Care_of_the_Diabetic_Client_Powerpoint_Brunner.ppt - Care of the Diabetic Client NUR 3215 Process I Delores B Lawson RN DSN 1 Diabetes Mellitus Group of

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Unformatted text preview: Care of the Diabetic Client NUR 3215 Process I Delores B. Lawson, RN., DSN 1 Diabetes Mellitus Group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia) Results from defects in insulin secretion and/or insulin action 2 Classification of Diabetes Type 1 – (previously IDDM, Type I) 5-10%; Tx - exogenous insulin Type 2 – (previously NIDDM, Type II) 90-95%; Tx – diet, exercise (oral hypoglycemic agents and/or insulin - control, acute physiologic stress) Type 1 – 90% beta cells destroyed by autoimmune process (little or no insulin, require insulin injections to control BG levels) Type 2 - < sensitivity to insulin (insulin resistance), impaired beta cell functioning from < insulin production (>30 y/o and obese) 3 Diabetes Mellitus Old terms & Roman #’s - classification based on tx not underlying etiology. Use numbers - helps reduce confusion Many differences within each category (Type 2 can move from one category to another (gestational) Borderline diabetes – impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) BG levels fall bet/w normal levels and levels considered dx for diabetes 4 Incidence Affects 17+ million; 5.9 million undx Especially prevalent in elderly AA, minority groups > risk for development, complications & > death rates 5 Incidence Leading cause - nontraumatic amputations, blindness, end stage renal disease 3rd leading cause death by disease (CVA) Economic cost > (> health cost, aging pop.) $100 billion/yr – direct & indirect cost 6 Diabetes Mellitus Cause – unknown and no cure Nursing care- varies with type, client’s age & needs Lifelong changes in client’s lifestyle & health status Normal BG – 70-110 mg/dL 7 Pancreatic Hormones Necessary for metabolism & cellular utilization of CHO, protein & fat Islet of Langerhans – Alpha and Beta cells produce the endocrine hormones – Glucagon and Insulin 8 Alpha Cells Hormone Produces hormone Glucagon < glucose oxidation & > BG levels Action initiated when BG falls <70mg/dL Keeps BG level from < below certain level when fasting or bet/w meals Stimulates breakdown of glycogen in liver, formation of CHO in liver & breakdown of lipids in liver & adipose tissue 9 Beta Cells Hormone Secretes hormone Insulin (anabolic or storage hormone) Facilitates movement of glucose across cell membranes into cells, < BG levels Enters portal circulation, then liver & released into general circulation Rapidly bounds to peripheral tissues (muscles & fat cells) or destroyed by liver & kidney 10 Insulin Prevents excess breakdown of glycogen in muscle and liver Facilitates lipid formation Inhibits breakdown of stored fats Helps move amino acids into cells for protein synthesis 11 Insulin Controls level of glucose in blood by regulating production & storage of glucose Release regulated by BG levels Levels rises in mins when eat, peaks in 3060 mins, then returns to base line 2-3 hrs 12 Insulin Facilitates active transport of glucose into muscle & fat cells – used as energy source Causes excess glucose to be stored in fat cell, preventing glucose from accumulating in blood Increased plasma levels of amino acids & fatty acids stimulate insulin release 13 BG Homeostasis All body tissues and organs require constant supply of glucose Brain, liver, intestines & renal tubules do not require insulin to transfer glucose into their cells Skeletal muscle, cardiac muscle & adipose tissue require insulin for glucose to move into the cells 14 Additional Glucose Stimulants Additional stimulants that increase glucose during hypoglycemia, stress, growth, > metabolic demands: Epinephrine Growth hormone Thyroxine Glucocorticoids 15 Treatment Goals/Complications Primary goals: Control BG levels Prevent acute/long term complications Acute metabolic complications Diabetic ketoacidosis (DKA) Hyperglycemic hyperosmolar nonketoic syndrome (HHNS) Hypoglycemia 16 DM Complications Long term complications Angiopathies Macrovascular (CAD, CVA, PVD) Microvascular (kidney, eye) (nephropathy, retinopathy) Neuropathic (diseases of nerves) 17 Type 1 Characterized by destruction of pancreatic beta cells (90%) – exogenous insulin required Thought - combined genetic, immunologic, & possibly environmental (viral) factors contribute to beta cell destruction Destruction results in < insulin production, unchecked glucose production by liver & fasting hyperglycemia Only inherit genetic predisposition (tendency) in those with certain HLA (genes) types (DR3 & DR4) 18 Type 1 Characterized by: hyperglycemia (> BG levels) breakdown of body fats & proteins (Insufficient/no insulin to transport glucose into muscles & fat cells – attempt to restore energy sources) development of ketosis (oxidation of fatty acids) 19 Clinical Manifestations 3 P’s Polyuria - > urination d/t osmotic diuresis Polydipsia - > thirst (excess < flds) Polyphagia - > appetite d/t catabolic state induced by insulin deficiency & protein & fat breakdown 20 Type 1 Manifestations Classic – 3 P’s, wt loss, malaise, fatigue (d/t lack of insulin to transport glucose across cell membrane into cell - < energy) Hyperglycemia – glucose molecules accumulate in circulating bld = osmotic diuretic Serum hyperosmolality – hyperglycemia draws H2O from IC space into general circulation Polyuria – > UA output d/t hyperglycemia & > bld vol. & > renal blood flow 21 Type 1 Glucosuria – BG level exceeds renal threshold (180-200 mg/dL) for glucose – excess glucose excreted in urine Dehydration – < in IC vol. & > urinary output (polydipsia, > thirst) Polyphagia – > food intake, wt loss d/t loss of H2O, breakdown proteins & fats (attempt to restore energy sources) 22 Type 1 Ketones – byproducts of fat breakdown (acids) Ketone bodies – disturb A/B balance of body when accumulated in excessive amts. DKA – acute complication – Metabolic acidosis s/s - abdominal pain, N, V, hyperventilation, fruity breath odor Tx – insulin, f/e, K+ Untx – altered LOC, coma, death 23 Type 2 Insulin resistance & impaired insulin secretion Exact cause - unknown, genetic factors thought to play a role Insulin resistance - < tissue sensitivity to insulin (norm - insulin bind to special receptors on cell surfaces & initiate series of reactions involved in glucose metabolism) 24 Type 2 Diminished intracellular reactions, insulin less effective at stimulating glucose uptake by tissues & at regulating glucose released by liver Beta cells can’t keep up with > demand of insulin, glucose levels >, & type 2 diabetes develops Enough insulin present to prevent breakdown of fat & production of ketone bodies DKA uncommon – uncontrolled cases may lead to HHNS 25 Type 2 Slow, progressive glucose intolerance May go undetected for many years S/S – frequently mild may include fatigue, irritability, polyuria, polydipsia, skin wounds, vaginal infections, blurred vision 26 Type 2 Primary tx – weight loss Exercise – enhances insulin effectiveness Oral antidiabetic agents – may be needed Insulin therapy – temporary or on-going 27 Clinical Manifestations Type 2 Onset slow, 2 P’s (polyuria, polydipsia) Fatigue & weakness Sudden vision changes - blurred Tingling or numbness (hands or feet) Dry skin, skin lesions, slow healing wounds Recurrent infections 28 Type 2 Acute complication – HHNS Tx – f/e, insulin, IV potassium Monitor skin turgor, I&O, CVP, LOC, cardiac activity, BG levels 29 Assessment & Dx Findings Dx basic criterion - abnorm > BG level Dx DM – Fasting plasma glucose (FPG) 126mg/dL or > Random plasma glucose level >200 mg/dL more than once OGTT/IGTT – not recommended for routine clinical use 30 Gerontologic Considerations >BG levels – appears to be age-related 50 y/o & > - common Cause – age related DM unknown (changes in CHO metabolism) maybe d/t poor diet, < exercise, < lean body mass (ingested CHO may be stored), altered insulin secretion, > fat tissue (> insulin resistance) 31 Management Main goal – normalize insulin