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Diabetes Mellitus in children for medical students

Diabetes Mellitus in children for medical students

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Diabetes Mellitus in children for medical students

  1. 1. Definition • It’s a chronic metabolic disorder characterized by hyperglycemia as a cardinal biochemical feature, caused by deficiency of insulin or its action, manifested by abnormal metabolism of carbohydrates, protein and fat
  2. 2. Epidemiology • Peaks of presentation occur in 2 age groups: at 5-7 yr of age (infectious) and at the time of puberty (gonadal steroids ). • Girls and boys are almost equally affected • There is no apparent correlation with socioeconomic status.
  3. 3. Incidence rates of type 1 diabetes mellitus by region and country
  4. 4. Diagnosis of diabetes is made when: • Symptoms + • random BGL ≥ 11.1 mmol/L (≥200 mg/dl) (or) • Fasting BGL ≥ 7mmol/L (≥ 126 mg/dl)
  5. 5. ETIOLOGIC CLASSIFICATIONS OF DIABETES MELLITUS Type I diabetes: (β-cell destruction, usually leading to absolute insulin deficiency) -Immune mediated. -Idiopathic. Type 2 diabetes: (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance). Other specific types : Genetic defects of β-cell function:Chromosome 7, glucokinase (MODY2) Genetic defects in insulin action:Rabson-Mendenhall syndrome Diseases of the exocrine pancreas: Pancreatitis Endocrinopathies: Cushing disease Drug- or chemical-induced : Glucocorticoids Infections:Cytomegalovirus Uncommon forms of immune-mediated diabetes :Stiff-man” syndrome Other genetic syndromes sometimes associated with diabetes :Down syndrome Gestational diabetes mellitus Neonatal diabetes mellitus
  6. 6. Physiology • The main function of insulin are: • 1. Reduce glucose by: • ↓ gluconeogenesis • ↓ glycogenolysis • ↑ uptake of glucose by cell • 2. Inhibit fat breakdown (lipolysis) • 3. Inhibit protein breakdown (proteolysis)
  7. 7. Insulin deficiency will lead to: 1. Hyperglycemia: increase glucose→ osmotic diuresis → polyuria → dehydration → compensatory polydepsia. 2. Proteolysis: → weight loss → Polyphagia. 3. Lipolysis: ↑ free fatty acids and accumulation of acetyl Co-A → Liver → keton bodies → ketonemia → ketonuria & Metabolic acidosis.
  8. 8. Presentation: 1. Although most symptoms are nonspecific 2. polyuria , polydepsia, Polyphagia & weight loss. 3. Recurrent infection: skin or UTI. 4. Diabetic Ketoacidosis
  9. 9. Investigations: • Blood glucose : Fasting glucose > 126 mg/dl & Random > 200 mg/dl. • HbA1c: (glycated haemoglobin) average over the last 2-3 months. Measures amount of glucose that attaches to haemoglobin, The target HbA1c < 7.5% (58 mmol/mol). • Ketone testing: either urine strips, or blood. • Urine: glucosuria & Ketonuria if DKA suspected.
  10. 10. Management • Need team & Special diabetic Clinic? • Medical: specialist • Specialist Nurses: • Dietitian. • Psychologist • Equipments: insulin, glucometer, Ketones meter and good maintenance. • Good follow up.
  11. 11. Treatment Insulin Nutrition
  12. 12. Types of Insulin
  13. 13. Types of presentation If newly diagnosed: 1. DKA: according to Guideline. 2. Only hyperglycemia. Already diabetes on insulin therapy with: 1. DKA: according to Guideline. 2. Presence of ketonemia? 3. Only hyperglycemia? Not controlled?
  14. 14. 1. Diabetic Ketoacidosis (DKA): • Occurs when there is profound insulin deficiency. • It frequently occurs at diagnosis and also in children and youth with diabetes if insulin is omitted, or if insufficient insulin is given at times of acute illness. • The biochemical criteria for DKA are:  Hyperglycaemia (blood glucose >11mmol/l (~200 mg/dl))  Venous pH <7.3 or bicarbonate <15 mmol/l  Ketonaemia and ketonuria
  15. 15. Management of DKA • Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications . • Fluid infusion should precede insulin administration by 1–2 hours; • an initial bolus of 20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 10% dehydration. • Insulin administration (0.1 U/kg/h) • Potassium (K) must be replaced early and sufficiently. • Bicarbonate administration is contraindicated.
  16. 16. Treatment
  17. 17. 2. New-Onset Diabetes without Ketoacidosis • Ideally, therapy can begin in the outpatient setting, with diabetic team. (we prefer admission). • There are many Insulin regimens for treatment with many advantages and disadvantages • We have to select one ??
  18. 18. Insulin regimens A. Conventional Insulin therapy: Twice daily mixed Insulin. B. Intensive Insulin therapy: 1. Basal – Bolus(3 Injections): o 2 bolus of short acting before breakfast and lunch + o Mixture of short acting and Intermediate acting at evening meal. 2. Basal – Bolus(3 +1 Injections): o 3 bolus of short acting before breakfast + lunch + evening meal + o Intermediate acting before bedtime. 3. Basal – Bolus(3 +1 Injections): o 3 bolus of Rapid acting before breakfast + lunch + evening meal + o Long acting before bedtime. 4. Basal – Bolus(3 +1 Injections): o Long acting before bedtime. o Rapid acting before meal according to Carbohydrate Counting and Insulin Correction
