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Nutrition Notes

by: Ashley Stanek

Nutrition Notes NTR 341

Ashley Stanek
GPA 3.75
Intro to Therapeutic Diets
Dr. Morse

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All in class nutrition notes for NTR 341. Arizona State University
Intro to Therapeutic Diets
Dr. Morse
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Date Created: 10/10/15
Chapter3 Nutrition Assessment 91214 325 PM Nutritional Status 0 Altered when stored of energy protein water vitamins or minerals uctuate as a result of increased need increased utilization altered intake or altered utilization 0 Determination of nutritional risk involves the attempt to predict potential problems based on the client s current health status Nutrition Assessment and Screening 0 Areas 0 Food and Nutrition related history Biochemical data Medical tests and procedures Anthropometric measurements NutritionFocused physical ndings Client history OOOOO Arginine Vasopressin AVP Previously known as antidiuretic hormone that acts on the renal tubules to reduce urine output in response to dehydration and hyperosmolarity Ascites Abnormal accumulation of uid in the abdominal cavity Baroreceptor In general any sensor of pressure changes Colloid Osmotic Pressure oncotic pressure The osmotic pressure attributed to proteins and other macromolecules Cyclosporine An immunosuppressant drug Dehydration A de cit of water in the body Diabetes Insipidus Chronic excretion of very large amounts of pale urine of low speci c gravity Dieresis The production of excessive amounts of urine Edema The accumulation of excess uid in cells tissues or a cavity resulting in swelling Electrolytes Those substances that bear on electrical charge ions Extracellular Fluid ECF the interstitial uid and the plasma constituting about 20 of the weight of the body sometimes used to mean all uid outside the cell Facultative Urine Excess water that is excreted through urination Hypercalcemia High serum CALCUIM Hyperkalemia High serum POTASSIUM Hypermagnesmia High serum MAGNESIUM levels Hypernatremia Abnormally high levels of serum SODIUM Hyperosmolar Hyperglycemic Nonketotic Syndrome A complication of Type 2 Diabetes Mellitus that usually develops after a period of hyperglycemia combines with inadequate uid intake Hyperphosphatemia High serum PHOSPHORUS Hypervolemia increased blood volume Hypocalcemia Low serum CALCIUM Hypokalemia Low serum POTASSIUM Hypomagnesemia Low serum MAGNESIUM levels Hyponatremia Abnormally low concentration of SODIUM ions in the circulating blood Hypophosphatemia Low serum PHOSPHORUS Hypovolemia decreased blood volume Insensible Losses Fluid loss that cannot be easily measured sweat lntraceuar Fluid ICF Fluid within cell tissues Kayexalate A medication used to reduce high serum potassium exchanged sodium for potassium in the intestine Leukocytosis High white blood cell count Metabolic Water Water that is produced through nutrient metabolism Obligatory Urine The amount of uid necessary for the body to excrete waste products and solutes Osmolality The number of osmols per kg of solvent Osmolarity The number of osmols per L of solvent Total Body Water 0 60 of total body weight in males 0 50 Female o 75 infants 0 Less than 50 elderly 0 Fat tissue has the lowest of water 0 As fat increased body water decreases Fluid Compartments 23 Intracellular 13 Extracellular o Interstitial Surrounds cells 0 lntravascular Found within blood 0 Transcellular Secretions with organs gastrointestinal cerebrospinal intraocular quotThird Spacesquot Fluid accumulation within body cavities Movement of Fluid Fluids move freely between uid compartments by osmosis and ltration Osmosis Only water moves between compartments Filtration Water and solutes besides proteins and red blood cells move 0 2 Pressures o Osmotic low concentration high concentration Determined by the number of solute particles in the solution o Hydrostatic Exerted by the uid on the membrane Exampleblood pressure Movement Between ECF and lCF Directed by osmotic pressure l osmotic equilibrium Fluid Intake 0 Anything uid at room temperature will be considered uid intake Fluid Output Sensible measurable lnsensible not seen or measured Types of Solutes Electrolytes 0 Sodium Potassium Calcium Magnesium Chloride Bicarbonate Phosphate Sulfate Distribution Anions Negative charge 0 ECF Chloride and bicarbonate o ICF Phosphate Cation Positive charge 0 ECF Sodium o ICF Potassium Factors In uencing Movement of Solutes Molecular Size Electrical Charge Hydrostatic Pressure Method of Transportation active transport is easier than diffusion Thirst Mechanism Triggered by the hypothalamus Elderly and Elite athletes are an exception RenalFuncUon Blood volume increases hydrostatic pressure increases 0 Then increases pressure resulting in large amount of uid moving through capillaries into renal tubules Then excreted as urine by the kidneys Hormonal In uence SEE CHART ON PAGE 125 Pharmacotherapy The use of drugs for treatment of disease and health maintenance Medical Drug medicine A chemical used fore the diagnosis prevention treatment of symptoms or a cure of a disease Cassi ed by 0 Structure Pharmacological action Pharmacoogy The study od drugs their properties and their effects Pharmacokinetics The study of drug absorption distribution metabolism and excretions Role of Nutrition Therapy in Pharmacotherapy Drug nutrient interactions are de nes as quotundesirableharmful interactions between food and OTC medications prescribed medications herbals botanicals andor dietary supplements that diminished enhances or alters the effect of nutrients andor medications Drug Mechanisms Binding of drug to speci c receptors of the cell membrane l speci c enzyme reactions React with a cellular receptor site due to the design and shape 0 Most drugs can interact with more than one cell receptor which is a result of many side effects that could occur Administration of Drugs 0 Oral Sublingual or Buccal 0 Under the tongue or in the cheek o Absorbed across mucous membranes into the circulatory system o Parenteral Injection into the body through routes that are subcutaneous intradermal intramuscular intraperitoneal intravenous 0 Tropical Applied to the skin Can also be absorbed via skin or mucous membranes 0 Inhalation Act with the respiratory system or to have systemic effect Can also be placed on target sites such as eyes ears or spinal chord Pharmacokinetics Absorption of Drugs 1 Is transferred from the administrative site to the circulatory or lymphatic system 2 Passive diffusion facilitated diffusion and active transport 3 The rate and effectiveness of absorption is based on o Solubility of the medication determines where in the gastrointestinal tract the medication will be dissolved and then be absorbed Dissolution or dissolving occurs before absorption 0 Excipients are substances added to formulations of medications that affect dissolution Binders lubricants coating agents decrease dissolution Disintegrants easily dissolved in water increase dissolution o The amount of time a medication is present in a speci c portion of the GI tract the pH of that portion of the GI tract and the surface area The largest surface area for drug absorption is located in the small intestine and the lungs O 0 Chemical properties of the drug the integrity of the GI tract and other tissues circulation and blood supply Highest regions of blood ow small intestine lungs muscle and buccal amp nasal cavities have the efficient rates of absorption and distribution Chemical properties of medications related to drug absorption include the solubility of the drug in lipid or water and the ionization of medication Lipid based drugs absorb across cell membrane quickly because cell membranes are lipid based Drugs that are not ionizedfast Distribution After absorptionljDistribution The movement of the drug throughout the body to the target sites where it can act Affected by O 0000 The binding of the drug to proteins within the circulation Capillary permeability The drug s solubility in water The binding of the drug to other tissues Physiological or anatomical features Metabolism of Drugs Biotransformation changing the physical form inactive l excreted by urine or bile The liver is the major site Cytochrome P450 isoenzymes are responsible for metabolizing drugs Interacts with CP450 as inhibitor or inducer o Inhibitor Reacts with speci c enzyme by competition for the receptor site Decreases metabolism and increases the drug effect 0 Inducer Stimulates