Presentation is loading. Please wait.

Presentation is loading. Please wait.

1 Paediatric And Adolescent Diabetes Care Dr Noman Ahmad 3 rd February 2011 Cork University Hospital.

Similar presentations


Presentation on theme: "1 Paediatric And Adolescent Diabetes Care Dr Noman Ahmad 3 rd February 2011 Cork University Hospital."— Presentation transcript:

1 1 Paediatric And Adolescent Diabetes Care Dr Noman Ahmad 3 rd February 2011 Cork University Hospital

2 2 Presentation Outline Definition Classification Pathophysiology Clinical Presentation Insulin types and regimens Insulin dose in different age groups Follow-up/Monitoring

3 3 Learning Objectives Understanding of insulin pharmacokinetics Right insulin regimen Aims of glycaemic control Complexity of management in different age groups

4 4 Definition Diabetes mellitus is group of metabolic diseases characterised by chronic hyperglycaemia resulting from defects in insulin secretion, action or both International society of paediatric and adolescent diabetes

5 5 Insulin Physiology

6 6 Classification Type 1 diabetes (IDDM) Type 2 diabetes (NIDDM) Monogenic diabetes (MODY) Neonatal diabetes (Transient first 3 months) Mitochondrial diabetes Cystic fibrosis related diabetes (CFRD) Drug induced hyperglycaemia

7 7 Pathophysiology T1DM Autoimmune destruction (T1A DM) Non autoimmune destruction (T1B DM) Multiple genes HLA genes (DR, DQ alpha, DQ beta) Autoantigen (Islet cells, Insulin, glutamic acid decarboxylase GAD 65, Isulinoma associated protien 2 IA-2, Zinc transporte ZnT8

8 8 Pathophysiology T1DM Environmental factors Viruses (Entero, Coxsackie, EBV) Cow’s milk Perinatal factors Vitamin D

9 9 Pathophysiology T1DM Association with other autoimmune diseases Thyroid 20% Adrenal 1.7% Coeliac disease 10% Polyglandular autoimmune disease

10 10 Pathophysiology T1DM Genetic predisposition HLA associations Environment Viruses, toxins, cow’s milk Immune dysregulation GAD 65, IA-2,Insulin, ZnT8,Islet cells Beta islet cell destruction Insulin deficiency Type 1 diabetes

11 11 Pathophysiology of T2DM

12 12 Presentation of T1DM Classic (most common)  Polyuria, polydipsia and weight loss Diabetic ketoacidosis  Hyperglycaemia, metabolic acidosis and ketonuria Silent  Usually siblings of known cases

13 13 Presentation of T2DM Girls 1.7 times more common Obesity, signs of insulin resistance (acanthosis nigricans) Strong family history, LBW, gestational diabetes Insulin resistant states (puberty, PCOS) Impaired OGTT Elevated A1C DKA Hyperosmolar coma with no ketunuria

14 14 Acanthosis Nigricans

15 15 INSULIN TYPES Short acting Regular Analogs (Novorapid,Humolog,Apidra) Intermediate acting NPH Long acting Detemir (Levemir) Glargine (Lantus)

16 16 Pharmacokinetics

17 17 Pharmacokinetics

18 18 Insulin Regimens Conventional  Premixed (Mixtard 30, Novomix 30)  Short acting(Novorapid) and intermediate acting (NPH) Intensive  MDI (Lantus or Levemir and Novorapid)  Insulin pump (CSII)

19 19 Insulin Regimens Conventional  Positives Twice a day No carbohydrate counting Good for new patients and school going kids Less chance of DKA  Negatives Non physiological Less flexible More risk of hypoglycaemia Loose glycaemic control

20 20 Conventional Regimen Novorapid Insultard (NPH) 0 304 61216 18

21 21 Insulin Regimen (MDI)

22 22 Insulin Regimen (MDI) Intensive  Positive Physiological Flexible Less risk of hypoglycaemia Good for teenagers Less long term side effects Better glyceamic control  Negatives More injections Carbohydrate counting More risk of DKA

23 23 Insulin Pump Continuous basal infusion Bolus with every meal or snack Correction bolus Regular or rapid insulin

24 24 Insulin Pump

25 25 Insulin Pump

26 26 Insulin Pump Advantages  Flexible  Precise  Better glycaemic control  Less variability  Less Hypoglycemia  Less long term complication

27 27 Insulin Pump Disadvantage  Tethered with device  Cost  Infection  Equipment failure  Carbohydrate counting  DKA  Hinder in some activities

28 28 Injection Sites Fast absorption in abdomen Slow in legs Intermediate in arms Subcutaneous fat Skin very slow absorption Muscles too fast

29 29 High Insulin Doses Growth Puberty Sickness Stress Active/competitive sports Steroid therapy No physical activity

30 30 Target Blood Glucose Preprandial  CDA 2008 0-6 years6-12 6-12 years4-10 >12 years4-7  ISPAD 2009 5-8 for all kids 2 hours postprandial 5-10 for all kids

31 31 Target HbA1C CDA 2008  <6 years8.5%  6-12< 8%  >12 years≤ 7% ISPAD 2009  < 7.5% for all kids

32 32 Clinic Visit History  Glucose diary  Hypoglycaemia  Intercurrent illness  Thyroid, adrenal, coeliac  Exercise  Hypoglycaemia supplies

33 33 Clinic Visit Examination  Growth, weight, BP  Thyroid  Injection sites  Finger poke sites  Pubertal exam  Retinal exam  Prayer signs

34 34 Clinic Visit Investigations  HbA1C every 3 months  TSH annually  Coeliac screen  Lipid profile  Albumin creatinine ratio  Eye exam

35 35 Infants And Toddlers Brain is very sensitive to hypoglycaemia Sensitive to Regular/rapid insulin Picky eater May need to give insulin after meals

36 36 Adolescents Insulin resistance Non compliance Fabrication Denial Eating out and snacking Family conflicts Alcohol Eating disorders

37 37 QUESTIONS


Download ppt "1 Paediatric And Adolescent Diabetes Care Dr Noman Ahmad 3 rd February 2011 Cork University Hospital."

Similar presentations


Ads by Google