activity & BG levels (< development of vascular & neuropathic complications) Therapeutic goal – achieve norm BG levels (euglycemia) without hypoglycemia & without seriously disrupting usual lifestyle & activities 32 Management 5 components of management nutrition, exercise, monitoring, pharmacologic therapy & education (client & family) Requires - constant assessment & modification of tx plan (nurse) & daily adjustments (client) 33 Nutritional Management Objective – control total caloric intake 5 Goals – Provide food for optimal nutrition Meet energy needs Achieve & maintain reasonable wt Maintain BG level & prevent complications Maintain serum lipids levels (macrovascular risks) 34 Nutrition Management Type 1 – maintain consistency in amt of calories & CHO at different meal times & time intervals bet/w meals with snacks if necessary Type 2 – 10% wt loss may reduce/eliminate need for antidiabetic meds Obese clients – (type 2) wt loss key to treatment Overweight – BMI 25-29 (body mass index - wt-to-ht ratio calculated by dividing body wt by square of ht) Obesity- 20% > ideal body wt or BMI = or > than 30 35 Nutrition Meal plan – food preferences, lifestyle, usual eating times & ethnic & cultural background Intensive insulin therapy – greater flexibility - timing & content of meal (adjust insulin dosage for changes in eating & exercise habits) Old concept – maintain constant dose of insulin adjusting schedule to insulin actions & duration Teaching – use various educational tools, materials and approaches 36 Nutrition Teaching Initial – consistent eating habits, relationship bet/w food & insulin, individualized meal plan Follow-up – management skills (restaurant eating, reading labels, adjusting meal plan for exercise, illness, special occasions) Nurse – communicates pertinent information to dietitian and reinforces ct understanding 37 Caloric Requirements Calories distributed - CHO, protein & fats, meal plan developed Caloric controlled diets – energy needs & cal requirements calculated based on age, gender, ht & wt Activity element - provides actual # cal required for wt maintenance 38 Caloric Requirements Promote 1-2 lb loss weekly – 500 to 1000 cal subtracted from daily total Calorie-controlled diets – may be confusing & difficult to comply (measure precise portions, specific foods & amounts) More realistic – base plan, usual eating habits & lifestyle to control glucose & wt loss or maintenance Work closely dietitian - assess current eating habits to achieve realistic, individualized goals 39 Caloric Distributions Focus - CHO, Proteins & Fats Recommended caloric intake CHO–50-60% (CHO counting - gm) Protein – 10% Fats – 20-30% (unsaturated - cholesterol < 300mg/day) Fiber – < BG & lipid levels Fiber - (soluble - legumes, oats) > stool bulk & prevents constipation (insoluble – wholegrain breads & cereals) 40 Food Classification Systems Several systems for meal planning (3) 1. Exchange Lists - 6 main exchange lists: Bread/starch, Vegetable, Milk, Meat, Fruit, & Fat Food items on 1 list contain = amts cal & approx gm protein, CHO & fat; may be interchanged with one another Combination & convenient foods, desserts, snacks, & fast foods included on list 41 Food Guide Pyramid 2. Food Guide Pyramid - Common Type 2 difficult time complying with calorie controlled diet 6 food groups: Bread, cereal, rice, pasta; Fruits; Vegetables (< cal & fat, > fiber); Meat, poultry, fish, eggs, dry beans, nuts; Milk, yogart, cheese; Fats, oils, sweets (use sparingly) 42 Glycemic Index 3. Glycemic Index – monitor amt given food > BG level Main goal - avoid sharp, rapid > in BG levels after food eaten Establish own glycemic index – monitor BG level after ingesting a particular food 43 Alcohol Consumption Moderation recommended (with food) Danger – hypoglycemia (taking insulin) May > norm physiologic reactions in body that produce glucose (gluconeogenesis) ETHO on empty stomach > likelihood of <BG occurring 44 Alcohol Consumption Type 2 – taking sulfonylurea agent chlorpropamide (Diabinese), side effect