NutritionInterventionChapter4.pdf NTR 341
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This 37 page Reader was uploaded by Ashley Stanek on Friday January 23, 2015. The Reader belongs to NTR 341 at a university taught by Dr. Morse in Fall. Since its upload, it has received 385 views.
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Date Created: 01/23/15
Nutrition Intervention Chapter 4 12315 322 PM Intervention Nutrition Prescription Determined after evaluation of patient s nutritional status and needs Assessment States the patien individualized plan for best meeting nutritional needs must be specific 0 Regular diet 0 Ground foods with gravy and thickened liwuids 0 Low sodium diet with a 1200 mlday fluid restriction o 1600 calorie to promote weight gain Causes for Poor PO intake Medications Unacceptable food Inappropriate diet orders Unfamiliar schedules Pain Fear and anxiety Medical Testing FoodNutrient Delivery Appendix C3 Therapeutic diets are bases on a general adequate diet modified as necessary 0 House or regular diet General diet 0 Therapeutic diets Maintain or restore health and nutrition Accommodate changes in digestion absorption or organ function Provide nutrition therapy though nutrient content changes Vary from normal as little as possible Recognize personal eating patterns and food preferences Diet prescription 0 Energy 0 Protein 0 Minerals and vitamins o Fluids 0 How do we change the house dietquot 0 Calorie level increase or decrease Food restriction add snacks 0 Protein level increase or decrease 0 Consistency liquid soft low fiber high fiber thickened pureed o Rearrange number size and or frequency or meds o Fluid restriction Table 44 Nutrition Interventions to Increase Nutrient Densty o Adjustments to accommodate disease or health risks Adjust level ratio or balance of protein fat and carbs diabetes renal cholesterollowering Signal or multiple nutrient manipulation sodium restricted lactoserestricted highfiber highprotein Feeding Assistance and Feeding Environment Appendix C3 0 Food choice trayfood preparation mouth care 0 Adaptive equipment 0 Lighting odors distractions Food Nutrient Delivery C3 0 Addition of supplements Medical Food Supplementsquot 0 Commercial Supplements or Homemade Goal increase nutrient density without increase volume Kcal andor protein increase Enteral or parenteral nutrition supportquot 0 Modify rate concentration composition or schedule 0 Nutrition Related Medication Managementquot 0 Drugnutrient interactions 0 Coordination of medication with meal planning 0 Appetite stimulants Nutritional Care for Hospitalized Patient To improve PO intake 0 Honor patient preferences 0 Attention to color texture composition and temperature of foods 0 Patient selection of menus increase consumption Standard HospitalHealth Care Diets Sips and Chips 0 O O O O O O 0 Clear Liquid Diet Seldom used today Fluids some electrolytes and some energy Inadequate in calories fiber and all other essential nutrients Use for short periods only Full Liquid Diet Milk based soups liquids Lactose free options RegularGeneral Diet Basic and adequate No restrictions Consistency modifications 0 Adequate 0 Food Intake Pureed ground aka mechanical soft 0 Monitoring intake to prevent iatrogenic malnutrition If intake is inadequate provide other foods or supplements 0 Can include forbidden foodsquot 0 Communicate with nursing medical and food service personnel 0 Where 0 Issues with calorie counts Nutrition Education C3 0 Group classes individual instruction written instruction via phone or electronic communication 0 Outpatient setting more conductive to understanding and overall compliance 0 Impatient setting survival skillsquot Counseling C3 0 Supportive Processes collaborative goal setting and individualized action plans 0 Extension of Nutrition Education 0 Ultimate goals is for the patient s to take responsibility for behavior Coordination of Nutrition Care 0 Discharge documentation includes 0 0 00000 Summary of nutritional therapies and outcomes Pertinent information such as weight lab results dietary intake Potential drugnutrient interactions Expected progress or prognosis Recommendations for followup services Extremely important when patient discharge on nutrition support Main goals maintain comfort and quality of life Attempt to maintain the patient s ability to function independenUy Communication with family members PO intake may be poor Pain Overall prognosis Dietary restrictions are rarely appropriate Termination of life support advance directives RDs work with numerous other health care professionals Successful transition from health care facility to the pateints Team effortTeam meetings Pharmacology 12315 322 PM Problems with Food and Drugs Druqnutrient interactions specific changes to pharmacokinetics of a drug caused by nutrients