DKA-1 - DIABETIC KETOACIDOSIS Andrew J Bauer Pediatric...

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DIABETIC KETOACIDOSIS Andrew J. Bauer Pediatric Endocrinology WRAMC
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GOALS REVIEW TYPE 1 DIABETES AND METABOLISM AS THEY RELATES TO DKA CLINICAL DIAGNOSIS and MISLEADING LABS TREATMENT and CONTROVERSIES TREATMENT GUIDELINES
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Type 1 DM Autoimmune destruction of the pancreatic islet cell Hallmark = lymphocytic infiltration of islets Progresses over years Leads to insulin deficiency Later may be associated with glucagon deficiency as well
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Progression to Type 1 DM Autoimmune destruction “Diabetes threshold” Honeymoon 100% Islet loss
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Typical Presentation Polyuria, polydypsia, weight loss Vomiting Rapid-deep respiration CNS depression – coma Precipitating event
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“Typical” Setting…. . 9 yo boy presents to clinic with CC “ 6 day history of stomach pain and diarrhea.” “Vomiting started 2 days ago and has persisted.” (+) weight loss PE: HR 140, RR 28, T97.8 Weight: 27 Kg Tachy mucous membranes Abd - soft, (+)BS, mild left CVA tenderness DX: viral gastroenteritis with mild dehydration Returned to ER 24 hours later PE: cachectic, quiet, tired, cooperative, (+) ketotic breath
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Background 15-30% of new diabetics present in DKA < 4 yrs of age = 40% with DKA @ diagnosis Most common cause of death in diabetics less than 20 years of age 70% of related deaths in diabetics less than 10 yrs of age Mortality: 5-15% (1-2% at MEDCEN) Preventable
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Diagnostic Criteria Blood glucose > 250 mg/dl pH < 7.35 • HCO 3 < 20 mEq/L Anion Gap > 12 ketonemia
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Etiology Results from inadequate insulin Accidental or intentional omission Inappropriate intervention when stressed
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Etiology DKA violates rules of common sense Increased insulin requirement despite decreased food intake Marked urine output in setting of dehydration Catabolic state in setting of hyperglycemia and hyperlipidemia
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Insulin Deficiency is the Primary defect Stress hormones accelerate and exaggerate the rate and magnitude of metabolic decompensation Pathophysiology Counter-Regulatory Hormones Pathophysiology Hormone Impaired insulin secretion Epi Anti-insulin action Epi, cortisol, GH Promoting catabolism All Dec glucose utilization Epi, cortisol, GH
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Islets of Langerhans β -cell destruction Insulin Deficiency Adipo- cytes Muscle Liver Increased Production Glucagon Increased Protein Catabolism Increased Ketogenesis Gluconeogenesis, Glycogenolysis IncreasedLipolysis Hyperglycemia Ketoacidosis HyperTG Polyuria Volume Depletion Ketonuria Amino Acids FattyAcids Stress E p i , C o r t s l G H Threshold 180 mg/dl
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Pathophysiology Insulin Glucagon Epinephrine Cortisol Growth Hormone
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Pathophysiology Dec Glucose Utilization Lipolysis Insulin Glucagon Epinephrine Cortisol Growth Hormone
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DKA - Early Relative Insulin Deficiency Glycogenolysis & gluconeogenesis restrained Peripheral glucose uptake Elevates blood glucose Decreased Utilization post-prandial and Stress-Induced hyperglycemia
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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DKA-1 - DIABETIC KETOACIDOSIS Andrew J Bauer Pediatric...

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