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Antidiabetic Medications & The Nursing Process

Antidiabetic Medications & The Nursing Process. Karen Ruffin RN, MSN Ed. Is it Diabetes or is it Hyperglycemia???????????????. Is there a difference and if so what is it??. What is ???????. Hyperglycemia Insulin The primary source of energy for our bodies. What is the difference between.

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Antidiabetic Medications & The Nursing Process

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  1. Antidiabetic Medications&The Nursing Process Karen Ruffin RN, MSN Ed.

  2. Is it Diabetes or is it Hyperglycemia??????????????? Is there a difference and if so what is it??

  3. What is ??????? • Hyperglycemia • Insulin • The primary source of energy for our bodies

  4. What is the difference between • Basel Insulin • Prandial Insulin

  5. Optimal Levels of Blood Sugars • Preprandial-110 mg/dl • Postprandial-180 mg/dl

  6. What happens to our bodies when we are hyperglycemic? Blood Glucose >110 Insulin Resistance Decreased Insulin Increased Free Fatty Acid Oxidative Stress

  7. Oxidative Stress Nitric Oxide Nitric oxide Tissue factor Plasminogen Activator Prostaccyclin Nitric Oxide Angiotensinll Endothelin-1 Activation of activator protein -l Angiotensinll Vasoconstriction Inflammation Thrombosis hypertension Release of chemokines Release of cytokines Expression of cellular adhesion molecules Vascular smooth muscle cell growth Hyper coagulation Platelet Activation Decreased Fibrinolysis

  8. So what disease states are you at risk for??? • MI • DVT • PE • Stroke • AAA • Retinopathy

  9. What happens to our bodies when we are hyperglycemic? Metabolic Stress Response Stress hormones and peptides Increased Glucose Decreased Insulin

  10. Increased Glucose Decreased Insulin Increase in: Ketones Free Fatty Acids Lactate Immune Dysfunction Reactive 02 Species Cellular Injury Inflammation Tissue Damage Altered Tissue Healing Acidosis Thrombosis Global Infarction Ischemia Infection Dissemination Increase Transcription Factors Leads to Secondary Meadiators

  11. DID YOU KNOW ANY BLOOD SUGAR >200 Stuns your ???????? for 2week

  12. Criteria for Diagnosis of DMDM Screening • Symptoms of diabetes + casual plasma glucose level less than or equal to 200 mg/dL OR • Fasting plasma glucose higher than or equal to 126 mg/dL OR • 2-hour postload glucose level higher than or equal to 200 mg/dL during an oral glucose tolerance test • Impaired glucose tolerance (IGT) • FPG <110 mg/dL: normal fasting glucose • FPG ≥110 mg/dL but <126 mg/dL: impaired fasting glucose (IFG) • FPG ≥126 mg/dL: provisional diagnosis of diabetes mellitus

  13. What is a HbA1c? • It is a test that allows healthcare providers to see how diabetics have managed their blood glucose level over the last 2-3 months…. • Why do you think this is important????

  14. At what blood glucose level do we start treating with sliding scale? ??????? So, what do you think we are doing to our patients???

  15. What is the Difference?? • Type 1 diabetes • Type 2 diabetes

  16. Type 1 Diabetes • Lack of insulin production OR • Production of defective insulin • Affected patients need exogenous insulin • Complications • Diabetic ketoacidosis (DKA) • Hyperosmolarnonketotic syndrome • Oral antidiabetic drugs not effective

  17. Diabetes Mellitus • Symptoms • Polyuria • Polydipsia • Polyphagia • Glycosuria • Unexplained weight loss • Fatigue • Hyperglycemia

  18. Type 2 Diabetes • Most common type • Caused by insulin deficiency and insulin resistance • Many tissues are resistant to insulin • Reduced number insulin receptors • Insulin receptors less responsive • These people respond to oral hypoglycemics

  19. Type 2 Diabetes • Several comorbid conditions • metabolic syndrome OR insulin-resistance syndrome OR syndrome X • Obesity • Coronary artery disease • Dyslipidemia • Hypertension • Microalbuminemia (protein in the urine) • Enhanced conditions for embolic events (blood clots) • Insulin Resistance

  20. Coronary Artery Disease

  21. Treatment DIfferences • Type 1 • Exogenous insulin • Dietary control • Type 2 • Lifestyle changes • Dietary control • Weight reduction • Exercise • May require oral hypoglycemic therapy or exogenous insulin • Insulin when oral hypoglycemic medications can no longer provide glycemic control

  22. Gestational Diabetes • Hyperglycemia that develops during pregnancy • Insulin must be given to prevent birth defects • 4% of all pregnancies • Must be reclassified if it persists 6 weeks post-delivery • Usually subsides after delivery • 30% of patients may develop Type 2 DM within 10 to 15 years