or changes to he kinetics of nutrients cause by a drug 0 Fooddruq interactions broader term that also includes effects of medication on nutritional status 0 Medication use widespread o Prescriptions o Complementary and alternative medicine CAM 0 Over the counter medications Role of Nutritional Therapy is Pharmacotherapy Pharmacotherapy use of drugs for the treatment of disease and health maintenance 0 Nutrition can affect drug action 0 Drug action can affect nutrition The processing of Drugs in the Body 0 Same basic processes as food and nutrients 0 Anything that can affect digestion of food can also affect digestion of drugs 0 Anything that can affect nutrient absorption can also affect drug absorption 0 Anything that can affect nutrient metabolism can also affect drug metabolism 0 Anything that can affect excretion of nutrients can also affect excretion of drugs How do food and Drugs interact Digestion and Absorption of Drugs 0 Any condition or process that can affect nutrient digestion and absorption can affect or alter drug absorption May need to alter drug dose Effects of food on Drug Therapy 0 Presence or absence of food can alter drug 0 Absorption o Bioavailability 0 Important to note specific guidelines regarding administration with or without food 0 Additional Concerns 0 Effects or fiber fat and other food component on drug therapy Chelation Adhesion of food component to medication fiber 0 Caution with duodenal administration of medications that require an acid environment Other Effects 0 Drug distribution of protein bound drugs 0 Malnutrition Decrease serum albumin binding sites cause altered drug effects May need to alter drug dose Metabolic Rate and Nutrient Metabolism 0 Metabolic rate altered increase or decrease 0 Change kcal goals 0 Nutrient metabolism may be altered o Dilantin inhibits folate and vitamin D metabolism 9 megaloblasitc anemia INH blocks activation of vitamin B6 therefore supplementation requited 0 TB rare but still see cases from Mexico or Central America Effects of Drugs on Food and Nutrition 0 Nutrient absorption or excretion may be altered Damage intestinal mucosa from the drug 0 Antineoplastic drugs affect cells with rapid turnover Intestinal mucosa 0 Increase or decrease excretion from the drug o Lasix and hypokalemia Modification of Drug Action by food and Nutrients JCAHO National Patient Saftey Goals Enhance or oppose drug effects MAOI s and pressor agents dopamine tryamine o MAOI s inhibitants breakdown of pressors which increases blood pressure Avoid tryamine containing foods aged chesses cured meats Warfarin Coumadin and vitamin K No chance in Vitamin K intake Coumadin Clinics to monitor INR s Side Effects of Drugs on Nutritional Status and Health Oral taste and smell effects 0 Altered or decrease in taste GI effects Nausea vomiting constipation or diarrhea Irritation and ulceration Destruction of intestinal bacteria Appetite suppressants Not diet pillsquot 0 Growth retardation in children Appetite stimulants undesirable and desirable o Psychotropics and increased appetite Glucose levels 0 Hypoglycemia o Hyperglycemia steroids Risk Factors for FoodDrug Interactions Polypharmacy Elderly Chronic disease Cancer and AIDS GI tract alterations Malnutrition 0 Body Composition 0 Fetus infant pregnant women 0 Consequences can be severe Medications and Enteral Nutrition Interactions 0 Drugs put in feeding tubes or added to eternal formulas may cause 0 Gel formation 0 Separation or formula 0 Clogged feeding tubes Interruption of delivery Bioavailability of drugs administered via feeding tubes 0 Phenytoin Dilantin May need a 1 to 4 hour feeding free interval a couple of ties per day Most adjust feeds to insure adequate nutrition provided 0 Excipients and FoodDrug Interactions Excipient Inactive ingredient added as a buffer binder filer diluent disintegrant flavoring dye preservative suspending agent coating Allergies and enzyme deficiencies o Lactose o Gluten sensitivity Nutritionally significant amounts od excipient nutrients 0 Ca Mg Al some vitamins propofol Sorbitol content of Elixers o 10 g dosediarrhea in adults Medical Nutrition Therapy 0 Nutrition Assessment 0 Factors that could affect absorption distribution metabolism or excretion 0 Nutrition Diagnosis food medication interactionquot 0 Nutrition Intervention 0 Modifications of diet or medication to reduce risk of interactions 0 Patient education 0 Nutrition Monitoring and evaluation 12315 322 PM AcidBase Balance 101614 Basic Concepts Acids Bases Buffers Acids 0 Donate or give up H ions 0 Acids generated from ingestion and metabolism of foods and toxins o Volatile acids Can be converted to gas and eliminated by the lungs C02 indirect measure of Carbonic Acid H2CO3 o Nonvolatile acids or fixed acids Acids produced via metabolism of CHO3 protein lipid Protein metabolism