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Diabetes Mellitus

Diabetes Mellitus. Diabetes Mellitus epidemiology. World WHO 2004 > 150 million China at present > 40million The second in the word annual gain >10%. concept.

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Diabetes Mellitus

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  1. Diabetes Mellitus

  2. Diabetes Mellitus epidemiology • World WHO 2004 > 150 million • China at present > 40million • The second in the word • annual gain >10%

  3. concept • Diabetes Mellitus is a syndrome with chronic hyperglycemia due to either a deficiency of insulin secretion or to a combination of insulin resistance and inadequate insulin secretion to compensate and leads to dysmetabolism of proteins, lipid as well as many other metabolites and elements.

  4. Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an autoimmune process , and these patients are prone to ketoacidosis. • Type 2 diabetes is the more prevalent form and results from insulin resistance with a defect in compensatory insulin secretion.

  5. CLASSIFICATION AND PATHOGENESIS • Clinical findings • Differential Diagnosis • Treatment : Diabetes MellitusDiet

  6. CLASSIFICATION AND PATHOGENESIS • Diabetes is now classified according to its etiology recommended by the American Diabetes Association (ADA) in 1997 and revised by WORLD Health Organization in 1999(usually referred to WHO/1999 Recommendation

  7. TYPE 1 DIABETES MELLITUS • The form of diabetes is immune –mediated in over 90% of cases and idiopathic in less than 10% .The rate of pancreatic B cell destruction is quite variable ,being rapid in some individuals and slow in others

  8. TYPE 1 DIABETES MELLITUS • It can occur at any age but most commonly arises in children and young adults with a peak incidence before school age and again at around puberty before last century

  9. TYPE 1 DIABETES MELLITUS • It is a catabolic disorder in which circulating insulin is very low or virtually absent . • The insulin secretion, due to the pancreatic B cell destruction ,fails to meet the requirement of nutrient absorption.

  10. TYPE 1 DIABETES MELLITUS • Exogenous insulin is therefore required to reverse the metabolic state, prevent ketosis, reduce the hyperglucagonemia ,and maintain glucose homeostasis.

  11. TYPE 1 DIABETES MELLITUS • Certain human leukocyte antigens (HLA) are strongly associated with the development of type 1 diabetes. • About 95% of type 1 patients possess either HLA-DR3 or HLA-DR4, compared with 45%-50% of white controls

  12. TYPE 1 DIABETES MELLITUS • HLA-DQ genes with even more specific ,markers of type 1 susceptibility, since a particular variety (HLA-DQB1*0302 )is found in the DR4 patients with type 1,while a “protective ”gene (HLADQB1*0602) is often present in the DR4 controls.

  13. TYPE 1 DIABETES MELLITUS • Recently it was found the freqency of “susceptible” genotype decreases and the frequency of “protective ”genotype increased as the onset age of a subject becomes older.

  14. TYPE 1 DIABETES MELLITUS • In addition , most patients with type 1 diabetes at diagnosis have circulating antibodies to islets (islet cell antibodies, ICA), insulin antibodies(IAA) ,glutamic acid decarboxylase (GAD 65),and to tyrosine phosphatases(IA-2 and IA2-b, IA is the abbreviation for insulinoma associated antigen).

  15. TYPE 1 DIABETES MELLITUS • The antibody levels decline with increasing duration of the disease. • Also, once patients are treated with insulin ,low levels of anti-bodies develop.

  16. TYPE 1 DIABETES MELLITUS • More recently regulatory T cell and cytotoxic T cell abnormality were considered to be critical in the development of isletitis and b cell destruction.

  17. TYPE 1 DIABETES MELLITUS • The polymorphism in gene encoding cytotoxic lymphocyte antigeng4 (CTLA-4) was found related to development of autoimmune diabetes as well as autoimmune thyroiditis. • B-cell reactive T cell avidity was proposed at the beginning of isletitis.

  18. TYPE 1 DIABETES MELLITUS • Certain unrecognized patients with a milder expression of type 1 diabetes initially retain enough b cell function to avoid ketosis but later in life develop increasing dependency on insulin therapy as b cell mass diminishes (usually 6 years after dignosis).

  19. TYPE 1 DIABETES MELLITUS • Islet cell antibody survey among northern Europeans indicate that up to 15% of “type 2”patients may actually have this mild form of type 1 diabetes (latent autoimmue diabetes of adulthood, LADA)

  20. TYPE 2 DIABETES MELLITUS • This presents a heterogeneous group comprising milder forms of diabetes that occur predominantly in adults but occasionally in juveniles. • More than 90% of all diabetes in the United States and China are included under this classification . • In most cases of this type of diabetes, this cause is unkown.

  21. TYPE 2 DIABETES MELLITUS • The pathogenesis currently received is illustrated in (Figure 6-18-1 ) • Tissue insensitivity to insulin has been noted in most type 2 patients irrespective of weight and has been attributed to several interrelated factors

  22. Figure 6-18-1 pathogenesis of type 2 diabetes mellitus

  23. TYPE 2 DIABETES MELLITUS • These include a putative(and as yet undefined ) genetic factor ,which is aggravated in time by additioal enhancers of insulin resistance such as aging ,a sedentary lifestyle, and abdominal –visceral obesity . • In addition ,there is an accompanying deficiency in the response of pancreatic b cells to glucose .

