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2003summary of Power Point Outline.doc
 

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    2003summary of Power Point Outline.doc 2003summary of Power Point Outline.doc Document Transcript

    • Identification of Nutrition Problem(s) sDiabetes is in poor control –hypoglycemic episodes –weight loss –little knowledge of Db and diet Setting Objectives sFormulate a plan for dealing with the problem(s) –Greatest attention to the most severe problem –Plan should be stated in objectives that are quantifiable or measurable –They should be patient centered –Realistic –concise and brief Objectives sWhich of the following offers a pt centered, quantifiable, concise, brief, and realistic statement? sA. I will teach the pt how to select a 1500 kcal diet from the hospital menu sB. Pt will be able to select a 1500 kcal diet from the hospital menu after 3, 1/2 hour education sessions. Realistic Objectives sImportant to take into account –Education level of pt –limitations, physical, mental, emotional –resources –family support Relationship: Nutrition Problems & Objectives sAt least one objective for each problem, in some cases more than one objective sExample: Problem--- Hypoglycemia sObjectives: –1. Find out when Hypoglycemic attacks occur •Diagnostic(Dx) –2. Pt will modify diet following education to reduce incidence of hypoglycemia •Prescriptive(Rx) Objectives sPt will demonstrate an understanding of hypoglycemia following a 1/2 hr education session –Education(Ed) Problem 2: Weight loss sPt will stop weight loss pattern and regain 10# following diet education. Pt wt will be monitored weekly for 3 months. Problem 3:Lack of Understanding of Diabetic Diet sObjective: pt will demonstrate an understanding of CHO Counting by selecting a 1500 Cal diet with 186 grams of CHO evenly distributed over three meals(3 grams per meal) Implementation of Plan sThis includes all of the activities that enable the pt to meet the objectives –Diet prescription –nutrition education –food and nutrient supplements –vitamin and mineral supplements
    • –activities such as referrals (WIC, Food Stamps, social worker, further Dx to clarify causes, etc.) Interventions follow Objectives sObjective 1: Pt will modify diet to avoid pm hypoglycemia –Intervention 1.1: CHO will be distributed throughout the day as follows while in Hospital •Breakfast (8am) 80 g •Lunch (12noon) 85 g •pm Snack (3 pm) 30 g •dinner (6:30 pm) 85 g Interventions: sIntervention 1.2: Pt will be able to select foods from the hospital menu to meet the above pattern following 2, 1/2 hour education sessions on Carbohydrate Counting. Measurement of Success sIf the Objectives and Interventions are written well, in a measurable fashion, evaluation of success is straightforward. –Intervention 1.2: After educating the pt, can he successfully select the appropriate foods to meet the goal? •If he can, then you can proceed. •If not,then a determination of what next is needed may be done Nutritional Index: Evaluation of Intake sIf the pt selects the correct menu, it is not guaranteed that the foods selected will be consumed. Nutritional Index –100 x Actual Intake of nutrient - Desirable – Desirable –If exceeds: % is + –If it is below: % is negative Calorie Count sAs meals are served, RD can’t always be present, so nursing staff records the amounts eaten of the foods served sBased on 1 to 3 days of records, the amount of CHO consumed can be estimated and then compared to the goals. –If they meet the goals, positive feedback to pt –If not, work with the pt to solve problem Nutrition Care Record sDocumentation in pt record of nutritional care process. Offers the following advantage: –1. Helps ensure care will be relevant, complete and effective by recording the problem –2. Allows entire health care team to understand problems and intervention –3. Allows entire team to participate in intervention Nutrition Care Record sAll these work toward helping the pt understand the nutrition care and to be an active participant Factors Describing Contents of Medical Records sAll entries should be labeled: “Nutrition Note”, or what is accepted for your institution sSign Entry; sIf hand written, use black ink Factors to consider in Records sClearly state, don’t imply. sDescribe accurately, and concisely sState relevant info to pt problem