synthesis of the enzyme increases action potential Increases metabolism and decreases the drug effect Excretion Metabolismexcretion Urine or bowel Altered GI absorption 0 Consumption of food and medication 0 Vomiting and Diarrhea o Decreases time availability for solubility and dissolution Disease or health conditions 0 Interrupt normal transit time or surface area will decrease the effectiveness of absorption Altered Distribution Circulation 0 Age and diseases 0 Body size and body composition 0 Elderly decrease in muscle mass lower dosage 0 Increase in body fat slower distribution of drug Altered Metabolism Age Genetics Altered Urinary Excretion pH has an effect 0 Changes in creative clearance alter the effect of medication Nutritional Assessment 1 Medical History 2 Labs for kidney function and glucose levels 3 Side effects from drugs 4 ALL drugs taken at time should be listed Fluid and Electrolytes Balance September4 Fluid and Electrolytes Balance Water 0 Water is the largest single component of the body 0 Essential component of nutrition assessment Homeostasis involves the GI tract kidneys and brain Distribution of Body Water 0 Total Body Water 0 5060 of Total Body Weight 0 In uenced by fatlean mass 0 Fluid compartments Intracellular uid 80 Extracellular uid 20 n Interstitial Between cells n Intravascular Abnormal Fluid Accumulation o Abnormal Interstitial Fluid 0 Edema abnormal accumulation of uid in interstitial space 0 Anasarca excessive accumulation of uid in interstitial space o Ascites excessive accumulation of uid in the abdominal cavity Normal Anatomy 0 Movement of Fluid between blood and interstitial compartments 0 Osmosis Decrease concentrationincrease concentration 0 Two Types of Pressure 0 Osmotic Colloid osmotic pressure oncotic Fluid moves to keep concentration of solutes and colloids equal Colloid does not dissolve Albumin levels have in uence 0 Hydrostatic Pressure on membrane walls Water Intake and Balance 0 Daily intake should losses 0 Intake of 1450 to 2800 milliliters of water is usually o Liquids at room temperature 550 to 1500 ml 0 Foods 700 to 1000 ml 0 Metabolic water approximately 200 to 300 ml 0 Water found in uid and foods 0 Output 0 Sensible losses Urine feces o Insensible losses sweat Water Requirements 0 Water needs to replace losses from urine sweat lung vapors 0 Minimum needs 500mlday Infants 0 15 mlkcal o 150 mlkg Children 0 5060 mlkg Athletes 0 15 mlkgday Adu s o 1 mlkcal o 1 mlkcal 100ml1g N 1800 kcal amp 70 g protein 1800 ml 70 g625 pro perg N 112 g N 112 x 100 1120 ml 1800 1120 2920 ml 0 3035 mlkg BW Additional uids required to replace excessive losses 0 Replacement of GI losses vomiting and diarrhea o 600 to 700 ml extra daily for lactation 0 Burns wounds exudates Parkland Formula 4 ml per kg of body weight XTotal body surface area 80 kg amp 50 TBSA320 ml x 50 16000 ml Half calculated volume given over rst 8 hours1000hr x 8 hour Remainder given over next 16 hours 500hr x 16 hr Body Solutes Electrolytes Other molecules 0 Glucose protein urea lactate organic acids 0 Maintaining physiologic functions Electrolyte Requirements amount needed to maintain normal serum levels Sodium 136 to 146 mEqL Potassium 35 to 50 mEqL Chloride 98106 mEqL Normal Electrolyte Concentration GI tract and kidneys regulate balance 0 Electrolytes follow water Losses vomiting sweating burns Replacements oral vs IV Abnormal Values manifestations associated with electrolyte funcUons Electrolyte Requirements o If labs are low Give MORE o If labs are high Give LESS Mg to mEq Hyperhigh blood levels 0 Lower feeding of the dietary content Hypolow blood levels 0 Higher feeding of the dietary content Physiological Functions 0 Renal function 0 Alters uid retention or excretion Hormonal In uence Renin AngiostensionAldosterone System and Vasopressin o Baroreceptors o In uences kidney to retain Na pulling uid back into the blood 0 Arginine vasopressin o Other solutes more with water Thirst o Thirst mechanism hypothalamus prompts us to drink when it is stimulated by 0 Increased concentration of salt and other dissolved substances in the blood increase blood electrolytes o A reeducation in blood volume and blood pressure such as during profuse sweating vomiting or low uid intake 0 Dry mouth and throat from reduced saliva o Arginine vasopressin signal the kidneys to retain water 0 Increase blood volume and pressure 0 Thirst works for most people not as effective in the elderly or during strenuous exercise Physiological Regulation 0 Sodium RAAS Potassium Aldosterone 0 Calcium and Phosphorus PTH intestinal absorption exchanges between EC uid and bones renal excretion Medications some diuretics eliminate Na and K others spare Lasix vs adactone Disease can play a role in altered regulation not necessarily dietary intake Disorders Alterations in uid balance 0 Fluid Volume 0 Electrolyte concentration Increase or decrease electrolytes Typically occur together 0 Treatment includes identifying the Causes Clinical manifestations Lab ndings critical values 0 Hypervolemia Fluid overload Excess water intracellular uid volume osmolar dilution results a Electrolyte levels must be maintained within a narrow range a Signi cant dilution unable to maintain functions 0 Sodium Imbalance Na 0 Hyponatremia low From dietary restrictions or medications diuretics Effect on uid status 0 Hypernatremia High Dehydration alterations in regulatory mechanisms Effect on uid status Chloride Imbalance CI 0 Hyperchloremia high Toxicity symptoms vomiting part of HCI o Hypochloremiaow Potassium Imbalance K 0 Acid base balance protective against high blood pressure DASH Calcium Ca 0 Albumin is carrier l decrease calcium levels when albumin decreases Corrected calcium when albumin levels are low 0 HypocalcemiaLow o HypercalcemiaHigh Phosphorus P 0 Component of ICF 0 Role in energy metabolism in adenosine triphosphate ATP Phosphorylation reactions in cell ICF Magnesium Mg 0 Hypermagnesemia low Chronic alcoholism medications lincrease renal losses 0 Hypermagnesemia high Toxicity symptoms a Only from nonfood sources a Diarrhea alkalosis dehydration loss of re exes slurred speech blurred vision Must assess for factors that affect uid and electrolyte balance 0 Disease or injury Kidney disease GI Losses Medication or treatment Fluid Status 0 Daily weight assists in assessing uid status NOT body weight 0 If uid status decreases rehydrate Nutrient Status 0 If blood levels decrease REPLACE o If blood levels increase RESTRICT medications or treatments to remove or increase excretion Oral Intake 0 Balance total intake vs output 0 PO enternal lv vs urine insensible losses other losses wounds ect Improving Health and Nutritional Status through Nutrition Care Nutrition Care Process involves Nutrition assessment 0 Nutrition interventions o How do we x the problems uncovered Monitoring and evaluation of our assessments Purpose 0 Nutrition Assessment Comprehensive evaluation of nutritionhealth history 0 De nes nutritional status by evaluating all pertinent factors Medical social nutritional and medication histories Process 0 4 Steps ADIME 1 Assessment 2 Diagnosis 3 Intervention 4 Monitoring amp Evaluation Steps of NCP 0 Nutrition diagnosis MUST be related to nutrition PES statement Problemdiagnostic labeling Etiologycause or existence of particular problem Signs or symptomsde ning characteristic The problem p related to the etiology e as evidenced by the signs and symptoms 5 Example Involuntary weight loss p related to inadequate energy intake e as evidenced by eight pounds weight loss within four weeks 5 PES statements 0 Evaluate the nutrtion assessment 0 Identify the problems 0 State them each clearly and singularly 0 Focus on those that can be treated by nutritional interviewing 0 Do patients only have one problem Final Steps Discharge plans and recommendations 0 Diet education Reevaluation of labs 0 Discharge diet or nutritional support 0 Permanent or Temporary 0 Recommended times frames for follow up and reevaluation Documentation Standardized Language and Medical Abbreviations o JCAHO unacceptable symbols and abbreviations o Misinterpretation of fatal errors possible 0 JCAHO has broad and vague standards 0 Use Nutrition Diagnostic Terminology o Developed and encouraged by AND 0 Not required byJCAHO o If individual facility has requirement for nutrition diagnostic terminology in policies then they must be used Charting 0 Organization of Nutrition Documentation 0 SOAP Subjective Data Objective Data Assessment Plan Re ects nutrition care process Assessment Diagnosis