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    1 : Diabetes Mellitus Priyadarshini.R
    2 : Diabetes mellitus (DM) is a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both. The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. The effects of diabetes mellitus include long–term damage, dysfunction and failure of various organs. What is diabetes?
    3 : STATISTISTICAL REVIEW Prevalence Physiological Impact Financial Impact
    4 : PREVALENCE 16 million Americans have DM 6 million of these are undiagnosed Represents 6% of US population 800,000 new cases annually Increased prevalence is multifactoral Older US population Increased risk factors Ethnic/racial variations African Americans , Hispanics, Asian Americans, and Native Americans are at increased risk for DM
    5 : PHYSIOLOGICAL IMPACT 2-4 x greater risk of death d/t heart disease 6th leading cause of death by disease Compounding Decreases life expectancy of middle-aged people by 5-10 years factors include: duration of disease, glycemic control, HTN, smoking, dyslipidemia, decreased activity, and obesity Leading cause of blindness in 25-74 year olds Leading cause of non-traumatic amputations Responsible for 25-30% of all new dialysis patients
    6 : FINANCIAL IMPACT Estimated to cost $99-$105 billion annually Adult DM patients have a 2.4 x > hospitalization rate than the general population Children with DM have a 5.3 x > hospitalization rate than the general population of children
    7 : Physiology of Energy Metabolism All body cells use glucose for energy. To maintain this constant source of energy, blood glucose levels must be kept between 3.3-6.1 mmol/L. Several hormones, help to maintain this level between 3.3-6.1mmol/L, include insulin, glucagon. The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver. The glucagon is released when blood glucose levels decreased (e.g. between meals and over the night) and stimulate the liver to release stored glucose.
    8 : Insulin Diabetes is a disease which deals with insulin. A healthy pancreas releases 40-50 units of insulin daily, still keeping several hundred units available in storage to be released if the blood glucose levels rise. When insulin enters the bloodstream, it binds to insulin receptors on the membranes of the liver, muscle, and fat cells. In these cells, insulin encourages glucose uptake by causing a shift of another insulin sensitive glucose transporter, GLUT 4, to the surface of cells.
    9 : Pathophysiology of Diabetes Mellitus Diabetes mellitus is not a single disease but a complex syndrome characterized by hyperglycemia resulting from altered carbohydrate, fat, and protein metabolism. This altered metabolism is secondary to insulin insufficiency, insufficient insulin activity, or both. Because of the altered fuel metabolism, diabetes is characterized by vascular and neurologic changes throughout the body. Absence of insulin or ineffective insulin activity prevents glucose from entering liver, muscle and fat cells
    10 :
    11 : Subclasses of Diabetes Mellitus Type 1 Type 2 Gestational Diabetes Mellitus Malnutrition Related Diabetes Mellitus Secondary Diabetes Mellitus Impaired Fasting Glucose and Impaired Glucose Tolerance
    12 : Type 1 Diabetes Mellitus Constitutes 5-10% of DM diagnosis Age of onset usually <30 yo and most <20yo Signs and symptoms occur when 90% of beta cells are destroyed resulting in severe or complete insulinopenia 3 “Ps”-polyuria, polydipsia, and polyphagia Ketonuria-DKA PRONE Rapid weight loss Hyperglycemia (ADA criteria)
    13 : Type 1 causes and treatment Suspected causes Genetic predisposition Immunologic Environmental Treatment Insulin
    14 : Type 2 Diabetes Mellitus Constitutes 90-95% of DM diagnosis Age of onset usually >30 yo -MODY Signs and symptoms usually mild or absent at time of diagnosis (ADA criteria) Occurs due to defects in insulin function Insulin resistance/not islet cell antibodies Decreased insulin secretion (rarely DKA) Hepatic glucose overproduction May be multifactoral
    15 : Gestational Diabetes Mellitus Hyperglycemia diagnosed during pregnancy Occurs in 2-5% of pregnancies Occurs due to placental hormone changes that effect insulin function (greater resistance) Screening usually occurs during the 24th-28th week in high risk patients Criteria for diagnosis is different than for Type 1 and Type 2 Dietary changes are initial treatment and insulin is the only BG lowering agent used Concern is both for maternal and fetal well-being Postpartum BG levels usually return to normal Increased risk for Type 2 diabetes (30-50%)
