Metabolic acidosis chronic

For patients with bladder drainage, enteric conversion may be required for refractory problems, such as dehydration, metabolic acidosis, chronic urethritis caused by trypsinogen derivation, urinary tract infections, and recurrent reflux pancreatitis. This uivolves an anastomosis between the graft duodenal segment and the recipient small bowel. 

The regulation of NHE2 is multifactorial. Chronic exposure to nitric oxide and gamma-interferon decrease NHE2 activity, whereas metabolic acidosis and chronic stimulation with epidermal growth factor (EGF) increase activity. 

Metformin is contraindicated in patients with heart failure, renal disease, hypersensitivity to metformin, and acute or chronic metabolic acidosis, including ketoacidosis. The drug is also contraindicated in patients older than 80 years and during pregnancy (Pregnancy Category B) and lactation. 

Stimulation of basolateral Na /H exchanger transport activity in LLC-PK] cells during chronic metabolic acidosis is accompanied by a parallel increase in NHE-1 transcript abundance [80]. Chronic metabolic acidosis also increases the abundance of Na /H exchanger transcripts in rat renal cortices [81] and SV40-transformed mouse proximal tubule cells [82]. 

Chronic or large ingestions of propylene glycol have been associated with the development of hyperosmolar anion-gap metabolic acidosis, renal dysfunction, hemolysis, cardiac arrhythmias, and seizures. 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

GSH-S deficiency is a more frequent cause of GSH deficiency (HI7), and more than 20 families with this enzyme deficiency have been reported since the first report by Oort et al. (05). There are two distinct types of GSH-S deficiency with different clinical pictures. In the red blood cell type, the enzyme defect is limited to red blood cells and the only clinical presentation is mild hemolysis. In the generalized type, the deficiency is also found in tissues other than red blood cells, and the patients show not only chronic hemolytic anemia but also metabolic acidosis with marked 5-oxoprolinuria and neurologic manifestations including mental retardation. The precise mechanism of these two different phenotypes remains to be elucidated, because the existence of tissue-specific isozymes is not clear. Seven mutations at the GSH-S locus on six alleles—four missense mutations, two deletions, and one splice site mutation—have been identified (S14). 

The major manifestation of chronic metabolic acidosis is bone demineralization with the development of rickets in children and osteomalacia and osteopenia in adults. 

Respiratory and metabolic acidosis can develop in patients with cardiorespiratory arrest, with chronic lung disease and shock, and with metabolic acidosis and respiratory failure. 

A chronically iU patient on long-term (home) parenteral nutrition develops metabolic acidosis, a grayish pallor, scaly dermatitis, and alopecia (hair loss). These symptoms subside upon addition of the B vitamin biotin to the alimentation fluid. 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

Roderick P, Willis NS, Blakeley S, Jones C, Tomson C. Correction of chronic metabolic acidosis for chronic kidney disease patients. Cochrane Database Syst Rev 2007. 

Chronic use or overdosage may result in electrolyte disturbances, such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis, persistent diarrhea, malabsorption, and weight loss. Electrolyte disturbance may produce vomiting and muscle weakness. 

Acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma... 

Hong, J.-J., Lin, J.-L., Wu, M.-S., Huang, C.-C. Verberckmoes, R. (1996) A chronic glue sniffer with hyperchloraemia metabolic acidosis, rhabdomyolysis, irreversible quadriplegia, central pontine myelinolysis, and hypothyroidism. Nephrol. Dial. Transpl., 11, 1848-1849... 

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. 

Acetazolamide can cause a metabolic acidosis in 50% of elderly patients (SEDA-11,199) occasionally (particularly if salicylates are being given or renal function is poor) the acidosis can be severe. It does this by inhibiting renal bicarbonate reabsorption. This effect is of particular use in treating patients with chronic respiratory acidosis with superimposed metabolic alkalosis. Life-threatening metabolic acidosis is rarely observed in the absence of renal insufficiency and/or diabetes mellitus. In three patients with central nervous system pathology alone conventional doses of acetazolamide resulted in severe metabolic acidosis (34). After withdrawal it took up to 48 hours for the metabolic acidosis and accompanying hyperventilation to resolve. 

The major risk resulting from topical treatment of psoriasis with salicylic acid is the potential chronic or acute systemic intoxication with the symptoms of burning of oral mucosa, frontal headache, CNS symptoms, pH deviation (metabolic acidosis), tinnitus, nausea, vomiting, and gastric symptoms.28-30 These symptoms may occur in topical treatment of large body surfaces, especially in children.31-33 Even lethal cases have been reported.34,35 Therefore, a concentration higher than 10%, and an application on larger surfaces especially in children are not suitable. Salicylic acid should not be applied to more than 20% of the body surface area.13 It should be noted that some topical treatments of psoriasis such as calcipotriol are inactivated by salicylic acid.36... 

Baseline and periodic serum bicarbonate levels to monitor for hyperchloremic, nonanion gap metabolic acidosis (i.e., decreased serum bicarbonate below the normal reference range in the absence of chronic respiratory alkalosis)... 

In contrast to the studies of glutamine transport, several studies have suggested a potential role for the malate/a-ketoglutarate transporter in chronic acidosis [135,297]. Although Cheema-Dhadli and Halperin [135] were unable to demonstrate activation of the dicarboxylate (malate/phosphate) transporter in kidney cortex mitochondria from rats with chronic metabolic acidosis, Brosnan et al. [297] demonstrated that the malate/a-ketoglutarate carrier was activated in chronic acidosis. Additional studies are required to characterize this effect fully and to determine its role in the overall process of augmented ammonia formation in metabolic acidosis. However, it is... 

Alcohol-induced ketoacidosis must be differentiated from a similar metabolic complication in diabetes melli-tUS (E.S. Dillon et al., 1940 D.W. Jenkins et al., 1971). With chronic alcohol consumption and concurrent malnutrition, metabolic acidosis is caused by a still unclear multifaceted pathogenesis (hypoinsulinaemia, lipolysis, extreme increase in free fatty acids, rise in ketone bodies). The clinical picture shows nausea, vomiting, dehydration, hyperventilation, fruity odour on breath, aceton-uria and acetonaemia as well as a moderate form of hyperglycaemia. This syndrome probably occurs more often than has been hitherto assumed. (54)... 

Boon, L., Blornmpart, R, Meijer, A., Lainers, W., and Schoolwerth. A, C. 119%). Response of hepatic amino acid consumption to chronic metabolic acidosi.s. Am. j. Pfr siol. 271, F198-F202. 

Chronic acetazolamide therapy is associated with greater spinal bone mineral density. This is probably the result of metabolic acidosis urine calcium is increased and serum phosphate reduced. Osteomalacia has been reported during long-term therapy in combination with barbiturates in two patients. 

A 50-year-old woman with chronic renal insufficiency treated with acetazolamide for simple glaucoma developed confusion, cerebellar ataxia, and metabolic acidosis 2 weeks after starting to take aspirin for acute pericarditis (30). A diagnosis of salicylism was made despite low serum salicylate concentrations. 

Henger A, Tutt P, Hulter HM, Krapf R. Acid-base effects of inhibition of aldosterone and angiotensin II action in chronic metabolic acidosis in humans. J Am Soc Nephrol 1999 10 121A. 

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