Intervention MonitoringEvaluation Re ects nutrition care process Sign all entries and include credentials Include date time and service 0 Document at the tie of service never in advance 0 Identify late entries Complete sentences are not necessary 0 Use correct spelling and grammar Entries should be consistent and noncontradictory o No personal opinions or criticism Errors Omissions o For omissions write quotsee addendumquot date time and initial 0 Errors must be noted quotincorrect chartquot Keeping a personal medical notebook 0 Your own system of keeping notes 0 No required format or terminology o Kept con dentialHIPPA 0 Not a legal document and not admissible in court Guidelines for ALL charting o Standardize guidelines no matter what organizational style you use 0 No correct way to chart 0 Con dentiality HIPPA Assessment for Protein Calorie Malnutrition Prognostic indicators based on nutritional depletion Hormonal and cell mediated response to stress Acute injury or iHness 0 Negative acute phase respondents Albumin transferrin prealbumin retinol binding protein 0 Positive acute phase respondents C reactive protein crp Nitrogen balance lmmunocepentenceimpaired 0 Presence of infection Albumin 0 Long half life 1020 days 0 23 weeks to see effect of nutritional repletion o Prognostic indicator 0 Negative acutephase respondent Acute or chronic stress decrease values 0 Surgery trauma burns infections 0 Renal or hepatic disease Fluid status effects values 0 Acute changes may be due to uid status Manufactured by the liver 0 Major function is to maintain oncotic pressure 0 Pressure at vessel is maintained by dissolved proteins in plasma and interstitial uids 0 Adequate albumin prevents uid leaking from plasma to interstitial spaces 0 Low albumin Fluid leads to interstitial space quotthird spacingquot Transports many compounds in the blood 0 Hormones enzymes mineral vitamins Large serum pool when serum values decrease a large amount has already been lost 0 Not a good marker of changes in nutritional status in acute care setting Transferrin 0 Intermediate half life 810 days 0 Re ective of protein status over last 2 weeks 0 Prognostic indicator 0 Negative acute phase respondent 0 Acute or chronic stress decreases value Surgery trauma burns infections Hepatic disease 0 Plasma protein that transports iron Re ects iron and protein status 0 Indicator of protein status only when iron status WNL normal ferritin 0 Levels increase in iron de ciency PreAlbumin Short life 23 days 0 More sensitive indicator of protein status 0 Not precursor of albumin and not affected by exogenous albumin administration 0 Prognostic indicator 0 Negative acute phase respondent 0 Acute of chronic stress disease vaue Surgery trauma burns infections Renal disease and corticosteroid false positive Synthesized in the liver Binds and transports nutrients CRP C Reactive Protein 0 Positive acute phase protein 0 Primary role is to assist the compliment system 0 Plasma concentration increase when conditions producing in ammation present burns infection surgery trauma cardiac stress 0 Re ects presence and intensity of in ammation 0 Levels increase rapidly in response to trauma infection and in ammation and decrease rapidly as issues resole o Slight increase indicated heart attack risk Synthesized in the liver 0 Effect of liver disease How do albumin prealbumin and CRP Interact with each other 0 For wound healing or recovery to occur protein de ciencies must be corrected Transcapillary escape of albumin increase in stress as part of SIRS Systemic In ammatory Response System 0 Decrease albumin associated with increase severity of illness and worse prognosis Prealbumins short life rapid decrease in synthesis and decrease in serum levels lmmunocompetence Antibodiesproteins Decrease immunocompetence associated with protein energy malnutrition Bottom line Lab Values 0 Never look at just one item 0 Glucose 0 Always look at multiple labs to determine true problem 0 CMP Never look at just one set of numbersaka one date 0 Always look at lab trends Medical Nutrition Therapy for Cardiovascular Disease Sept 19 14 Anatomy and Physiology of the Cardiovascular System 0 The Heart 0 3 Layers Myocardium middle layermuscle contraction Myocardial Infarction Ml Damage to later in muscle contraction o 4 chambers Left and right Atria Left and right Ventricles Left ventricular hypertrophy LVH n Enlargement of the left ventricle seen in HTN and CHF cognitive heart failure 0 The Vasculature o Arteries and Veins o Capillaries microvasculature The Cardiac Cycle 0 Repeating contractionrelaxation of the heart Systole contraction Diastole relaxation Exerted force on the walls of blood vessels terms quotsystolic blood pressure and diastolic blood pressure Regulation of Blood Pressure Sympathetic nervous system short term control 0 With decrease in BP norepinephrine release to produce vasoconstriction and increase BP 0 Kidney long term control 0 Controls uid volume 0 Secretes renin which activates reninangiotensin system to Increase Na and water retention Hype engon Systolic contraction BP above 140 and diastolic above 90 Persistently high arterial BP 0 Silent Killer Strong positive relationship between BP and risk of CVD events 0 Increase risk for CHF kidney failure Ml stroke vision problems Cerebrovascular l stroke PeripheralVasculature n Decrease profusion l extremity pain cold limbs decrease pulse rest pain and or blackened toes due to tissue necrosis Renal System decrease ltration l renal failure a Damage to microvasculature capillaries seen with renal failure Retinopathy l visual disturbances n Damage to microvasculature capillaries Etiology of HTN MultiFactorial Genetic 0 High prevalence in African Americans 0 Family history of HTN and CVD o Maleshigher risk 0 Secondary result of another chronic condition involved in regulation of BP 0 Sympathetic nervous system de cits o Overstimulated reninangiotensin system 0 Chronic in ammatory response 0 Obesity higher BMI l risk of HTN 0 DM 0 Lifestyle FactorsSmoking exercise diet 0 Low Potassium diet 0 Sodium Chloride Intake 0 Individuals who are no salt sensitive may not experience signi cant effects on BP when consuming a high sodium chloride diet Obesity is associated with salt sensitivity 0 When following a decrease sodium chloride diet the decrease in BP most signi cant in high risk individuals African Americans the elderly obese or those with additional co morbidities like DM chronic in ammation 0 Goal Healthy People 2020 achieve BP control 0 0 gt30 of adult US population with HTN 2012 o 5 of pediatric population Prevalence increases with age Related to pediatric obesity The Role of Atherosclerosis Blood pressure is a function of cardiac output multiplied by peripheral resistance Affected by diameter of blood vessel 0 Decrease diameter l increase pressure Atherosclerosis decreases diameter increase blood pressure 0 Increase LDL increase total cholesterol decrease HDL l risk due to blood vessel blockage Genetics exercise diet play a role 0 Need to minimized risk of atherosclerosis Drug therapy increases diameter lowers blood pressure Medical Medication Lifestyle modi cations 0 Weight reduction PA nutrition therapy PharmacologicalTherapy o Diuretics Promote uid and therefore Na loss Thiazide produce increase K losses Kprotective Aldactone potassium sparing diuretic o B Blockers Block effects epinephrine Help blood vessels open up to improve blood ow 0 Calcium channel blockers Affects movement of calcium to promote relaxation of blood vessels Help blood vessels open up to improve blood ow 0 Drug Treatment Nutrition Therapy 0 Nutrition Assessment 0 Through evaluation of medical social dietary and lifestyle factors 0 Evaluate need for weight control and dietary medications o Prioritized methods to meet DASH dietary goals 0 Nutrition Diagnosis 0 Excessive energy intake 0 Excessive or inappropriate intake of fatsspecify 0 Excessive sodium intake 0 Inadequate calcium ber potassium or magnesium Nutrition Intervention DASH Diet Dietary Approaches to Stop Hypertension 0 GOO 000 O Grains 6 to 8 day Vegetables 4 to 5 day Fruits 4 to 5 day Fat Free or low fat milk and milk products 2 to 3 servings day Lean meats poultry and sh 6 oz or less day Nuts seeds and legumes 4 to 5 servings per week Fats and oils 2 to 3 tsp day Sweets and added sugars 5 or less servingsweek Weight loss and PA 0 Salt restriction O 0000 AHA Recommendations aim to eat lt1500 mg sodiumday 10 added in cooking at home and at table 10 5 naturally occurring in foods Decrease