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Diabetes Mellitus

Diabetes Mellitus. Zoya Minasyan RN-MSN- Edu. Diabetes Mellitus. A chronic multisystem disease related to Abnormal insulin production Impaired insulin utilization Or both 7 th leading cause of death in the USA

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Diabetes Mellitus

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  1. Diabetes Mellitus ZoyaMinasyan RN-MSN-Edu

  2. Diabetes Mellitus • A chronic multisystem disease related to • Abnormal insulin production • Impaired insulin utilization • Or both • 7th leading cause of death in the USA • Leading cause of adult blindness, end-stage renal disease, and non traumatic lower limb amputation. • Major contributing factor • Heart disease • Stroke

  3. Diabetes MellitusEtiology and Pathophysiology • Genetic • Autoimmune • Viral • Environmental Regardless of it’s cause, Diabetes is primarily a disorder of glucose metabolism r/t absent or insufficient insulin supply and/or poor utilization of the insulin that is available.

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

  5. Etiology and Pathophysiology • Normal insulin metabolism • Produced by the  cells • Islets of Langerhans of the pancreas. • Released continuously into bloodstream in small amounts; with larger amounts released after food. • Stabilizes glucose range to 70 to 120 mg/dL • Counter regulatory hormones-glucagon, epinephrine, growth hormone and cortisol work to oppose the effect of insulin; work to increase blood glucose level by stimulating glucose production and output by liver, and decreasing the movement of glucose into the cells.

  6. Insulin • Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell • Decreases glucose in the bloodstream • ↑ insulin after a meal • Stimulates storage of glucose as glycogen in liver and muscle • Inhibits gluconeogenesis • Enhances fat deposition • ↑ protein synthesis

  7. The Pancreas Pancreas Exocrine Endocrine pancreas pancreas releases digestive releases hormones juices through a into the blood duct to the duodenum

  8. Endocrine pancreas: Islets of Langerhans Alpha Beta cells Delta cells PP cells cells Insulin Pancreatic Glucagon Somatostatin and amylin polypeptide

  9. Functions of Pancreatic Hormones • Glucagon: causes cells to release stored food into the blood • Insulin: allows cells to take up glucose from the blood • Amylin: slows glucose absorption in small intestine; suppresses glucagon secretion • Somatostatin: decreases GI activity; suppresses glucagon and insulin secretion

  10. Question Which pancreatic hormone decreases blood glucose levels? • Glucagon • Insulin • Amylin • Somatostatin

  11. Answer • Insulin Insulin allows cells to take glucose from the blood and use it for energy/to make ATP. Because it stimulates movement of glucose out of the blood and into the cells, blood levels decrease when insulin is released.

  12. Question Tell whether the following statement is true or false: Type 2 DM is more common than Type 1 DM.

  13. Answer True Type 1 DM is autoimmune (juvenile diabetes is Type 1), and affects only 5% to 10% of the diabetic population. Type 2 DM is associated with risk factors like obesity, poor diet, and sedentary lifestyle; 90% to 95% of diabetics suffer from this type.

  14. Insulin • Skeletal muscle and adipose tissues are Insulin-dependent tissues; have receptors for insulin • Other tissues (brain, liver, blood cells) do not directly depend on insulin for glucose transport; but require adequate glucose for normal fx. Liver has receptor sites for hepatic uptake of glucose and its conversion to glycogen.

  15. Type 1 Diabetes Mellitus • “juvenile-onset” or “insulin-dependent” diabetes, occurs in people younger than 40 years of age, and in younger children. • Progressive destruction of pancreatic  cells by body’s own T cells • Caused by • Genetic predisposition • Related to human leukocyte antigens (HLAs) • Exposure to a virus • Manifestations develop when pancreas can no longer produce insulin.

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

  17. Prediabetes • Individuals already at risk for diabetes • Blood glucose is high but not high enough to be diagnosed as having diabetes • Characterized by • Impaired fasting glucose (IFG) • Impaired glucose tolerance (IGT) • 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%. • Must watch for diabetes symptoms • Polyuria • Polyphagia • Polydipsia

  18. Type 2 Diabetes MellitusEtiology and Pathophysiology • Usually occurs in • people over 35 years of age, • overweight, • increases with age, • genetic basis.