of consumption - a disulfiram (Antabuse) type reaction Consumption may lead to excess wt gain, hyperlipidemia & > BG levels (mixed drinks) Teach – use < calorie or less sweet drinks (light beer/dry wine & eat food with ETOH) Antabuse reaction - (facial flushing, warmth, HA, N, V, sweating or thirst within min. of consuming ETOH 45 Sweetners Use in moderation – avoid potential adverse effects 2 main types – nutritive & non-nutritive Nutritive - contain calories (fructose, sorbitol, xylitol – cal. amt. similar to sucrose (table sugar), causes less > BG than sucrose Non-nutritive - few/no cal., produce minimal/no > BG - Saccharin (no cal.), Aspartame (NutraSweet) 4 cal/pk, loses sweetness with heat, Acesulfame-K (Sunnette) contains 1 cal/pk, Sucralose (Splenda) Splenda – no calories - about 600 times sweeter than sugar. FDA approves it for use in baked goods, nonalcohoic beverages, chewing gum, coffee, confections, frostings and frozen dairy products 46 Food Labels Teach to read labels: Sugarless or sugar free Dietetic Health foods/snacks Sugarless/sugar free - may contain cal. = to sugar containing products (contain nutritive sweetners) Should not consider sugarless or sugar free foods as “free” foods (eat unlimited) Dietetic foods – not necessarily reduced-calorie (< Na, >sugar & fat) Health foods/snacks– often contain CHO, saturated vegetable fats 47 Exercise Benefits <BG & <CV risk factors > uptake of glucose by body muscles & improves insulin utilization Improves circulation & muscle tone Alters blood lipid levels, > high density liproproteins, < total cholesterol & triglycerides Enhances loss of body fat 48 Exercise Precautions Should not exercise - BG > 250 mg/dL, ketones in urine Teach - Initially (insulin) – eat 15g CHO snack or complex CHO with protein before moderate exercise (prevent unexpected hypoglycemia) Teach – On-going - monitor BG to determine if extra food needed & amt. before, during or after exercise If BG > 250 mg exercise causes (> secretion of glucagon, growth hormone & catecholamines, liver then releases more glucose & > BG) 49 Exercise Exercise & wt loss improves insulin sensitivity & may < need for insulin or oral agents – obese, type 2 Glucose tolerance may eventually return to normal - type 2 Type 2 not taking insulin or oral agent may not need extra food before exercise Precautions: Use proper footwear; avoid in extreme heat or cold; inspect feet daily afterwards; avoid during periods of poor metabolic control 50 Exercise Recommendations Regular, same time (BG at peak), same amt Slow, gradual increase with MD approval Daily walking – safe, beneficial >30 y/o – 2 or more risk factors of heart disease (HTN, obesity, smoker, male, family hx., abnorm EKG, > cholesterol) exercise stress test recommended 51 Monitoring Glucose Levels & Ketones SMBG – self monitoring BG Useful for managing self-care Enables adjustment of tx regimen (optimal BG control) Allows detection & prevention (hypo/hyper) Plays role in normalizing BG levels May < risk of long-term complications 52 Monitoring Various SMBG methods Most – drop bld, apply to special reagent strip (5-30 sec.), meter gives digital readout of BG value Meters offers different features & benefits (visual impairments – audio components) 53 SMBG Systems Teach technique - initially (newly dx) Evaluate technique - experienced Compare meter with simultaneous lab measured BG level (q 6-12 mons) Assess meters & strips with control solutions specific to meter when new strips open or validity of reading in doubt 54 Candidates for SMBG Key tx for any intensive insulin therapy regimen (2-4 injections/day or insulin pumps) Recommended: Unstable DM Tendency for severe ketosis or hypo Hypo without warning symptoms Not taking insulin (monitor effects of exercise , diet & oral meds) Type 2 – periods of suspected hyper or hypo 55 SMBG Frequency Require insulin 2-4 X/day (ac meals & hs) At least 3X/day ac meals (determine each dose) No required insulin - 2-3X/wk & 2 hr postprandial test Whenever hypo or hyper suspected