processed foods increase fresh foods Nutrition Intervention Affecting BP 0 Potassium O Involved in uid balance muscle contraction 0 Greater effect seen with African Americans 0 DASH diet l K intake decrease NA intake 0 Calcium 0 Involved in muscle contraction Magnesium Lipids Bene ts of Intervention Nutrition education 0 Increase fruits and vegetables increase ber intake decrease total fat intake 0 Weight loss promotes decrease in BP 0 Comparing DASH diet vs Typical US Diet in CVD risk in patients with pre HTN or stage 1 HTN who were receiving no medication 0 DASH group decrease total serum cholesterol decrease LDL cholesterol increase HDL decrease BP Hypertension in Children and Adolescence Framingham Children s Study 0 4 servings of fruits and veggiesday 0 2 servings dairyday 0 Lower blood pressure than those who consume less HTN associated with obesity and intake of high calorie high salty foods 0 Increase fast foods 0 Increase processed foods increase Na decrease K 0 Increase risk of adverse cardiovascular events in adulthood Lifestyle modi cations produced bene ts 0 Control weight gain 0 Exercise 0 DASH diet Limit Na intake fast and processed foods Older Adults 0 Nutrition and Lifestyle Modi cations Same as for younger adults 0 Lifestyle modi cations alcohol and exercise 0 Weight restriction 0 Salt restrictions 0 Trial of Nonpharmacological Interventions in the Elderly TONE Stroke 0 It is important to note that a stroke is cause by a cardiovascular event 0 HTN o Atherosclerosis o Preventative measures include methods to prevent HTN and CVD o DASH diet 0 Weight loss 0 Effects of a stroke are more neurological in nature 0 Hemiplegia partial paralysis o Dysphagia difficulty swallowing o Slurred Speech Atherosclerosis Thickening of the blood vessel walls caused by presence of plaque AS 0 Arteriosclerosisincludes loss of vascular elasticity 0 Results in restriction of blood ow Myocardial Infarction Ml CAD Peripheral Vascular Disease CHF 0 Risk Factors 0 Obesity Dyslipidemia Hype engon Physical Inactivity Atherogenic Diet OOOO 0 Diabetes Mellitus 0 Metabolic Syndrome Abdominal Obesity Increase TG Increase cholesterol HTN Type 2 DM 0 Cigarette Smoke Framingham Study and Risk Factors Largest epidemiological study of CAD risk factors in wold o MultigenerationalStudy 0 Now evaluating 3rd generation 0 Identi ed multiple risk factors 0 1960 cigarette smoking found to increase the risk of heart disease 0 1961 Cholesterol level BP and electrocardiogram abnormalities found to increase heart problems Development of Plaque Vascular endothelial cells ideally smooth 0 In ammation damages endothelial cells Damages endothelium enables plaque deposits 0 Increase cholesterol or increase glucose l increase in ammation l athrogenesis Pathophysiology of Atherosclerosis 0 Clinical Manifestations o Asymptomatic In ammatory response Injury to endothelial lining Attracts platelets Form small clot l thrombi Continued migration of cells to the area Proliferation of the plaque Rupture of brous cap may occur and unstable plaque can break off blockage elsewhere in the vasculature l ischemic heart disease decrease blood ow In ammatory Markers of CAD Fibrinogen 0 Protein involved in normal blood clotting 0 Increase with smoking obesity HTN elevated TG sedentary lifestyle 0 Directly cause athrogenesis marker of endothelial damage 0 Strong evidence increase levels predictor of CVD and stroke 0 C Reactive Protein 0 Acute phase respondent and measure of in ammation 0 gt3 mgdl associated with cardiovascular risk 0 Recommended for individuals with Framingham Global risk assessment of 1020 0 Increase body wt increase glucose or insulin requirements l increase CRP o CRP infusion in health adults with NOT l in ammation Homocysteine 0 Increase levels associated with risk of CVD 0 Associated with endothelial damage 0 Increase levels associated with in ammation 0 Genetics de ciency of cystathoinine B synthase prevents complete metabolism of methionine l increase homocysteine o Nitric Oxide NO 0 Produced in endothelial cells relation of smooth muscles in arteries 0 Increase oxidative stress l decrease NO and in ammation Blood Lipids and Liproproteins Triglycerides 0 Excessive CHO or kcal intake l increase 0 EtOH intake l increase 0 Total cholesterol amount in all lipoprotein fractions HDL LDL VLDL VLDL Transport endogenous triglycerides and cholesterol TG5 VLDL 0 LDL Major cholesterol transport lipoprotein 0 Deposits cholesterol 0 HDL Reverse cholesterol transport O 0 Protective In uenced by exercise genetics positive or negative 0 Apolioproteins Protein portion of the lipoprotein 0 A1 values show a protective effect associated with HDL O B values associated with LDL and atherosclerosis Atherosclerosis Medical Management 0 NCEP ATP lll Guidelines 0 00000 0 Step 1 Analyze lipoprotein levels Step 2 Presence of CHD and risks Step 3 Analyze other risk factors smoking family history ect Step 4 and 5 Determine risk category from 13 above Step 6 Initiate TLC Guidelines Step 7 Add medications Diet MAY minimize need for drugs May not help with genetic causes Step 8 Identify and treat Metabolic Syndrome Atherosclerosis Medical Treatment and Pharmacological Management Type of Medications Bile acid sequestrates cholestyramine Nicotinic Acid decrease CRP in ammation decrease Tg and cholesterol increase HDL o HMG CoA reductive inhibitor stains eg lovastatin pracastatin Nutrition Therapy 0 Evaluate diet lifestyle family history 0 Use TLC Therapeutic Lifestyle Change 0 Dietary fat 0 Saturated fat 0 Exercise 0 Weight reduction MEDFICTS assessment tool 0 Meats Eggs Dairy Fried Foods ln baked goods Convenience foods Table fats Snacks 0 Dietary CAGE question Assess saturated fat and cholesterol Nutrition Therapy for Atherosclerosis Saturated Fatty Acids lt7 0 Animal Fat 0 Trans fatty acids increase food shelf life 0 Tropical Oils Coconut short chain 0 Not all saturated fats affect lipid pro le that same 0 Dietary Cholesterol lt200 mgday 0 Animal sources 0 Affects LDL levels 0 Recommendation to decrease saturated fat 0 Skim milk and milk products 0 Trim fat or remove skin before cooking 0 Limit portions Nutrition Therapy for Atherosclerosis 0 Total Fat intake 2535 kcal 0 Saturated fat 7 kcal o Remaining Fat Intake 18 28 kcal o Polyunsaturated fatty acids Veggie oils Lowers LDL Monosaturated fatty acids Positive effect 0 Olive oil ax and Mediterranean Diet 0 Lowers LDL and TG levels No impact on HDL Omega 3 Fatty Acids o Inhibit VLDL synthesis 0 Linolenic EFA 0 Fatty Fish EPA and DHA Best source Salmon Mackerel Trout 0 Plant Source ALA Walnuts axseed Canola Oil Body must convert ALA to DHA not as effective 0 Caution with sh oil supplements may contain mercury contaminants 0 Omega 3 Omega 6 Ratio High omega 6 l decrease bodies ability to convert to ALA to DHA and EPA lnsoluble Fiber No effect Soluble ber Oat legumes 0 Strong evidence 713 gd decrease cholesterol and LDL o Binds bile in GI tract 0 GI bacteria ferment l SCFA s which inhibit cholesterol synthesis lncrease fresh fruits and vegetables l increase potassium o Antioxidants Strong evidence Vitamin E C and Beta Carotene supplements provide no bene t Limit processed foods to decrease sodium intake Strong evidence Plant stanol sand sterols nuts inhibit absorption of dietary cholesterol Pharmacological Management Standard care Drug therapy 0 Drug cocktail or a combination drug components Aspirin Anticoagulant decrease in ammation Statin drug to lower cholesterol Medications to decrease blood pressure and decrease in ammation Bonus Years Diet by Dr Chef Ralph Felder Red Wine Sozday o Decrease risk by 32 o Decrease LDL adherence to vasulature endothelium Garlic 1 cloveday o Decrease risk by 25 0 Fruits and Veggies 4 cupsday o Decrease risk by 21 0 Salmon 5 oz 3 timesweek o Decrease by 14 0 Nuts 2 ozday o Decrease by 12 0 Dark Chocolate 2ozday o Decrease by 11 0 Combined decreased CVD risk by 75 Nutrition Therapy for Atherosclerosis Registered Dietitian RD 0 Studies that science of how food and nutrients are associated with health Food components Label reading Cooking methods 0 Strong evidence time spent with RD 0 Decrease total cholesterol 0 Decrease LDL 0 Dependence on prescription treating CVD Job Security lschemic Heart Disease Inadequate supply to the heart 0 Occlusion cause by atherosclerosis may be asymptomatic o Angina chest pain 0 Can precipitate Ml causing necrosis of these Etiology 0 Acute coronary syndrome acute MI or unstable angina Plaque erosions rupture of plaque forming thrombus vasoconstriction 0 