STRESS-INDUCED HYPERGLYCEMIA方案介绍.pptVIP

STRESS-INDUCED HYPERGLYCEMIA 成大醫院 內科部 內分泌新陳代謝科 TOPICS PREVALENCE PATHOPHYSIOLOGY EFFECTS OF HYPERGLYCEMIA MANAGEMENT OF HYPERGLYCEMIA SUMMARY TOPICS PREVALENCE PATHOPHYSIOLOGY EFFECTS OF HYPERGLYCEMIA MANAGEMENT OF HYPERGLYCEMIA SUMMARY Prevalence Quite common in critically ill patients; varied prevalence Undiagnosed diabetes vs pure stress-hyperglycemia A manifestation of the stress response Most often evident shortly after admission to the ICU Resolve as the underlying catabolic illness subsides Hepatic insulin resistance is more important than peripheral (skeletal muscle) resistance in the genesis of stress hyperglycemia Study 1 Infusion of cocktail of epinephrine, glucagon, cortisol for 3 days Sustained increase in PG (60-80 %), glucose production (100%) despite hyperinsulinemia Synergistic effect of hormones Study 2 Infusion of counterregulatory hormones and glucose (4.5 mg/kg/min) vs glucose infusion only PG: 360 mg/dl vs 130 mg/dl Substrate for accelerated hepatic gluconeogenesis Alanine: from skeletal muscle proteolysis Lactate: from peripheral tissue glycolysis Glycerol: from adipocyte lipolysis Renal gluconeogenesis Account for 1/3 change in glucose turnover Glucose clearance in critical illness Non-insulin dependent tissue: increased Reticuloendothelial system Insulin dependent tissue: decreased Skeletal muscle, myocardium, adipose tissue Impaired glucose uptake Normal cellular glucose oxidation Impaired glycogen synthesis Hormone Mechanism Glucagon Increased gluconeogenesis Increased hepatic glycogenolysis Epinephrine Increased gluconeogenesis Increased skeletal muscle and hepatic glycogenolysis Increased lipolysis-increased free fatty acid Skeletal muscle insulin resistance by altering postreceptor signaling Direct suppression of insulin secretion Norepinephrine Increased gluconeogenesis but hyperglycemia not marked except at high concentrations Increased lipolysis Glucocorticoid Gluconeogenesis increased, through provision of substrate Increased l