Increase frequency - changes in meds, activity, diet, with stress or illness 56 Responding to SMBG Results Keep log (BG patterns, alter tx regimen) Test at peak med times (evaluate dose adjustments needs) Test ac meals – evaluate basal & determine bolus doses Test 2 hrs pc meals - titrate bolus doses, regular or lispro Type 2 – test ac & 2 hrs pc largest meal of day or ….. Test 3am wkly - take insulin hs or have insulin pump (document BG level not < during hs) 57 Glycosylated Hemoglobin HgbA1C or A1C – bld test reflects ave BG level over past 2-3 months Normal range 4-6% Glucose molecules attach to HBG in RBC when BG levels > Life of RBC - approx 120 days 58 Urine Testing for Glucose Use limited - don’t/cannot perform SMBG Less expensive & non invasive Apply urine to reagent strip or tab & match colors on stripe with color chart Disadv: False-negative readings Don’t reflect BG level at time of test Some meds interfere with results (ASA, vit C) 59 Testing for Ketones Ketones (ketone bodies) – UA signals control deteriorating & DKA risk high (type 1) Byproducts of fat breakdown (breakdown stored fat for energy when almost no effective insulin available) Accumulate in bld & UA UA testing – dipstick most common method for self-testing (ketonuria) Perform – type 1 - glucosuria or persistently > BG level (>240mg/dL 2 consecutive times, illness, gestational DM) 60 Pharmacology Therapy Insulin therapy – SMBG cornerstone of therapy Type 1 - exogenous must be administered for life Type 2 – may be necessary if diet & oral agents fail, during illness, infection, pregnancy, surgery or other stressful events. Insulin – secreted by beta cells, works to lower the BG level after meals by facilitating the uptake & utilization of glucose by muscle, fat & liver cells. In absence of adequate insulin, pharmacologic therapy is essential 61 Insulin & Regular acting Insulin Group in several categories (onset, peak & duration of action) Human insulin – shorter duration of action than insulin from animal sources Rapid acting insulin lispro (Humalog) & insulin aspart (Novolog) produce more rapid effect (short duration) than regular insulin Onset 5-15 mins., peak 1 hr, duration 2-4 hrs Eat 5-15 minutes after injection 62 Regular Insulin Short acting (R), clear, onset 30 min - 1 hr, peak 2-3 hrs, duration 4-6 hrs. (Humulin R, Iletin Regular, Novolin R) Usually administered 20-30 min. before meal, alone or in combination with longer-acting insulin 63 Intermediate Insulin NPH insulin (neutral protamine Hagedorn) or Lente insulin Humulin N, Iletin NPH, Novolin N = NPH insulins Humulin L, Iletin L, Novolin L = Lente insulins Onset 3-4 hrs, peak 4-12 hrs., duration 16-20 hrs. White & cloudy Eat around onset & peak 64 Long-acting Insulin Ultralente insulin Sometimes called peakless insulin (has long slow sustained action) Onset 6-8 hrs., peak, 12-16 hrs, duration 20-30 hrs. 65 Peakless Insulin Insulin Glargine (Lantus) – peakless insulin, approved to use as basal insulin – absorbed very slowly over 24 hrs & given once a day Suspension with pH of 4 – cannot be mixed with other insulin (cause precipitation) Onset – 1 hr., peak continuous (no peak), duration 24 hrs. Used for basal dose 66 Insulin Nurse must focus on which meals/snacks are being covered by which insulin doses Rapid & short acting insulin - expected to cover rise in glucose levels after meals (immediately after the injection) Intermediate acting insulin – expected to cover subsequent meals Long-acting insulin - provides relatively constant level of insulin & act as a basal insulin 67 Source and Manufacturers Human insulin widely used – produced by recombinant DNA technology 2 manufacturers in US – Eli-Lilly & Novo Nordisk Usually interchangeable, concentration, species & type are same Human insulin are by different companies, have different brand names 68 Insulin Regimen Varies from 1-4 injections/day Usually combination - short acting & longer acting Goal – mimic normal pattern of insulin secre...
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