Diabetes and Acute and Chronic Complications of Diabetes PDF

DIABETES, ACUTE AND CHRONIC COMPLICATIONS OF DIABETES DIABETES MELLITUS FOR CONTENT RELATED TO MEDICATIONS, IF THERE IS A CONFLICT WITH YOUR TEXT AND WHAT YOUR PHR AND ANS I PROFESSORS PROVIDE TO YOU, CONTENT THAT YOUR PROFESSORS PRESENT ARE THE STANDARD FOR YOUR ANSWERS (FOR EXAMPLE, ONSET...

DIABETES, ACUTE AND CHRONIC COMPLICATIONS OF DIABETES DIABETES MELLITUS FOR CONTENT RELATED TO MEDICATIONS, IF THERE IS A CONFLICT WITH YOUR TEXT AND WHAT YOUR PHR AND ANS I PROFESSORS PROVIDE TO YOU, CONTENT THAT YOUR PROFESSORS PRESENT ARE THE STANDARD FOR YOUR ANSWERS (FOR EXAMPLE, ONSET AND DURATION OF MEDICATION)  WHAT IS DIABETES? Diabetes mellitus Definition: a group of metabolic disorders characterized by increased levels of glucose in the blood (hyperglycemia) resulting from Defects in insulin secretion Defects in insulin action Or both American Diabetes Association, 2013  INSULIN  Action: ◦ promotes glucose entry into muscle and fat cells ◦ the key that opens the lock so glucose can enter the cell  Main Targets: ◦ Muscle cells ◦ Adipose cells ◦ Liver ◦ The body uses insulin 24 hours a day  TYPES OF DIABETES Type 1 (5% of DM) Type 2 (90 -95% of DM) Formerly known as “juvenile Most prevalent type of diabetes onset” or “insulin dependent” 90 - 95%of people with diabetes diabetes have Type 2 Most often occurs in people Usually, > 35 years of age under 80% to 90% of patients are 30 years of age overweight or obese Peak onset between ages 11 and 13 Typically seen in a lean body type  OTHER TYPES OF DIABETES Gestational Diabetes Any degree of glucose intolerance that develops during pregnancy, increasing the risk of pregnancy complications Increases risk of developing DM II later Secondary Diabetes Hyperglycemia that occurs because of another underlying medical condition or treatment of a medical condition Medical conditions: Cushing syndrome, hyperthyroidism, cystic fibrosis, recurrent pancreatitis, hemochromatosis Meds/treatments: TPN, corticosteroids, thiazide diuretics, phenytoin, some uncommonly prescribed antipsychotics DM I Characteristics DM I Age of onset Usually childhood or adolescents ( 30 years (changing…) Speed of onset Gradual Family history Frequently positive Prevalence 90-95% Etiology Unknown- hereditary? Strong family link Primary defect Insulin resistance and inappropriate insulin secretion Insulin levels Low (deficiency), normal or high (indicating resistance) Treatment Oral anti-diabetic, non-insulin injectable, or insulin medications. Combine with reduced calorie diet and exercise Blood glucose More stable than Type I Symptoms Same but may be asymptomatic initially Body composition Frequently overweight or obese Ketosis Uncommon: occurs only if beta cells have been destroyed  PREDIABETES (ASSOCIATED WITH DM2) Prediabetes, or Insulin Resistance Defined as impaired glucose tolerance, impaired fasting glucose, or both. Individuals diagnosed with prediabetes are at increased risk for developing Type 2 Diabetes. Intermediate stage between normal glucose homeostasis and diabetes Glucose levels are elevated, but not high enough to meet the criteria for diabetes Can be reversible or management may delay onset of DM 2 Usually, asymptomatic What are the nursing implications for this diagnosis?  