Which of the following statement(s) is/are true concerning the derangement of metabolic acidosis?

a. A major source of acid production of the body is sulfuric acid

b. Excessive loss of bicarbonate can occur with intestinal or pancreatic fistulas

c. Ketoacidosis can occur in conditions of either hyper-or hypoglycemia

e. Lactic acidosis can be associated with ethanol toxicity 

Most clinically significant metabolic acidosis is related to the net loss of bicarbonate, which occurs when consumption due to either loss or titration is greater than bicarbonate generation. Under normal circumstances of ingestion of the average amount of protein in an American diet, about 70 mEq acid is generated daily. The major source of acid production is sulfuric acid from the metabolism of sulphur-containing amino acids. Increased protein intake and tissue catabolism resulting in greater metabolism of sulphur containing amino acids may lead to a generation of increased amounts of sulfuric acid. This excess acid utilizes excess bicarbonate for neutralization. Diarrhea, intestinal or pancreatic fistulas, and burns can cause metabolic acidosis secondary to loss of bicarbonate. The two most common types of organic acidosis are ketoacidosis and lactic acidosis. The abnormality primarily responsible for ketoacidosis is deficiency of insulin whether primary, as in diabetic ketoacidosis, or secondary to hypoglycemia. Under normal conditions a small amount of ketoacids is produced. During prolonged starvation, production of ketoacids increase to modest levels, providing an important source of energy to nonhepatic tissues, particularly the brain. In ketoacidosis, the ketoacid production is excessive because of insulin deficiency. In diabetic acidosis, insulin deficiency also contributes to hyperglycemia by decreasing the metabolism of glucose by extrahepatic tissue and increasing hepatic production of glucose.

 Lactic acidosis can be divided into type A, caused by tissue hypoxia, and type B, caused by other mechanisms. Hypoxia, the most common cause of lactic acidosis, impairs the mitochondrial oxidation of NADH to NAD that is necessary for glycolysis. Normal serum lactate concentration is below 2 mEq/L. Lactate acidosis is secondary to hypoxemia, usually due to an increased production of lactate as well as decreased use, and serum lactate concentrations greater than 6 mEq/L. The most common cause of type B lactate acidosis is ethanol intoxication.