Diabetes Mellitus

1. Diabetes Mellitus Ella’s Story (7 min 28 seconds) https://www.youtube.com/watch?v=jniek-5BRg4

2. ETIOLOGY • Diabetes – ‘like a sieve or siphon’ • Mellitus – ‘sweet or r/t honey’ • A systemic metabolic disorder that involves improper metabolism of CHO, fats and proteins

3. ETIOLOGY • Chronic multisystem disease r/t: • 1. a decrease or absolute lack of insulin production by the beta cells of the islets of Langerhans in the pancreas, or • 2. by impaired insulin utilization, or • 3. Both

4. ETIOLOGY • Exact cause: unknown • Contributing factors: • Genetic • Virus • Aging process • Diet, lifestyle , ethnicity

5. ETIOLOGY • Other contributing factors: • Obesity • T-lymphocytes may play a role in the autoimmune destruction of the pancreatic insulin-producing cells

6. TYPES OF DIABETES • 2 main types: “Type 1” and “Type 2” • Type 1 was formerly called: • Juvenile or juvenile-onset • Insulin Dependent Diabetes Mellitus (IDDM) • Type 2 was formerly called: • Adult-onset diabetes or Maturity-onset diabetes • Non-insulin dependent Diabetes Mellitus (NIDDM)

7. Type 1 Diabetes Absence of endogenous insulin An autoimmune process, possibly triggered by a viral infection, destroys beta cells in the pancreatic islets  deficient insulin production Pt. retains normal sensitivity to the action of insulin Within 5 years of diagnosis, all of the pt.’s beta cells will have been destroyed and no insulin is produced Affected people require exogenous insulin for the rest of their lives

8. TYPE 2 Diabetes • MAIN PROBLEM: an abnormal resistance to insulin action • Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose chronically elevated blood glucose • Controlled by diet and exercise; may require oral hypoglycemic agents or exogenous insulin http://www.bing.com/videos/search?q=youttube+bach+music&FORM=VIRE3#view=detail&mid=C55B52AB9E21E0B2205EC55B52AB9E21E0B2205E (an hour of BACH study music)

9. Type 1/Type 2 Type 1 Diabetes Type 2 Diabetes More gradual onset Usually occurs in 35+ years old with most dx. >55 yr. old and overweight Decreased response to insulin = insulin resistant Oral hypoglycemics utilized Diet change and weight loss can often reverse this process • s/sx more rapid and acute • Usually appears before 30 years of age • Significant decrease or lack of insulin production • Exogenous insulin needed

10. Youtube.com Diabetes Type 1 https://www.youtube.com/watch?v=_OOWhuC_9Lw (2 minutes 14 sec) Diabetes Type 2 http://www.youtube.com/watch?v=OXAe3eOjqCk (8 minutes)

11. METABOLIC SYNDROME Metabolic syndrome Thought to be a precursor to diabetes Includes: Impaired glucose tolerance, high serum insulin, hypertension, elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue

12. METABOLIC SYNDROME • Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM • Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress

13. PATHOPHYSIOLOGY of DM • In normal metabolism, the end products of digestion (glucose, fatty acids and glycerol, and amino acids) are absorbed into the venous circulation and carried to the liver where they can be used immediately or stored for later use. • The liver can change glycerol and fatty acids into glucose which serves as fuel for muscles and as an energy source for the brain. • Insulin must be present for muscles and other body cells to utilize glucose

14. Pathophysiology • In the diabetic person, lack of proper amounts of insulin or it’s inadequate utilization, impairs the use of glucose in the body. • The excess glucose accumulates in the bloodstream, and hyperglycemia results. • To get rid of this abnormal amount of glucose, the kidneys excrete it in the urine (glycosuria). • Glycosuria necessitates an extra amount of water intake to dilute the urine

15. Pathophysiology • The patient then develops: • Polyuria • Polydipsia • Even though excess glucose is available in the bloodstream, the body cannot utilize it without the help of insulin cells are not properly nourished  polyphagia develops

16. Pathophysiology • Ketone bodies: Fatty acids (normal metabolic products from which acetone may spontaneously arise) may also be changed by the liver into glucose and ketone bodies. • Because CHO cannot be utilized properly, protein and fats are broken down ketone bodies and used for heat and energy  diabetic ketoacidosis/diabetic coma may develop

17. Role of Insulin Glucose Insulin stimulates active transport of glucose into cells If insulin absent, glucose remains in the bloodstream Blood becomes thick, which increases its osmolality Increased osmolality stimulates the thirst center Increased fluid does not pass into body tissues; high serum osmolality retains fluid in the bloodstream As blood passes through the kidneys, some glucose eliminated Osmotic force created by glucose draws extra fluid and electrolytes with it, causing abnormally increased urine volume

18. Role of Insulin Fatty acids Without adequate insulin, fat stores break down and increased triglycerides are stored in the liver Increased fatty acids in the liver can triple the production of lipoproteins; promotes atherosclerosis

