childhood diabetes presentation

CHILDHOOD DIABETES

BYDR.AKINBI

OLUBAYODE.O

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.

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.

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

DIAGNOSTIC CRITERIA THE OGTT ( oral glucose tolerance test)-200mg/dl means diabetes-140 -199,9mg/dl means prediabetesLess than 140mg/dl means normal

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

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

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

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

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

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.

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

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:

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

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

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

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

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

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

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

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

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

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

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.

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

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

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)

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.

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

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

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

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

COMPLICATIONS OF DIABETES Macrovascular

Heart and blood vessels: High cholesterol Hypertension Atherosclerosis

Microvascular Retinopathy Nephropathy NeuropathyOthersKetoacidosis , infections, stroke, etc

THANK YOUMCI

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