Diabetes Mellitus In-Class Content PDF

CHAPTER 53 DIABETES MELLITUS IN CLASS CONTENT Shelly Hopko MSN-Ed, RN, PCCN, CNE  DIABETES MELLITUS CLINICAL MANIFESTATIONS Type 1 Type 2 Rapid onset of symptoms Gradual onset of symptoms bu...

CHAPTER 53 DIABETES MELLITUS IN CLASS CONTENT Shelly Hopko MSN-Ed, RN, PCCN, CNE  DIABETES MELLITUS CLINICAL MANIFESTATIONS Type 1 Type 2 Rapid onset of symptoms Gradual onset of symptoms but could Polydipsia have similar onset of symptoms as type 1 (polydipsia, polyuria, and polyphagia) Polyuria Fatigue Polyphagia Recurrent yeast infections Weight loss Prolonged wound healing Weakness Visual changes Fatigue Ketoacidosis  DIABETES MELLITUS DIAGNOSTICS One of four methods A1C of 6.5% or higher A1C is the percent of glycosylated hemoglobin Fast blood glucose > 126 mg/dL Fasting means no caloric intake for 8 hours 2 hour oral glucose tolerance test OGTT using a 75gm load of glucose In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis-a random blood glucose ≥200mg/dL  DIABETES MELLITUS INTERPROFESSIONAL CARE Goals of Diabetes Management How do we meet these goals? Reduce symptoms By keeping blood glucose at near Promote well-being normal levels as much as possible Prevent acute complications Education of patients and related to high and low blood caregivers enables them to make glucose good choices regarding food, exercise and medications. Prevent or delay the onset and progression of long-term Allow and encourage patient to be complications an active participant in own health ABC’s of Diabetes management A1C, BP, Cholesterol  DIABETES MELLITUS MEDICATIONS YOU NEED TO KNOW YOUR MEDS!!!!! 3 types of Diabetes Medications Insulin Oral agents Non-insulin injectables  DIABETES MELLITUS MEDICATIONS – INSULIN Exogenous (injected) insulin is Different types of insulin vary in needed when patient’s own insulin timing of onset, peak and duration is inadequate May need multiple injections a day or a continuous sub cutaneous pump Review table and figure 53.4 Types of insulin Rapid acting Short acting Intermediate acting Long acting  TYPES OF INSULIN Rapid acting Rapid or short acting insulins mimic Lispro(Humalog), aspart (Novolog), the release of insulin from the and glulisine (Apidra) pancreas when a meal is eaten Onset 10-30 min Should be given 15 minutes before Peak 30 min to 3 hour a meal Duration 3-5 hours Requires BG checks more often Short acting Regular (Humulin R, Novolin R) Onset 30min to 1 hour Peak 2-5 hours Duration 5-8 hours  TYPES OF INSULINS Intermediate acting Intermediate and long-acting insulins NPH (Humulin N, Novolin N) act in the background to provide a Onset 1.5 to 4 hours constant release on insulin Peak 4 to 12 hours Long-acting insulin helps control BG in Duration 12 to 18 hours between meals and overnight by releasing a continuous and steady Long acting amount of insulin Glargine (Lantus) detemir (Levemir) degludec (Tresiba) Intermediate insulin can be mixed with short and rapid acting insulins, must be Onset 0.8 to 4 hours agitated before drawing it up, and can Peak- less defined/ no peak minimize injections a patient needs Duration 16 to 24 hours (combination therapy)  TYPES OF INSULIN OTHER CONSIDERATIONS Storage of Insulins Store needles upward to avoid Avoid heat and freezing (alters clumping of medication in the molecular structure and makes it needle less effective) Gentle roll syringe in your hands to Opened vials and pens can be warm it before giving stored at room temperature for 4 weeks Avoid direct sunlight Unopened pens and vials in fridge Prefilled syringes in fridge for up to 1 week (mixed) and 30 days (not mixed)  INSULIN PUMP THERAPY Delivers insulin continuously Uses rapid acting insulin, loaded into the reservoir Programmable to run a basal rate Can be adjusted for number of carbs or to give bolus dose Must check BG 4-8 times a day Offers tighter glucose control (because the pump works like the pancreas)  INHALED INSULIN Afrezza Rapid acting Taken in beginning of meal or within 20 minutes of starting the meal Must be in combination with long acting insulin in type 1 DM Not for patients with chronic lung disease  PROBLEMS WITH INSULIN THERAPY Hypoglycemia- low blood glucose Allergic reactions Itching, redness, burning at injection site True allergies to insulin is rare Zinc, protamine and latex allergies from preservatives and stopper on vial Lipodystrophy- atrophy (wasting) or hypertrophy (thickening) of the subcutaneous tissue May occur if injections sites are not rotated COST!  