Traditional risk factors of AS apply to HD o CReactive protein CRP food predictor Clinical Manifestations 0 Stage angina Indigestion nausea vomiting sweating shortness of breath weakness fatigue 0 Rhythmic abnormalities Sudden onset bradychardia palpations dizziness Some part of coronary circulation blocked schemia decrease blood ow leads to muscle destruction infarction Diagnosis ECG blood levels of enzymes speci cally related to cardiac muscle damage Treatment 0 Oxygen aspirin morphine 0 Bed rest post MI 0 Slow increase in physical activity Post Infarction Nutrition 0 1st 24 hrs no caffeine liquid diet nausea and choking Drugs that contain nausea digitalis morphine 0 Small frequent meals soft or liquid diet 0 Na restriction if BP and uid status indicated 0 Follow TLC diet recommendations Heart Failure 0 Impairment of the ventricles capacity to eject blood from the heart or to ll with blood 0 Progressive disease related to decreased blood ow and oxygen profusion 0 Clinical Manifestations o Dyspnea SOB fatigue weakness exercise intolerance poor adaptation to cold 0 Fluid retention pulmonary congestion edema hepatomegaly splenomegaly ascites Cardiac edema 0 Treatment 0 Treat underlying cause and control symptoms 0 Medications 0 Exercise as tolerated 0 Nutrition therapy Nutrition Therapy for Heart Failure 0 Cardiac cachexia syndrome of malnutrition 0 Extreme skeletal muscle wasting somatic What do you expect from visceral proteins 0 Fatigue 0 Anorexia Complications leading to nutrition problems 0 GI slowed peristalsis and early satiety o Impairment of nutrition absorption 0 Side effects from drugs 0 Nutrient de ciencies 0 Nutrition Assessment and Diagnosisterminoogy related to o Malnutrition Sodium and uid Early satiety weight loss Drug nutrient interactions 0 Nutrition nterventionterminology related to Nutritional repletion 0 Sodium o Fluid 0 DrugNutrientlnteraction 0 Regulation of Energy Balance Hunger VS Appetite o Appetite o Hypothalamus neurological response to sight and smell of foods Psychological component Social component 0 Secretions of pancreatic and GI hormones Increase and decrease appetite and food intake Hormones affection hunger and food intake 0 As blood glucose levels increase Insulin and Amylin l decrease appetite and food intake 0 In response to expanding stomach chime entering small bowel Neural signals l decrease appetite Glucagon Cholecystokinin CCK Glucagon like peptide 1 Peptide YY l decrease appetite o Ghrelin Gain 0 Leptin Lean Ghrelin Protein produced by stomach cells 0 Increase appetite and energy storage 0 Decrease energy expenditure 0 Increase before meal decrease rapidly after eating 0 Lean individuals increase ghrelin to promote appetite and energy storage 0 Anorexia signi cant increase in ghrelin Opposite action of leptin Generic Causes of Obesity Adiponectin produces by fat cells stimulate storage 0 Levels increase as stored fat decreases Signals quotneed to store morequot 0 Leptin o Ob gene l protein leptin o Leptin produced by fat cells Affects energy stores signals quotstored enoughquot lncrease leptin l decrease appetite and increase energy expenditure 0 If de cient extremely overweight o More research needed 0 Opposite action of ghrelin o Prader Willi Syndrome 0 Generic disorder characterized byquot lncrease appetite Morbid obesity lncrease ghrelin levels increase adiponectin decrease leptin Adipose Tissue Storage site 90 energy reserves T6 0 White adipose energy reserve 0 Brown adipose temperature regulation 0 Body fat re ects 0 Number of fat cells 0 Sixe of fat cells 0 Fat cell development 0 Hypertrophy increase size of cells 0 Hyperplasia increase number of cells Harder to decrease and maintain weight if hyperplasia is present Adipose Tissue Hormonal Regulation 0 Fat storage and release 0 From dietary triglycerides and lipogenesis o Lipoprotein lipase LPL Found on adipose and muscle cell membranes Promotes fat storage Obese have more fat cells LPL activity After weight loss LPL activity increases a Adiposity or BMI rebound o Hormone Sensitive Lipase HSL Hydrolyze stored triglycerides within adipocytes for release into circulation for utilization Mobilization and utilization for fat Body Composition or Weight Components 0 Two compartment model fat vs fat free mass 0 Essential body fat Necessary for physiologic function Men need less 0 Storage body fat Under skin Around internal organs to protect from trauma Considered expendable Fat free mass 0 Skeletal muscles water bone organs Assessment of Body Weight Determines underweight VS WNL 0 May determine overweight 0 Evaluation standards determine health risks 0 O 0 Ideal Body Weight IBW Hamwi equation Body Mass Index BMI Use of height and weight BMI commonly used to assess obes y Cinica judgment should be used a Look at your patient Obese gt30 Regional Distribution of Fat and Metabolic Syndrome Genetic men VS women 0 Apple or Android excess subcutaneous truncalabdonminal fat 0 More common in men increase with age 0 Correlated with insulin resistance metabolic syndrome DM and CVD risk Pear or Gynoid excess gluteofemoral fat 0 More common in premenopausal women 0 Estrogen in uences deposition 0 New Research 0 Increase risk of death from CVD with increase belly fat 0 Risk seen with thin cardiac patients normal BMI Assessment of Body Weight 0 Evaluation standards determine health risks 0 Key concept fat deep within abdomen and around intestines and liver increased disease risk 0 Waist to hip ratio 0 Disease risk increase WHR gt095 in males and gt08 in females Waist circumference 0 gt40 in males gt35 in in females quothigh riskquot Health Risks Type 2 Diabetes 0 CVD 0 Hypertension o Hyperlipidemia Gallbladder disease 0 Some cancers Nonalcoholic fatty liver disease 0 Reproductive disorders 0 Increased mortality Etiology of Obesity 0 Chronic energy intake exceeding energy expenditure 0 Environmental generic psychological cultural and physiologic factors Genetic Causes of Obesity Contributing factors 0 gt4050 of BMI explained by genetics 0 In uences taste appetite intake expenditure location of stored fat 0 Multiple genes involved 0 Predictive in families parents and twins 80 with 2 obese parents 40 with 1 obese parent 0 Weight of offspring between and after bariatric surgerysigni cant difference Child born after the surgery and weight loss had better genes Etiology of Obesity Obesigenic environment 0 Toxic food environment available of low cost tasty energy dense foods in large portions 0 Contributing factors Plate sizes sedentary lifestyle Evidence supports low energy dense foods for satiety 0 Soups fruits vegetables cooked whole grains 0 Barriers cost and convenience Goals of Weight Management Achievement of ideal body weight may not be possible or desirable Bene cial to maintain present weight or achieve moderate loss 5 to 10 Effects of rapid weight loss starvation response and metabolic aberrations that can lead to death Popular Diets K State Professor l weight decreased 0 Commercial programs 0 Weight watchers regular foods 0 Jenny Craig prepackaged foods Eatlimit speci c foods or groups Cabbage soup 0 Latest and Greatest 0 Dr 02 o Hcg very low kcal and limited foods Diet Therapy developed 19505 January 2011 FDA reports hcg drops fraudulent Pharmaceutical Management CNSacting agents 0 Sibutramine Meridia Inhibits reuptake of norepinephrine and serotonin to increase satiety decrease hunger and decrease drop in REE commonly associated with weight loss Sympathetic stimulant and l cardiovascular side effects Pulled from the marked October 8 2010 due to increased risk of heart attack stroke and death Diet Drug approved 62812 Lorcaserin Belviq a CNS agent o Auguments diet exercise and behavior therapy 0 Created satiety after consuming smaller amounts of food 0 MD supervision and speci c BMI criteria 0 Was rejected by an FDA advisory panel in 2010 over safety 0 Most recently the FDA advisory panel decided that the bene ts of the drug outweighed the risks 0 Manufacturer is required to conduct six studies including Long term cardio trial to assess the affect of a heart attack stmia o Auguments diet exercise and behavior therapy 0 Created satiety after consuming smaller amounts of food 0 Combination of two drugs Phentermine an appetite suppressing stimulant Topiramate an anti seizure medication that enhances satiety 0 MD supervision and speci c BMI criteria NonCNSacting agents 0 OrlistatAlli inhibits GI lipase 13 fat malabsorption Concern over fat soluble vitamins diarrhea and atus Su rgical Procedu res Bariatric surgery for morbidly