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CHILDHOOD DIABETES MELLITUS

الكلية كلية التمريض     القسم قسم التخصصات التمريضية     المرحلة 2
أستاذ المادة عبد المهدي عبد الرضا حسن الشحماني       24/10/2014 08:48:46
CHILDHOOD DIABETES MELLITUS

الدكتور عبد المهدي عبد الرضا حسن الشحماني
كلية التمريض / جامعة بابل
PhD, pediatric & Mental Health Nursing
DEFINITION
? The term diabetes mellitus describes
a 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.
DIABETES EPIDEMIOLOGY
? Diabetes is the most common endocrine problem & is a major health hazard worldwide.
? Incidence of diabetes is alarmingly increasing all over the globe.
? Incidence of childhood diabetes range between 3-50/100,000 worldwide; in Oman it is estimated as 4/100000 per year.
OLD CLASSIFICATION (1985)
? Type 1, Insulin-dependent (IDDM)
? Type 2, Non Insulin-dependent (NIDDM)
– obese
– non-obese
– MODY
? IGT
? Gestational Diabetes
WHO CLASSIFICATION 2000
? Is based on etiology not on type of treatment or age of the patient.
? Type 1 Diabetes
(idiopathic or autoimmune ?-cell destruction)
? Type 2 Diabetes
(defects in insulin secretion or action)
? Other specific types
WHO CLASSIFICATION/2
? Both type 1 & type 2 can be further subdivided into:
? Not insulin requiring
? Insulin requiring for control
? Insulin requiring for survival
? Gestational diabetes is a separate entity
? Impaired Glucose Tolerance (IGT) indicates blood glucose levels between normal & diabetic cut off points during glucose tolerance test.
DIAGNOSTIC CRITERIA
? Fasting blood glucose level
? Diabetic
? Plasma >7.0 mmol
? Capillary >6.0 mmol
? IGT
? Plasma 6.0-6.9 mmol
? Capillary 5.6-6.0 mmol
? 2 hours after glucose load
(Plasma or capillary BS)
? IGT
? 7.8-11.0
? Diabetic level
? > 11.1 (200 mg)
Types of Diabetes in Children
? Type 1 diabetes mellitus accounts for >90% of cases.
? Type 2 diabetes is increasingly recognized in children with presentation like in adults.
? Permanent neonatal diabetes
? Transient neonatal diabetes
? Maturity-onset diabetes of the young
? Secondary diabetes e.g. in cystic fibrosis or Cushing syndrome.
MODY
? Usually affects older children & adolescents
? Not rare as previously considered
? 5 subclasses are identified, one subclass has specific mode of inheritance (AD)
? Not associated with immunologic or genetic markers
? Insulin resistance is present
TRANSIENT NEONATAL DIABETES
? Observed in both term & preterm babies, but more common in preterm
? Caused by immaturity of islet ?-cells
? Polyuria & dehydration are prominent, but baby looks well & suck vigorously
? Highly sensitive to insulin
? Disappears in 4-6 weeks
PERMANENT NEONATAL DIABETES
? A familial form of diabetes that appear shortly after birth & continue for life
? The usual genetic & immunologic markers of Type 1 diabetes are absent
? Insulin requiring, but ketosis resistant
? Is often associated with other congenital anomalies & syndromes e.g. Wolcott-Rallison syndrome.
TYPE 1 DIABETES: ETIOLOGY
? Type 1 diabetes mellitus is an autoimmune disease.
? It is triggered by environmental factors in genetically susceptible individuals.
? Both humoral & cell-mediated immunity are stimulated.

GENETIC FACTORS
? Evidence of genetics is shown in
? Ethnic differences
? Familial clustering
? High concordance rate in twins
? Specific genetic markers
? Higher incidence with genetic syndromes or chromosomal defects
AUTOIMMUNITY
? Circulating antibodies against ?-cells and insulin.
? Immunofluorescent antibodies & lymphocyte infiltration around pancreatic islet cells.