  19. Type 2 Diabetes MellitusEtiology and Pathophysiology • Four major metabolic abnormalities • 1. Insulin resistance • Body tissues do not respond to insulin which results in hyperglycemia. • 2. Pancreas ↓ ability to produce insulin • β cells fatigued from compensating • β-cell mass lost • 3. Inappropriate glucose production from liver • 4. Alteration in production of hormones

  20. Type 2 Diabetes MellitusEtiology and Pathophysiology Individuals with metabolic syndrome also known as syndrome X or insulin resistance syndrome are at increased risk for type 2 diabetes • risk for cardiovascular disease and diabetes characterized by insulin resistance Individuals with metabolic syndrome • Elevated insulin levels, ↑ triglycerides, LDLs, ↓ HDLs, hypertension • Risk factors • Central obesity, sedentary lifestyle, urbanization, certain ethnicities(African Americans, Native Americans, Hispanics, Asians)

  21. 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(will discuss later)

  22. Gestational Diabetes • Develops during pregnancy • Detected at 24 to 28 weeks of gestation • Usually normal glucose levels at 6 weeks post partum • Increased risk for cesarean delivery, and neonatal complications • Increased risk for developing type 2 in 5 to 10 years • Therapy: First- nutritional, second -insulin

  23. Specific Types of Diabetes • Results from • Another medical condition • Cushing syndrome • Hyperthyroidism • Pancreatitis • Parenteral nutrition • Cystic fibrosis • 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 • Drugs that can alter blood glucose levels are listed in Table 49-8.

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

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

  26. Diabetes MellitusDiagnostic Studies • Four methods of diagnosis • AIC ≥ 6.5% • Fasting plasma glucose level >126 mg/dL • Random plasma glucose measurement ≥200 mg/dL • Two-hour OGTT(oral glucose tolerance test) level ≥200 mg/dL when a glucose load of 75 g is used • 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 • Ideal goal • ADA ≤7.0% • American College of Endocrinology <6.5% • Normal A1C reduces risks of retinopathy, nephropathy, and neuropathy.

  27. Diabetes Mellitus • Goals of diabetes management • Decrease symptoms • Promote well being • Prevent acute complications • Delay onset and progression of long term complications • Patient teaching • Self-monitoring of blood glucose • Nutritional therapy • Drug therapy • Exercise

  28. Drug Therapy: Insulin • Insulin differ with regard to onset, peak action, and duration. • Characterized as rapid-acting, short-acting, intermediate-acting, and long-acting • Rapid-acting: Lispro (Humalog), Aspart (Novolog), and glulisine (Apidra) • Short-acting: Regular • Intermediate-acting: NPH • Long-acting: Glargine (Lantus), detemir (Levemir)

  29. Drug Therapy: Insulin

  30. Drug Therapy: Insulin • Insulin preparations • Rapid-acting (bolus) • Lispro, aspart, glulisine • Injected 0 to 15 minutes before meal • Onset of action 15 minutes • Short-acting (bolus) • Regular • Injected 30 to 45 minutes before meal • Onset of action 30 to 60 minutes • Long-acting (basal) • Injected once a day at bedtime or in the morning • Released steadily and continuously • No peak action • Cannot be mixed with any other insulin or solution

  31. Drug Therapy: Insulin • Storage of insulin • Do not heat/freeze. • In-use vials may be left at room temperature up to 4 weeks. • Extra insulin should be refrigerated. • Avoid exposure to direct sunlight. • Administration of insulin • Cannot be taken orally • Subcutaneous injection for self-administration • IV administration • Fastest absorption from abdomen, followed by arm, thigh, and buttock • Abdomen is the preferred site. • Rotate injections within one particular site. • Do not inject in site to be exercised.

  32. Drug Therapy: Insulin • Administration of insulin • Hand washing • Do not recap needle • 45- to 90-degree angle, depending on fat thickness of the patient • Insulin pens preloaded with insulin are now available.

  33. Drug Therapy:Insulin

  34. Drug Therapy:Insulin • Insulin pump • Continuous subcutaneous infusion; Battery-operated device • Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall

  35. Drug Therapy:Insulin • Problems with insulin therapy • Hypoglycemia • Allergic reaction • Lipodystrophy(atrophy of SQ tissue) • Somogyi effect( during the sleep hrs-decline in blood glucose in respond to insulin; counterregulatory hormones causes gluconeogenesis which causes rebound hyperglycemia and ketosis at night and in the morning; sweats or nightmares, and high blood glucose in am(recheck BG at 2 and 4 pm again) • Dawn phenomenon( growth hormone and cortisol: hyperglycemia in the morning)

  36. Drug Therapy Oral Agents • Sulfonylureas • ↑ insulin production from pancreas • ↓ chance of prolonged hypoglycemia • Ex: glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta, Glynase), and glimepiride (Amaryl). • Meglitinides • Increase insulin production from pancreas • Taken 30 minutes before each meal up to time of meal • Should not be taken if meal skipped • Ex: repaglinide (Prandin) and nateglinide (Starlix).