19. Role of Insulin Protein Without adequate insulin, protein storage halts; large amounts of amino acids dumped into the bloodstream High levels of plasma amino acids place people with diabetes at risk for development of gout Changes in protein metabolism lead to extreme weakness and poor organ functioning

20. CLINICAL MANIFESTATIONS • Type 1 – 3 classic “polys”: • Polyuria • Polydipsia • Polyphasia As ketone bodies accumulate in the bloodstream, imbalances of Na+, K+, and bicarbonate result

21. CLINICAL MANIFESTATIONS • Type 2 • Asymptomatic in early disease • But later may c/o sx Type 1 DM • May not seek medical care until severe complications such as: kidney involvement, retinopathy, impotence, neuropathy, or gangrene

22. ASSESSMENT • Subjective Data: • Pt. c/o hunger, thirst, and nausea • Frequent and large amt. urination • Weakness and fatigue • Blurred vision • Decreased sensation to pain and temperature in the feet; numbness and tingling of the LE • C/O his or her body and his/her ability to cope with the illness

23. ASSESSMENT • Objective Data: • Assess skin, wound healing, ulcerations, etc • Women: freq. UTI’s and vaginal infections; bothersome vaginal discharge • Obesity • Legs and feet cold to touch; ↓ hair present on LE • Ability and compliance with glucose testing and proper use of medication – oral and insulin s.q.

24. DIAGNOSTIC TESTS • The patient with the following results should be further evaluated: • random blood glucose > 200mg/dL • a FBS >126 mg/dL • a 2 hr post prandial level > 200mg/dL • See p. 512 Box 11-2 for Diagnostic Tests

25. DIAGNOSTIC TESTS • ADA recommends self-monitor blood glucose instead of urine testing • However, urine testing for ketonuria is valuable in determining the advent of DKA • Recommended for Type 1 diabetics experiencing hyperglycemia and acute illness.

26. MEDICAL DIAGNOSIS • For “Diabetes Mellitus”: • One or more of the following criteria needs to be met on 2 separate occasions: • Polyuria, polydipsia, polyphagia, unexplained weight loss + random glucose level = or > 200 mg/dL • FBS = or > 100mg/dL (after 8 hrs fast , minimum) • 2 hr Post Prandial blood sugar = or > 200mg/dL during an oral glucose tolerance test (OGTT)

27. MEDICAL DIAGNOSIS • For “Prediabetes”: • Impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) • Individuals should receive education on weight reduction and increasing physical activity

28. MEDICAL MANAGEMENT • SUMMARY: • Education • Monitoring • Meal Planning • Medication • Exercise

29. MEDICAL MANAGEMENT • OVERALL GOAL • Assist people with diabetes in making changes in nutrition and exercise habits leading to improved metabolic control • Additional goals: • Maintenance of as near-normal blood glucose levels as possible • Achievement of optimal serum lipid levels • Provision of optimal calories for maintaining or attaining reasonable weight and normal growth and development rates for children and adolescents and pregnancy

30. MEDICAL MANAGEMENT • ADDITIONAL GOALS cont. • Prevention and treatment of acute complications • Improvement of overall health through optimal nutrition • IMPORTANCE OF THE NURSE AS A TEACHER In supporting Diabetes Self Care: • Dietary information • Medication routine • SMBG • Exercise

31. DIET • Nutritional Therapy • Aimed at achieving a normal glucose leves of < 126 mg/dL • Attaining a reasonable body weight • Ensuring proper growth and maintenance • Reduce total fat –esp. saturated fat • Monitor Lab results: esp. HgbA1c, SMBG results, and lipids

32. DIET • DIETICIAN REFERRAL – inpatient and outpatient • Diets based on ADA recommendations • Home Care Issues • Ability to choose, shop, and pay for groceries • Prepare food, store leftovers • Ability to follow dietary regimen

33. DIET • Glycemic Index • Different CHO foods affect the blood glucose level in different ways • This varying effect is termed the “glycemic index” • What is the glycemic index of the foods that are being consumed? • Check labels for “low glycemic index”

34. DIET • Other diets: Quantitative and Qualitative • Quantitative Diet: follow the food choices and number of servings recommended by the MyPyramid food planning tool • 45-50% of total kilocalories from CHO • 10-20% of total kilocalories from protein • 30% of total kilocalories from fats • Qualitative Diet: unmeasured and unrestricted; stressing moderation when selecting foods from My Pyramid food planning tool • Reduce use of simple CHO, saturated fat, and alcohol

35. DIET • Insulin-dependent diabetics • Snacks midafternoon and bedtime • Evenly distribute food intake throughout the day