    16 : Risk factors of gestational diabetes Over the age of 30 Obesity Family history of diabetes Having previously given birth to a very large child (over 9 pounds, 14 ounces), having previously given birth to a stillborn child or a child with a birth defect Having too much amniotic fluid Having gestational diabetes in a previous pregnancy Having high blood pressure
    17 : Malnutrition Related Diabetes Mellitus Usually seen in developing countries Age of onset usually 10-40 yo Hyperglycemia exists without ketosis Usually require insulin
    18 : Secondary Diabetes Mellitus DM occurs as a result of another problem (primary) Diseases Conditions Medications Thiazides Diuretics Beta blockers Steroids Hyperglycemia is diagnostic for DM Treatment of the primary cause may resolve the DM but lifestyle modifications and medications may be needed as well
    19 : Impaired Fasting Glucose Defined as a fasting plasma blood glucose of >/= to 110 but < 126 Increased risk for DM Must educate regarding risks and need for lifestyle modifications
    20 : Clinical manifestations of diabetes Polyuria – increased urination Polydispia – increased thirst, which occurs as a result of excess loss of fluid associated with osmotic diuresis. Polyphagia – increased appetite which results from the catabolic state induced by insulin deficiency
    21 : Type I S&S Increased thirst Frequent urination Fatigue Excessive weight loss Nausea and vomiting Having dry, itchy skin Feeling of numbness and tingling in the feet Blurry eyesight Constant hunger Abdominal pain if DKA (Diabetic Ketoacidosis) have occurred
    22 : Type II S & S Fatigue Frequent urination Increased thirst and hunger Blurred vision
    23 : Gestational diabetes S & S Generally, gestational diabetes may not cause any symptoms; however, the woman may experience Excessive weight gain, Excessive hunger or thirst, Excessive urination Recurrent vaginal infections
    24 : Diagnosis of diabetes DM is indicated by typical S&S and confirmed by measurement of plasma glucose. Fasting plasma glucose (FPG): measurement after an 8-12h fast. Oral glucose tolerance testing (OGTT): 2h after ingestion of a concentrated glucose solution. OGTT is more sensitive for Dx DM and impaired tolerance but is more expansive and less convenient and reproducible than FPG. It is rarely used routinely, except for Dx of gestational DM. HbA1c : testing for glycosylated hemoglobin. HbA1c levels reflect glucose control over the preceding 2-3 months. HbA1c is not considered as reliable as FPG or OGTT testing for Dx DM and used mainly for monitoring DM control.
    25 : Diagnosis of diabetes (con’t) Diagnostic criteria for DM and impaired glucose regulation
    26 : Management of Diabetes
    27 : Good Diabetes Management Regular Blood Glucose Monitoring Healthy Nutrition  Regular Exercise
    28 : Management components of DM Education Nutrition Exercise Monitoring Medications
    29 : Educating the patient with DM Learner assessment Health hx of patient and family Personal characteristics Lifestyle Psychosocial issues Current DM knowledge Values/beliefs Teaching plan Must include the learner Goals-short and long term Objectives-determined by methods of teaching Outcomes-determine future goals and objectives Utilizes the nursing process
    30 :
    31 : Diet is a basic part of management in every case. Treatment cannot be effective unless adequate attention is given to ensuring appropriate nutrition. Dietary treatment should aim at: ensuring weight control providing nutritional requirements allowing good glycaemic control with blood glucose levels as close to normal as possible correcting any associated blood lipid abnormalities A. Diet
    32 : Food Guide Pyramid Fats/Sugars Milk, Eggs, Cheese/Meats Vegetables/Fruits Starches Based on dietary recommendations of obtaining 50-60% of calories from CHOs, 20-30% from fats, and 20% from protein Suggest a range of servings in each group w/o serving size recommendations specified
    33 : Weight Management and DM Cornerstone of Type 2 management in 80% of cases IBW calculations vs reasonable body weight goals – must be patient determined if possible Obesity is defined as 20% above IBW 10-15lbs of wt loss can improve IGT 10% total body wt loss may significantly improve glycemic control Key is calorie control initially with careful monitoring of BG
