java barcode scanner library METABOLIC ACIDOSIS in Objective-C

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METABOLIC ACIDOSIS
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Decreased HCO3 with acidemia Classified into high anion gap acidosis and normal anion gap acidosis The highest anion gap acidoses are seen in lactic acidosis, ketoacidosis, or toxins Normal anion gap acidosis is mainly caused by gastrointestinal HCO3 loss or RTA Urinary anion gap may help distinguish between these causes
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The hallmark of metabolic acidosis is decreased HCO3 , seen also in respiratory alkalosis (see above), but the pH distinguishes between the two disorders Calculation of the anion gap is useful in determining the cause of the metabolic acidosis (Table 21 14) The anion gap represents the difference between readily measured anions and cations
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Table 21 14 Anion gap in metabolic acidosis1
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Decreased (< 6 mEq) Hypoalbuminemia (decreased unmeasured anion) Plasma cell dyscrasias Monoclonal protein (cationic paraprotein) (accompanied by chloride and bicarbonate) Bromide intoxication Increased (>12 mEq) Metabolic anion Diabetic ketoacidosis Alcoholic ketoacidosis Lactic acidosis Chronic kidney disease (advanced stages) (PO43 , SO42 ) Starvation Metabolic alkalosis (increased number of negative charges on protein) Drug or chemical anion Salicylate intoxication Sodium carbenicillin therapy Methanol (formic acid) Ethylene glycol (oxalic acid) Normal (6 12 mEq) Loss of HCO3 Diarrhea Recovery from diabetic ketoacidosis Pancreatic fluid loss ileostomy (unadapted) Carbonic anhydrase inhibitors Chloride retention Renal tubular acidosis Ileal loop bladder Administration of HCl equivalent or NH4Cl Arginine and lysine in parenteral nutrition
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that the anion gap increases Normochloremic metabolic acidosis generally results from addition to the blood of nonchloride acids such as lactate, acetoacetate, -hydroxybutyrate, and exogenous toxins Unmeasured anions such as isocitrate, alpha-ketoglutarate, malate and d-lactate, may further contribute to the anion gap of lactic acidosis, diabetic ketoacidosis, and acidosis of unknown etiology An exception is uremia (CKD stage 5), with underexcretion of organic acids and anions
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A Lactic Acidosis
Lactic acid is formed from pyruvate in anaerobic glycolysis Therefore, most of the lactate is produced in tissues with high rates of glycolysis, such as gut (responsible for over 50% of lactate production), skeletal muscle, brain, skin, and erythrocytes Normally, lactate levels remain low (1 mEq/L) because of metabolism of lactate principally by the liver through gluconeogenesis or oxidation via the Krebs cycle Furthermore, the kidneys metabolize about 30% of lactate In lactic acidosis, lactate levels are at least 4 5 mEq/L but commonly 10 30 mEq/L The mortality rate exceeds 50% There are two basic types of lactic acidosis, both associated with increased lactate production and decreased lactate utilization Type A is characterized by hypoxia or decreased tissue perfusion, whereas in type B there is no clinical evidence of hypoxia Type A (hypoxic) lactic acidosis is the more common type, resulting from poor tissue perfusion; cardiogenic, septic, or hemorrhagic shock; and carbon monoxide or cyanide poisoning These conditions not only cause lactic acid production to increase peripherally but, more importantly, hepatic metabolism of lactate to decrease as liver perfusion declines In addition, severe acidosis impairs the ability of the liver to extract the perfused lactate Type B lactic acidosis may be due to metabolic causes, such as diabetes, ketoacidosis, liver disease, renal failure, infection, leukemia, or lymphoma, or it may occur as a result of toxicity from ethanol, methanol, salicylates, isoniazid, or metformin Propylene glycol, used as a vehicle for intravenous agents such as nitroglycerin, etomidate, and high-dose diazepam, may cause lactic acidosis from liver metabolism Nutritional problems are important causes of lactic acidosis Parenteral nutrition without thiamine causes severe refractory lactic acidosis from the deranged metabolism of pyruvate Patients with short bowel syndrome may develop D-lactic acidosis with encephalopathy due to carbohydrate malabsorption in the intestine and subsequent fermentation by colonic bacteria AIDS without AIDS-related lymphoma is associated with type B lactic acidosis Treatment of HIV patients with nucleoside analog reverse transcriptase inhibitors may cause lactic acidosis due to mitochondrial toxicity Idiopathic lactic acidosis, usually in debilitated patients, has an extremely high mortality rate (For treatment of lactic acidosis, see below and 27)
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