  24. TYPE 2 DIABETES MELLITUS • Both the tissue resistance to insulin and the impaired b cell response to glucose appear to be further aggravated by increased hyperglycemia (glucose toxicity), and both defects are ameliorated by treatment that reduces the hyperglycemia toward normal

  25. TYPE 2 DIABETES MELLITUS • Most epidemiologic data indicate strong genetic influences. • Attempts to identify genetic markers for type 2 have as yet been unsuccessful.

  26. Other specific types of diabetes mellitus • Other specific types of diabetes mellitus is relatively rare • Maturity –onset diabetes of the young (MODY) is a subgroup due to monogenic disorder characterized by non-insulin –dependent diabetes with autosomal dominant inhenritantance and an age at onset of 25 years or younger.

  27. Other specific types of diabetes mellitus • Diabetes due to mutant insulin is a very rare subtype of nonobese type 2 diabetes ,with no more than ten families having been described.

  28. Other specific types of diabetes mellitus • Diabetes duo to a mutation of mitochondrial DNA that impairs the transfer of leucine or lysine into mitochondrial , proteins has been described.

  29. Other specific types of diabetes mellitus • Since sperm do not contain mitochondria, only the mother transmits mitochondrial genes to her offspring.

  30. Gestational diabetes mellitus (GDM) • GDM is defined as any degree of glucose intolerance with onset or first reconition during pregnancy. • The definition appleies regardless of whether insulin or only diet modification is used for treatment or whether the condition persists after pregnancy.

  31. Gestational diabetes mellitus (GDM) • It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancies. • The prevalence may range from 1%-14%of pregnancies, depending on the population studied

  32. Gestational diabetes mellitus (GDM) • GDM represents nearly 90% of all pregnancies complicated by diabetes. • Insulin is recommended as the only modality of treatment even trial of oral agents that are undertaken showed safe.

  33. Gestational diabetes mellitus (GDM) • Deterioration of glucose tolerance occurs normally during pregnancy , particularlyi n the 3rd trimester.

  34. Clinical findings • Symptoms and signs • Laboratory findings

  35. Clinical findings • Symptoms and signs • The principal clinical features of the two major types of diabetes mellitus are listed for comparison in (Table 6-18-3)

  36. Diabetes Mellitus: Signs & Symptoms • Three polys: polyphagia, polyuria, & polydipsia Weight loss Fatigue Hyperglycemia

  37. Clinical findings • Symptoms and signs • Patients with type 1 diabetes present with a characteristic symptom complex. • An absolute deficiency of insulin results in accumulation of circulating glucose and fat acids,with conseqent hyperosmolality and hyperketonemia.

  38. Clinical findings • Symptoms and signs • Patients with type 2 diabetes may or may not present with characteristic features. • The presence of obesity or a strongly positive family history for mild diabetes suggests a high risk for the development of type 2 diabetes.

  39. Laboratory findings • Urinary analysis • Blood test procedures • B cell Reserve Evaluation • Autoantibodies • Lipoprotein Abormalities in Diabetes

  40. Clinical findings • Laboratory findings • Urinary analysis • Glycosuria and ketonuria can be found in diabetic patients.

  41. Clinical findings • Laboratory findings • Blood test procedures • A. Glucose Tolerance Test • B. Glycated Hemoglobin (Hemoglobin A1) measurements • C. Serum Fructosamine • D. Self –Monitoring of Blood Glucose • E.Continuous Glucose Monitoring Systems

  42. Blood test procedures • A. Glucose Tolerance Test • Criteria for laboratory confirmation of diabetes mellitus if the fasting plasma glucose level is 7.0 mmol/L(126mg/dL) or higher on more than one occasion , further evaluation of the patient with a glucose challenge is unnecessary .

  43. Blood test procedures • A. Glucose Tolerance Test • However ,when fasting plasma glucose is less than 7.0 mmol/L(126mg/dL) in suspected cases ,a standardized oral glucose tolerance test may be ordered .

  44. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements Glycated hemoglobin is abnormally high in diabetics with chronic hyperglycemia and reflects their metabolic control. It is produced by nonenzymatic condensation of glucose molecules with free amino groups on the globin component of hemoglobin.

  45. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements The higher the prevailing ambient levels of blood glucose, the higher will be the level of glycated hemoglobin. The major form of glycohemoglobin istermed hemoglobin A1c,which normally comprises only 4%-6% of the totalhemoglobin

  46. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements • Since glycohemoglobins circulate with in red blood cells whose life span lasts up to 120 days, they generally reflect the state of glycemia over the preceding 8-12 weeks, thereby providing an improved method of assessing diabetic control.

  47. Blood test procedures B. Glycated Hemoglobin(HemoglobinA1) measurements • Measurements should be made in patients with either type of diabetes mellitus at 3-to 4 month intervals so that adjustment in therapy can be made if glycohemoglobin is either subnormal or if it is more than 2% above the upper limits of normal for a particular laboratory.

  48. Blood test procedures • C. Serum Fructosamine • Serum fructosamine is formed by nonenzymatic glycosylation of serum proteins (predominantly albumin).

  49. Blood test procedures • C. Serum Fructosamine • Since serum albumin has a much shorter half-life than hemoglobin, serum fructosamine generally reflects the state of glycemic control for only the preceding 2 weeks.

  50. Blood test procedures • C. Serum Fructosamine • Normal values vary in relation to the serum albumin concentration and are 1.5-2.4mmol/L when the serum albumin level is 5 g/dL

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