? Evidence of immune system activation. Circulating immune complexes with high IgA & low interferon levels.
? Association with other autoimmune diseases.
ENVIRONMENTAL INFLUENCE
? Seasonal & geographical variation.
? Migrants take on risk of new home.
? Evidence for rapid temporal changes.
? Suspicion of environmental agents causing disease which is confirmed by case-control experimental animal studies.
ENVIRONMENTAL SUSPECTS
? Viruses
? Coxaschie B
? Mumps
? Rubella
? Reoviruses
? Nutrition & dietary factors
? Cow’s milk protein
? Contaminated sea food
OTHER MODIFYING FACTORS
? The counter-regulatory hormones:
? glucagon
? cortisol,
? catecholamines
? thyroxin,
? GH & somatostatin
? sex hormones
? Emotional stress
ETIOLOGIC MODEL
? The etiologic model of type 1 diabetes resembles that of Rheumatic fever.
? Rheumatic fever was prevented by elimination of the triggering environ. factor (?-streptococci).
? Similarly type 1 diabetes may be prevented by controlling the triggering factors in high risk persons.
CLINICAL PRESENTATIONS
? Classical symptom triad:
? polyuria, polydipsia and weight loss
? DKA
? Accidental diagnosis
? Anorexia nervosa like illness
DIAGNOSIS
? In symptomatic children a random plasma glucose >11 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.
NATURAL HISTORY
? Diagnosis & initiation of insulin
? Period of metabolic recovery
? Honeymoon phase
? State of total insulin dependency
METABOLIC RECOVERY
During metabolic recovery the patient may
Develop one or more of the following:
• Hepatomegaly
• Peripheral edema
• Loss of hair
• Problem with visual acuity
These are caused by deposition of glycogen & metabolic re-balance.
HONEYMOON PERIOD
? Due to ?-cell reserve optimal function & initiation of insulin therapy.
? Leads to normal blood glucose level without exogenous insulin.
? Observed in 50-60% of newly diagnosed patients & it can last up to one year but it always ends.
? Can confuse patients & parents if not educated about it early.
COMPLICATIONS OF DIABETES
? Acute:
? DKA
? Hypoglycemia
? Late-onset:
? Retinopathy
? Neuropathy
? Nephropathy
? Ischemic heart disease & stroke
TREATMENT GOALS
? Prevent death & alleviate symptoms
? Achieve biochemical control
? Maintain growth & development
? Prevent acute complications
? Prevent or delay late-onset complications
TREATMENT ELEMENTS
? Education
? Insulin therapy
? Diet and meal planning
? Monitoring
? HbA1c every 2-months
? Home regular BG monitoring
? Home urine ketones tests when indicated
EDUCATION
? Educate child & care givers about:
? Diabetes
? Insulin
? Life-saving skills
? Recognition of Hypo & DKA
? Meal plan
? Sick-day management
INSULIN
? A polypeptide made of 2 ?-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 INSULIN
? Insulin 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.
TYPES OF INSULIN
? Short acting (neutral, soluble, regular)
? Peak 2-3 hours & duration up to 8 hours
? Intermediate acting
? Isophane (peak 6-8 h & duration 16-24 h)
? Biphasic (peak 4-6 h & duration 12-20 h)
? Semilente (peak 5-7 h & duration 12-18 h)
? Long acting (lente, ultralente & PZI)
? Peak 8-14 h & duration 20-36 h
INSULIN CONCENTRATIONS
? Insulin 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 REGIMENS
? Twice 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.
INSULIN ANALOGS
? Ultra short acting
? Insulin Lispro
? Insulin Aspart
? Long acting without peak action to simulate normal basal insulin
? Glargine
NEW INSULIN PREPARATIONS
? Inhaled 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 INSULIN
? Hypoglycemia
? Lipoatrophy
? Lipohypertrophy
? Obesity
? Insulin allergy
? Insulin antibodies
? Insulin induced edema
PRACTICAL PROBLEMS
? Non-availability of insulin in poor countries
? injection sites & technique
? Insulin storage & transfer
? Mixing insulin preparations
? Insulin & school hours
? Adjusting insulin dose at home
? Sick-day management
? Recognition & Rx of hypo at home
DIET REGULATION
? Regular meal plans with calorie exchange options are encouraged.
