Diabetes Lecture - Nursing Theory PDF

NSG 5130: Level III Nursing Theory Med-Surg Week 10: Diabetes Mellitus Rachael Jaffray, RN, MScN Diabetes Diabetes Abnormal insulin production, impaired insulin utilization, or both Various factors involved: Genetic, autoimmune, viral and environmental (lifestyle, obesity, stress) L...

NSG 5130: Level III Nursing Theory Med-Surg Week 10: Diabetes Mellitus Rachael Jaffray, RN, MScN Diabetes Diabetes Abnormal insulin production, impaired insulin utilization, or both Various factors involved: Genetic, autoimmune, viral and environmental (lifestyle, obesity, stress) Leads to acute and/or chronic complications 65% - 80% of people with Diabetes Mellitus will die as a result of heart disease or stroke Most common Type 1 (10% of people with DM) Type 2 Other types Gestational, prediabetes, secondary (11 categories in total) (Lewis et. al., 2019  Patho Review: Glucagon, Insulin and the Pancreas Glucagon Insulin Synthesized and released from The principal regulator of pancreas in response to low blood metabolism and storage of carbs, glucose, protein ingestion and fats and proteins exercise Insulin facilitates glucose transport Increases blood glucose across cell membranes into tissues Glucagon and insulin work together (lowering blood glucose) to maintain normal blood glucose An increase in blood glucose levels stimulates insulin release In periods of fasting, glucagon After a meal, insulin is responsible breaks down stored complex fuels to for the storage of nutrients provide glucose Skeletal muscle and adipose tissue are insulin dependent tissues (have specific insulin receptors) (McMillan, 2020) Patho Review: Glucagon, Insulin and the Pancreas Think of insulin as if it were a pump. It is continuously released (“basal rate”) into the bloodstream, but delivers “boluses” when food is ingested Insulin lowers blood sugar Target BS levels: 4-6/7 Things that work to OPPOSE insulin by stimulating glucose production and release: Glucagon, epinephrine (fight or flight), growth hormone, cortisol (stress response hormone) (McMillan, 2020)  Diabetes: Glucose mmol/L 7 Normal range Hypoglycemic Hyperglycemic Goals vary depending on client May require emergency management when hypo or extremer hyper (later on in lecture) Type 1 Occurs most often in people 35 Now seeing it more in children/adolescents 80-90% are overweight at time of diagnosis. Risk can be cut anywhere from 60-70% by moderate daily exercise and losing 5-7% of body weight Obesity is the highest risk factor (abdominal & visceral fat surrounding organs) (Lewis et. al., 2019 Type 2: Risk Factors High blood pressure High levels of cholesterol or other fats in the blood A high or are overweight (especially if that weight is mostly carried around the tummy) Prediabetes (impaired glucose tolerance or impaired fasting glucose) Polycystic Ovary Syndrome (PCOS) Psychiatric disorders (schizophrenia, depression, bipolar disorder) Obstructive sleep apnea Darkened patches of skin called acanthosis nigricans Membership with high risk population (next) (Diabetes Canada, 2020) DM: Cultural Considerations High-Risk Population for Type 2 Indigenous, Latin American, South Asian, Asian, African Complex relationship: mixture of genetics, cultural practices (food/lifestyle), social determinants of health Consider preferences of cultural group when meal planning Practice healthy eating within pre-existing cultural Education and access to resources Type 2: Clinical Manifestations Usually gradual onset Complications may arise before client know they have a problem Often nonspecific May or may not experience classic type 1 symptoms (polyuria, polydipsia, polyphagia, weight loss) Most common symptoms Fatigue Recurrent infections/prolonged wound healing time (diminished peripheral blood flow) Visual changes (tiny eye vasculature damaged) Painful peripheral neuropathy in feet (nerve are affected by uncontrolled glucose levels) (Lewis et. al., 2019 DM: Diagnostics 1) Hemoglobin AIC (>=6.5%) Glucose levels over time Glucose attached to a hemoglobin molecule (part of an RBC) RBC life cycle is 120 days, test is effective in measuring overall glucose control for 90-120 days (3-4 months) 2) Fasting plasma glucose (>= 7) Blood glucose left in blood stream after no glucose Higher levels means insulin is either not being produced/released to regulate 3) Random plasma glucose (>=11), with classic symptoms Works by showing how much glucose circulates in the blood regardless of meals 4) Two-hour OGTT level (>=11.1), using a glucose load of 75g ( Oral glucose tolerance test) Results show how well the body metabolizes glucose (it’s ability to produce/synthesis insulin) (McMillan, 2020) DM: Clinical Management Insulin All people with Type 1 require exogenous insulin Only some individuals with Type 2 require exogenous insulin Oral antihyperglycemic agents (OHA) Lifestyle changes Nutrition, weight loss, exercise are (often not effective alone, need OHA +/- insulin) Insulin Types of insulin are categorized based on: Onset, peak, duration Often made of the “basal” “bolus” routine that mimics how the body should be endogenously regulating insulin Insulin Mealtime insulins Rapid acting insulins (Humolog, Novorapid) given 0-15 minutes before a meal Regular/short acting insulin (Humulin R) given 30-45 minutes prior to meals Intermediate acting (Humulin N, NPH) Peak is 4-10hrs, so can be harder to manipulate with meals and rapid acting Often given twice daily (mixed with short acting in the morning) Long action acting (Lantus) Given once daily at bedtime (no peak in action) (Lewis et. al., 2019 Insulin Combination therapy: Short/rapid acting (clear) + intermediate (NPH) (cloudy) Either prepared by patient/nurse/caregiver or premixed commercially Draw up clear before cloudy Why? Insulin Administration Require a physician order Often mix of sliding scale and scheduled Reassessed daily in pediatric facilities HIGH RISK medication May require a co-signature What to do when patient has their own pens? Use their own glucometers? Assess site and rotate within the site Assess for infection, lipodystrophy Adverse events: Hypoglycemia Somogi Effect Dawn Phenomenon Antihyperglycemic Agents OHAs work in the following ways: Increase pancreas stimulation Increase insulin production Enhances insulin sensitivity and absorption at cellular level Reduce glucose production in liver Slow down carbohydrate absorption Allows certain hormones (Incretin) to stay in blood stream longer increases Insulin synthesis For them to be effective there must be some level of circulating insulin Common OHAs include Gluconorm Metformin (Lewis et. al., 2019 Nutrition Nutritional therapy focuses on Blood sugar regulation Serum lipid control BP control Reminder! ‘Carb counting’ technique for some patients Dieticians Balanced diet consists of are a great resource!!!! Reducing total fat (saturated especially) Increase fiber Decrease in simple sugars Small meals t/o day versus 3 large ones Can use the Glycemic Index Diet The rise in blood sugar level after eating specific carbohydrates Higher the rise, the more insulin is needed (McMillan, 2020) DM- Safety Tips Exercise: Safety Tips See doctor for pre-exercise assessment Listen to your body! If you take insulin or medications that increase insulin levels: Monitor blood sugar levels before, during and many hours after activity Glucose lowering can happen up to 48hours after exercise Eat before exercising Emergency fast-acting carbohydrate in case of with hypoglycemia Recommend 30min, 5 times a week Aerobic and resistance (Diabetes Canada, 2020 DM and Alcohol Alcohol has an inhibitory affect on glucose production Risk for severe hypoglycemia in patients taking insulin or OHAs that increase insulin production Other potential adverse effects: Alcohol and Metformin lactic acidosis Reduced risk for hypoglycemic event by: No more than 1 to 2 drinks per day Eating food when drinking alcohol Use sugar free mixes Drink dry, light, wines