  19. 19. 2. New-Onset Diabetes without Ketoacidosis Insulin regimens 50% of the total daily dose Rapid -acting insulin (NovoRapid Pen) divided up between 3 pre- meal boluses 50% of the total daily dose long-acting insulin (Lantus® (insulin glargine Pen) single evening injection Insulin requirements: Start with 0.5 IU/kg/day Pre-pubertal 0.7-1.0 IU/kg/day. During puberty 1 and even up to 2 U/kg/day. The correct dose of insulin is that which achieves the best glycaemic control
  20. 20. BLOOD GLUCOSE MONITORING • Blood glucose monitoring should ideally be carried out 4-6 times a day, however, this is dependent on the availability of testing strips. • Recommended target blood glucose levels: Blood Glucose Targets for Most People with Diabetes During the day 4.5-7mmol/l 80-125mg/dl Overnight & pre breakfast 5.5 -8mmol/l 100-145 mg/dl
  21. 21. Exercise • Regular exercise; improves glucoregulation by increasing insulin receptor number. • No form of exercise, including competitive sports, should be forbidden to the diabetic child. • In patients who are in poor metabolic control, vigorous exercise may precipitate ketoacidosis because of the exercise-induced increase in the counter-regulatory hormones. • A major complication of exercise in diabetic patients is the presence of a hypoglycemic reaction during or within hours after exercise.
  22. 22. • The major contributing factor to hypoglycemia with exercise is an increased rate of absorption of insulin from its injection site. • In anticipation of vigorous exercise, additional carbohydrate exchange may be taken before exercise, and glucose should be available during and after exercise. • The total dose of insulin may be reduced by about 10-15% on the day of the scheduled exercise. Exercise
  23. 23. Diet • There are 3 main nutrients in foods—fats, proteins, and carbohydrates. • Fats: Fat typically doesn't break down into sugar , and in small amounts, it doesn't affect blood glucose levels. • Proteins: Protein doesn't affect blood glucose unless the patient eat more than the body needs. • Carbohydrates: Carbohydrates affect blood glucose more than any other nutrient.
  24. 24. Diet • The same total caloric intake as usual in normal child is given with the same ratio • 50% CHO • 35% Fat • 15% Proteins • Number of meals is preferred to be three fixed major with two snakes in between.
  25. 25. Patient Education
  26. 26. Family Education
  27. 27. Dietary Education
  28. 28. Nurse Advices & Education
  29. 29. Nurse Advices & Education
  30. 30. Psychological support & Education
  31. 31. Screening for complications and associated conditions • height and weight & state of injection sites at each clinic visit. • Thyroid disease & coeliac disease at diagnosis and annually. • annual foot care reviews. • Regular dental and eye examinations every 2 years. • from the age of 12 years: blood pressure, retinopathy, microalbuminuria & S.Creatinine.
  32. 32. Special consideration • Partial Remission or Honeymoon Phase in Type 1 Diabetes • Somogi Phenomena • Dawn Phenomena. • Management of DM during Infection.
  33. 33. Partial Remission or Honeymoon Phase in Type 1 Diabetes • Insulin requirements can decrease transiently following initiation of insulin treatment. • This has been defined as insulin requirements of less than 0.5 units per kg of body weight per day with an HbA1c < 7%. • Ketoacidosis at presentation and at a young age reduce the likelihood of a remission phase. • It is important to advise the family of the transient nature of the honeymoon phase to avoid the false hope that the diabetes is spontaneously disappearing. • Treatment by reduce the dose of Insulin Accordingly.
  34. 34. • In children with High dose of Insulin at Night (Long acting) develop late night(3-4 a.m) Hypoglycemia Counter regulatory hormon will increase Early morning Hyperglycemia. • Treatment: Reduce the dose of Long acting Insulin at Night . Somogyi Phenomenon
  35. 35. • In children with Normal dose of Insulin at Night & Normal midnight glucose (Normoglycemia), Counter regulatory hormone may normally increase Early morning Hyperglycemia. • Treatment: Increase the dose of Long acting Insulin at Night . Dawn Phenomenon
  36. 36. • Infection may precipitate hyperglycemia or DKA. • Mild infection should be treated + increase the dose of Insulin by 10 – 15%. • Sever infection necessitate hospitalization. Management during Infection
  37. 37. Important information • Do not shake the insulin as this damages the insulin? • After first usage, an insulin vial should be discarded after 3 months if kept at 2-8 C or 4 weeks if kept at room temperature. • Intermediate-acting and short-acting/rapid- acting insulin, can be combined in one Syringe. • Use 4mm needle for injection of Insulin SC.
  38. 38. THANKS FOR YOUR Attention

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Diabetes Mellitus in children for medical students


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