Pathology of Ketoacidosis in Emergency of Diabetic Ketoacidosis and Alcoholic Ketoacidosis: A Retrospective Study

Figure 6

(a) Pathophysiology of diabetic ketoacidosis. DKA results in excessive amounts of glucose and glycogen due to absolute insulin deficiency, which finally leads to hyperglycemia. Hyperglycemia causes osmotic diuresis, leading to dehydration. In addition, in DKA, the enormous supply of fatty acyl CoA and deficiency in oxaloacetate overwhelm these normal biochemical pathways. Under the conditions, excessive amounts of acetyl-CoA derivatives are oxidized to form ketone bodies, and large quantities of β-OHB and AcAc are released into the blood stream. (b) Pathophysiology of alcoholic ketoacidosis. AKA is caused by various factors such as poor intake of carbohydrate and suppression of insulin with increased counterregulatory hormones. Low glycogen storage and suppression of gluconeogenesis lead to hypoglycemia. NAD is reduced to NADH during the metabolism of alcohol. Alcohol is metabolized to acetate, which consequently forms acetyl-CoA. AcAc tends to metabolize into β-OHB when a NADH/NAD ratio is high, which causes ketoacidosis with a high β-OHB/AcAc ratio.

(a)

(b)