2.5.2.1 - Diabetes Mellitus pada Anak (1).ppt

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DIABETES MELLITUS DIABETES MELLITUS PADA ANAK PADA ANAK Eka Agustia Rini Eka Agustia Rini

Transcript of 2.5.2.1 - Diabetes Mellitus pada Anak (1).ppt

  • DIABETES MELLITUS PADA ANAKEka Agustia Rini

  • DIABETES MELLITUSHigh levels of blood glucose : defects in insulin production, insulin action, or both

    Type 1 Diabetescells that produce insulin are destroyed results in insulin dependence

    Type 2 DiabetesLack of insulin productionInsufficient insulin action (resistant cells)

  • Diabetes - DiagnosisSymptoms of diabetes plus random plasma glucose >200mg/dl (11.1mmol/l) orFasting plasma glucose >126 mg/dl (7.0 mmol/l) or 2 hour plasma glucose >200 mg/dl during an oral glucose tolerance testAmerican Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.

  • GEJALA KLINISHIPERGLIKEMIPoliuriaPolidipsiPoli fagiaKOMPLIKASIKetoasidosisHipoglikemiMikrovaskularMakrovaskular

  • Type 1 DMWhat Causes Type 1 Diabetes?Autoimmune ResponseGenetic Abnormalities Viruses Cows milk

  • Etiology80%-85% no affected family memberAutoimune destruction of pancreas islet Multiple genetic (predisposition)Enviromental factors (trigger)viral infection, diet and toxinsInsulin secretionor

  • PathogenesisDestruction of -cell is quite variable.

    Fasting hyperglycemia can rapidly change to severe hyperglycemia or ketoacidosis (in infection or other stress).

    Manifestation little or no insulin secretion low or undetectable C-peptide

  • Pathophysiology Utilization glucose decreased postprandial hyperglycemiaGlycogenolysis and gliconeogenesis fasting hyperglycemiaGlucosuriaLoss of calorie and electrolyte, dehydrationInsulinopenia

  • Clinical ManifestationPhase of type 1 DMPrediabetesPresentation of diabetesPartial remission or honeymoonChronic phase of lifelong dependency on administrated insulin

  • Clinical manifestationPolyuria or nocturia glucosuriaPolydipsiaPolyphagia calories lost in urineWeight loss Monilial vaginitis glucosuria

  • DiagnosisSymptoms and casual plasma glucose 200 mg/dL orFPG 126 mg/dL or2-h postload glucose 200 mg/dLLow or undetectable C-peptideICA positive

  • MANAGEMENT OF T1DMDiabetes education.Insulin replacement.Nutritional plan.Psychological adjustmentExerciseDiabetes camp

  • Diabetes Management PrinciplesAn effective insulin regimen Monitoring of glucoseAs flexible with food and activity as possibleMust remember Young children need routine and rulesYoung children need to develop autonomyYoung children need to explore and experienceYoung children need to begin to make decisions

  • The aims of DM management:

    Optimal metabolic (glycaemic) control.Normal growth and development.Optimal psychosocial adjustment.An individualised plan of diabetes care incorporating the particular needs of the child or adolescent and the family.

  • Diabetes educationThe cause of diabetes.Insulin replacement ; adjustment, storage, inj. techniquesBlood glucose measurement.Exercise.Diabetes and exercise.Psychological and family adjustment.Hypoglycaemia and its management.Diabetes management during illness.Travel.Dietetic principles.Contraception.Alcohol and Drugs.Diabetes complications. Driving.Smoking.

  • INSULIN REPLACEMENTInsulin types

    Rapid-acting Lyspro, aspart, glulysineShort-acting Regular InsulinIntermediate - Lente, NPHLong-acting - Ultralente, Glargine, Detemir

  • Physiologic Insulin Therapy

  • Fixed dose regimens: requires scheduled meals and snacks and is not flexible enough for most young children

    Basal bolus regimens:MDIuseful only if child is willing to take frequent injectionsInsulin pumps (CSII)child must be willing to wear the pumpInsulin management

  • On Target!Location of injection

  • Insulin pump therapyBased on what body does naturally - Small amounts of insulin all the time (basal insulin)- Extra doses to cover each meal or snack (bolus insulin)

    Rapid or Short-Acting InsulinPrecision, micro-drop insulin deliveryFlexibility Considered as a treatment optionInitiated and supervised by a specialised multidisciplinary

  • Nutritionadequate energy and nutrients, optimal growth and development, avoid hyperglycemia or hypoglycemia.Number of recommended meal : 6/day 3 main meal (25/20, 25/30 and 20/20) and 3 snacks (10%). Caloric:1000 cal + 100 cal / year ageIdeal BW + activity (
  • Emergency conditionsDiabetic ketoacidosisHypoglycemia

    Longterm complications Cardiovascular Neuropathy, Vascular Injury, and Amputations. Eye Complications. Kidney Damage (Nephropathy). Other Complications. Specific Complications in Women. Diabetes appears to affect female hormones. Specific Complications for Adolescents.

