Interventions for Clients with Diabetes Mellitus Overview What is Diabetes? Why is it a major public health concern? Pathophysiology Endocrine Pancreatic Hormones Islets of Langerhans Alpha cells - glucagon Beta cells - insulin Delta cells - somatostatin Blood Glucose Homeostasis Classification Type 1 Diabetes Type 2 Diabetes Other Specific Types Gestational Diabetes Normal Insulin Production Physiologic Response to Insufficient Insulin Hyperglycemia –(F&E imbalances ) Polyuria Polydipsia Polyphagia Lipolysis Formation of ketones Hemoconcentration = hypovolemia Hyperviscosity of blood More Effects of Insufficient Insulin Hypoperfusion Hypoxia Hypokalemia Kussmaul respirations Metabolic acidosis Type 1 – Diabetes (IDDM) Autoimmune Process - Beta cells destroyed - Insulin deficiency Idiopathic - No known cause - Genetic predisposition Manifestations of Type 1 DM Hyperglycemia 3 P’s Polyuria Polydipsia Polyphagia Weight loss Glycosuria Fatigue Type 2 – Diabetes (NIDDM) Insulin resistance Obesity Physical inactivity Genetic predisposition Manifestations of Type 2 DM Hyperglycemia Polyuria Polydipsia Blurred vision Fatigue Paresthesias Skin infections Other specific types of DM Genetic defects of beta cells Genetic defects in insulin action Diseases of the exocrine pancreas Endocrine disorders Drug or chemical induced Infections Gestational Diabetes Glucose intolerance during pregnancy Diagnostic Tests Diagnostic criteria recommended by ADA: Fasting blood glucose test <110 mg/dL Glucose tolerance test <140 mg/dL Glycosylated hemoglobin (A1C) 4% to 6% Lab Assessment Blood tests 1. Fasting Blood Glucose Test 2. Oral Glucose Tolerance Test 3. Glycosylated Hemoglobin Assays 4. Glycosylated Serum Proteins and Albumin Urine Tests 1. Urine testing for Ketone Bodies 2. Tests for Renal Function 3. Urine Testing for Glucose ADA Treatment Goals Hgb A1C maintained at 7% or below Premeal blood glucose level 70 to 110mg/dl Blood glucose at bedtime 100-140mg/dl Management Nonsurgical Management 1. Dietary interventions 2. Monitoring of blood glucose levels 3. Exercise program 4. Medications to lower blood glucose Diet Therapy Meal planning strategies Exchange System-(Carbohydrates, Protein, and Fat) Carbohydrate counting-1unit/15g CHO Exercise Therapy Increases insulin sensitivity, improves cell uptake of glucose, a nd promotes weight loss. Insulin Therapy Types of Insulin Rapid acting (Lispro, Humalog - clear Short acting (Regular) - clear Intermediate (NPH) - cloudy . Long acting (Lantus/Glargine) - clear - can’t mix with other insulins Pre-Mixed Insulin Humulin or Novolin - 70/30 - 70% NPH / 30% Regular Novolog - 70/30 - 70% NPL / 30% Novolog Humalog - 75/25 (75% NPL / 25% Humalog - 50/50 (50% NPH / 50% Regular - Give immediately before meals Drug Therapy Sulfonylurea Agents - glipizide (Glucotrol) – stimulate insulin production - Give 30 min before meals - Watch for photosenitivity Meglitinides Agents - repaglinide (Prandin) – stimulate insulin production Cont. - Give 30 min before meals - Causes weigh gain Biguanides Agents - glucophage (Metformin – decrease hepatic glucose production - Take with meals - Increase weight loss - monitor renal function Alpha-Glucosidase Inhibitors - acarbose (Precose) – block sugar absorption - gas forming (rarely prescribed) - take with first bite of each of the 3 main meals - monitor liver function tests Thiazolidinedione Agents – sensitize muscle to insulin - rosiglitazone (Avandia) - pioglitazone (Actos) - high incidence pregnancy after menapause - use birth control - monitor weigh & assess for edema Surgical Management Whole-Pancreas Transplantation 1. Transplant pancreas alone (PTA) 2. Transplant pancreas after kidney (PAK) 3. Simultaneous pancreas and kidney(SPK) Islet Cell Transplantation-(experimental) Insulin Pump Common Nursing Diagnosis Risk for injury R/T hyperglycemia Risk for injury R/T sensory alterations Chronic Pain R/T diabetic neuropathy Ineffective renal tissue perfusion R/T diabetic