    • sUse appropriate technical language sCorrect spelling, grammar: complete sentences are not always necessary sUse objective style: Pt vs he or she Records sWrite legibly sUse of correct abbreviations –Medical terminology Types of Medical Records s2 Types commonly used –Sources Oriented Medical Record(SOMR) •not as common •each discipline has their own entry area –Problem Oriented Medical Record •more common •consists of 4 parts –1. Data Base 2. Problem List –3. Initial Care Plan 4. Progress Notes Data Base sEstablished at the time care is initiated sIncludes: –Pt profile •description of pt with environmental, social & family factors •Med Hx •family Med Hx •review of systems concerning problems •existing nutrition assessment Problem List sEstablished by Physician Based on Data sDefines Problems –Anything that requires •Dx •or management –Known allergies and intollerances should also be listed Initial Care Plans sPlans for dealing with each problem listed are written by the Physician sOrders made by the physician sThese may include nutrition intervention sThese are most commonly written in SOAP format –Sometimes in DAP format SOAP sAn emulsifiying agent which helps to cleanse and degrease or sA format to record relevant data and plans about the pt being considered sS: Subjective: info from pt, family or other difficult to measure source –e.g.: Pt states, “I hate milk” SOAP sO: Objective –Data from tests, blood values, –ht, wt, age, desired wt –current diet order
    • –medications SOAP sA:Assessment: –Interpretation of pt status base on S and O –Evaluation of Diet Hx –Assessment of Comprehension and Motivation –Practicality of Diet Prescription –Anticipated problems with pt compliance SOAP sP: Plan –Problems listed above in A –Plan or intervention is documented in P to deal with problems –These may be Diagnostic Dx –Therapeutic or prescriptive Rx –Educational Ed SOAP sPhysician will develop plan in SOAP format –Plan may included nutrition intervention –When this happens, then RD does a nutrition assessment based on available data, interview with pt, etc. •This is also written in SOAP format SOAP sOnce initial assessment and problem list is established by each discipline, the plan is implemented –Periodic progress notes are added to describe how plan is progressing –This is where evaluation is stated –These notes also follow SOAP format SOAP = DAP sMore correctly stated: –SO = D –in some medical records, the S and O material is all recorded as Data (D) Assessment: Calorie Needs sHarris Benedict Equation: sMales: 66.47+(13.75xwt)+(5xht)--(6.76xa) sFemales:655.1+(9.56xwt)+(1.85xht)--(4.68xage) sht in cm; wt in kg; age in years sThis results in BEE sTEE=BEE x activity factor x injury factor Activity and Injury Factors sIn bed: 1.2 Ambulatory: 1.3 sInjury: sSurgery: Minor 1.1; Major 1.2 sInfection: Mild 1.2; Mod 1.4; Severe 1.6 sBurns: 40% of body: 1.5; 100% 1.9 sTrauma: Skeletal 1.35; Head 1.6; Blunt 1.35 Energy Needs: Another Method sMaintenance: 25-30 kcal/kg sMaintenance w/ activity: 30-35
    • sElective surgery: 28-30 sAnabolism: 35-40 sTrauma: 35-40 sSevere Trauma, burns: 45-55 sSepsis: 45-55 Children: Calorie needs sAge(yrs) REE per kg per day s0-0.5 320 108 650 s0.5-1 500 98 850 s1-3 740 102 1300 s4-6 950 90 1800 s7-10 1130 70 2000 Adolescence: Calorie Needs sAge REE per kg per day smales s11-14 1440 55 2500 s15-18 1760 45 3000 sfemales s11-14 1310 47 2200 s15-18 1370 40 2200 Medical Terminology Types of Terminology Root Words Modifiers General Abbreviations Unit Abbreviations Root Words Examples of Words Meanings Arterio- Artery Lith- Stone Poly- Many or much Cardi- Heart Sclero- Hard Arterio-Sclerosis hard arteries Modifiers: Prefixes and Suffixes Tachy- Rapid or fast –Tachy-cardia Rapid heart beat –Brady-Cardia Slow heart beat -it is inflammation -emia in blood -stenosis narrowing –arteriostenosis narrowing of artery General Abbreviations ARF Acute renal failure A-V Arteriovenous CBC complete blood count SOB shortness of breath TIA transcient ischemic attack WNL Within normal limits Frequency Designations q.h. every hour q.d. Every day