produces the most acids Lungs cannot eliminate Bases 0 Accept or recieve H ions 0 Bicarbonate HCO3 o Kidneysprimary regulation Buffers Reacts with acid or base to decrease effect neutralize pH 0 Intracellularproteins and phosphate pH 0 Measures acidity or alkalinity of a fluid 1acidic to 14basic Water is neutral70 Basic Concepts 0 Terms Describing pH 0 Acidosis Accumulation to acid or loss of base 0 Acidemia patient acidotic pH lt735 0 Alkalosis Accumulation of base or loss of acid 0 Acids can donate H o H2Co3 9 H and HCO3 Carbonic Acid 9 Hydrogen and Bicarbonate o A base can accept H 0 CH0 protein and fat metabolism produce H2CO3 carbonic acid 0 Respiration presents increase C02 accumulation acidosis Regulation of Acid Base Balance 0 Acid base balance state of equilibrium of H ion concentration 0 Body tries to restore normal pH by developing compensatory responses to offset the effects of primary disorder 0 Chemical buffering o Bicarbonate Carbonic Acid Buffer System Alters rate and depth of breathing I Increase of decrease expiration of C02 Reabsorption or regeneration of CHO3 in the kidneys o Other Chemical Buffers o Disodiummonosodium phosphate buffer system 0 Intracellular proteins 0 Hemoglobin within the RBC Regulation of Acid Base Balance 0 Respiration Control 0 Alters rate and depth of breathing o Regulate C02 concentration via expiration 0 Release or retention of C02 Acidosis increase ventilation 9 C02 acid loss 9 increase pH Alkalosis decrease ventilation 9 C02 acid retention 9 decrease pH Shorter time for results Regulation of Acid Base Balance 0 Renal Control 0 Regulate concentration of HCO3 in blood via reabsorption of HCO3 bicarbonate Increase or decrease excretion based on need o Regulate excretion of acids H ions Increase or decrease excretion based on need 0 Renal failure 9 decrease HCO3 reabsorption Kidneys o Acidosis 9 increase HCO3 base reabsorption 9 increase pH 0 Alkalosis 9 decrease HCO3 base reabsorption 9 decrease pH 0 Longer time for results Regulation of Acid Base Balance 0 Effect of Acid and Base shifts on electrolyte balance 0 Hydrogen and bicarbonate both have electrical charges 0 Other electrolytes affected to maintain electroneutrality Shifts in potassium chloride sodium concentration Alteration in pH electrolyte shifts affect cellular and metabolic functions Assessment of Acid Base Balance 0 Body attempts to self correct changes in pH making assessment difficult 0 pH alone not adequate 0 Need to determine underlying cause to correct problem 0 Common lab measures 0 ABG s Arterial Blood Gasses 0 Serum electrolytes levels Acid Base Balance Disorders 0 Diagnosis and treatment 0 Metabolic VS respiratory etiology 0 Metabolic AcidosisAlkalosis primary changes in bicarbonate level 0 Respiratory AcidosisAlkalosis primary changes in dissolved C02 levels Respiratory Acidosis 0 Excess acid in blood secondary to carbon dioxide retention 0 Due to respiration dysfunction 0 Remember renal regulatory systems compensate Acidosis decreased ventilation and consequent C02 retention from respiratory dysfunction 0 Overfeeding NOTjust excessive CH0 0 Sleep apnea 0 Asthma o COPD o Propofol overdose 0 Chest wall injury 0 ARDS Labs 0 Decrease pH elevated pCOZ 0 Slightly elevated bicarbonate due to renal compensation o Alerted electrolytes Treatment 0 Correct underlying condition 0 Increase oxygenation 0 Mechanical ventilation if needed Respiratory Alkalosis 0 Relative excess amount of base from reduction of C02 Hyperventilation can be cause Alkalosis increased ventilation and elimination of C02 0 TBI treatment to depress brain swelling 0 Hypoxemia o Stimulant overdose 0 Anxiety Labs 0 pHgt745 0 Plasma HCO3 low in chronic PaCO3 low in acute Treatment 0 Correct underlying condition Metabolic Acidosis All types not caused by excessive C02 Diarrhea most common cause 0 Fluid and electrolyte losses Excessive loss of bicarbonate lower GI tract 0 Bicarbonate carbonic acid buffer system is stimulated Acidosis increased generation of accumulated acids or bicarbonate losses from kidney or GI tract 0 Diabetic Ketoacidosis DKA or Starvation o Lactic Acidosis 0 Renal failure 0 Diarrhea or fistula drainage loss of GI fluids Labs 0 Increase C02 9hyperventilation o DKA increase beta hydroxybuteric acid Treatment 0 Treat underlying cause DKA provide insulin Mechanical ventilation Raise pH to safe level not too quickly OOO Metabolic Alkalosis Excess amount of base Fluid imbalance with or without total volume decrease Underlying event determines pathophysiology Alkalosis administration or accumulation of bicarbonate excessive acid loss 0 Gastric Suctioning or Hyperemesis Loss of HCI 0 Loss of ECF as from diuretics Hypokalemia 0 Excessive antacid intake Labs 0 No specific signs or symptoms 0 pH gt 745 elevated HCO3 o Electrolytes and total volume may be altered Treatment 