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DIABETES MELLITUS TYPE 1 & MANAGEMENT OF DIABETIC KETOACIDOSIS

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  • DIABETES MELLITUS TYPE 1 & MANAGEMENT OF DIABETIC KETOACIDOSIS PRESENTED BYDR ASHISH SHARMA GUIDED BYDR MEENA PATEL

  • DEFINITION Metabolic disorder of multiple etiologies characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects of insulin secretion, insulin action or both.

  • OLD CLASSIFICATION (1985)Type 1, Insulin-dependent (IDDM)Type 2, Non Insulin-dependent (NIDDM)obesenon-obeseMODY IGTGestational Diabetes

  • WHO CLASSIFICATION 2000Is based on etiology not on type of treatment or age of the patient.Type 1 Diabetes (idiopathic or autoimmune b-cell destruction)Type 2 Diabetes (defects in insulin secretion or action)Other specific types

  • Both type 1 & type 2 can be further subdivided into:Not insulin requiringInsulin requiring for controlInsulin requiring for survival

  • Type 1 Diabetes Mellitus Formerly called insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes

    T1DM is characterized by low or absent levels of endogenously produced insulin

  • EPIDEMIOLOGY The onset occurs predominantly in childhood, with median age of 7-15 yr, but it may present at any age.

    Indian data suggest an incidence of 10.5/100,000/yr .

    India would have 79 million diabetes by 2030, the highest for any country in the world.

  • Pathogenesis & Natural history The natural history includes distinct stages Initiation of autoimmunity Preclinical autoimmunity with progressive loss of -cell functionOnset of clinical diseaseTransient remission( Honeymoon period)Established diseaseDevelopment of complications

  • Both genetic ,environmental and autoimmune factors contribute to the pathogenesis.

    Genetic factors- Genetic susceptibility to T1DM is determined by several genes .HLA complex accounts for almost 50 % of genetic risk for type 1 diabetes.Some of the known associations include the HLA DR3/4-DQ2/8 genotype

  • Association with DR3 has been reported in Indians.Risk of diabetes is also increased when a parent has diabetes and this risk differs between the 2 parents; the risk is 2% if the mother has diabetes, but 7% when the father has diabetes.In monozygotic twins, the concordance rate ranges from 30-65%, whereas dizygotic twins have a concordance rate of 6-10%.

  • Envoirmental factors

    Many envoirmental agents are thought to trigger the development of type 1 diabetes including,Viral infections- Enterovirus , mumps , rubella Diet- Breast-feeding may lower the risk of T1DM. Early introduction of cow's milk protein and early exposure to gluten have both been implicated in the development of autoimmunity

  • Autoimmune factors

    Whatever the triggering factor, it seems that in most cases of T1DM that are diagnosed in childhood.The 1st signs of autoimmunity appear before age 2yr.Insulin associated antibodies (IAA) Glutamic acid decarboxylase 65kd (GAD65) &tyrosine phosphatase insulinoma-associated

  • . The earliest antibodies are predominantly of the IgG1 subclass

    The appearance of autoimmunity is followed by progressive destruction of cells.

    Antibodies are a marker for the presence of autoimmunity, but the actual damage to the cells is primarily T-cell mediated

  • PathophysiologyInsulin performs a critical role in the storage and retrieval of cellular fuel.

    In normal metabolism, there are regular swings between the postprandial, high-insulin anabolic state and the fasted, low-insulin catabolic state that affect liver, muscle, and adipose tissue

  • Pathophysiology.T1DM is a progressive low-insulin catabolic state in which feeding does not reverse but rather exaggerates these catabolic processes.

    At even lower insulin levels, the liver produces excessive glucose via glycogenolysis and gluconeogenesis, and fasting hyperglycemia begins.

  • Pathophysiology.Hyperglycemia produces an osmotic diuresis (glycosuria) when the renal threshold is exceeded (180mg/dL; 10mmol/L). The resulting loss of calories and electrolytes, as well as the persistent dehydration, produce a physiologic stress with hypersecretion of stress hormones (epinephrine, cortisol, growth hormone, and glucagon)

  • Pathophysiology.These hormones, in turn, contribute to the metabolic decompensation by promoting glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis (glucagon, epinephrine, growth hormone, and cortisol) while decreasing glucose utilization and glucose clearance.