? 50-60% of required energy to be obtained from complex carbohydrates.
? Distribute carbohydrate load evenly during the day preferably 3 meals & 2 snacks with avoidance of simple sugars.
? Encouraged low salt, low saturated fats and high fiber diet.
EXERCISE
? Decreases insulin requirement in diabetic subjects by increasing both sensitivity of muscle cells to insulin & glucose utilization.
? It can precipitate hypoglycemia in the unprepared diabetic patient.
? It may worsen pre-existing diabetic retinopathy.
MONITORING
? Compliance (check records)
? HBG tests
? HbA1 every 2 months
? Insulin & meal plan
? Growth & development
? Well being & life style
? School & hobbies
ADVANCES IN MONITORING
? Smaller & accurate meters for intermittent BG monitoring
? Glucowatch continuous monitoring using reverse iontophoresis to measure interstitial fluid glucose every 20 minutes
? Glucosensor that measures s/c capillary BG every 5 minutes
? Implantable sensor with high & low BG alarm
ADVANCES IN MANAGEMENT
? Better understanding of diabetes allows more rational approach to therapy.
? Primary prevention could be possible if the triggering factors are identified.
? The DCCT studies proves beyond doubt that chronic diabetic complication can be controlled or prevented by strict glycemic control.
TREATMENT MADE EASY
? Insulin pens & new delivery products
? Handy insulin pumps
? fine micro needles
? Simple accurate glucometers
? Free educational material
? computer programs for comprehensive management & monitoring
TELECARE SYSTEMS
? IT has improved diabetes care
? Internet sites for education & support
? Web-based systems for telecare are now available. The patient feeds his HBGM data and get the physician, nurse & dietician advice on the required modification to diet & insulin treatment.
PITFALLS OF MANAGEMENT
? Delayed diagnosis of IDDM
? The honey-moon period
? Detection & treatment of NIDDY
? Problems with diagnosis & treatment of DKA & hypoglycemia
? Somogi’s effect (dawn phenomenon) may go unrecognized.
FUTURE PROMISES
? The cure for IDDM is successful islet cell transplantation, which will be available in the near future.
? Primary prevention by a vaccine or drug will be offered to at risk subjects identified by genetic studies.
? Gene modulation therapy for susceptible subjects is a promising preventive measure.
Pancreas & Islet Cell Transplantation
? Pancreas transplants are usually given to diabetics with end stage renal disease.
? Islet cell transplants, the ultimate treatment of type 1 diabetes is under trial in many centers in the US & Europe with encouraging results but graft rejection & recurrence of autoimmunity are serious limitations.
IMMUNE MODULATION
? Immunosuppressive therapy for
? Newly diagnosed
? Prolonged the honey moon
? For high risk children
? Immune modulating drugs
? Nicotinamide
? mycophenolate
GENE THERAPY
? Blocks the immunologic attack against islet-cells by DNA-plasmids encoding self antigen.
? Gene encode cytokine inhibitors.
? Modifying gene expressed islet-cell antigens like GAD.
PREDICTION OF DIABETES
? Sensitive & specific immunologic markers
? GAD Antibodies
? GLIMA antibodies
? IA-2 antibodies
? Sensitive genetic markers
• HLA haplotypes
• DQ molecular markers
PREVENTION OF DIABETES
? Primary prevention
• Identification of diabetes gene
• Tampering with the immune system
• Elimination of environmental factor
? Secondary prevention
• Immunosuppressive therapy
? Tertiary prevention
• Tight metabolic control & good monitoring
Dreams are the seedlings of realities


المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .