diabetesoutpatmgmt

diabetesoutpatmgmt - Outpatient Management of Diabetes...

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Outpatient Management of Diabetes Mellitus Gary L. Francis, MD, PhD Professor and Associate Chair for Research USUHS
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The Face of IDDM In 1920 was not Encouraging
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1921 – Banting and Best Began to Isolate the “Internal Secretion of the Pancreas”
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1923 Banting and Best Awarded Nobel Prize for Discovery And Use of Insulin in the Treatment of IDDM
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Islets of Langerhans β -cell destruction Insulin Deficiency Adipo- cytes Muscle Liver Decreased Glucose Utilization Glucagon Excess Increased Protein Catabolism Increased Ketogenesis Gluconeogenesis IncreasedLipolysis Hyperglycemia Ketoacidosis Polyuria Volume Depletion Ketonuria
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Classification of Different Forms of Diabetes Mellitus
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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 also be associated with glucagon deficiency
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Progression to Type 1 DM Autoimmune destruction “Diabetes threshold” Honeymoon 100% Islet loss Autoimmune markers (ICA, IAA, GAD
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Disease-Free Survival is Shortened with More Numerous Antibodies
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EPIDEMIOLOGY Most common metabolic disease in childhood Annual incidence 15 new cases per 100,000 in children < 18 yrs Frequency increases with increasing age. 1: 1400 at age 5 yrs 1: 400 at age 16 yrs Males and females equally affected No correlation with socioeconomic status
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IDDM RISK OF CONCORDANCE Offspring of IDDM parent: 2-5% overall risk Offspring of diabetic mother: 2% risk Offspring of diabetic father: 5% risk
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Type I - IDDM 1.9/100,000 school age children 1/1430@ 5 yr of age 1/360 @ 16 yr of age ID twins 50% concordance risk Dizygotic twins 20% concordance risk Two shared HLA haplotypes (DR3 + DR4) 12-20% risk One shared HLA haplotype (DR3 or DR4) 5-7% risk No shared HLA haplotypes 1-2% risk HLA DQ(beta) Asp 57 virtual protection HLA DQ(beta) non-Asp 57 100 X increased risk
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DIABETES MELLITUS CLINICAL MANIFESTATIONS Classic Presentation: Polyuria Polydipsia Polyphagia Weight loss. Insidious Onset of lethargy and weakness. Duration of symptoms usually < 1 month.
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DIABETES MELLITUS - TYPE I Body Systems Involved GU Urinary frequency GI Nausea, vomiting, constipation abdominal pain Respiratory Acidosis, Kussmaul breathing Cardiovascular Vascular collapse, dehydration tachycardia CNS Cerebral edema Musculoskeletal Glycogen depletion, K loss muscle weakness
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DIABETES MELLITUS - TYPE 1 THERAPEUTIC OBJECTIVES Achieve metabolic control Maintain normal growth and sexual Maturation Prevent acute and chronic complications Prevent ketoacidosis
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IDDM: OPTIMIZING GLYCEMIC CONTROL Hypoglycemia: May be unaware School grades Early am symptoms Headache Nightmares Look for at camp Reduce dose 10% Hyperglycemia: Few symptoms Nocturia Dawn phenomenon Adolescent insulin resistance Increase dose 10%
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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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diabetesoutpatmgmt - Outpatient Management of Diabetes...

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