    34 :
    35 : Exercise Benefits Lowers BP Lowers BG – readily available and stored Improves Lipids Raises HDL Lowers triglycerides Lowers total cholesterol Enhances insulin sensitivity Contributes to weight loss Strengthens cardiac health Contributes to reduction in medication use Improves overall well-being
    36 : Self-Practice Monitoring Self Monitoring Blood Glucose (SMBG) Urine for Ketones Urine for Glycosuria Daily Foot Care Periodic Medical Exams
    37 : Daily Foot Care Benefits Promotes health of skin and nail integrity Daily cleansing Daily lotion application Periodic nail care Promotes early intervention for problems Education Teach how to examine feet Teach when to examine feet (personally and professionally) Teach how to care for feet Cleansing Lotion application Footwear Teach when to seek medical evaluation
    38 : Periodic Medical Exams Routine check-ups with health care provider Physical exam Ht, wt, BP Foot exam (microfilament and vibratory testing) Multi-system review and exam Diagnostic Exams Laboratory /Screenings Hgb A1C quarterly to biannually Annual lipids, TSH, urine for microalbuminuria, and BMP Testing of other functions depends on medications, new GXT or other cardiac work-up Specialist Ophthalmologist annually Podiatrist Nephrologist Endocrinologist
    39 : Pharmacology for Diabetes Mellitus Oral Diabetic Medications Sulfonylureas Biguanides Alpha-Glucosidase Inhibitors Nonsulfonylurea Secretagogues Meglitinide D-phenylalanine derivatives Thiazolidinediones (TZDs) Insulins Mealtime Insulins Rapid Acting Short Acting Basal Insulins Intermediate Acting Long Acting Premixed
    40 : Sulfonylureas Act by stimulating the pancreatic secretion of insulin Side Effects Wt gain Hypoglycemia GI disturbances skin reactions Two Classes 1st Generation 2nd Generation
    41 : 1st Generation Sulfonylureas Rarely prescribed due to increases in side effects Examples Dymelor Diabinese Tolinase Orinase
    42 : 2nd Generation Sulfonylureas Most commonly prescribed sulfonylureas Glimepiride (Amaryl) 1-8mg qd in single dose FDA approval in combination tx with insulin Glipizide (Glucotrol and Glucotrol XL) Dosage 2.5mg-40mg qd for Gluctrol 5-10mg qd for Glucotrol XL Now generic Used in mild hepatic and renal failure safely Glyburide (Glynase Prestab, Micronase, and Diabeta) 1.25 mg to 20mg qd for Diabeta 1.5-6mg qd for Glynase 1.25-20mg qd
    43 : Biguanides Glucophage and Glucophage XR Method of Action Suppresses hepatic glucose production Increases peripheral glucose uptake Frequently prescribed d/t action-excellent choice for obese patients with Type 2 DM Side Effects GI disturbances – usually dose related Lactic Acidosis – creatinine clearance level must be known prior to tx Dosing 250-2250mg Glucophage 500-2000mg Glucophage XR Glucovance – New! (combines metformin with Glyburide)
    44 : Alpha-Glucosidase Inhibitors Delay absorption of glucose from GI tract by slowing the breakdown of complex CHOs– no systemic absorption Must be taken at the beginning of the meal Side Effects GI disturbances Hypoglycemia with combination tx possible-must not be treated with sucrose 2 Brands Acarbose (Precose): dose is titrated up as tolerance is developed starting with 25mg qd and increasing to 50-100mg TID Miglitol (Glyset): dose is titrated up as tolerated starting with 25mg qd and increasing to 25-50mg tid
    45 : Nonsulfonylurea Secretagogues Stimulate pancreatic insulin secretion but uses a fast action with short duration Must be taken at the beginning of each meal and avoided if meal is missed Side Effects Hypoglycemia – rare with monotherapy Wt gain 2 classes of drugs with one medication in each class Meglitinide Class Repaglinide (Prandin) given .5-4mg ac meals 1-4xqd D-phenylalanine Derivative Class Nateglinide (Starlix) given ac meals
    46 : TZDs Decreases peripheral insulin resistance and hepatic glucose production Considered 1st line tx for Type 2 early onset DM patients and in others where insulin resistance is a problem Side Effects Peripheral Edema Wt gain Caution in use with patients in advanced CHF Caution with liver failure-monitoring liver fxn imperative 2 Brands available Pioglitazone (Actos) given in 15-45mg dose qd Rosiglitazone (Avandia) given in 4-8mg qd Rezulin is no longer available