Be honest and open with health care providers (McMillan, 2020) Acute Complications Hypoglycemia Hypoglycemia Occurs when Too much insulin in proportion to glucose in the blood Blood glucose level less than 4 mmol/L Causes More common with insulin therapy, but can happen with OHAs Mismatch in timing Food intake and peak action of insulin or oral hypoglycemic agents Too much insulin, not enough food, delay in timing (Lewis et. al., 2020 Hypoglycemia: Clinical Manifestations If untreated can progress to irritability, difficulty speaking, confusion, loss of consciousness, seizures, When brain coma, and death does not have enough glucose Hypoglycemic unawareness Not everyone experiences these symptoms. Related to autonomic neuropathy. (Lewis et. al., 2020  Hypoglycemia: Treatment Nurse needs to acts quickly – can usually be reversed with effective and rapid treatment Diagnosis: Capillary blood glucose if no glucometer available, suspect hypoglycemia based on symptoms Physical examination Treatment depends on severity and symptoms Glucose level, level of consciousness **Once corrected, then investigate cause** Hypoglycemia: Treatment Hypoglycemia: Treatment Acute Complications Hyperglycemia Events: Diabetic Ketoacidosis Hyperosmolar Hyperglycemic Syndrome Diabetic Ketoacidosis (DKA) Acute metabolic complication Metabolism of fats in the absence of insulin causing: Hyperglycemia Ketosis (breakdown of fat for energy) Metabolic acidosis Severe dehydration (volume depletion) Precipitating Factors: Illness Infection Inadequate insulin dosage Undiagnosed type 1 Poor self-management (Lewis et. al., 2020 DKA: Clinical Manifestations Polyuria, polydipsia Abdominal pain Lethargy/weakness Kussmaul’s respirations Early symptoms Rapid deep breathing Attempt to reverse Dehydration metabolic acidosis Poor skin turgor Sweet fruity odour Dry mucous membranes Tachycardia Orthostatic hypotension (Lewis et. al., 2020 Hyperosmolar Hyperglycemic Syndrome (HHS) Medical Emergency: Life-threatening syndrome, high mortality rate Less common than DKA, often occurs in older clients with type 2 DM Client has enough circulating insulin that ketoacidosis does not occur. Clinical manifestations: Produces fewer symptoms in earlier stages. Neurological manifestations occur because of ↑ serum osmolality. (Lewis et. al., 2020 Hyperosmolar Hyperglycemic Syndrome (HHS) Usually, history of: Inadequate fluid intake Increasing mental depression Polyuria Laboratory values Blood glucose >34 mmol/L Increase in serum osmolality Absent/minimal ketone bodies (Lewis et. al., 2020 Management of DKA and HHS Chronic Complications Chronic Complications Vascular damage Accumulation of damaging substances in vessels byproducts of glucose metabolism (sorbitol) impact nerve cells Formation of abnormal glucose molecules in smallest blood vessels impacting eye & kidney vessels Oxidative stress Creates free radicals that disproportionality damages retina Leads to retinopathy (Calderon et al., 2017) Can be ‘macro’ or ‘micro’ concerns Damage to large vessels or small vessels (Lewis et. al., 2019 Focus on Feet DM and Complications of the Foot Those with DM 20 times more likely to be hospitalized with nontraumatic lower limb amputations Various association risk factors: PVD, clotting abnormalities, impaired immune function, sensory neuropathy (loss of protective sensation = LOPS) Can lead to leg ulcers gangrene amputation Nurses and Annual (or more frequent) screening recommended patients - Get support from a Education of foot care foot care specialist for guidance! (Lewis et. al., 2019 Foot Care Tips: Examine your feet and legs daily for cuts or sores Care for your nails regularly (Cut and file nails evenly) Apply lotion if your feet are dry (but not between the toes) Wear properly fitting shoes Test your bath water with your hand or elbow before you step in to make sure it’s not too hot, use mild soaps Do not leave your feet to soak Dry feet after washing (Canadian Diabetes Association, 2014)