Please enable JavaScript.
Coggle requires JavaScript to display documents.
Diabetes Mellitus Type 1: Primary B-cell Defect or Failure - Coggle Diagram
Diabetes Mellitus Type 1: Primary B-cell Defect or Failure
Categories of Increased Risk
FPG 100-125mg/dl
2-h PG 140-199 mg/dl during OGTT
HbA1C 5.7%-6.4%
Etiology
Insulin resistance at diagnosis is unusual, but may occur as individual ages and gains weight
Autoantibodies to insulin and to glutamic acid decarboxylase (GAD65)
Autoimmune: genetic and environmental factors, resulting in gradual process of autoimmune destruction in genetically susceptible individuals
Nonautoimmune: Unknown
Severe insulin deficiency or no insulin secretion at all
Diagnostic criteria
FPG > or = 126 mg/dl; fasting is defined as no caloric intake for at least 8 hours
2-h plasma glucose > or = 200mg/dl during OGTT
HbA1c > or = 6.5 %
In an individual with classic symptoms of hyperglycemia or or hyperglycemic crisis, a random plasma glucose > or = 200 mg/dl
Characteristics
little or no insulin secretion
Individual prone to ketoacidosis
Insulin dependent
75% of individuals develop before 30 years of age; can occur up to the 10th decade
Cellular-mediated autoimmune destruction of pancreatic B cells
Usually not obese
Pathophysiology
Idiopathic Diabetes Mellitus type 1
Less common than autoimmune
Strong genetic component
Occurs mostly in people of Asian or African descent
Affected individuals have no evidence of B cell autoimmunity and have varying degrees of insulin deficiency
Autoimmune diabetes mellitus type 1
Strong genetic associations with histocompatibility leukocyte antigen (HLA) class 2 alleles HLA-DQ and HLA-DR
Environmental factors that have been implicated include exposure to certain drugs, foods and viruses
Slowly progressive disease that destroys B cells of the pancreas
Gene-environment interactions result in the formation of autoantigens that are expressed on the surface of pancreatic B cells and circulate in the blood stream and lymphatics
Cellular immunity (T-cytotoxic cells and macrophages) and humoral immunity (autoantibodies against islet cells, insulin, glutamic acid decarboxylase (GAD), and other cytoplasmic proteins) are stimulated, resulting in B-cell destruction and apoptosis
Over time, 80% to 90% of the insulin secreting B cells of the islet of Langerhans are destroyed, insulin synthesis declines, and hyperglycemia develops
Clinical Manifestation
Polyphagia
Weight loss
Polyuria
Fatigue
Polydipsia
Recurrent infection
Prolonged wound healing
Genital pruritis
Visual changes
Paresthesias
cardiovascular symptoms