0 Treat underlying condition Treatment of Acid Base Disorders 0 Treat underlying cause of the problem 0 Don39t just treat symptoms Underlying problem will not disappear and can make acid base disorders become lethal 0 Example DKA Avoid overfeeding increase C02 production or excessive HCO3 administration Diabetes 101614 Insulin and Counterregulatory Hormones 0 Review and know Table 172 Summary of hormonal control of energy metabolism Insulin anabolic hormone decrease blood glucose 0 Pancreatic beta cells 0 Promotes glucose utilization o Promotes energy storage glycogen and T6 0 Stress hormones catabolic stimulate gluconeogenesis and increase blood glucose 0 Contribute to hyperglycemia associated with stress response 0 Pancreatic alpha cells Glucagon o Adrenal gland Cortisol Epinephrine adrenaline Norepinephrine Endocrine Control of Energy Metabolism Insulin 0 Controls CHO pro and fat storage and suppresses mobilization of stores Normal Blood Glucose Control 0 Insulin o Secreted in response to rise in blood glucose 0 Binds to receptor sites on cell membranes to facilitate uptake of glucose Tryosine kinase Phosphate ATP tyrosine Insulin binding to aunits gtgt Bunit autophosphorylation to active receptor Activate receptor phosphorylates intracellular transporter GLUT4gtgt glucose uptake 0 Mitochondria of cell 0 Glucose utilization for energy or triglyceride production Endocrine Control of Energy Metabolism Glucagon catabolic hormone Diabetes Mellitus o A group of diseases characterized by high blood glucose concentrations due to defects in o Insulin secretion 0 Insulin action 0 Combination of decrease insulin secretion and action 0 Genetic components for type 1 and type 2 DM 0 Long term damage correlated with failure of eyes kidneys nerves heart blood vessels Elevated Blood Glucose Normal fasting serum glucose 0 lt100 Hyperglycemia Fasting Blood Glucose FBG gt 125 0 DM 0 Stress infections 0 Excessive nutritional support Greater effect with adults 0 Type 1 Diabetes 0 Destruction of pancreatic beta cells 0 Pre Diabetes FBG between 100 125 or impaired glucose tolerance after 75 g glucose load 0 New 2010 diagnosis 0 Expect increase due to increase incidence of obesity 0 Type 2 Diabetes 0 Insulin resistance related to obesity other factors 0 Gestational Diabetes 0 Insulin resistancesuppression from placental hormones 0 Increase nutritional intake Type 1 Diabetes Epidemiology 0 510 of diagnosed cases o Pancreatic autoantibodies are characteristic of type 1 diabetes and should be obtained in ALL individuals with suspected DM 0 Genetic component General US incidence 003 Family member with Type 1 5 Screen for celiac disease a Immune mediated disorder increase frequency in patients with type 1 DM n Up to 16 of individuals compared with 03 1 in the general population 0 Lack of insulin production 0 Immune mediated beta cells destroyed by autoimmune process 0 Idiopathic cause of beta cell function loss unknown 0 Pancreatic disease or resection o Variability of glucose intolerance based on degree of pancreatic damage 0 Symptoms upon initial diagnosis 0 Decrease in insulin 9 hyperglycemia therefore cells starve 9 polyphagia hunger o Lipolysis and Fatty acids transformed to ketones 9 Ketoacidosis and pH falls Metabolic acidosis o Gluconeogenesis 9 increase hyperglycemia o Polyuria and excess glucose in urine glycosuria and Ketosuria ketones in urine 9Polydipsia thirst 0 Weight loos dehydration electrolyte disturbance 0 Increase respirations to get rid of acids Diagnosis Type 1 Diabetes 0 Classic signs and symptoms of hyperglycemia 0 Oral glucose tolerance test 2 hour FBG gt 200 FBG gt126 5 Type 1 Diabetes related autoantibodies o Glutamic acid decarboxylase autoantibodies o Islet cells autoantibodies o Insulin autoantibodies 0 Diabetic Ketoacidosisprobably present Type 1 Diabetes Mellitus Medical Treatment DMSE Diabetes Self Management Education 0 Risk factors and treatment for short and long term complications 0 Exogenous insulin required Honeymoon Phase Recovery endogenous insulin secretion after initial diagnosis and treatment and insulin requirements may decrease for up to 1 year 0 Nutritional modifications based on medication administration required 0 Exercise 0 Coordinated team effort 0 Individualized management plan Insan Essential to survive in type 1 diabetes 0 May be needed in type 2 diabetes 0 Types may vary by onset peak and duration of actin Inhaled insulin Insulin pump Individualized type and timing of insulin regimen based on eating and exercise habits body weight blood glucose levels Table 175 Types of Insulin Type 1 Diabetes Through the Life Span Goals Most individuals with type 1 diabetes should 0 Be treated with multiply daily insulin injections 3 or more injections per day of prandial insulin and one to two injections of basal insulin 0 Be educated in