obese only BMI gt40 or BMI gt35 with comorbidities 0 Previous failure of comprehensive programs 0 Evaluate physiologic and medical complications psychological problems and motivation before proceeding Gastroplasty restrictive and gastric bypass malabsorptive Liposuction Vertical Band Gastric Bypass Sleeve ln vertical banded gastroplasty the surgeon constructs a small stomach pouch and restricts the outlet from the stomach to the intestines ln bypass the surgeon constructs a small stomach pouch and creates an outlet directly to the jejunum The sleeve you remove a good portion of the stomach Stomach is in a shape Second step after weight loss then they go back 6 months to a year and do the bypass not everyone has second step done Gastric Surgeries for Obesity Surgical weight loss can lessen degree of obesity related co morbidities 400 gastric bypass patients with comorbidities 330 months post Op 0 2165 with comorbidities o HTN increase lipids DM sleep apnea GERD improved or resolved in 80100 of patients Perceived improved quality of life 0 6 weeks postop 34 o 18 months postop gt80 Less complications with Gastric Sleeve O 2 phases 1st sleeve 2nCI by pass Surgical weight loss can lead to potential nutritional and medical complications 0 0000000 Dehydration Nutritional de ciencies and malnutrition Dumping syndrome Weight loss failure Intestinal obstruction Abdominal pain Enterocutaneous stulas Depending on degree of obesity or weight loss nutritional de ciencies l MOF and death Gastric Bypass Diet Postop stomach volume reduced to about 1 ounce or 2 tablespoons Over time stomach volume will stretch until it can hold 4 to 8 ounces 12 to 1 cup Concentrated sweets l dumping syndrome Start with clear liquids full liquids l pureed l regular Need 6 small mealsday for kcal and adequate nutrients Nutrition Therapy for Weight Management Nutrition Assessment 0 O O Anthropometric Measurements Client History FoodNutrientRelated History Intervention O 0000 Avoid additional weight fain once goal is reached Reduce energy intake Low energy dense foods Focus on a speci c macronutrient intake controversial Physical Activity Important component of weight loss therapy Minimizes loss of LBM Decrease LDL cholesterol increase HDL cholesterol Improved insulin sensitivity Improves physical tness Nutrition Monitoring and Evaluation Diseases of the Cardiovascular System These diseases include high blood pressure coronary heart disease cerebrovascular disease peripheral vascular disease and congenital heart defects Anatomy and Physiology of the Cardiovascular System The role is to regulate blood ow to the tissues in order to deliver oxygenated blood and nutrients as well as to retrieve waste products from cellular metabolism Thermoregulation hormone transport maintenance of uid volume regulation of pH to control acidosis and alkalosis and gas exchange The Heart Three Layers o Epicardium Outer layer 0 Myocardium Middle layer responsible for muscle contraction that pumps the blood from the heart 0 Endocardium Inner layer 4 Chambers 0 Left and Right Atria 0 Left and Right Ventricles 0 Right atrium and ventricle pump blood through the pulmonary circulation for oxygenation 0 Left atrium and ventricle pump oxygenated blood through the systemic circulation Right Atrium l right ventricle l pulmonary trunk l pulmonary circulation lungs l carbon dioxide is removed and oxygen is added l returns to the heart via the pulmonary veins and enters the left atrium l left ventricle l pumped into the systemic circulation through the aorta smaller arteries to the body vena cava Electrical Activity of the Heart lntercalated discs Membranes that connect heart cell muscles that allow electrical impulses to pass from one cell to another Sinoatrial node SA where electrical activity starts Depolarization in the SA node cases contraction of the atria Then carried from the atria to the ventricles by the atrioventricular node AV located in the base of the right atrium The depolarization of the AV node is carried into the ventricles by the atrioventricular bundle bundle of His which splits into the right and left bundle branches Then carried down the bundle branches and then spread throughout the ventricles by the Purkinji Fibers Cardiac Cycle Systole Contraction Diastole Relaxation Cardiac Function 0 Stroke Volume The volume of blood ejected with each contraction of the left ventricle 0 End Diastolic Volume EDV The amount of blood in the ventricles at the end of diastole o Referred to as preload o The greater EDV the more the ventricles are stretched Regulation of Blood Pressure 0 Resistance is dependent upon the radius of the arterioles length of vessel and the blood viscosity 0 The radius is controlled by local metabolic controls in skeletal muscles within a particular region of the body may cause vasodilation and increase blood ow to those muscles in order to match metabolic needs 0 Vasodilation would decrease resistance by increasing the radius and increase resistance by increasing the radius of the vessels Vasopressin and angiotensin II also affect blood pressure 0 Vasopressin Antidiuretic hormone is stored in the posterior pituitary gland and is controlled by the hypothalamus When there is a water de cit vasopressin is released causing and increase in the reabsorption of water increase BP 0 Angiotensin II is part of the reninangiotensinaldosterone system When there is a decrease in sodium plasma volume and arterial BP the hormone renin is secreted by the kidneys Baroreceptors Pressure sensors that monitor blood pressure Nutrition Therapy for Hypertension Lifestyle Modi cations 0 Nutrition Therapy 0 Increase PA smoking cessation and weight loss reduction of Sodium alcohol intake primary strategies Nutrition Assessment Food and Nutrition Intake Knowledgebeliefsattitudes Behavior Physical Activity and Function Biochemical Data DASH Diet Nutrition Intervention Educann DASH Diet Weight Loss 0 Approximately 20lbs lost will reduce BP Sodium 0 Limit intake to 2300 mgday Alcohol 0 Reduce to less than 2 drinks per day Potassium Calcium and Magnesium Physical Activity 0 30 minsday does decrease BP 49mmHg Smoking Cessation Atherosclerosis Thickening of the walls of the vessels and a loss of vascular elasticity Development of plaque in the vascular wall that will occlude the lumen of the vessel and creates ischemic conditions Factors 0 Family History 0 Age and Sex Men Higher risk gt65 Obesity Dyslipidemia Hype engon Physical Inactivity Atherogenic Diet Diabetes Mellitus Impaired Fasting Glucose and Metabolic Syndrome Obstructive Sleep Apnea OOOOOOOO Nutrition Therapy Assessment History Diagnosis Intervention Weight loss Physical activity Total Dietary Fat Saturated Fat Trans Fatty Acids Monounsaturated fats Omega 3 Fatty Acids Linolenic Acid Polyunsaturated Fats Cholesterol Fiber Nuts PIantSterols Phytosterols Foate Nutrition EducationNutrition Counseling Ischemic Heart Disease 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 xed acids Acids produced via metabolism of CHO3 protein lipid Protein metabolism produces the most acids Lungs cannot eliminate Bases 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 uid 1acidic to 14basic 0 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 Acids can donate H o H2Co3 l H and HCO3 Carbonic Acid l Hydrogen and Bicarbonate A base can accept H CHO 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 Other Chemical Buffers o Disodiummonosodium phosphate buffer system 0 Intracellular proteins 0 Hemoglobin within the RBC Regulation of Acid Base Balance Respiration Control 0 Alters rate and depth of breathing o Regulate C02 concentration via expiration 0 Release or retention of C02 Acidosis increase ventilation l C02 acid loss increase pH Alkalosis decrease ventilation l C02 acid retention l 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 0 Regulate excretion of acids H ions Increase or decrease excretion based on need 0 Renal failure l decrease HCO3 reabsorption Kidneys o Acidosis l increase HCO3 base reabsorption l increase pH 0 Alkalosis l decrease HCO3 base reabsorption l 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 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 Asthma COPD Propofol overdose Chest wall injury ARDS Decrease pH elevated pC02 Slightly elevated bicarbonate due to renal compensation Alerted electrolytes 0 Treatment 0 Correct underlying condition 0 Increase oxygenation 0 Mechanical ventilation if needed 0 0 000300000 Respiratory Alkalosis Relative excess amount of base from reduction of C02 