PROBLEMS WITH INSULIN THERAPY Somogyi effect Hyperglycemia in the morning High dose of insulin produces a drop in BG, counterregulatory hormones are released to correct this (stimulating release of glucose) Patient wakes with high BG (rebound hyperglycemia) If patient has high am BG, check BG between 2 and 4 am for hypoglycemia Bedtime snack or decreasing insulin dose can help  PROBLEMS WITH INSULIN THERAPY Dawn Phenomenon Also hyperglycemia in the morning Counterregulatory hormones (growth hormone and cortisol) are excreted in increased amounts in the early morning hours Most common in adolescents and young adults Checking the BG between 2-4 am may be high Insulin doses may need increased  ORAL AGENTS AND NONINSULIN INJECTABLES FOR DIABETES MELLITUS These drugs work on 3 defects of Read table 53.8 for the oral agents type 2 diabetes and non-insulin injectables. Look Insulin resistance for unusual nursing considerations Decreased insulin production and drug alerts! Increased hepatic glucose production May be used in combination with other oral agents or insulin  ORAL AGENTS Biguanides Thiazolidinediones Metformin Pioglitazone, rosiglitazone Sulfonylureas Dipeptidyl peptidase-4 inhibitors Glipizide, glyburide, glimepiride Linagliptin, saxagliptin, sitagliptin, alogliptin Meglitinides Nateglinide, repaglinide Dopamine receptor agonists bromocriptine a-Glucosidase inhibitors Acarbose, miglitol Sodium-glucose co-transporter 2 inhibitors Canaglifozin, dapaglifozin, empaglifozin  NON INSULIN INJECTABLES Glucagon-like peptide-1 receptor Amylin Analogs agonists Pramlintide (Symlin) GLP-1 Exenatide (Byetta) Exenatide extended release(Bydureon) Liraglutide (Victoza) Albiglutide (Tanzuem) Dulaglutide (Trulicity) Lixisenatide(Adylxin)  ACUTE COMPLICATIONS OF DIABETES MELLITUS Hyperglycemia Too little insulin circulating in blood Hypoglycemia Too much insulin circulating in blood Worsens rapidly if not corrected Review table 53.18 for a comparison between hyperglycemia and hypoglycemia  DIABETIC KETOACIDOSIS Caused by a profound deficiency When there is not enough insulin, of insulin and is characterized by glucose can’t be used properly for hyperglycemia, ketosis, acidosis and energy dehydration The body compensates by breaking Can occur in both type 1 and 2 but down fat stores (ketones are a by most likely type 1 product of this process) Precipitating factors can include Excess ketones illness, infection, inadequate insulin Alter pH balance (acidosis) dose, undiagnosed type 1, poor Are excreted in urine management and neglect Cause electrolyte imbalance  DIABETES KETOACIDOSIS Insulin deficiency impairs protein synthesis Excessive protein degradation Insulin deficiency stimulates the production of glucose from amino acids in the liver (making the glucose level even higher) If left untreated, electrolytes are depleted (Na+, K+, Cl, Mg+, Phos) Hypovolemia to shock to renal failure to dehydration to comatose to death  DIABETIC KETOACIDOSIS Clinical manifestations Diagnostics Early signs- lethargy and weakness Blood glucose ≥ 250 mg/dL Dehydration- poor turgor, dry ABG pH level < 7.3 mucous membranes, tachycardia, Serum bicarb < 16.mEq/L and orthostatic hypotension Large or moderate amounts of Sever dehydration- loose dry skin, ketones present in urine sunken eyes, possible abdominal pain, nausea, vomiting, anorexia, Kussmaul’s respirations (rapid and deep) acetone on breath  DIABETIC KETOACIDOSIS Interprofessional Care Blood glucose should be lowered May or may not require slowly to prevent cerebral edema! hospitalization Reduce BG by 36- 54 mg/dL/hr to Emergency management avoid complications IV fluids and electrolytes Airway management Fluids should be changed to 5-10% Insulin gtt with fluids dextrose to prevent hypoglycemia Aim of fluids and electrolytes is to and cerebral edema replace extracellular and Monitor for fluid overload intracellular water to correct deficits of sodium, chloride, bicarb, potassium, phosphate, magnesium and nitrogen  HYPEROSMOLAR HYPERGLYCEMIC SYNDROME - HHS Considered a medical emergency Clinical manifestations and has a high mortality rate! Somnolence, coma, seizures, Management is similar to DKA hemiparesis, and aphasia Main difference between DKA and HHS HHS is that HHS has enough BG> 600 mg/dL circulating insulin to prevent Increase in serum osmolality ketoacidosis Little to no ketones present Fewer problems initially so BG climbs very high before patient is symptomatic  HYPEROSMOLAR HYPERGLYCEMIC SYNDROME Interprofessional care IV fluids IV insulin infusion Electrolyte replacement Assess VS, I&O, turgor, labs, and cardiac rhythm Monitor BG and urine tests (ketones)  HYPOGLYCEMIA Low blood glucose, too much insulin in circulation BG less than 70mg/dL Counterregulatory hormones are released and activate the autonomic nervous system Epinephrine is released, causing shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor  HYPOGLYCEMIA Brain needs glucose too! Hypoglycemia unawareness Mental functioning, difficulty Patient does not experience speaking, visual disturbances, symptoms until the BG is critically stupor, confusion, coma low What else does this sound like? Patients at risk Untreated Repeated episodes of hypoglycemia, older patients, Loss of consciousness, seizures, patients who take beta blockers coma, eventually death Patient’s goal BG is higher than a normal level  HYPOGLYCEMIA Causes Mismatch in timing of food intake and peak action of insulin or other DM medication Too much med Too little food Unusually amount of exercise Can also occur when high BG falls too quickly- patient can’t tolerate the sudden shift  HYPOGLYCEMIA- RULE OF 15 Nursing management and Avoid carbs with fat (slows Interprofessional care absorption of glucose) At first sign- STOP AND CHECK BG! Do not overtreat (to avoid If 70, check for other causes of symptoms In acute care, use glucose gels, tabs, IM or IV dextrose 50% Rule of 15 If less than 70, treat with 15 to 20 g of a simple, fast-acting carb Recheck BG in 15 min Repeat until BG >70 Call HCP if still