    47 : Insulins 3 main characteristics determine classes of insulin Time of action Species Manufacturer Route- IV or SQ (syringe/jet/or CSII pump) Always indicated in Type 1 DM and in certain situations in Type 2 SMBG is necessary Side Effects Hypoglycemia Lipodystrophy/lipohypertrophy Allergic reactions (local vs systemic)/Resistance Teaching insulin administration is
    48 :
    49 : Methods of delivery insulin Intravenous (IV) Syringes (SC) Pens Jet injectors Insulin pumps
    50 : Site Selection: Where can I give the Injections? 4 major areas: Arms-posterior surface Abdomen-avoid 1 inch area around navel Thighs-anterior surface Hips Note: Systematic rotation of injection sites within an anatomic area to prevent lipodystrophy. Administering each injection 0.5-1inch away from the previous injection.
    51 : Storing and Handling Insulin Stored at room temperature (15 to 30°C). If stored in a refrigerator, unopened bottles are good until the expiration date printed on the bottle. Opened bottles that are stored in a refrigerator should be used within one month of being opened. Protect your insulin (bottles, pens, and cartridges) from extremes of hot and cold. Never store your insulin in the freezer - once insulin is frozen, it loses its potency.
    52 : Chronic Complications of DM Diabetic Neuropathies Microvascular Disease Retinopathy Diabetic nephropathy Macrovascular Disease CAD CVA PVD Infection Lower-limb amputations
    53 : Patients should be educated to practice self-care. This allows the patient to assume responsibility and control of his / her own diabetes management. Self-care should include: Body weight monitoring Foot-care Blood glucose monitoring Personal hygiene Healthy lifestyle/diet or physical activity Identify targets for control Stopping smoking Self-Care
    54 : Diabetic Neuropathies (con’t) Peripheral neuropathy Paresthesias (prickling, tingling, or hightened sensation) on feet and fingers. Burning sensations (especially at night) The feet become numb as the neuropathy progress. Decreased sensations of pain and temperature. (risk for injury and undetected foot infection) A decrease in proprioception (awareness of posture and mov’t of body and of position and wt. of objects in relatio to the body) A decrease sensation of light touch (may lead to unsteady gait)
    55 : Macrovascular Disease Blood vessel walls thicken, atherosclerosis, and become occluded by plaque. CAD The most common cause of death in those with type II, also common in those with type I. MI (coronary artery occlusion) CHF CVA-hypertension; accelerated atherosclerosis, formation of an embolus ** S&S of CVA may be similar to symptoms of acute diabetic complications e.g. HHNS. It is important to rapidly assess the CBG so that testing and tx of CVA can be initiated if indicated. PVD: gangrene occurs. Occlusions of the small arteries and arterioles lead to the gangrene of the lower extremities results in patchy areas of the feet and toes. Amputation of foot or leg.
    56 : Microvascular Disease Persistent exposure to hyperglycemia is an important factor in the development of diabetic microvascular complications. Microvascular changes are unique to diabetes. Microangiopathy (Diabetic microvascular disease) :Thickening of capillary basement membrane results in decreased tissue perfusion. Hypoxia and ischemia of various organs may result from microangiopathy: two areas often affected are the retina and the kidney. (persistent increased blood glucose levels are responsible for the thickening of the basement of membrane) Renal retinal syndrome: the vast majority of individuals with DM have some degree of retinopathy, and retinopathy is closely associated with diabetic nephropathy. Retinopathy Diabetic Nephropathy
    57 : Retinopathy Diabetic retinopathy is the leading cause of blindness in people b/w 20 and 74 years old. A change in vision (caused by the rupture of small microaneurysms in retinal vessels.) Blurred vision (macular edema) Sudden loss of vision ( retinal detachment) Cataracts ( lens opacity)
    58 : Diabetic Nephropathy Renal disease secondary to diabetic microvascular changes in the kidney. A common complication of diabetes. About 20 % to 30% of people with type I or type II diabetes develop nephropathy. With the blood glucose levels elevated, the kidney’s filtration mechanism is stressed. The earliest sign is a thickening in the glomerulus, allowing blood proteins to leak into the urine. As a result, the pressure in the blood vessels of the kidney increases. The elevated pressure stimulates the development of nephropathy.
