Version May 2024
| Increased lactate production |
| Increased pyruvate production |
| Enzymatic defects in glycogenolysis or gluconeogenesis (as with type 1 glycogen storage disease) |
| Respiratory alkalosis, including salicylate intoxication |
| Pheochromocytoma |
| Beta-agonists |
| Sepsis |
| Impaired pyruvate utilization |
| Decreased activity of pyruvate dehydrogenase or pyruvate carboxylase |
| • Congenital |
| • Possibly a role in diabetes mellitus, Reye syndrome |
| Altered redox state favoring pyruvate conversion to lactate |
| Enhanced metabolic rate |
| • Grand mal seizure |
| • Severe exercise |
| • Hypothermic shivering |
| • Severe asthma |
| Decreased oxygen delivery |
| • Shock |
| • Cardiac arrest |
| • Acute pulmonary edema |
| • Carbon monoxide poisoning |
| • Severe hypoxemia (PO2 <25 to 30 mmHg) |
| • Pheochromocytoma |
| Reduced oxygen utilization |
| • Cyanide intoxication (decreased oxidative metabolism), which may result from cyanide poisoning or, during a fire, from smoke inhalation of vapors derived from the thermal decomposition of nitrogen-containing materials such as wool, silk, and polyurethane |
| • Drug-induced mitochondrial dysfunction due to zidovudine or stavudine |
| • Sepsis |
| D-lactic acidosis |
| Primary decrease in lactate utilization |
| Hypoperfusion and marked acidemia |
| Alcoholism |
| Liver disease |
| Mechanism uncertain |
| Malignancy |
| Diabetes mellitus, including metformin in the absence of tissue hypoxia |
| Acquired immunodeficiency syndrome |
| Hypoglycemia |
| Idiopathic |
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