Pathophysiology: The primary disturbance in the diabetic ketoacidotic (DKA) patient is an absolute or relative deficiency of insulin and elaboration of counter-regulatory hormones such as glucagon, cortisol, epinephrine, norepinephrine, and growth hormone. This constellation of hormonal changes mirrors many of the metabolic adaptations in the patient with starvation (with a few exceptions). A decrease in the insulin/glucagon ratio contributes to decreased peripheral utilization of glucose and breakdown of glycogen stores through activation of glycogenolytic enzymes; hyperglycemia results. As the body is "fooled" into thinking that a state of starvation exists; further metabolic adaptations (increases in cortisol) are geared at increasing glucose levels through proteolysis to provide substrate for gluconeogenesis. Additionally, activation of hormone sensitive lipase results in lipolysis and the release of free fatty acids. Without the presence of insulin, hepatic ketogenic enzymes are induced to produce ketones as opposed to re-esterifying triglycerides and incorporation into lipoproteins. These changes in carbohydrate, protein, and fat metabolism have direct relationships to the progression and clinical signs of ketoacidosis.
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