  • CLINICAL PRESENTATIONSClassical symptom triad: polyuria, polydipsia and weight lossDKAAccidental diagnosisAnorexia nervosa like illness

  • DIAGNOSTIC CRITERIAFasting blood glucose levelDiabeticPlasma >7.0 mmol/ 126mg/dlCapillary >6.0 mmolIGTPlasma 6.0-6.9 mmolCapillary 5.6-6.0 mmol2 hours after glucose load(Plasma or capillary BS)IGT7.8-11.0Diabetic level> 11.1 (200 mg)

  • DIAGNOSISIn symptomatic children a random plasma glucose >11.1 mmol (200 mg) is diagnostic.A modified OGTT (fasting & 2h) may be needed in asymptomatic children with hyperglycemia if the cause is not obvious.Remember: acute infections in young non-diabetic children can cause hyperglycemia without ketoacidosis.

  • COMPLICATIONS OF DIABETESAcute:DKAHypoglycemiaLate-onset:Retinopathy NeuropathyNephropathyIschemic heart disease & stroke

  • TREATMENT GOALSPrevent death & alleviate symptomsAchieve biochemical controlMaintain growth & developmentPrevent acute complicationsPrevent or delay late-onset complications

  • TREATMENT ELEMENTSEducationInsulin therapyDiet and meal planningMonitoringHbA1c every 2-monthsHome regular BG monitoring Home urine ketones tests when indicated

  • EDUCATIONEducate child & care givers about: Diabetes Insulin Life-saving skills Recognition of Hypo & DKA Meal plan Sick-day management

  • INSULINA polypeptide made of 2 b-chains.Discovered by Bants & Best in 1921.Animal types (porcine & bovine) were used before the introduction of human-like insulin (DNA-recombinant types).Recently more potent insulin analogs are produced by changing aminoacid sequence.

  • FUNCTION OF INSULINInsulin being an anabolic hormone stimulates protein & fatty acids synthesis.Insulin decreases blood sugar By inhibiting hepatic glycogenolysis and gluconeogenesis.By stimulating glucose uptake, utilization & storage by the liver, muscles & adipose tissue.

  • Characteristics of InsulinThere are three characteristics of insulin:

    Onset- Is the length of time before insulin reaches the bloodstream and begins lowering blood glucose.Peaktime- Is the time during which insulin is at maximum strength in terms of lowering blood glucose.Duration- Is how insulin continues to lower blood glucose.

  • The Basics of Insulin: 4 TypesRapid-acting insulin

    Regular or short-acting insulin

    Intermediate-acting insulin

    Long-acting insulin

  • Rapid-acting InsulinExamples: insulin lispro or insulin aspart

    Onset: Begins to work at about 5 minutes

    Peaktime: Peak is about 1 hour

    Duration: Continues to work for about 2-4 hours

  • Regular or Short-acting InsulinExamples: insulin lispro, Aspart

    Onset: Reaches the bloodstream within 30 minutes after injection.

    Peaktime: Peaks anywhere from 2-3 hours after injection.

    Duration: Effective for approximately 3-6 hours.

  • Intermediate-acting InsulinExamples:NPH, Lente

    Onset: Reaches the blood stream about 2 to 4 hours after injection.

    Peaktime: Peaks 4-12 hours later.

    Duration: Effective for about 12 to 18 hours

  • Long-acting Insulin

    Examples: insulin glargine

    Onset: Reaches the bloodstream 6-10 hours after injection Duration: Usually effective for 20-24 hours

  • INSULIN CONCENTRATIONSInsulin is available in different concentrations 40, 80 & 100 Unit/ml.WHO now recommends U 100 to be the only used insulin to prevent confusion.Special preparation for infusion pumps is soluble insulin 500 U/ml.

  • Insulin Pump TherapyContinuous subcutaneous insulin infusion (CSII) via battery-powered pumps provides a closer approximation of normal plasma insulin profiles.It accurately deliver a small baseline continuous infusion of insulin, coupled with parameters for bolus therapy. The bolus insulin determined by amount of carbohydrate intake and blood sugar level

  • INSULIN REGIMENSTwice daily: either NPH alone or NPH+SI.Thrice daily: SI before each meal and NPH only before dinner.Intensive 4 times/day: SI before meals + NPH or Glargine at bed time.Continuous s/c infusion using pumps loaded with SI.

  • NEW INSULIN PREPARATIONSInhaled insulin proved to be effective & will be available within 2 years.Nasal insulin was not successful because of variable nasal absorption.Oral insulin preparations are under trials.

  • ADVERSE EFFECTS OF INSULINHypoglycemiaLipoatrophyLipohypertrophyObesityInsulin allergyInsulin antibodiesInsulin induced edema

  • PRACTICAL PROBLEMSNon-availability of insulin in poor countriesinjection sites & techniqueInsulin storage & transferMixing insulin preparationsInsulin & school hoursAdjusting insulin dose at homeSick-day managementRecognition & Rx of hypo at home

  • DIET REGULATIONRegular meal plans with calorie exchange options are encouraged.50-60% of required energy to be obtained from complex carbohydrates.Distribute

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