how to match prandial insulin dose to CHO intake permeable blood glucose and anticipated activities 0 Use insulin analogs to reduce hypoglycemia risk All Individuals with type 1 diabetes should be taught how to manage blood glucose levels under carrying circumstances o Sickness 0 Receiving glucocorticoids o If using a pumps need how to trouble shoot pump problems arise Child caregivers and school personnel should be taught how to administer insulin when a child cannot self manage and is out of the care and control of his or her parents Type 1 DM Insulin Dosing Determining Insulin Doses 0 Algorithm based on body weight 0 Adjusting based on blood glucose patterns 0 Advanced CHO Counting Ratio of insulin units to cover x g CHO consumed 500 Rule SODTotal Daily Insulin Dose g CHO per untinsan Example 50050 total units per day 10 g CHO per units of insulin 6 units for 60 g CHO or 4 CH0 Servings Type 1 DM Medical Treatment Insulin Regimens FixedConventionalStandard o Constant dose of basal insulin 0 With short or rapid bolus insulin 0 Mixed dose or split mixed dose 0 Must synchronize insulin with food intake 0 Flexible 0 Multiple daily injections Bolus insulin before meals Basal insulin once or twice daily More flexibility in alterations in activity or food intake schedule OOO Nutrition Therapy for Type 1 and Type 2 DM 0 Table 175 Nutrition therapy for DM 0 Nutrition Diagnosis PES o Impaired nutrient utilizationquot Carbohydrates Altered nutrition related lab valuesquot specify glucose 0 Food and nutrition related knowledge deficitquot Nutritional Intervention GOALS 0 Obtain optimal metabolic outcomes 0 Address individual nutritional needs and PA 0 Nutrition Prescriptions INTERVENTION 0 Nutrition recommendations for general population are appropriate 0 Carbohydrate individualized o No diabetic dietquot or ADA dietquot 0 Meal Planning Intervention Education 0 Individualized based on insulin regimen customary food intake preference 0 Consider meals and snacks o Carbohydrate counting and exchange lists Keys to CH0 Counting and Meal Planning 0 15 gram portions of CHO 1 CH0 serving 0 Check exchanges for grams CHO per exchange Total amount of carbs intake not source is focus Consistent amounts of carb and meals and snacks n 15 g counts as one choice a Total grams per meal 0 Sugars do not increase glycemia more than isocaloric amounts of starch 0 Count total grams of CHO Carb Counting o Portions of food containing 15 g carb Low CHO diets are not recommended 0 Insulin 0 Meals CHO ingestions need to be planned around insulin peaks Diet Intervention CH0 and Fiber 0 Strong evidence when looking at high fiber intakes and glycemic control 0 Excessive amounts of fiber needed for improved glycemia Difficult due to volume of food required GI effects 0 No improvement with RDA of 24gday o Oat fiber will decrease cholesterol 0 Current fiber recommendations gt5 gday Inconclusive Evidence 0 Evidence is inconclusive for an ideal CHO intake for people with DM 0 Strong Evidence amount of CH0 and available insulin may be the most important factor influencing glycemic response after eating Diet Intervention Protein Fat and Alcohol 0 Protein No effect on blood glucose levels in wellcontrolled DM 0 Uncontrolled DM 9 gluconeogenesis from boy protein 0 Recommended usual protein intake 15 to 20 of kcals May need to be adjusted if renal complications develop 0 Fat People with diabetes have similar risk of CVD to non diabetics with a past history of CVD 0 Diet to decrease risks of CVD recommended TLC DASH 0 Alcohol Moderate amounts of alcohol with food have minimal effect of glucose and insulin 0 Need to count caloric load provided 0 Substitute for nutrient dense foods 0 Excessive alcohol 3 drinksday 9 hyperglycemia Nutrient Intervention The Exchange System Foods with CHO Appendix L1 p A 109 Glycemic Control 0 Summary of A1C recommendations for nonpregnant people with diabetes to decrease complications risk Youth lt18 75 Adults 70 Older adults Healthy 75 Complex issues 80 Very complexpoor health 85 Physical ActivityExercise Integral part of treatment plan for all individuals with diabetes 0 Enhances glucose uptake and improves insulin sensitivity 0 Reduces cardiovascular risk factors 0 Weight control 0 May decrease risk of type 2 diabetes in high risk individuals Diabetic Ketoacidosis Initial diagnosis of Type 1 DM noncompliance or stress Insulin deficiency and increased gucagon 9 guconeogenesis o Hyperglycemia 0 Increased ketone production 0 Ketone Production fro increase fat cataboism Metabolic Derangements of DKA 0 Metabolic Acidosis decrease pH 0 Increased ketone levels and C02 production acids 0 Hyperventilation to compensate Osmotic Diuretics o Hyperglycemia 9 increased serum osmoarity 0 Sodium buffers ketones 9 increased serum sodium Increased intravascular fluid 9 increased fluid to