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Diabetes Mellitus

Diabetes Mellitus. Dr. Meg- angela Christi Amores. Diabetes Mellitus. refers to a group of common metabolic disorders that share the phenotype of hyperglycemia Factors: reduced insulin secretion decreased glucose utilization increased glucose production. Classification. Diagnosis.

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Diabetes Mellitus

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  1. Diabetes Mellitus Dr. Meg-angela Christi Amores

  2. Diabetes Mellitus • refers to a group of common metabolic disorders that share the phenotype of hyperglycemia • Factors: • reduced insulin secretion • decreased glucose utilization • increased glucose production

  3. Classification

  4. Diagnosis • Criteria for the diagnosis of DM • Symptoms of diabetes plus random blood glucose concentration > 200 mg/dL • Fasting plasma glucose > 126 mg/dL • Two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test • FPG is the most reliable and convenient test for identifying DM in asymptomatic individuals

  5. Risk Factors for Type 2 DM • Family history of diabetes (i.e., parent or sibling with type 2 diabetes) • Obesity (BMI 25 kg/m2) • Habitual physical inactivity Race/ethnicity • Previously identified IFG or IGT • History of GDM or delivery of baby >4 kg (>9 lb) • Hypertension (blood pressure 140/90 mmHg) • HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L) • Polycystic ovary syndrome or acanthosisnigricans • History of vascular disease

  6. Insulin biosynthesis, Secretion, Action • produced in the beta cells of the pancreatic islets • PREPROINSULIN • PROINSULIN • A or B chains of INSULUN

  7. Secretion • Glucose is the key regulator of insulin secretion by the pancreatic beta cell • Glucose levels > 70 mg/dL stimulate insulin synthesis

  8. transport into the beta cell by the GLUT2 glucose transporter • phosphorylation by glucokinase • rate-limiting step that controls glucose-regulated insulin secretion • metabolism of glucose-6-phosphate via glycolysis generates ATP • inhibits the activity of an ATP-sensitive K+ channel • opens voltage-dependent calcium channels • stimulates insulin secretion

  9. Action • Once insulin is secreted into the portal venous system, ~50% is degraded by the liver • Unextracted insulin enters the systemic circulation where it binds to receptors in target sites • initiate a complex cascade of phosphorylation and dephosphorylation reactions • resulting in the widespread metabolic and mitogenic effects of insulin

  10. Action • Glucose homeostasis reflects a balance between hepatic glucose production and peripheral glucose uptake and utilization • Insulin is the most important regulator of this metabolic equilibrium

  11. Type I DM • the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency • rate of decline in beta cell mass varies widely among individuals, with some patients progressing rapidly to clinical diabetes and others evolving more slowly

  12. Type I DM • Features of diabetes do not become evident until a majority of beta cells are destroyed (~80%)

  13. Type II DM • Insulin resistance and abnormal insulin secretion are central to the development of type 2 DM • has a strong genetic component • polygenic and multifactorial since in addition to genetic susceptibility, environmental factors (such as obesity, nutrition, and physical activity) modulate the phenotype

  14. Type II DM • Obesity, particularly visceral or central (as evidenced by the hip-waist ratio), is very common • In the early stages of the disorder, glucose tolerance is normal, pancreatic beta cells compensate by increasing insulin output

  15. Acute complications • Diabetic ketoacidosis • HyperglycemicHyperosmolar State

  16. Chronic Complications

  17. Approach to patient • HISTORY • DM-relevant aspects such as weight, family history of DM and its complications, risk factors for cardiovascular disease, exercise, smoking, and ethanol use • Symptoms of hyperglycemia: • polyuria, polydipsia, weight loss, fatigue, weakness, blurry vision, frequent superficial infections (vaginitis, fungal skin infections), and slow healing of skin lesions after minor trauma • Blurred vision

  18. Approach to patient • PHYSICAL EXAMINATION • weight or BMI, retinal examination, orthostatic blood pressure, foot examination, peripheral pulses, and insulin injection sites • Blood pressure > 130/80 mmHg is considered hypertension • peripheral neuropathy, calluses, superficial fungal infections, nail disease, ankle reflexes, and foot deformities

  19. Treatment Overall goals of therapy • (1) eliminate symptoms related to hyperglycemia • (2) reduce or eliminate the long-term microvascular and macrovascular complications of DM • (3) allow the patient to achieve as normal a lifestyle as possible

  20. Treatment • Patient education • nutrition, exercise, care of diabetes during illness, and medications • fruits, vegetables, fiber-containing foods, and low-fat milk is advised • Consumption of foods with a low glycemic index • Reduced calorie and nonnutritive sweeteners are useful

  21. Assignment: • List foods with a LOW GLYCEMIC INDEX

  22. Treatment • Achieve normoglycemia • Insulin • Glucose-lowering agents • Sulfonylurea (Gliclazide) • Biguanides (Metformin) • a glucosidase inhibitors (Acarbose) • Thiazilidinediones

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