1 / 22

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.

zeheb
Download Presentation

Diabetes Mellitus

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  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

More Related