DIABETES TYPE 2 Risk Factors Age ≥45 (increasing incidence in children) 1st degree family history Overweight (BMI 25 – 29.9), or obese (BMI > 30) Metabolic Syndrome (next slide) Certain ethnicities: African American, Hispanic American, Native American, Native Hawaiians or other Pacific Islanders H/O gestational diabetes, or having an infant weighing >9lbs at birth Hypertension Elevated lipid levels  METABOLIC SYNDROME Patients with metabolic syndrome are at increased risk for developing type 2 diabetes 5 components Elevated glucose levels Abdominal obesity Elevated blood pressure High levels of triglycerides Decreased HDLs A patient must have 3 of the five to have metabolic syndrome Overweight individuals with metabolic syndrome can prevent or delay diabetes with weight loss and regular physical activity  DM TYPE 2: PATHOPHYSIOLOGY Problem Insulin resistance Impaired insulin secretion (but there is enough insulin present to prevent ketosis) Key differentiating factor from Type 1 = some endogenous insulin produced in DM 2 Onset: gradual (years) Often undetected and untreated 18  DM 2 PATHOPHYSIOLOGY: FOUR METABOLIC FACTORS Insulin Resistance Pancreatic dysfunction Inappropriate glucose production by the liver Altered production of hormones and cytokines by adipose tissue (adipokines) which cause chronic inflammation Medications for DM 2 target theses defects  DM 2: INSULIN RESISTANCE Insulin less effective at stimulating glucose uptake by the tissues and in regulating glucose release by liver Increased amounts of insulin secreted to maintain the glucose at a normal level Coexisting hyperglycemia and hyperinsulinemia, and both damage blood vessels!  DM 2: PANCREATIC DYSFUNCTION If beta cells can’t keep up with the increased demand for insulin, glucose level rises (hyperglycemia) When insulin improperly used, glucose transport into cell impeded, resulting in hyperglycemia DM2: INAPPROPRIATE GLUCOSE PRODUCTION BY THE LIVER Insulin is ineffective in moving adequate amounts of glucose into the cells Cell starvation signals the liver to release more glucose into the bloodstream  DM 2: ALTERED PRODUCTION OF HORMONES AND CYTOKINES BY ADIPOSE TISSUE (ADIPOKINES) Alteration in production of hormones and cytokines by adipose tissue results in chronic inflammation (a factor in insulin resistance, DM 2 and cardiovascular disease)  DM TYPE 2: CLINICAL MANIFESTATIONS Often nonspecific May include some classic type 1 symptoms Including polydipsia, polyuria, and polyphagia More common Fatigue Frequent infections: genital, vaginal, skin and gums Prolonged wound healing Visual changes (retinopathy) Peripheral neuropathy May go undetected for long time because of the few symptoms (because body still producing insulin)  DM TYPE 2: MANAGEMENT AND COLLABORATIVE CARE Nutritional therapy Balance between usual food intake and insulin therapy Exercise therapy Moderate – 20g/hr. extra carbohydrates required Strenuous – can further increase an elevated BG because stress response may be evoked Drug therapy Oral hypoglycemics, noninsulin injectables, insulin Self-Monitoring of blood glucose Facilitates making self-management decisions Teaching & follow-up Characteristics DM I DM 2 Age of onset Usually, childhood or adolescents Usually > 30 years (changing…) Speed of onset Abrupt Gradual Family history Frequently negative Frequently positive Prevalence 5-10% 90-95% Etiology Autoimmune or idiopathic process, possible Unknown- hereditary? Strong family link genetic and environmental influences Primary defect Loss of pancreatic beta cells Insulin resistance and inappropriate insulin secretion Insulin levels Reduced early in the disease and Low (deficiency), normal or high (indicating completely absent later resistance) Treatment Insulin replacement is mandatory with strict Oral anti-diabetic, non-insulin injectable, or insulin dietary control medications. Combine with reduced calorie diet and exercise Blood glucose Levels fluctuate widely in response to More stable than Type I infection, exercise, and changes in insulin dose and caloric intake Symptoms Polyuria, polydipsia, polyphagia, weight loss Same but may be asymptomatic initially Body Usually thin and undernourished at Frequently obese composition diagnosis Ketosis Common, especially if insulin dose is too Uncommon: occurs only if beta cells have been low destroyed BREAK DIAGNOSIS AND COLLABORATIVE CARE OF THE DIABETIC PATIENT  DM MANAGEMENT GOALS Hemoglobin A1c