renal tubes 9 increase urine output Polyuria and poydipsia Hypervolemia shock Electrolyte Abnormalities o Electrolytes follow water 0 Increased urine output 9 increased electrolyte losses 0 Treatment 0 Insulin o Bicarbonate o Fluid electrolyte replacement 0 Mechanical variations Short and Long Term Complications Type 1 and Type 2 0 Sick Days 0 Food and metabolism 0 Gastroporesis Macrovascular diseased o Dyslipidemia CVD Risk 0 Hypertension Microvascular diseased o Nephropathy renal failure 0 Retinopathy blindness o Neuropathy decreased sensation 0 Poor wound healing Type 2 Diabetes lt60 non traumatic amputations due to DM 0 Most common form of DM accounting for 90 to 95 of diagnosed cases 0 Multiple cases Etiology 0 Genetic component autosomal dominant 0000 2014 Study 14 sets of identical twins and only with 1 with type 2 DM Twin with DM Genes involve in inflammation were up regulated and genes involved in fat and glucose metabolism were down regulated Fount 1400 places on identical twins DNA with a difference in DNA methylation between the diabetic and the non diabetic twin Theorize that difference in DNA methylation are due to difference in lifestyle and this confirms the theory that type 2 DM is strongly linked to lifestyle Obesity central body adiposity Physical inactivity High or low birth weight Poor placental growth Pathophysiology Multiple factors can produce glucose intolerance 9 hyperglycemia 0 Combination of insulin resistance andor beta cell failure insulin deficiency 0 Initial increase in pancreatic insulin secretion to compensate for insulin resistance at target cells hepatic muscle adipose o Insulin deficiency Eventual decrease in insulin secretion with possible need for exogenous insulin 0 Exogenous insulin required during times of stress 0 Commonly present before diagnosis Early symptoms may be difficult to detect 0 Typically screening of hyperglycemia trauma admits 0 May be asymptomatic for 610 years 0 Diagnosis HgbAlC OG39IT Medications may not be required Acute Complications NKHHS Nonketotic hyperosmolar hyperglycemia syndrome Type 2 0 Acute increase in glucose and serum osmolality without ketone production 0 Do see polyuria polydipsia and weight decrease 0 Type 2 DM produces some insulin therefore no fat burning 9 ketones o Infections 0 Treat Rehydration electrolyte replacement and treat underlying condition 0 DKA Type 1 Hyperglycemia Type 1 and Type 2 0 Down phenomenon Increased fasting blood glucose and need for insulin upon rising Somogyi effect n Rebound hyperglycemia after episode of hypoglycemia due to insulin over dosage and counterregulatory hormones glucagon stimulating hepatic glucose production Type 2 SM Medical Treatment 0 Medical Treatment DMSE Diabetes Self Management Education 0 Individualized management plan Addresses risk factors and treatment for short and long term complications 0 Exercise Achieve and maintained weight goals Modest weight loss 0 Medications likely Oral agents Exogenous insulin may be needed Oral Medications for Type 2 Diabetes 0 Glucose lowering medications used alone or in combination in Type 2 diabetes 0 4 classes with different mechanisms of action Insulin secretagogues 0 Promote insulin secretion by BCells 0 Promote drip and gush based on PO intake Drip slow insulin release between meals Gush increased insulin secretion with PO 0 Sulfonylureas Produce both drip and gush o Meglitinides only produce gush brief stimulation therefore frequent dosing required Insulin Sensitizers 2 Classes 0 Enhance insulin action Insulin on Steroids 0 Required presence of exogenous or endogenous insulin 0 Bigunanides metformin suppresses hepatic glucose production and decrease insulin resistance 0 Thiazides decrease insulin resistance Injectable Medications Pramlintide Symlin synthetic for of amylin o Hormone normally secreted with insulin by pancreatic beta cells in response to food intake 0 Decreases glucagon production and hepatic glucose releases therefore decreasing postprandial hyperglycemia Exenatide Byetta Incretin Mimetic or incretin line agent Early Use of Incretins in Type 2 0 Clinical trials Preliminary reports that incretins are 0 Delaying the progression of pre diabetes to Type 2 DM 0 Earlier use in pre diabetes to Type 2 DM 0 Appear to be delaying Beta cell damage 0 Preliminary Findings 0 Beta cell failure in occurs earlier and s more severe than previously thought Exercise 0 Prescribed for all 0 Enhances blood glucose uptake and improves insulin sensitivity 0 Glycemic responses to exercise in type 1 and type 2 DM 0 Type 1 Variable glycemic response depending on typical glucose control food intake intensity of exercise Well controlled DM Hypoglycemia from increase muscular uptake of glucose mediated by insulin Poorly controlled DM Hyperglycemia from increase FFA and glucose due to decrease circulating