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TYPE 2 DIABETES MELLITUS

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Title: TYPE 2 DIABETES MELLITUS


1
TYPE 2 DIABETES MELLITUS
  • BY
  • JEROME ELUSIYAN
  • PAED. ENDOCRINOLOGY FELLOWSHIP, KENYA

2
OUTLINE
  • INTRODUCTION
  • EPIDEMIOLOGY
  • PATHOPHYSIOLOGY
  • CLINICAL FEATURES
  • DIAGNOSIS
  • TREATMENT
  • CONCLUSION

3
INTRODUCTION
  • Increasing awareness of non type1 DM since1916
  • Changing pattern of food consumption and
    exercise, life style westernization
  • Increasing incidence of Overweight and Obesity
  • Matter of concern long term complications and
    public health concern

4
EPIDEMIOLOGY
  • Common in American Indians, African Americans,
    and Hispanics and whites
  • Prevalence and incidence is increasing WORLD-
    WIDE
  • 10 fold increase in incidence in the past decade
  • prevalence of 22.3 per 1000 (10-14 yrs) 50.9 per
    1000 (15-19yrs) among Pima Indians

5
EPIDEMIOLOGY CTD
  • accounts for approximately 15 to 45 of all new
    cases of childhood diabetes

6
RISK FACTORS
  • Obesity (85 are obese)
  • family history ( 75-100 have a positive family
    history in10 or 20 relative)
  • female gender,
  • puberty
  • Genetic ( complex and incompletely defined 100
    concordance among twins)

7
PATHOGENESIS / PATHOPHYSIOLOGY
  • Precise mechanism is poorly understood
  • Insulin resistance of skeletal muscle
  • Enhanced hepatic glucose production
  • Decreased glucose-induced insulin secretion(
    glucotoxicity and lipotoxicity on ß-cell
    function)
  • Under expression of IGF-II in-utero leading to
    reduced ß-cell mass

8
OBESITY DM
  • Adipose tissue synthesize and secretes
    metabolites signalling proteins that alter Ins.
    secretion, sensitivity even cause I resistance
  • Metabolites Fatty acids, Glycerol and Acetate
  • Signalling Proteins Leptin, Adipsin, Acylation
    stimulating Protein,Plasminigen-activator-inhibito
    r1, interleukin-6,-8, TNFœ, Adiponectin,
    Renin-angiotensinogen, Resistin, Progstaglandin

9
CLINICAL FEATURES
  • Presence of risk factors
  • Elevated RBS, OR Positive urine glucose on
    Routine screening
  • Mild polyuria and polydipsia in some
  • Girls may complain of candida infection
  • 1/3rd may have ketonuria, and 5-25 may have
    ketoacidosis at presentation

10
CLINICAL FEATURES
  • Non ketotic hyperglycaemic coma
  • Immunologic markers of type1 DM are usually
    absent but may be positive in up to 1/3rd of
    Adolescents
  • Insulin and/ or C peptide may be normal or
    elevated
  • May have Acanthosis nigricans and
    hyperandrogenism are also seen( as marker of
    insulin resistance)

11
TREATMENT
  • The treatment goal for type 2 diabetes is to
    correct metabolic imbalance and maintain
    euglycemia in order to avoid short- and long-term
    complications and maintain physical and
    psychological well-being.

12
TREATMENT
  • Multidisciplinary
  • Comprehensive self-management education
  • Dietary counseling (culturally appropriate)
  • Physical Exercise
  • Follow-up
  • Drugs often time are NEEDED

13
TREATMENT
  • Initial treatment depends on presentation
  • May require Insulin, if there is significant
    hyperglycaemia, ketosis or ketoacidosis
  • Once metabolically stable, oral agents are
    introduced and weaned off insulin
  • Limited experience with drugs in children
  • Start with Metformin 500mg B.D
  • May require addition of 1or more drugs

14
Drug Class Mechanism of Action Examples Important Side Effects
Biguanides-- Decrease hepatic glucose output-- Enhance hepatic insulin sensitivity Metformin-- Abdominal cramping and diarrhea Lactic acidosis
Sulfonylureas Promote insulin secretion Acetohexamide, chlorpropamide, gliclazide, glipizide, glyburide, others Hypoglycemia
Meglitinide Promotes glucose-mediated insulin secretion Repaglinide Hypoglycemia
Glucosidase inhibitors Slows hydrolysis and absorption of complex carbohydrates Acarbose, miglitol Abdominal cramping and diarrhea
Thiazolidenediones Enhance peripheral insulin sensitivity Troglitazone, rosiglitazone, pioglitazone Hepatic toxicity (common to drug class?)
15
TREATMENT CTD.
  • Monitoring and follow up helps maintain
    motivation, reinforce healthy habits, and
    identify unmet needs.
  • Quarterly glycosylated haemoglobin monitoring
  • Regular BP monitoring
  • Yearly screening for microalbuminuria,
    retinopathy, and lipid abnormalities helps early
    detection and treatment

16
TREATMENT
  • PREVENTION OF OBESITY-lifestyle changes in
    physical activity and food intake are implemented
    in individuals at risk
  • Efforts should be directed toward the individual,
    the family, and society as a whole
  • particular attention must be given to the school
    setting.

17
  • screening recommendations proposed recently by
    the American Diabetes Association.
  • testing should be done every 2 years starting at
    age 10 or at onset of puberty in an individual
    who is overweight and has any 2 of the following
    risk factors

18
  • Family history of type 2 diabetes in first- and
    second-degree relatives
  • Membership in a high-risk ethnic group
  • Signs of insulin resistance or conditions
    associated with insulin resistance
  • a fasting plasma glucose or a 2-hour postprandial
    glucose is a suitable test.

19
Maturity onset diabetes of youth (MODY)
  • This is a genetically and clinically
    heterogenous subtype of Type 2 DM characterised
    by early onset between the ages of 9 and 25
    years, autosomal dominant inheritance and a
    primary defect in insulin secretion.
  • Criteria for diagnosis
  • - Type 2 DM in at least 3 generations
  • - autosomal dominant transmission and
  • - diagnosis before age 25 years in at
    least one affected subject.

20
  • MODY 1Results from a mutation in the hepatocyte
    nuclear factor (HNF)-4a ( long arm of chrm 20)
  • MODY 2 results from a mutation in the gene for
    glucokinase (short arm chrm 7)
  • MODY 3 HNF-1a ( long arm chrm 12)
  • MODY 2 results in mild, chronic hyperglycaemia

21
MITOCHONDRIA GENE DEFECTS
  • Point mutation in mitochondrial DNA are
    associated with DM and deafness (mutation
    identical to MELAS mutation)
  • Wolfram Syndrome xterised by Diabetes insipidus,
    DM, optic atrophy, and deafness- DIDMOAD- occurs
    sequentially DM (1ST decade), DI Deafness (2nd
    decade),RTAnomally(3rd decade),neurologic
    complications (4th)

22
CONCLUSION
  • T YPE 2 DM has become a major problem in
    Paediatrics, coupled with the increasing
    incidence of TYPE 1 DM posses a lot of challenge
    to Child health
  • Efforts at preventing childhood obesity can not
    be too much if the incidence of Type 2 DM and
    its consequent effects are to be halted

23
THANK YOU ALL
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