    59 : Infections The individual with DM is at increased risk for infection throughout the body: Diminished sense Microvascular & macrovascular complications cause decreased O2 supply to tissue. The increased content of glycosylated hemoglobin in the red blood cell impedes the release of O2 to tissues. Pathogens are able to multiply rapidly because the increased glucose in body fluids provides an excellent source of energy. Decreased blood supply resulting from vascular changes, leads to decreased supply of WBC to the affected area The function of the WBC is impaired.
    60 : Foot and Leg problems Typical Diabetic foot ulcer
    61 : Management of hospitalized diabetic patients Avoid hyperglycemia during hospitalization Assess the pt’s usual home routine. Try to approximate as much as possible the home schedule of insulin, meals, and activities. CBG monitoring. The insulin doses must not be withheld when CBG are normal. IV antibiotics should be mixed in NS to avoid excess infusion of dextrose. Tx of hypoglycemia/hyperglycemia by following hospital protocol.
    62 : Management of hospitalized diabetic patients (con’t) Avoid hypoglycemia during hospitalization Hypoglycemia in a hospitalized pt. is usually the result of too much insulin or delays in eating. To avoid hypoglycemic reactions caused by delayed food intake, the nurse should arrange for a snack if meals are going to be delayed because of procedures, PT, or other activities.
    63 : Management of hospitalized diabetic patients (con’t) NPO For the pt who must have NPO in preparation for diagnostic or surgical procedure, the nurse must ensure that the usual insulin dosage has been changed. Even when no food is taken, glucose levels may rise as a result of hepatic glucose production, especially in pts with type I diabetes. Elimination of the insulin dose may lead to the development of DKA. ** Administering insulin to the patient with type I diabetes who is NPO is an important nursing intervention. Because DKA does not develop when insulin doses are eliminated in type II diabetes pts, skipping the insulin dose may be safe, but close monitoring is essential. Glucose testing and insulin administration should be at regular intervals usually 2-4 times per day. Pts should receive dextrose infusion to provide some calories and limit ketosis. To prevent these problems resulting from the need to withhold food, diagnostic tests and procedures and surgery should be scheduled early in the morning if possible.
    64 : Management of hospitalized diabetic patients (con’t) Hygiene Must focus attention on oral hygiene and skin care, because diabetic pts are at increased risk for periodontal disease. Keep the skin clean and dry, especially in areas of contact b/w two skin surfaces (eg, groin, axilla, and in obese women, under the breasts). For the bedridden diabetic pt, nursing care must emphasize the prevention of skin breakdown at pressure points. The heels are particularly susceptible to breakdown. Feet should be cleaned, dried, lubricated with lotion (but not b/w the toes), and inspected frequently. Teach the pt about diabetes self-management, including daily oral, skin, and foot care. Female diabetic pts should also be instructed about measures for the avoidance of vaginal infections, which occur more frequently when blood glucose levels are elevated.
    65 : Management of hospitalized diabetic patients (con’t) Diabetes and the risk of blood clots Higher risk of DVT formation than non-diabetic pts. The factors that increase the risk of DVT. Age: >60 years Recent major surgery Poor circulation: Lack of adequate circulation in the deep veins can lead to a blood clot. Obesity: Being significantly overweight affects your circulation and your activity levels. Infections Interventions: Anticoagulant e.g. Heparin T.E.Ds Encourage ambulation/leg exercise
    66 : Conclusions The rate of people being diagnosed with Type 2 DM is on the rise New Treatments and even cures are continuously being explored Early detection and intervention hold the key to delaying or even avoiding the development of DM DM management is crucial to preventing complications
    67 : Being a Nurse is being an Educator
    68 : Thank You

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