| How is immune regulation in T1DM? | Autoantibodies to insulin (IAA), GAD65 (GADA - glutamic acid decarboxylase), IA-2A
These may present several years after hyperglycemia, and pt w/positive beta cell autoantibodies have varying degrees of beta cell dysfunction
Presence of the three antibodies together increases risk more than 1 of them alone, and they are important to differential classification of diabetes in adults (Type 1 or 2) (mainly GAD)
First antibody made is IAA
Associated w/other disorders (hashimoto, celiac, addison's, pernicious anemia, Addison's, ovarian failure, MG)
ABO incompatibility and hyperbilirubinemia are associated w/increased risk of T1DM |
| What are signs and symptoms of T1DM? | Polyuria (due to high glucose concentration in blood, incomplete glucose reabsorption in urine, increased urine osmotic pressure and inhibition of water reabsorption)
Dehydration (Due to water loss in urine - causes polydipsia)
Polyphagia (increased apetite due to low glucose to muscles, tissues and body)
Weight loss and weakness (no krebs cycle, uses fat instead)
Vision changes (change in shape of the lens) |
| How is epidemiology of T1DM? | Increasing worldwide and is an epidemic in some countries, evidence of annual increase of 2-7%. (sweden didn't increase but shifted to a younger age (Belgium as well)
It is controversial whether BMI increases risk of T1DM or not. |
| What are signs and symptoms of T1DM? | Polyuria (due to high glucose concentration in blood, incomplete glucose reabsorption in urine, increased urine osmotic pressure and inhibition of water reabsorption)
Dehydration (Due to water loss in urine - causes polydipsia)
Polyphagia (increased apetite due to low glucose to muscles, tissues and body)
Weight loss and weakness (no krebs cycle, uses fat instead)
Vision changes (change in shape of the lens) |
| What are main features of T1DM? | Sudden onset, severe symptoms (ketoacidotic coma), weight loss, lean, spontaneous ketosis, absent C peptide, markers of autoimmunity
Genes, environment and immune regulation all play a role in causing autoimmunity leading to T1DM |
| What is the natural hx of T1DM? | Genetic predisposition, then we get overt immunologic abnormalities that lead to decrease in normal insulin secretion, with this decrease we reach a point where we get abnormal glucose concentrations and C peptide still present (overt diabetes), which progresses to get into no C peptide at all. |
| How is the trigger for autoimmunity occurring? | Genetic suseptibility needs an environmental trigger in order to start autoimmunity
These include (viruses [rubella, coxsackie, enterovirus, mumps] Food [nitrosamine, milk proteins]) |
| How is immune regulation in T1DM? | Autoantibodies to insulin (IAA), GAD65 (GADA - glutamic acid decarboxylase), IA-2A
These may present several years after hyperglycemia, and pt w/positive beta cell autoantibodies have varying degrees of beta cell dysfunction
Presence of the three antibodies together increases risk more than 1 of them alone, and they are important to differential classification of diabetes in adults (Type 1 or 2) (mainly GAD)
First antibody made is IAA
Associated w/other disorders (hashimoto, celiac, addison's, pernicious anemia, Addison's, ovarian failure, MG)
ABO incompatibility and hyperbilirubinemia are associated w/increased risk of T1DM |
| How is T1DM occurring in pt <1years old? | Rare, often develops rapidly, vague symptoms (breathing, GI), important for pt w/ unclear GI symptoms to test urine and plasma glucose, manage carefully because of cerebral edema. |
| What is the recommended standard of care for T1DM? | Glycemic control (HbA1C <7% without getting into hypoglycemia)
lower HbA1C reduces risk of microvascular and macrovascular complications benifits as soon as 3 years |