insulin available for glucose uptake by exercising muscles 0 Type 2 Improved glucose control from decrease insulin resistance Potential Problems 0 Exercise guidelines 0 Frequent blood glucose monitoring before during and after exercise 0 Reduce insulin or ingest carbohydrate to prevent Hypoglycemia if using insulin or insulin secretagogues Hyperglycemia Due to greater than normal increase in counterregulatory hormones causing hepatic glucose release Exercise Recommendations 0 Add 15 g CH0 1 Serving for every 30 to 60 minutes of activity depending on intensity 0 No adjustment for exercise lt30 mins 0 Add CHO if preexercise glucose level lt100 No supplementary CHO if not receiving insulin or secretagogues CHO ingestion during prolonged exercise improved performance Aerobic Training and Insulin Sensitivity Aerobic training appears to improve muscle glucose disposal 0 Via improved insulin sensitivity 0 Exercise stimulated GLUT4 translocation 0 Increased utilization of FFA s 0 Research 0 Found improved insulin resistance with both moderate and high intensity aerobic exercise Nutritional Goals 0 Nutrition Intervention 0 Weight management Carbohydrates Protein Fat Fiber OOOO Gestational Diabetes Mellitus CDM Glucose intolerance with symptoms of hyperglycemia 0 Screen between 2628 weeks gestation due to alterations in insulin secretion 0 OGTF 0 Associated complications HTN preterm delivery increase C section rate increase birth weight 0 High risk for type 2 diabetes later in life 0 Hyperglycemia may resolve after delivery 0 Pathophysiology similar to TZDM GDM affects fetus o Induces fetal hyperglycemia and hyperinsulinemia Gestational DM 0 Intervention o Individualize and adjust meal plan throughout pregnancy to promote fetal growth and development Carbohydrate controlled meal plan Adequate energy for weight gain Increased protein and 2nd and 3rd trimesters Monitoring and Evaluation 0 Dietary compliance and knowledge 0 Normoglycemia and absence of ketone production 0 Glucose levels 6 weeks post delivery MNT for Preexisting Diabetes and Pregnancy 0 Preconception counseling 0 Hormonal changes in first trimester lead to erratic 86 levels 0 Frequently adjust meal plan Increased need for insulin in second and third trimesters Adjust meal plan to promote fetal growth and development Avoid hypoglycemia and ketosis Acute Complications Hypoglycemia Type 1 and Type 2 o Autonomicadrenergic symptoms shakiness sweating palpations anxiety hunger 0 Cause Improper medication dose food intake or both 0 Symptoms slow performance MNT for Type 1 and Type 2 DM Maintain BG levels in or near normal rage lowrisk lipid and lipoprotein profile low risk blood pressure Individual treatment goals 0 Lifestyle modifications energy needs and nutrition care based on metabolic profile 0 To prevent or slow down development of chronic DM complications 0 Dependent upon changes person is willing and able to make Self management training for individuals during episodes of acute iHness Nutrition therapy is recommended as an effective component of the overall treatment plan 0 Individualized MNT as need provided by an RD familiar with the components of diabetes MNT Nutrition Support 1030 Nutrition Support 0 Delivery of formulated enteral or parental nutrients to maintain or restore nutritional status 0 Enteral nutrition 0 Provision of nutrients into GI tract through tube or catheter when oral intake is inadequate or not possible 0 Parenteral nutrition 0 Provision of nutrients intravenously when the GI tract is not functioning Rationale and Criteria 0 Enteral nutrition 0 Appropriate when function of small bowel present Supplement intake when PO inadequate o Postop small bowel motility returns before gastric or colonic motility allows early enteral feeding 0 Feed through OR trophic feeds immediately postop Parenteral nutrition 0 Not appropriate when adequate GI function present 0 Reserved for nonfunctional or severely diminished small bowel Distal enterocutaneous fistulas intractable diarrhea short bowel syndrome Enteral Nutrition 0 Better GI bacteria function 0 Preserved GI immunity 0 Preserved gut associated lymphoid tissue activity 0 Feeing through the GI tract via tube catheter or stoma delivering nutrients distal to oral cavity 0 Tube feeding bypassing the mouth Indicated for patients with functioning GI but unable to self feed or unable to eat enough 0 Feed into the stomach Conditions that Often Require Enteral Nutrition 0 Inability to consume any oral nutrition o Facial oral or esophageal cancer or trauma respiratory failure traumatic brain injury with deficits comatose states major GI surgery 0 Inability to consume adequate nutrition orally 0 Hyperemesis or pregnancy hypermetabolic states as burns trauma cachexia spinal cord injury Impaired digestion absorption metabolism 0 Severe gastroparesis inborn