). This can have serious metabolic consequences, particularly in the very young and the elderly. Fluid and electrolyte losses are increased if vomiting also occurs. 

Gastrointestinal symptoms of metabolic acidosis include loss of appetite, nausea, and vomiting. Severe acidosis (pH <7.1) interferes with carbohydrate metabolism and insulin utilization, and results in hyperglycemia. Metabolic acidosis alters potassium homeostasis and contributes to the development of hyperkalemia. The magnimde of the effect on serum potassium depends on the type of acidosis Acidosis caused by mineral acids (e.g., hydrochloric acid) are associated with a greater change in potassium levels than acidosis caused by organic acids (e.g., lactic acidosis), in which the increase in potassium attributable to the acidosis per se is minimal. 

Chronic pulmonary failure may be further complicated by metabolic disturbances tending to metabolic alkalosis or metabolic acidosis. The mechanism leading to alkalosis is not always clear, but among the factors that may influence it are the loss of hydrogen and Cl ions, because of vomiting or because of selective Cl and potassium depletion as a result of undernourishment, and prolonged treatment with diuretics. It is usually assumed that severe respiratory acidosis is always accompanied by metabolic acidosis. This reasoning is based on the fact that when the same CO2 tensions are achieved in the blood in vivo and in vitro,the plasma concentration of bicarbonate for identical pH s is lower in vivo than in vitro. In reality, this bicarbonate deficit seems to result because (I) the buffer curve of the blood CO2 has a lower slope in vivo than in vitro and (2) hyperventilation in vivo leads to lactic acid accumulation in he blood. 

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