Type 1 Diabetes
by Elizabeth Spaulding
1. Pathogenesis
1.1. Autoimmune
1.1.1. Autoimmune destruction of insulin producing beta cells
2. Risk Factors
2.1. Polymorphisms of Genes
2.1.1. HLA-DQalpha
2.1.2. HLA-DQbeta
2.1.3. HLA-DR
2.1.4. Preproinsulin
2.1.5. PTPN22
2.1.6. CTLA-4
2.2. Environmental
2.2.1. Stimulus, such as bacteria or virus provoke autoimmune responses which causes antibodies to attack beta cells of pancreas and cause insulitis
2.2.2. Higher birthweight
2.2.3. Offspring of older mothers
3. Incidence
3.1. More common in males than females
3.2. Presents in childhood and adolescence
3.3. Prevalence has increased globally for decades; most profound elevations in youngest of individuals
3.4. 1 million people in America have T1D
3.5. 30-50% twin concordance rate in monozygotic twins
4. Diagnostics
4.1. Glucose Tolerance Test
4.2. Fasting Plasma Glucose Test (FPG)
4.3. Urinalysis
5. Treatments
5.1. Restore fluid imbalance
5.2. Lower blood glucose levels with insulin
5.3. No cure
5.4. Management
5.4.1. Subcutaneous insulin administration
5.4.1.1. Daily injections
5.4.1.2. Continuous infusion with battery pump
6. Clinical Manifestations
6.1. Abrupt onset
6.2. Polydypsia
6.3. Polyphasia
6.4. Polyuria
6.5. Hyperglycemia
6.6. Ketoacidosis
6.7. Weight loss
6.8. Muscle wasting
6.9. Long term
6.9.1. Cardiovascular disease
6.9.2. Retinopathy
6.9.3. Renal failure
6.9.4. Neuropathy
6.9.4.1. Numbness and pain in hands and feet
6.10. High risk of infection
6.10.1. Elevated glucose levels encourage bacterial growth