childhood diabetes presentation
TRANSCRIPT
![Page 1: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/1.jpg)
CHILDHOOD DIABETES
BYDR.AKINBI
OLUBAYODE.O
![Page 2: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/2.jpg)
DEFINATION
Diabetes mellitus - a chronic metabolic disorder of multiple aetiologies characterized by chronic hyperglcemia with disturbances of CHO, fat & protein metabolism resulting from defects in insulin secretion, action or both.
![Page 3: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/3.jpg)
EPIDEMIOLOGY Most common endocrine-metabolic
disease in childhood and adolescents Incidence of diabetes is alarming and
increasing all over the globe Incidence of childhood diabetes ranges
from 3-50/100,000 worldwide.
![Page 4: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/4.jpg)
DIAGNOSTIC CRITERIA THE A1C TEST-6.5% means diabetes-5-7-5.99% means prediabetes-less than 5.7% means normal THE FPG( fasting plasma glucose test)-126mg/dl means diabetes-100 – 125.99mg/dl means prediabetes-less than 100mg/dl means normal
![Page 5: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/5.jpg)
DIAGNOSTIC CRITERIA THE OGTT ( oral glucose tolerance test)-200mg/dl means diabetes-140 -199,9mg/dl means prediabetesLess than 140mg/dl means normal
![Page 6: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/6.jpg)
![Page 7: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/7.jpg)
CLASSIFICATION T1DM. - Most common type of DM in C &
adolescents accounts for 90% of cases. Epidemic of T2DM now being observed in
most societies around the world. (↑obesity, ↑cal diet, sedentary life style)
Permanent neonatal diabetes Transient neonatal diabetes Maturity-onset diabetes of the young Secondary diabetes e.g, cystic fibrosis,
cushing syndrome
![Page 8: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/8.jpg)
MODY Uncommon but distinct entity Presentation < 25yrs, often teenager Ass. with mutations of glucokinase gene
in chromosome 7 Not associated with immunologic or
genetic markers Insulin resistance is present
![Page 9: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/9.jpg)
TRANSIENT NEONATAL DIABETES
Observe in both term and preterm babies, but more common in preterm.
Caused by immaturity of islet of β-cells Polyuria & dehydration are prominent,
but baby looks well and suck vigorously Highly sensitive to insulin Disappears in 4-6 weeks
![Page 10: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/10.jpg)
PERMANENT NEONATAL DIABETES
A familial form of diabetes that appear shortly after birth and continue for life
The usual genetic and immunologic markers of type 1 diabetes are absent
Insulin requiring, but ketosis resistant Is often associated with other congenital
anomalies and syndromes e.g, walcott-Rallison syndrome
![Page 11: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/11.jpg)
TYPE 2DIABETES Previously known as Adult-onset, NIDDM,
MODY Usually obese;↑ incidence because of↑
childhood obesity Not Insulin-Dependent (except during
stress etc for symptomatic hyperglycemia)
Not ketosis-prone (severe infectns, stress Insidious presentation usually- (routine
medical exam or for other problems
![Page 12: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/12.jpg)
TYPE 2 DIABETES Minority of all DM pts in paediatric years
(10-20%) Inherited nature – stronger than T1DM Concordance for identical twins - >ter
(80-90%) No known HLA or ass. with autoimm
markers or dx.
![Page 13: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/13.jpg)
Hyperglycemia
Metabolic Defects in Type 2 Diabetes
Pancreas
Liver Muscle and Adipose
Hepatic Glucose Insulin Production - Resistance Glucose
Uptake Insulin
Resistance -
Progressive Insulin Secretory Defect
![Page 14: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/14.jpg)
SCREENING FOR TYPE2 DM IN CHILDREN
Criteria: overweight (BMI > 85th %ile for age and sex,
weight for height > 85th %ile, or weight > 120% of ideal for height)
Plus any two of the following risk factors:
![Page 15: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/15.jpg)
RISK FACTORS FOR TYPE 2• family history of type 2 diabetes in first- or
second-degree relative• race/ethnicity (American Indian, African-
American, Hispanic, Asian/Pacific Islander)• signs of insulin resistance (acanthosis
nigricans, hypertension, dyslipidemia, polycystic ovary syndrome
![Page 16: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/16.jpg)
MANAGEMENT OF TYPE2 DM
Cornerstone - Modify diet ↑dly exercise Pharmacologic tx if BG is frequently
>200mg/dl, HbA1c > 8% Sulphonylurea- ↑ Insulin secretion
(cheap, convenient & effective in 3-7 days)
SE- refraction, hypoglcemia
![Page 17: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/17.jpg)
MANAGEMENT OF TYPE2 DM
Metformin (glucophage) – biguanide -Now 1st line for T2DM -Mechanism- not fully known but 1oly
↓hepatic glucose production -SE- GIT symptoms, lactic acidosis -CI- liver, renal failure, metabolic acidosis
![Page 18: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/18.jpg)
MANAGEMENT OF TYPE2 DM
Thiazolinediones- ↓peripheral insulin resistance in muscle & fat
Glucosidase inhibitors- competitive inhibitors of enzymes on intestinal brush border. Hence limit CHO absorption & minimize post prandial hyperglycemia
![Page 19: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/19.jpg)
TYPE 1 DIABETES Autoimmune destruction of the beta cells
of the pancreas Insulin deficiency Insulin is necessary for survival
Diabetic Ketoacidosis (DKA) Usually an acute onset