errors of metabolism Crohn s disease short bowel syndrome with minimum resection some cancers 0 Severe wasting or depressed growth 0 Failure to thrive cerebral palsy cancers HIV cachexia Conditions that Often Require Parenteral Nutrition 0 Gastrointestinal Incompetence 0 Short bowel syndrome with major resection 0 Severe acute pancreatitis or necrotizing pancreatitis 0 Severe IBD inflammatory bowel disease small bowl ischemia 0 Severe liver failure GI Access for Enteral Nutrition 0 Temporary access route is described by where it enters the body and where the tip is located 0 Nasogastric or Orogastric 0 Short term up to 3 or 4 weeks 0 Normal stomach function No diabetic gastroporesis o Bolus intermittent or continuous infusions Nasointestinal o No bolus infusions caution with intermittent 0 Short term up to 3 or 6 weeks 0 Gastric motility disorders esophageal reflux or persistent nausea and vomiting 0 No guarantee thee is abnormal stomach function 0 More permanent types or ostomy o Surgically placed enterostomies Gastrostomies Gtube and jejuostomies Jtube Long term access months 0 Percutaneous endoscopic gastrostomy PEG or jejuostomy PEJ Nonsurgical Type of Tube or Enteral Feeding Depends on o Anticipated length of time of enteral feeding 0 Risk for aspiration or rube displacement o Presenceabsence of normal or partial GI function Bolus up to 500 ml rapid delivery via syringe 3 or 4 times daily I 5g I I I I I I I Trophic Very low rate for 24 48 hours small intestine very malnourished stimulate GI tract Continuous Via infusion pump at defined rate Enteral Nutrition Formulas 0 Based on subtates nutritent density osmolality and viscosity Protein Ca rb Lipids Formula Selection 0 Formula selection based on Functional status of GI tract Energy and nutrient content Digestion and absorption capability of patient Clinical considerations fluid and electrolyte status and organ function 0 Types of enteral formulas 0 Standard meet basic nutritional needs OOOO 0 High nitrogen for patients with high protein needs wounds 0 Specialized Expensive Low in fat low protein pre digested protein fragments Disease specific pancreitis HIVAIDS hepatic disease cardiopulmonary glucose intolerance Parenteral Nutrition 0 Provision of nutrients directly into bloodstream 0 Total Parenteral Nutrition TPN Catheter is large high blood flow vein such as superior vena cava or subclavian 0 Long Term Central Access Peripherally inserted central catheters PICC a Tip deposits feeds in large vein 0 Peripheral Parenteral Nutrition PPN Catheter in smaller vein typically arm Short term Cannot tolerate concentrated solutions Difficult to meet nutritional needs Parenteral Nutrition 0 Solutions 0 Two in one or three in one system 0 Protein 0 Crystalline amino acids 0 4 kcal g protein 0 Carbohydrate o Dextrose monohydrate 34 kcalg Lipid o 10 emulsions 11 kcalml o 20 emulsions 2 kcalml 0 Both provide minimum of 2 to 4 kcals as linoleic acid Electrolytes Vitamins Minerals and Fluids TPN Administration 0 Continuous infusion 0 Depending on tolerance increase incrementally over 24 hours to reach goal rate 0 Avoid abrupt cessation and rebound hypoglycemia 0 Cyclic infusion 0 Approximately 12 hours per day usually at night 0 Higher rate or more concentrated solution 0 Lower infusion rate 1st and last hour to prevent rebound hypoglycemia Complications 0 Need to monitor for complications frequently 0 Access Problems Tube displacement or obstruction Leakage in percutaneous or surgically placed tubes 0 Administration Aspiration or regurgitation Microbial contamination low risk with closed system 0 Gastrointestinal Complications Nauseavomiting delayed gastric emptying high gastric residuals constipation diarrhea malabsorption abdominal distention 0 Metabolic Complications Refeeding syndrome glucose intolerance 0 Mechanical Pneumothorax subclavian artery injury central veins thrombophlebitis air embolism catheter misplacement Infection and sepsis Catheter site 0 Metabolic Dehydration hyperosmolar nonketotic hyperglycemic coma rebound hypoglycemia electrolyte imbalance hyperglycemia azotemia hyperlipidemia o Gastrointestinal Cholestasis hepatic abnormalities GI villous atrophy Refeeding Syndrome Cachectic individuals at high risk 0 Can happen with parenteral or enteral feeds 0 Risk much higher with nutrition support than by mouth 0 Hypokalemia hypophosphatemia and hypomagnesaemia o Intake of intracellular electrolytes should be adequate and serum levels monitored frequently Transitional Feeding Parenteral to enteral 0 Duration of transition dependent on patient tolerance of enteral feeds 0 Stop parenteral when enteral reaches 5075 Parenteral to oral 0 Stop parenteral when oral reaches 5075 0 Enteral to oral 0 Duration of transition dependent on patient tolerance
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