Hyperventilation can be cause 0 Alkalosis increased ventilation and elimination of C02 0 TBI treatment to depress brain swelling 0 Hypoxemia o Stimulant overdose 0 Anxiety 0 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 0 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 stula drainage loss of GI uids 0 Increase C02 lhyperventilation o DKA increase beta hydroxybuteric acid Treatment 0 Treat underlying cause 0 DKA provide insulin 0 Mechanical ventilation o Raise pH to safe level not too quickly 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 0 No speci c 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 Insulin and Counterregulatory Hormones 0 Review and know Table 172 Summary of hormonal control of energy metabolism lnsulin anabolic hormone decrease blood glucose 0 Pancreatic beta cells 0 Promotes glucose utilization o Promotes energy storage glycogen and TG 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 o lnsulin 0 Controls CHO pro and fat storage and suppresses mobilization of stores Normal Blood Glucose Control 0 lnsulin 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 lnsulin binding to aunits gtgt Bunit autophosphorylation to active receptor Activate receptor phosphorylates intracellular transporter GLUT4gtgt glucose uptake o Mitochondria of cell 0 Glucose utilization for energy or triglyceride production Endocrine Control of Energy Metabolism Glucagon catabolic hormone Diabetes Mellitus 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 Gestational Diabetes 0 lnsulin resistancesuppression from placental hormones 0 Increase nutritional intake Type 1 Diabetes Epidemiology 0 510 of diagnosed cases 0 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 lmmune 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 O O O Immune mediated beta cells destroyed by autoimmune process Idiopathic cause of beta cell function loss unknown Pancreatic disease or resection Variability of glucose intolerance based on degree of pancreatic damage 0 Symptoms upon initial diagnosis 0 O O O O O Decrease in insulin l hyperglycemia therefore cells starve l polyphagia hunger Lipolysis and Fatty acids transformed to ketones l Ketoacidosis and pH falls Metabolic acidosis Gluconeogenesis l increase hyperglycemia Polyuria and excess glucose in urine glycosuria and Ketosuria ketones in urine lPolydipsia thirst Weight loos dehydration electrolyte disturbance lncrease respirations to get rid of acids Diagnosis Type 1 Diabetes 0 0 Classic signs and symptoms of hyperglycemia Oral glucose tolerance test 2 hour FBG gt 200 FBG gt126 5 Type 1 Diabetes related autoantibodies Glutamic acid decarboxylase autoantibodies lslet cells autoantibodies O Insulin autoantibodies Diabetic Ketoacidosisprobably present Type 1 Diabetes Mellitus 0 Medical Treatment DMSE Diabetes Self Management Education 0 O O O O O Insulin Risk factors and treatment for short and long term complications Exogenous insulin required Honeymoon Phase Recovery endogenous insulin secretion after initial diagnosis and treatment and insulin requirements may decrease for up to 1 year Nutritional modi cations based on medication administration required Exercise Coordinated team effort Individualized management plan 0 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 o Inhaled insulin Insulin pump 0 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 CH0 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 0 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 lnsulin 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 500Total Daily lnsulin Dose g CHO per unit insulin 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 FixedConventionaStandard 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 0 Bolus insulin before meals 0 Basal insulin once or twice daily 0 More exibility in alterations in activity or food intake schedule Nutrition Therapy for Type 1 and Type 2 DM 0 Table 175 Nutrition therapy for DM 0 Nutrition Diagnosis PES 0 quotImpaired nutrient utilizationquot Carbohydrates quotAltered nutrition related lab valuesquot specify glucose 0 quotFood and nutrition related knowledge de citquot o 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 quotdiabetic dietquot or quotADA 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 ber intakes and glycemic control 0 Excessive amounts of ber needed for improved glycemia Dif cult due to volume of food required GI effects 0 No improvement with RDA of 24gday o Oat ber will decrease cholesterol 0 Current ber recommendations gt5 gday lnconclusive 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 in uencing glycemic response after eating Diet Intervention Protein Fat and Alcohol 0 Protein No effect on blood glucose levels in wellcontrolled DM 0 Uncontrolled DM 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 l 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 o 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 de ciency and increased glucagon l gluconeogenesis o Hyperglycemia 0 Increased ketone production Ketone Production fro increase fat catabolism Metabolic Derangements of DKA Metabolic Acidosis decrease pH 0 Increased ketone levels and C02 production acids 0 Hyperventilation to compensate Osmotic Diuretics o Hyperglycemia l increased serum osmolarity 0 Sodium buffers ketones l increased serum sodium Increased intravascular uid l increased uid to renal tubes l increase urine output Polyuria and polydipsia Hypervolemia shock o Electrolyte Abnormalities o Electrolytes follow water 0 Increased urine output l 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 Gastroporesis Macrovascular diseased o Dyslipidemia CVD Risk 0 Hypertension Microvascular diseased Nephropathy renal failure 0 Retinopathy blindness o Neuropathy decreased sensation 0 Poor wound healing O lt60 non traumatic amputations due to DM Type 2 Dia betes Most common form of DM accounting for 90 to 95 of diagnosed cases 0 Multiple cases Etiology 0 Genetic component autosomal dominant 2014 Study 14 sets of identical twins and only with 1 with type 2 DM Twin with DM Genes involve in in ammation 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 con rms 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 OOOO Pathophysiology Multiple factors can produce glucose intolerance l hyperglycemia 0 Combination of insulin resistance andor beta cell failure insulin de ciency 0 Initial increase in pancreatic insulin secretion to compensate for insulin resistance at target cells hepatic muscle adipose o lnsulin de ciency Eventual decrease in insulin secretion with possible need for exogenous insulin 0 Exogenous insulin required during times of stress 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 HgbA1C OGTT Medications may not be required Acute Complications NKHHS Nonketotic hyperosmolar hyperglycemia syndrome Type 2 o O O O O 0 DKA Acute increase in glucose and serum osmolality without ketone production Do see polyuria polydipsia and weight decrease Type 2 DM produces some insulin therefore no fat burning l ketones Infections Treat Rehydration electrolyte replacement and treat underlying condition Type 1 o Hyperglycemia Type 1 and Type 2 0 Down phenomenon Increased fasting blood glucose and need for insulin upon rising Somogyi effect a 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 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 o 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 o Pramlintide Symlin synthetic for of amylin o Hormone normally secreted with insulin by pancreatic beta cells in response to food intake 0 Decreases gucagon production and hepatic glucose releases therefore decreasing postprandial hyperglycemia o Exenatide Byetta Incretin Mimetic or incretin ine agent Early Use of ncretins 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 ce failure in occurs earlier and s more severe than previously thought Exercise Prescribed for all o Enhances blood glucose uptake and improves insulin sensitivity 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 GLUT 4 translocation 0 Increased utilization of FFA s Research 0 Found improved insulin resistance with both moderate and high intensity aerobic exercise Nutritional Goals 0 Nutrition Intervention O 0000 Weight management Carbohydrates Protein Fat Fiber Gestational Diabetes Mellitus CDM Glucose intolerance with symptoms of hyperglycemia O 0 Screen between 2628 weeks gestation due to alterations in insulin secretion OG39IT 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 Pathophysiology similar to T2DM 