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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

Diabetes Mellitus

Dr. Meg-angela Christi Amores

diabetes mellitus1
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
  • 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
risk factors for type 2 dm
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
insulin biosynthesis secretion action
Insulin biosynthesis, Secretion, Action
  • produced in the beta cells of the pancreatic islets
  • A or B chains of INSULUN
  • Glucose is the key regulator of insulin secretion by the pancreatic beta cell
  • Glucose levels > 70 mg/dL stimulate insulin synthesis

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
  • 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
  • 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
type i dm
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
type i dm1
Type I DM
  • Features of diabetes do not become evident until a majority of beta cells are destroyed (~80%)
type ii dm
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
type ii dm1
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
acute complications
Acute complications
  • Diabetic ketoacidosis
  • HyperglycemicHyperosmolar State
approach to patient
Approach to patient
    • 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
approach to patient1
Approach to patient
    • 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

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
  • 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
  • List foods with a LOW GLYCEMIC INDEX
  • Achieve normoglycemia
    • Insulin
    • Glucose-lowering agents
      • Sulfonylurea (Gliclazide)
      • Biguanides (Metformin)
      • a glucosidase inhibitors (Acarbose)
      • Thiazilidinediones