  37. Drug Therapy Oral Agents • Biguanide • Reduce glucose production by liver • Enhance insulin sensitivity at tissues • Improve glucose transport into cells • Do not promote weight gain • Ex: Metformin (Glucophage) • α-glucosidase inhibitors • “Starch blockers” • Slow down absorption of carbohydrate in small intestine • Ex:Acarbose (Precose) and miglitol (Glyset) • Thiazaolidinediones • ↑ glucose uptake in muscle and ↓glucose production • Ex: pioglitazone (Actos) and rosiglitazone (Avandia).

  38. Drug Therapy Oral Agents • Dipeptidyl peptidase-4 (DDP-4) inhibitor • Slows the inactivation of incretin hormones(Gastric hormones-Ex:gastrin,secretin…) • Potential for hypoglycemia • Ex: Sitagliptin (Januvia) • Saxagliptin (Onglyza) Amylin analog • Hormone secreted by  cells of pancreas • Administered subcutaneously: thigh or abdomen • Slows gastric emptying • Ex: Pramlintide (Symlin) • Incretin mimetic • Synthetic peptide • Stimulates release of insulin from  cells • Subcutaneous injection • Suppresses glucagon secretion • Reduces food intake • Slows gastric emptying • Not to be used with insulin • Ex: Byetta • -adrenergic blockers • Mask symptoms of hypoglycemia • Thiazide/loop diuretics • Can potentiate hyperglycemia • By inducing potassium loss

  39. Diabetes: Nutritional Therapy • American Diabetes Association (ADA) • Overall goal • Assist people in making changes in nutrition and exercise habits that will lead to improved metabolic control. • Meal plan is based on individual’s usual food intake and is balanced with insulin and exercise patterns.

  40. Diabetes: Nutritional Therapy • Carbohydrates • Sugars, starches, and fiber • minimum of 130 g/day; whole grains, along with fruits, vegetables, and low-fat milk, should be included. • Fats • Less than 200 mg/day of cholesterol and trans fats • Protein • Alcohol • High in calories • No nutritive value • Detrimental effects on liver • Can cause severe hypoglycemia • Alcohol inhibits gluconeogenesis (breakdown of glycogen to glucose) by the liver. This can cause severe hypoglycemia in patients on insulin or oral hypoglycemic medications that increase insulin secretion. • Moderate alcohol consumption can sometimes be safely incorporated into the meal plan if blood glucose levels are well controlled, and if the patient is not taking medications that will cause adverse effects.

  41. Diabetes • Exercise • Essential part of diabetes management • ↑ insulin receptor sites • Lowers blood glucose levels • Contributes to weight loss • The ADA recommends that individuals with diabetes should perform at least 150 minutes per week of a moderate-intensity aerobic physical activity. • The ADA also encourages those with type 2 diabetes to perform resistance training 3 times a week in the absence of contraindications. • Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia. • Best done after meals • Exercise plans should be started after medical clearance • Slowly with gradual progression • Should be individualized • Monitor blood glucose levels before, during, and after exercise.

  42. Nursing ManagementNursing Assessment • Past health history • Viral infections • Medications • Recent surgery • Obesity • Weight loss • Thirst • Hunger • Poor healing • Kussmaul respirations (Rapid, deep breathing)

  43. Nursing ManagementNursing Diagnoses • Ineffective self-health management • Risk for injury • Risk for infection • Powerlessness • Imbalanced nutrition: More than body requirements

  44. Nursing ManagementPlanning • Overall goals • Active patient participation • Few or no episodes of acute hyperglycemic emergencies or hypoglycemia • Maintain normal blood glucose levels. • Prevent or delay chronic complications. • Lifestyle adjustments with minimal stress

  45. Nursing Management Nursing Implementation • Health promotion • Identify those at risk, routine screening • Acute intervention for • Hypoglycemia; Diabetic ketoacidosis; Hyperosmolar hyperglycemic nonketotic syndrome. • Stress of illness and surgery • ↑ blood glucose level • Continue taking oral agents and insulin. • Frequent monitoring of blood glucose • Patients undergoing surgery or radiologic procedures requiring contrast medium should hold their metformin on day of surgery and to 48 hour • Ambulatory and home care • Overall goal is to reach an optimal level of independence • Insulin therapy and oral agents • Personal hygiene • Medical identification and travel card • Patient and family teaching • Educate on disease process, physical activity, medications, monitoring blood glucose, diet, resources.

  46. Medical Alert

  47. Nursing ManagementEvaluation • Knowledge • Balance of nutrition • Immune status • Health benefits • No injuries

  48. Acute Complications • Diabetic ketoacidosis (DKA) • Hyperosmolar hyperglycemic syndrome (HHS) • Hypoglycemia • Table 49-17 compares the manifestations, causes, management, and prevention of hyperglycemia and hypoglycemia(page 1242)

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