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Focus on Diabetes Mellitus

Focus on Diabetes Mellitus. J Brinley. Objectives. Describe the pathophysiology and clinical manifestation of diabetes mellitus. Describe the difference between type 1 and type 2 diabetes mellitus. Describe the care of the patient with diabetes mellitus.

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Focus on Diabetes Mellitus

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  1. Focus onDiabetes Mellitus J Brinley

  2. Objectives Describe the pathophysiology and clinical manifestation of diabetes mellitus. Describe the difference between type 1 and type 2 diabetes mellitus. Describe the care of the patient with diabetes mellitus. Demonstrate teaching concepts to the diabetic patient. Explain the nursing management of a patient with newly diagnosed diabetes mellitus. Describe the nursing management of the patient with diabetes mellitus in the ambulatory and home care settings. Relate the pathophysiology of acute and chronic complication s of diabetes mellitus to the clinical manifestations. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetes mellitus.

  3. Definition • A chronic multisystem disease related to • Abnormal insulin production • Impaired insulin utilization • Or both

  4. Definition • Leading cause of • End-stage renal disease • Adult blindness • Nontraumatic lower limb amputations • Major contributing factor • Heart disease • Stroke

  5. Etiology and Pathophysiology • Theories link cause to single/ combination of these factors • Genetic • Autoimmune • Viral • Environmental

  6. Etiology and Pathophysiology • Two most common types • Type 1 • Type 2 • Other types • Gestational • Prediabetes • Secondary diabetes

  7. Etiology and Pathophysiology • Normal insulin metabolism • Produced by the  cells • Islets of Langerhans • Released continuously into bloodstream in small increments with larger amounts released after food • Stabilizes glucose range to 70 to 120 mg/dL

  8. Normal Insulin Secretion Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

  9. Etiology and Pathophysiology • Insulin • Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell • Decreases glucose in the bloodstream

  10. Etiology and Pathophysiology • Insulin • ↑ insulin after a meal • Stimulates storage of glucose as glycogen in liver and muscle • Inhibits gluconeogenesis • Enhances fat deposition • ↑ protein synthesis

  11. Knowledge Test • Insulin that is produced by a person’s body is ________. a. Exogenous. b. Genetic. c. Endogenous. d. Synthetic.

  12. Etiology and Pathophysiology • Skeletal muscle and adipose tissue—Insulin-dependent tissues • Other tissues (brain, liver, blood cells) do not directly depend on insulin for glucose transport.

  13. Etiology and Pathophysiology • Counterregulatory hormones • Oppose effects of insulin • Increase blood glucose levels • Provide regulated release of glucose for energy • Help maintain normal blood glucose levels • Examples • Glucagon, epinephrine, growth hormone, cortisol

  14. Question • What happens when alpha cells in the pancreas produce the hormone glucagon? • A. Epinephrine inhibits glycogen metabolism. • B. Glycogen is converted into glucose in the liver. • C. Free fatty acids are converted into triglycerides. • D. Glucose can’t enter cells because receptors are blocked.

  15. Another question • In idiopathic type I diabetes, what causes hyperglycemia? • A. Ketoacidosis • B. Insulin resistance • C. Beta cell destruction • D. Alpha cell destruction

  16. Altered Mechanisms in Type 1 and Type 2 Diabetes Fig. 49-2. Altered mechanisms in type 1 and type 2 diabetes mellitus.

  17. Type 1 Diabetes Mellitus • Formerly known as “juvenile-onset” or “insulin-dependent” diabetes • Most often occurs in people younger than 40 years of age • Occurs more frequently in younger children

  18. Type 1 Diabetes MellitusEtiology and Pathophysiology • End result of long-standing process • Progressive destruction of pancreatic  cells by body’s own T cells • Autoantibodies cause a reduction of 80% to 90% in normal -cell function before manifestations occur.

  19. Type 1 Diabetes MellitusEtiology and Pathophysiology • Causes • Genetic predisposition • Related to human leukocyte antigens (HLAs) • Exposure to a virus

  20. Type 1 Diabetes MellitusOnset of Disease • Long preclinical period • Antibodies present for months to years before symptoms occur • Manifestations develop when pancreas can no longer produce insulin. • Rapid onset of symptoms • Present at ED with ketoacidosis

  21. Type 1 Diabetes MellitusOnset of Disease • Will require exogenous insulin to sustain life • Diabetic ketoacidosis (DKA) • Occurs in absence of exogenous insulin • Life-threatening condition • Results in metabolic acidosis

  22. Prediabetes • Individuals already at risk for diabetes • Blood glucose high but not high enough to be diagnosed as having diabetes

  23. Prediabetes • Characterized by • Impaired fasting glucose (IFG) • Impaired glucose tolerance (IGT)

  24. Prediabetes • IFG: Fasting glucose levels are 100 to 125 mg/dL • IGT: 2-Hour plasma glucose levels are between 140 and 199 mg/dL • AIC is in range of 5.7% to 6.4%.

  25. Prediabetes • Long-term damage already occurring • Heart, blood vessels • Usually present with no symptoms • Must watch for diabetes symptoms • Polyuria • Polyphagia • Polydipsia

  26. Type 2 Diabetes Mellitus • Most prevalent type of diabetes • More than 90% of patients with diabetes • Usually occurs in people over 35 years of age • 80% to 90% of patients are overweight.

