Mixed acid-base disturbances

Important Causes of Mixed Acid-Base Disturbances ... 

Acid-base disturbances frequently coexist with two or more simple disorders (Table 39-2). In these settings, blood pH is either severely depressed (e.g., a patient with metabolic acidosis and respiratory acidosis) or normal. Both plasma HCOj and pH may be within normal limits when metabolic alkalosis and metabolic ketoacidosis coexist, as in a patient with diabetic ketoacidosis who is vomiting. In this situation, an elevated anion gap may be the initial abnormality that can be detected in the underlying mixed acid-base disturbance. 

Acid-base disturbance. Alkalosis or mixed alkalosis/ acidosis need no specific treatment. Metabolic acidosis is treated with sodium bicarbonate, which alkalinises the urine and accelerates the removal of salicylate in the urine (see p. 97). 

The primary acid-base disturbance observed with salicylate overdosage depends on age and severity of intoxication. Respiratory alkalosis predominates in children over age 4 and in adults, except in very severe cases that may progress through a mixed respiratory alkalosis-metabolic acidosis to metabolic acidosis. In 97 adult patients who had plasma salicylate concentrations greater than 700mg/L, 19% were found to have respiratory alkalosis, 61% had combined res-... 

Boron oxide particles were incorporated to silicone rubber-based mixes containing fumed silica (reinforcing filler) and reference mineral fillers - aluminum hydroxide, wollastonite, calcined kaolin, mica (phlogipite) and surface modified montmorillonite with dimethyl-dihydrogenatedtal-low quaternary ammonium salt. Acidic character of boron oxide, which can disturb the peroxide curing process, was compensated by addition of magnesium oxide. The influence of boron oxide particles on properties of composites was determined and mechanism of their ceramization process studied. 

Cysteamine has been shown to be effective in removing the lysosomal cystine in cystinosis. The weak base cysteamine tends to distribute within the acidic lysosomal space. A mixed disulfide of cysteamine and cysteine is formed by disulfide interchange and is transported out of the lysosomal space by the carrier for lysine. In cytosol the mixed disulfide is cleaved by reduced glutathione. Early introduction of cysteamine therapy can protect the kidneys from further progression of glomerular destruction. In end-stage renal failure replacement therapy (dialysis, transplantation) becomes necessary. Longterm survival of cystinotic patients is followed by additional late sequelae e.g. distal myopathy, loss of retinal function (blindness), disturbances of memory and other cerebral functions (for review see [3]). 

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