  • Diabetic KetoacidosisHyperglycemiaBeta Cell ToxicityInsulin secretion+Insulin resistance 2o obesityRelative Insulin DeficiencyLipolysisFree Fatty AcidsKetonemiaKetonuria

  • Manifestation of ketoacisodosisKetoacid accumulate when low insulin levelsAbdominal discomfortnausea & emesisDehydration, but still polyuriaSign of metabolic acidosisDiminish of neurocognitiv function comaThe biochemical criteria : hyperglycaemia (> 200 mg/dL), pH
  • Type 2 DM

  • Childhood Obesity The prevalence of childhood obesity is estimated to be 25 to 30 %. type 2 diabetes is increasing in children and adolescents obesity Family history of diabetes is strongly associated with type 2 diabetes in children

  • Insulin ResistanceObesity Metabolic SyndromeType 2DMNASHPCOSDyslipidemiaHypertension

  • Type 2 DiabetesDiagnosisElevated fasting insulin and hyperglycemia.Only 20% present with polyuria, polydipsia, and weight loss. EtiologyOne third of new diabetics presenting between 10-19 years had NIDDM.Pinhas-Hamiel J Pediatr 1996;128:608-615.

  • Acanthosis nigricans and polycystic ovarian syndrome (PCOS), disorders associated with insulin resistance and obesity, are common in youth with type 2 diabetes

    Currently, type 2 diabetes are usually diagnosed over the age of 10 years and are in middle to late puberty

  • Acanthosis NigricansDr. George Datto

  • Acanthosis NigricansHyperpigmentation and velvety thickening that occurs in neck, axilla, and other skin folds

    In pediatrics, commonly in obese children. Also seen in malignancies and other insulin resistant syndromes.

    Obese pediatric + acanthosis have higher fasting insulin and lower insulin sensitivity

  • Type 2 Diabetes - One End of the ContinuumGenetic PredispositionEnvironmental TriggerObesityInsulin ResistanceBeta HyperglycemiaType 2 DiabetesDysfunctionCell

  • Type 2 Diabetes - Risk factorsObesity 85% overweight or obese on diagnosisAmerican Diabetes Association: Type 2 diabetes in children and adolescents (Consensus Statement). Diabetes Care 23:381389, 2000).65% of children with type 2 diabetes have first degree relative with Type 2 diabetesPinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 61574%-100% have first or second degree relative with type 2 diabetesAmerican Diabetes Association: Type 2 diabetes in children and adolescents (Consensus Statement). Diabetes Care 23:381389, 2000).

  • Type 2 Diabetes Risk factorsAfrican American, Hispanic, Asian, Native American descentAmerican Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.Increased insulin resistance (puberty,ethnicity, inactivity,visceral fat distribution,PCOS) American Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.Female/male 1.7:1Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 615

  • Type 2 Diabetes- Prevalence4.1/100,000 for all 15-19 year old American Indians up to 50.9/100,000 for 15-19 yr old Pima IndianFagot-Campagna A, Pettitt DJ, Engelgau MM, Ros Burrows N, Geiss LS, Valdez R, et al. Type 2diabetes among North American children and adolescents: an epidemiological review and a public health perspective. J Pediatr 2000; 136: 664-672Estimated incidence of type 2 diabetes 7.2/100,000/yr (Ohio 1994)10 fold increase from 1982-1994 Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 615

  • Type 2 Diabetes - Risk

    Lifetime risk of diabetes for individuals born in 20001 in 3 for males2 in 5 for femalesNarayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF: Lifetime risk for diabetes mellitus in the United States. JAMA290 :1884 1890,2003

  • Components of the Met Syndr in ChildhoodAbnormal blood lipids (HDL cholesterol 150mg/dl LDL>130mg/dl).

    Impaired glucose tolerance (fasting glucose > 100 (110) mg/dl, random glucose >200mg/dl).Obesity (BMI >95% for age and sex)Elevated blood pressure (SBP or DBP > 90% for age).

  • Screening (ADA recomendation) 10 years /puberty

    BMI > p 85, BB > 120% Family history

    Special ethnic

    Insulin resistentOGTT every 2 years

  • Impaired glucose toleranceIncreased incidence of impaired glucose tolerance in obesity clinic population25% of obese children (aged 4-10yrs)21 % of obese adolescents (aged11-18 yrs) Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, Savoye M, Rieger V, Taksali S, Barbetta G, Sherwin RS, Caprio S: Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 346:802810, 2002

  • Diagnosis criteriaDiabetes mellitus1. Symptom DM + Glucose random > 200 mg/dl2. Fasting blood glucose > 125 mg/dl2. Blood glucose, 2 hr OGTT > 200 mg/dl

    Prediabetes1. Gula darah puasa terganggu (> 11O & 140 mg/dl & < > 200 mg/dl)

  • Treatment of Type 2 DM Lifestyle changes Pharmaceutical therapyBiguanidesSulfonylureasMeglitinide ThiazolidenedionesMonitoring for complicationsHypertension and hyperlipidemia treatment

  • Nutrisi treatmentChildren or adolescent calori requirement

    Carbohydrat : 55%-60%Protein : 10-20%Fat : 30%

  • **Insulin works best when it is injected into a layer of fat under the skin, above the muscle tissue.Rotating sites is important to insulin absorption.Common preferred sites are the abdomen, thighs, buttocks, and upper arms.Student should choose injection site.*****