  23. Major Long-Term Complications of DM (Both Types) • Macrovascular (atherosclerotic plaque) • Coronary arteries • Cerebral arteries • Renal arteries • Peripheral vessels • Microvascular (capillary damage) • Retinopathy • Neuropathy • Nephropathy

  24. Complications Associated with Diabetes Mellitus • Cardiovascular disease, including hypertension • Peripheral vascular disease • Delayed healing • Visual defects, including blindness • Renal disease • Infection • Neuropathies • Impotence

  25. Oral Hypoglycemics • Sulfonylureas (oldest) • Meglitinides • Biguanide • Thiazolidinediones

  26. Indications for Oral Hypoglycemics • They are used to lower blood sugar levels in patients that diet and exercise have failed. • The patient must have some pancreatic function left. • They can be used as a monotherapy or in conjunction with other oral hypoglycemics.

  27. Contraindications • Know drug allergy • Active hypoglycemia • Usually not used during pregnancy subq insulin's are used then. • Liver disease • Kidney disease • Depending on the metabolic pathways of the medication

  28. Sulfonylureas • First generation: • chlorpropamide (Diabinese), • tolazamide (Tolinase) • tolbutamide (Orinase) • Second generation: • glimepiride (Amaryl) • glipizide (Glucotrol) • glyburide (DiaBeta, Micronase)

  29. Sulfonylureas • Stimulate insulin secretion from the beta cells of the pancreas, thus increasing insulin levels • Beta cell function must be present • Improve sensitivity to insulin in tissues • Result: lower blood glucose levels • First-generation drugs not used as frequently now

  30. Adverse Effects • Sulfonylureas • Hypoglycemia • hematologic effects • nausea • epigastric fullness • heartburn • many others

  31. Interactions • Sulfonylureas • Hypoglycemic effect increases when taken with alcohol, anabolic steroids, many other drugs • Adrenergics (beta blockers) may mask many of the symptoms of hypoglycemia • Hyperglycemia: corticosteroids, phenothiazines, diuretics, oral contraceptives, thyroid replacement hormones, phenytoin, diazoxide and lithium. • Allergic cross-sensitivity may occur with loop diuretics and sulfonamide antibiotics • May interact with alcohol/OTC medication containing alcohol) - causing a disulfiram (Antabuse) -type reaction (facial flushing, pounding headache, feeling of breathlessness, and nausea)

  32. Meglitinides • Meglitinides • repaglinide (Prandin) • nateglinide (Starlix) • Meglitinides • Action similar to sulfonylureas • Increase insulin secretion from the pancreas

  33. Adverse Effects • Meglitinides • Headache • hypoglycemic effects • Dizziness • weight gain • joint pain • upper respiratory infection or flu-like symptoms

  34. Biguanides • Biguanides • metformin (Glucophage) • Biguanides • Decrease production of glucose • Increase uptake of glucose by tissues • Does not increase insulin secretion from the pancreas (does not cause hypoglycemia)

  35. Adverse Effects • Metformin • Primarily affects GI tract: abdominal bloating, nausea, cramping, diarrhea, feeling of fullness • May also cause metallic taste, reduced vitamin B12 levels • Lactic acidosis is rare but lethal if it occurs • Does not cause hypoglycemia

  36. Thiazolidinediones • Thiazolidinediones • pioglitazone (Actos), • rosiglitazone (Avandia) • Also known as “glitazones” • Thiazolidinediones • Decrease insulin resistance • “Insulin sensitizing drugs” • Increase glucose uptake and use in skeletal muscle • Inhibit glucose and triglyceride production in the liver

  37. Adverse Effects • Thiazolidinediones • Moderate weight gain • Edema • Mild anemia • Hepatic toxicity—monitor liver function tests

  38. Alpha-glucosidase Inhibitors • Alpha-glucosidase inhibitors • acarbose (Precose) • miglitol (Glyset) • Alpha-glucosidase inhibitors • Reversibly inhibit the enzyme alpha-glucosidase in the small intestine • Result: delayed absorption of glucose • Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)

  39. Adverse Effects • α-glucosidase inhibitors • Flatulence • diarrhea • abdominal pain • Do not cause hypoglycemia, hyperinsulinemia, or weight gain

  40. Insulins • Mechanism of Action • Substitute for & same effects as endogenous insulin • Restores the diabetic patient’s ability to: • Metabolize carbohydrates, fats, and proteins • Store glucose in the liver • Convert glycogen to fat stores • Some derived from porcine sources • Most now human-derived, using recombinant DNA technologies • Goal: tight glucose control • To reduce the incidence of long-term complications

  41. Indications • To treat both types of diabetes • Each patient requires careful customization of the dosing regimen for optimal glycemic control

  42. Contraindications • Anyone who is hypoglycemic?????

  43. Adverse Effects • Are all signs and symptoms of hypoglycemia including shock and death.

  44. Human-Based Insulins • Rapid-Acting • Most rapid onset of action • Shorter duration May be given SC or via continuous SC infusionpump (but not IV)

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