  27. Type 2 Diabetes • Prevalence increases with age. • Genetic basis • Greater in some ethnic populations • Increased rate in African Americans, Asian Americans, Hispanic Americans, and Native Americans • Native Americans and Alaskan Natives: Highest rates of diabetes in the world

  28. Type 2 Diabetes MellitusEtiology and Pathophysiology • Pancreas continues to produce some endogenous insulin. • Insulin produced is insufficient or is poorly utilized by tissues.

  29. Type 2 Diabetes MellitusEtiology and Pathophysiology • Obesity (abdominal/visceral) • Most powerful risk factor • Genetic mutations • Lead to insulin resistance • Increased risk for obesity

  30. Type 2 Diabetes MellitusEtiology and Pathophysiology • Four major metabolic abnormalities • 1. Insulin resistance • Body tissues do not respond to insulin. • Insulin receptors are either unresponsive or insufficient in number. • Results in hyperglycemia

  31. Type 2 Diabetes MellitusEtiology and Pathophysiology • 2. Pancreas ↓ ability to produce insulin • β cells fatigued from compensating • β-cell mass lost • 3. Inappropriate glucose production from liver • Liver’s response of regulating release of glucose is haphazard. • Not considered a primary factor in development of type 2

  32. Type 2 Diabetes MellitusEtiology and Pathophysiology • 4. Alteration in production of hormones and adipokines • Play a role in glucose and fat metabolism • Contribute to pathophysiology of type 2 diabetes • Two main adipokines • Adiponectin and leptin

  33. Question • Which factor does NOT increase the risk of developing insulin resistance? • A. Obesity • B. Sedentary lifestyle • C. Native American ethnic background • D. Family history of autoimmune Type I diabetes

  34. Type 2 Diabetes MellitusEtiology and Pathophysiology • Individuals with metabolic syndrome at increased risk for type 2 diabetes • Cluster of abnormalities that increase risk for cardiovascular disease and diabetes • Characterized by insulin resistance

  35. Type 2 Diabetes MellitusEtiology and Pathophysiology • Individuals with metabolic syndrome • Elevated insulin levels, ↑ triglycerides, LDLs, ↓ HDLs, hypertension • Risk factors • Central obesity, sedentary lifestyle, urbanization, certain ethnicities

  36. Type 2 Diabetes MellitusOnset of Disease • Gradual onset • Person may go many years with undetected hyperglycemia. • Osmotic fluid/electrolyte loss from hyperglycemia may become severe. • Hyperosmolar coma

  37. Gestational Diabetes • Develops during pregnancy • Detected at 24 to 28 weeks of gestation • Usually normal glucose levels at 6 weeks post partum

  38. Gestational Diabetes • Increased risk for cesarean delivery, perinatal death, and neonatal complications • Increased risk for developing type 2 in 5 to 10 years • Therapy: First nutritional, second insulin

  39. Secondary Diabetes • Results from • Another medical condition • Cushing syndrome • Hyperthyroidism • Pancreatitis • Parenteral nutrition • Cystic fibrosis • Hemochromatosis

  40. Secondary Diabetes • Treatment of a medical condition that causes abnormal blood glucose level • Corticosteroids (Prednisone) • Thiazides • Phenytoin (Dilantin) • Atypical antipsychotics (clozapine) • Usually resolves when underlying condition treated

  41. Clinical ManifestationsType 1 Diabetes Mellitus • Classic symptoms • Polyuria (frequent urination) • Polydipsia (excessive thirst) • Polyphagia (excessive hunger) • Weight loss • Weakness • Fatigue

  42. Clinical ManifestationsType 2 Diabetes Mellitus • Nonspecific symptoms • May have classic symptoms of type 1 • Fatigue • Recurrent infection • Recurrent vaginal yeast or monilia infection • Prolonged wound healing • Visual changes

  43. Diabetes MellitusDiagnostic Studies • Four methods of diagnosis • AIC ≥ 6.5% • Fasting plasma glucose level >126 mg/dL • Random or casual plasma glucose measurement ≥200 mg/dL plus symptoms • Two-hour OGTT level ≥200 mg/dL when a glucose load of 75 g is used

  44. Diabetes MellitusDiagnostic Studies • Hemoglobin A1C test • In 2010, recommended to be used as a diagnostic test • Useful in determining glycemic levels over time • Shows the amount of glucose attached to hemoglobin molecules over RBC life span • Approximately 120 days

  45. Diabetes MellitusDiagnostic Studies • Hemoglobin A1C (cont’d) • Regular assessments required • Ideal goal • ADA ≤7.0% • American College of Endocrinology <6.5% • Normal A1C reduces risks of retinopathy, nephropathy, and neuropathy.

  46. Diabetes MellitusCollaborative Care • Goals of diabetes management • Decrease symptoms. • Promote well-being. • Prevent acute complications. • Delay onset and progression of long-term complications.

  47. Diabetes MellitusCollaborative Care • Patient teaching • Self-monitoring of blood glucose • Nutritional therapy • Drug therapy • Exercise

  48. Drug TherapyInsulin • Exogenous insulin • Insulin from an outside source • Required for type 1 diabetes • Prescribed for patient with type 2 diabetes who cannot control blood glucose by other means

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