• Definition: HbA1c >6.5%, fasting plasma glucose >126 mg/dl and random blood glucose >200mg/dl

  • Screening for T2DM should start at age 35

  

  

  

  

  <aside> 🚭 Smoking cessation is by far the most effective preventive intervention in almost all patients, and this is especially true in those with diabetes.

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• Lifestyle modifications, metformin, an ACEI (or ARB), and an SGLT-2 inhibitor are indicated in diabetic patients.
• Statin therapy is indicated for the primary prevention of atherosclerotic cardiovascular disease in all patients age 40-75 years with diabetes mellitus, regardless of LDL level.
• follow up always involves foot exam + dilated eye exam
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• Additionally, a short course of basal insulin therapy should be considered for patients with symptomatic hyperglycemia, signs of a continued catabolic state (e.g., weight loss), initial glucose ≥ 300 mg/dL, or HbA1c > 10%.

Type 1 vs 2 Diabetes

The two cardinal defects involved in the pathophysiology of type 2 diabetes mellitus are increased insulin resistance and defective insulin secretion. Although still controversial, many researchers believe that increased insulin resistance is the primary abnormality in type 2 diabetes mellitus. Early in the pathogenesis of type 2 diabetes, glucose tolerance is thought to remain normal because of a compensatory increase in insulin secretion from beta cells. This compensatory insulin response by beta cells ultimately fails, causing poor glucose tolerance. A number of genetic and acquired factors are implicated in the beta-cell dysregulation of type 2 diabetes. Islet amyloid polypeptide (amylin) is one factor thought to be responsible for this beta cell dysfunction. Amylin is stored in insulin secretory granules and is co-secreted with insulin from pancreatic beta cells. Deposits of amylin are universally seen in the pancreatic islets of patients with type 2 diabetes mellitus. Amylin may play a causative role in beta cell apoptosis and defective insulin secretion; however, this theory is still controversial.

Type 1 and type 2 diabetes mellitus have very strong genetic components. Twin studies have shown a concordance rate of 50% in identical twins for diabetes mellitus type 1, and around 80% for diabetes mellitus type 2. The genes involved in the pathogenesis of diabetes mellitus type 2 remain largely unknown. Gene polymorphism within the major histocompatibility complex contributes to type 1 diabetes mellitus disease in humans. HLA-DQ and -DR are the most important determinants of type 1 diabetes mellitus. In the general population, DR3 and DR4 are seen in approximately 40% of subjects; however, in patients with type 1 diabetes mellitus, DR3 and DR4 haplotypes are seen in more than 90% of subjects.