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 2nCI and 3rd trimesters 0 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 Preconception counseling 0 Hormonal changes in rst trimester lead to erratic BG levels 0 Frequently adjust meal plan 0 Increased need for insulin in second and third trimesters Adjust meal plan to promote fetal growth and development 0 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 0 Maintain BG levels in or near normal rage lowrisk lipid and lipoprotein pro le low risk blood pressure 0 Individual treatment goals 0 Lifestyle modi cations energy needs and nutrition care based on metabolic pro le 0 To prevent or slow down development of chronic DM complications 0 Dependent upon changes person is willing and able to make 0 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 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 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 eary 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 stulas intractable diarrhea short bowel syndrome Enteral Nutrition 0 Better GI bacteria function Preserved GI immunity o 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 Inability to consume any ora nutrition 0 Facial oral or esophageal cancer or trauma respiratory failure traumatic brain injury with de cits comatose states major GI surgery 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 Gastrointestinal Incompetence 0 Short bowel syndrome with major resection 0 Severe acute pancreatitis or necrotizing pancreatitis 0 Severe IBD in ammatory 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 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 re ux or persistent nausea and vomiting 0 No guarantee thee is abnormal stomach function 0 More permanent types or quotostomyquot o Surgically placed enterostomies Gastrostomies Gtube and jejuostomies Jtube Long term access months 0 Percutaneous endoscopic gastrostomy PEG orjejuostomy 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 intermittent taFPWith LGQW mi and merease aHeiemted ZW as I I I Trophic Very low rate for 24 48 hours small intestine very malnourished stimulate GI tract Continuous Via infusion pump at de ned rate Enteral Nutrition Formulas 0 Based on subtates nutritent density osmoaity and viscosity Protein Carb Lipids Formula Selection 0 Formula selection based on 0 Functional status of GI tract 0 Energy and nutrient content o Digestion and absorption capability of patient 0 Clinical considerations uid and electrolyte status and organ funcUon Types of enteral formulas 0 Standard meet basic nutritional needs 0 High nitrogen for patients with high protein needs wounds 0 Specialized Expensive Low in fat low protein pre digested protein fragments Disease speci c 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 ow 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 Carbohydrate o Dextrose monohydrate 34 kcalg o 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 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 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 Nutrition Intervention Chapter 4 09092014 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 speci c 0 Regular diet 0 Ground foods with gravy and thickened Iiwuids 0 Low sodium diet with a 1200 mIday uid 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 0 Therapeutic diets are bases on a general adequate diet modi ed 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 0 Diet prescription 0 O O 0 Energy Protein Minerals and vitamins Fluids 0 How do we change the quothouse dietquot 0 O O O Calorie level increase or decrease Food restriction add snacks Protein level increase or decrease Consistency liquid soft low ber high ber thickened pureed Rearrange number size and or frequency or meds Fluid restriction Table 44 Nutrition Interventions to Increase Nutrient Density 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 high ber 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 quotMedical Food Supplementsquot 0 Commercial Supplements or Homemade Goal increase nutrient density without increase volume Kcal andor protein increase 0 quotEnteral or parenteral nutrition supportquot 0 Modify rate concentration composition or schedule 0 quotNutrition 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 Honor patient preferences Attention to color texture composition and temperature of foods Patient selection of menus increase consumption Standard HospitalHealth Care Diets Sips and Chips Clear Liquid Diet 0 Seldom used today 0 Fluids some electrolytes and some energy 0 Inadequate in calories ber and all other essential nutrients 0 Use for short periods only Full Liquid Diet 0 Milk based soups liquids o Lactose free options RegularGeneral Diet 0 Basic and adequate o No restrictions Consistency modi cations 0 Adequate o Pureed ground aka mechanical soft Food Intake 0 Monitoring intake to prevent iatrogenic malnutrition If intake is inadequate provide other foods or supplements 0 Can include quotforbidden 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 Outpatient setting more conductive to understanding and overall compliance 0 Impatient settingquotsurvival skillsquot Counseling C3 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 Summary of nutritional therapies and outcomes o Pertinent information such as weight lab results dietary intake Potential drugnutrient interactions Expected progress or prognosis 0 Recommendations for followup services Extremely important when patient discharge on nutrition support 0 Main goals maintain comfort and quality of life Attempt to maintain the patient s ability to function independenUy Communication with family members 0 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 CO 00000 Problems with Food and Drugs Drugnutrient interactions speci c changes to pharmacokinetics of a drug caused by nutrients or changes to he kinetics of nutrients cause by a drug Fooddrug interactions broader term that also includes effects of medication on nutritional status 0 Medication use widespread O O O Prescriptions Complementary and alternative medicine CAM 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 O O O 0 Anything that can affect digestion of food can also affect digestion of drugs Anything that can affect nutrient absorption can also affect drug absorption Anything that can affect nutrient metabolism can also affect drug metabolism Anything that can affect excretion of nutrients can also affect excretion of drugs How do food and Drugs interact o 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 speci c guidelines regarding administration with or without food 0 Additional Concerns 0 Effects or ber fat and other food component on drug therapy Chelation Adhesion of food component to medication ber 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 Metabolic rate altered increase or decrease 0 Change kcal goals 0 Nutrient metabolism may be altered o Dilantin inhibits folate and vitamin D metabolism l megaloblasitc anemia o 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 Increase or decrease excretion from the drug 0 Lasix and hypokalemia Modi cation of Drug Action by food and Nutrients JCAHO National Patient Saftey Goals Enhance or oppose drug effects MAOl s and pressor agents dopamine tryamine o MAOl s inhibitants breakdown of pressors which increases blood pressure 0 Avoid tryamine containing foods aged chesses cured meats Warfarin Coumadin and vitamin K No chance in Vitamin K intake Coumadin Clinics to monitor lNR 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 quotdiet 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 o Elderly Chronic disease 0 Cancer and AIDS 0 GI tract alterations o Malnutrition Body Composition Fetus infant pregnant women 0 Consequences can be severe Medications and Enteral Nutrition Interactions Drugs put in feeding tubes or added to eternal formulas may cause 0 Gel formation 0 Separation or formula 0 Clogged feeding tubes 0 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 Excipients and FoodDrug Interactions Excipient Inactive ingredient added as a buffer binder ler diluent disintegrant avoring dye preservative suspending agent coaUng Allergies and enzyme de ciencies o Lactose o Gluten sensitivity 0 Nutritionally signi cant 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 quotfood medication interactionquot 0 Nutrition Intervention 0 Modi cations of diet or medication to reduce risk of interactions 0 Patient education 0 Nutrition Monitoring and evaluation


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