36. EXERCISEhttp://www.webmd.com/diabetes/video/kahn-does-exercise-affect-diabetesEXERCISEhttp://www.webmd.com/diabetes/video/kahn-does-exercise-affect-diabetes • Yes! Exercise regularly • Promotes proper utilization of glucose • Important for overall functioning of C-V system • Increases sense of well-being • Can reduce insulin-resistance and increase glucose uptake; reduces BP and lipid levels

37. Stress of Acute Illness and Surgery • Emotional and physical stress can ↑ blood glucose level and  hyperglycemia • Acute Illness • May require extra insulin during times of stress • ↑ blood glucose monitoring during this time – even every 1-2 hrs • Diet modifications (solids to liquids for a period of time) • Monitor urinary output and degree of ketonuria

38. Stress of Acute Illness and Surgery • Increase fluid intake to prevent dehydration (minimum 4oz per hour for adult) • Call MD when CBG > 250mg/dL • Surgery • Preplan adjustments in diabetic regimen • IV fluids and insulin before, during, and after surgery when no oral intake • The type2 pt. who usually takes oral hypoglycemics will be on insulin during the surgical period

39. MEDICATIONS • INSULIN AND ORAL HYPOGLYCEMICS are the drugs of choice • INSULIN • Needed for all patients with Type 1 AND Type 2 diabetes whose condition cannot be controlled by diet, exercise or hypoglycemic meds alone

40. MEDICATIONS • INSULIN cont. • Today, only Biosynthetic insulin • A hormone • Given subcutaneously • IV administration when immediate action needed • Differ in regard to: • Onset • Peak • Action • Duration

41. MEDICATION • INSULIN cont. • By adding zinc, protamine, and acetate buffers to insulin in various ways, the onset of activity, peak, and duration times can be manipulated  availability of rapid-, short-, intermediate-, and long-acting insulins • Different combinations/premixed may be used • REVIEW Table 11-5 ppgs. 515 and 516 (((check book for accuracy of page numbers)))

42. MEDICATION • A human insulin formula: Insulin Lispro • Begins to take effect in less than half the time of regular, fast-acting insulin • May be administered 15 min before a meal • This timing mimics more closely the body’s own hormone activity

43. MEDICATION • When giving insulin: • Inject into the subcutaneous tissue (fat) • The Space between the skin and muscle layers • Requires the appropriate syringe • U-100 = 100u insulin per ml. • The concentration on the insulin bottle should match the syringe indication - a U-100 syringe should be used with an insulin that has printed on the label “U-100” • Other syringes available for those taking a smaller dosage: U-25, U-30, U-50

44. MEDICATION • Appropriate syringe cont. • NOTE: ONE IMPORTANT DISTINCTION • The U-100 syringe is marked in 2-unit increments, whereas • The 30 and 50 unit syringes are marked in 1-unit increments • The Joint Commission recommends using “units” instead of the abbreviation “U” on med orders and med administration records (MAR) • Needles: very fine: 25-30g • Other options: • Insulin Pens

45. MEDICATION • Insulin Injection sites • Abdomen (except for 2 inches around the navel) • Upper arms • Anterior or lateral aspects of the thighs • Hips and buttocks • Because of differing anatomical absorption rates of insulin, injections should be given in all the available sites in one area before moving to another site

46. MEDICATION • External Infusion Pump • P. 519 Figure 11-17 • A continuous, or basal rate of rapid- or short-acting regular insulin with bolus doses available • Basal rate is designed to keep the blood glucose level steady between meals and during sleep • Pump is programmed –at the touch of a button- to deliver a larger quantity to cover CHO at meals • Mimics the pancreas

47. MEDICATION • Refrigeration of Insulin • An open bottle of insulin in current use DOES NOT have to be refrigerated • Current thought: administer at room temp (not straight from the fridge) to help prevent insulin lipodystrophy(loss of local fat deposits) • Extra bottles: store in refrigerator

48. MEDICATION • Best Practice: Nurses administering insulin injections MUST ALWAYS have another licensed person check and document the dose drawn up in the syringe to prevent med errors • Be alert for s/sx hypoglycemia at the peak of action for whatever type of insulin is given • Educate the pt. and cgrs re: s/sx hypoglycemia and appropriate tx.

49. MEDICATION • Oral Hypoglycemics • Treat Type II DM • For pts. whose insulin production or utilization is inadequate • This is NOT oral insulin or a substitute for insulin

50. MEDICATIONhttp://www.webmd.com/diabetes/video/kahn-whats-future-treating-diabetesMEDICATIONhttp://www.webmd.com/diabetes/video/kahn-whats-future-treating-diabetes • 5 types: • Sulfonylureas: stimulate the pancreas to release insulin • E.g. Glypizides (Glucotrol), Glyburide (Micronase) • Meglitinides : stimulates increased insulin release from the pancreas • E.g. repalinide (Prandin) • Alpha-Glucosidase Inhibitors: inhibits delay of CHO absorption from the small intestine • E.g. Miglitol (Glycet)