nephropathy Potential for Hypoglycemia Potential for Diabetic Ketoacidosis Risk for Injury R/T Sensory Alterations Foot injury is the most common complication of diabetes leading to hospitalization. Diabetes is the leading cause of amputation worldwide. Diabetic Neuropathy About 60-70% of people with diabetes have mild to severe forms of nervous system damage, including: Impaired sensation or pain in the feet or hands Slowed digestion of food in the stomach Carpal tunnel syndrome Other nerve problems More than 60% of nontraumatic lower-limb amputations in the United States occur among people with diabetes. Foot Care Instructions Inspect your feet daily Do not wear the same pair of shoes 2 days in a row Wear clean cotton socks daily Do not go barefooted Trim your toenails straight across with a nail clipper Do not treat blisters, see your physician Chronic Pain Neuropathic pain 1. Anticonvulsant drugs (Neurontin) 2. Tricyclic antidepressants – (Elavil,Pamelor) 3. Capsaicin cream, Zostrix-HP - burning Ineffective Renal Tissue Perfusion ADA recommends yearly evaluation of kidney function 1. Spot urine collection – (albumin-creatinine ratio) 2. 24-hour urine collection (creatinine) 3. Timed urine collection Acute Complications of Diabetes HYPOGLYCEMIA Potential for Hypoglycemia Four common causes: 1. Excess insulin 2. Deficient intake or absorption of food 3. Exercise 4. Alcohol Symptoms of Hypoglycemia Responses of the ANS Hunger Irritability Shakiness Pale, cool skin Rapid pulse Hypotension Impaired Cerebral Function Headache Inability to concentrate Slurred speech Blurred vision Decrease in LOC Seizures/Coma Management of Hypoglycemia Hypoglycemic protocol Mild hypoglycemia (BG < 60 and symptomatic) - 10 to 15g of carbohydrate - Recheck BG in 15minutes Moderate (BG < 40 and symptomatic) -15 to 30g of rapidly absorbed CHO Severe (BG < 20 and unable to swallow) - 1mg of glucagon IM/SQ or amp of D50 IVP Diabetic Ketoacidosis (DKA) Pathophysiology Four Metabolic Problems Hyperosmolarity from hyperglycemia and dehydration Metabolic acidosis from an accumulation of ketoacids Extracellular volume depletion from osmotic diuresis Electrolyte imbalances Laboratory Findings for DKA BG >250mg/dl Plasma pH < 7.3 Plasma HCO3 < 15meq/L Presence of serum ketones Presence of urine ketones and glucose Abnormal levels of serum Na, K, Cl- Clinical Manifestations DKA Dehydration: polyuria, polydipsia, weight loss, dry skin, sunken eyes, lethargy, coma, rapid weak pulse, hypotension Metabolic Acidosis (ketosis): N/V, “fruity” breath, Kussmaul respirations, abdominal pain Treatment for DKA Frequent assessment of client: LOC, V/S, blood glucose levels, fluid and electrolyte status Correct fluid volume deficit 1 liter of isotonic saline over 1 hour 1 liter of hypotonic saline over 6 to 8 hrs 1 liter of hypertonic solution (D51/2NS) over 8 to 12 hrs. Drug therapy for DKA Insulin therapy: lower BG by 75-150mg/dl/hr Regular insulin IV bolus dose of .1u/kg followed by IV drip of .1u/kg/hr. SQ insulin when client can eat and ketosis has ended. Electrolyte replacement Potassium Bicarbonate Patho for HHS Metabolic Problems Laboratory Findings Clinical Manifestations Treatment Chronic Complications of Diabetes Mellitus Alterations in the CV System Macrovascular Cardiovascular Disease Cerebrovascular Disease Peripheral Vascular Disease Microvascular Nephropathy Retinopathy Diabetic Retinopathy Diabetic Nephropathy Alterations in the Peripheral and Autonomic Nervous Systems Diabetic Neuropathies Peripheral Neuropathies – Polyneuropathy and Mononeuropathy Visceral Neuropathies – Autonomic Neuropathies Client and Family Teaching Sick-Day Rules Notify your health care provider that you are ill. Monitor your blood glucose at least every 4 hours. Test your urine for ketones if BG>240. Continue to take your insulin or oral antidiabetic agents. Drink 8 to 12 ounces of sugarfree liquids every hour that you are awake. Continue to eat meals at regular times.