![Page 20: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/20.jpg)
TYPE 1 DIABETES Accounts for > 90% of Childhood &
Adolescent DM. 3-50/100,000 C < 15yrs dev T1DM annually
with wide global variations in incidence Whites of N. European descent more likely
than Blacks, Asians. Can manifest at any age (approx 50% at >
18yrs) Bimodal peak age distribution: 5-7yrs &
puberty Worldwide↑ in No of young C being
diagnosed with T1DM especially in ↓ 5yrs
![Page 21: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/21.jpg)
RISK FACTOR FOR TYPE1 Chronic Autoimmune dx – vast majority
(HLA DR3 & 4, B8,BW15 on chr 6) T-cell mediated autoimmune destruction
of pancreatic β-cells in genetically predisposed C. (Islet AB, Insulin AB)
Idiopathic - few
![Page 22: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/22.jpg)
RISK FACTOR FOR TYPE1 Siblings 5-6%, Mother 3-4%, Father 6%,
5-10% both parents, Monozygotic twins 30-40%, general population 0.4%
Seasonal factors-new cases > in winter/autumn
![Page 23: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/23.jpg)
PATHOPHYSIOLOGY OF TYPE 1 Insulinopenia→↓ glucose utiliztn (muscle, fat)
→post prandial hyperglcemia, at lower Insulin levels→ ↑hepatic glycogenolysis/ gluconeogenesis → fasting hyperglycemia → osmotic diuresis
→ glucosuria (> renal threshold-180mg /dl-10mM/L→calorie & E- loss →dehydratn
![Page 24: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/24.jpg)
PATHOPHYSIOLOGY OF TYPE 1 →physiological stress →↑epinephrine,
cortisol, GH, glucagon→ worsens metabolic decompensation→↑ lipolysis & impaired lipid synthesis → ↑FFA, cholest, TGA → ketones- (βOH butyrate, acetoacetate, acetone) →buffer depleted →metabolic acidosis (DKA) –Kussmaul resp- deep, rapid resp to excrete excess CO2
→ ketonuria → ↑ H2O & E-loss →hyper osmolality
→dec cerebral O2 use →impaired consc, coma
![Page 25: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/25.jpg)
MANAGEMENT Dreadful disease, requires team support:
paediatrician, nurse educator, dietician, mental health professional, social worker, peer discussion group, summer camps, role models, support groups
Aims of therapy: Provide N growth, puberty, psychomotor
development & well being Exercise is an integral component of
growth & dev. No sport is excluded.
![Page 26: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/26.jpg)
MANAGEMENT Nutrition- 1 of cornerstone of mx No sp nutrition required other than for
optimal growth & dev. Same food type as for gen populatn
Regular eating pattern for Insulin regimen Individual nutritional reqment & meal
plan based on age, sex, wt, activity, preferences
![Page 27: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/27.jpg)
MANAGEMENT Meal plan: 50% CHO- 70% as Complex eg
starch to prolong digestion & absorption for slow rise of BG
Avoid refined sugars, give high fiber diet eg veg, legumes, whole-meal bread, cereals diet & sugar- free carbonated drinks,
Lipids-30%- limit cholesterol; poly :unsat ≥2:1 –fat from plant( marg, veg oil to reduce LDL & cholest
20% protein (plant)- limit egg-yolk, give fish poultry, lean-cut meat
![Page 28: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/28.jpg)
MANAGEMENT BG target: fasting/ preprandial – 70-
130mg/dl After meals < 180mg/dl Night: not < 60mg/dl (early morning
headache- suggestive of hypoglycemia in the night)
![Page 29: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/29.jpg)
INSULIN Insulin is a hormone produced in the beta
cells of the Islets of Langerhans in the pancreas
FUNCTION: To allow glucose to pass into the cell To decrease physiological production of
glucose by the liver and muscle To turn off ketone production.
![Page 30: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/30.jpg)
INSULIN Insulin: replacement required in T1DM,
even the small no of T2D are usually txed Wide variations in regimen Single dly injection (intermediate –
acting) rarely successful Multiple dly injections or continuous s/c
infusions – offers flexibility
![Page 31: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/31.jpg)
TYPES OF INSULIN Rapid Acting:
Insulin lispro (Humalog) ® Insulin aspart (Novolog) ® Insulin glulisine (Apidra) ®
Short-acting: regular
Intermediate-acting: NPH (Neutral Protamine Hagedorn)
Long-acting: Insulin glargine (Lantus) ® Insulin detemir (Levemir
![Page 32: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/32.jpg)
INSULIN ADMINISTRATION
Syringes: short needle, mixing insulins Pen injectors: flexibility Insulin Pumps; Continuous subcutaneous
insulin infusion (CSII) devices Insulin to Carbohydrate ratio
Unit: Grams of CHO Example: 1 unit : 15 grams of CHO
![Page 33: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/33.jpg)
OUT-PATIENT MANAGEMENT
Goals Stabilize BG within target range Avoid metabolic decompensatn (DKA,
hypoglycemia) Ensure N growth & dev- physical &
emotnal Prevent long-term complicatn Preprandial BG- 80-120mg/dl 2hr pp < 180mg/dl Bedtime- 100-140mg/dl HbA1c within 1% of high normal for
method used
![Page 34: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/34.jpg)
COMPLICATIONS OF DIABETES Macrovascular
Heart and blood vessels: High cholesterol Hypertension Atherosclerosis
Microvascular Retinopathy Nephropathy NeuropathyOthersKetoacidosis , infections, stroke, etc
![Page 35: Childhood diabetes presentation](https://reader035.vdocuments.mx/reader035/viewer/2022062503/58ac6b231a28abd7488b5c6b/html5/thumbnails/35.jpg)
THANK YOUMCI
www.mediconsultinitiative.com