    • b.i.d. Twice daily q.id 4 x day qod every other day prn as required ad lib as desired Unit Abbreviations ml milliliter mcg microgram cc cubic centimeter hs hour of sleep mEq milliequivalent Diabetes Definition of Diabetes A group of diseases of endocrine system with similar symptoms –Hyperglycemia –premature vascular disease –kidney disease –retinal damage Incidence of Diabetes 3 % of middle aged adults 6.4 % of 65-75 yo: many are unaware 0.4% of young adults Acute care hospitals: –Diabetic patients most common therapeutic diet Public Health Significance: –Blindness, CVD, renal failure, amputations, reduced life expectancy Types of Diabetes D. Insipidus: large urine output D. Mellitus: Primary or Essential –Type 1 also called IDDM, juvenile onset –5 to 10 % of primary pts –appears suddenly –little or no insulin production –control requires diet and insulin therapy –those with poor control called brittle diabetics Diabetes: Types Type 2: also called adult onset, NIDDM about 90% of DM pts decreased sensitivity of insulin or inability to secrete: But insulin is present Onset is gradual Treatment: diet, exercise, hypoglycemic meds (diabenese), sometimes insulin Secondary Diabetes Other conditions cause diabetes to occur Examples: –Pancreatitis: inflamed pancreas due to alcoholism, or infection decreases insulin production –When pancreatitis is reduced, insulin production returns Secondary Diabetes Gestational Diabetes:
    • –During pregnancy, interaction between hormones and glucose metabolism •Human Placental Lactogen and Human Growth Hormone are insulin antagonists Primary Diabetes Genetic Related Disease –Predisposition vs a trait or disease –Dependent on environmental factors Type 1: results from destruction of Beta cells on islets of langerhans in pancreas –2 million cells produce insulin –identical twin studies: one has type one •50% chance of the other getting type 1 Type 1 genetic vs environment Certain viral agents are Beta cyto-toxic –Rubella, mumps, Epstein-Barr(mononucleosis) –Chemical agents: rodentocide Vacor Coupled with genetic factor: –Human Leukocyte Antigen (HLA) –Factors carried on 6th Chromosome –Combination of agent and certain HLA results in Beta Cell Destruction Destruction of Beta Cells HLA + agent = production of antibodies that destroy Beta cells on pancreas many allele HLAs –Each location or loci on the 6th Chromosome has several possible alleles •If certain alleles are present, then problems may arise if the person is exposed to the right environmental factor. Type 2: Environment vs Genetics Monozygotic twins: If one gets type 2, almost all of the other twins will get it. 75% of Type 2 are obese In other countries where obesity is low, so is incidence of Type 2 diabetes Type 2: Mechanism? Probably several –May include poor Beta Cell response to elevated BG –Insulin receptor down regulation Insulin receptors: insulin fills and this opens transport of glucose into insulin dependent cells Insulin Receptor Down Regulation With Obesity and Inactivity –Decrease Insulin Receptor Concentration on Cell Membrane •Fewer insulin filled insulin receptors •Less entry of glucose into cells •Buildup of blood glucose (hyperglycemia) With Increased Activity and Wt loss –Up Regulation of Insulin Receptors –Increased Uptake of Glucose and –Reduced Blood Glucose Pathology of Diabetes Normal Action of Insulin: –Lowers Blood Glucose Concentration •Moves Glucose into muscle and adipose cells
    • •reduces gluconeogenesis by liver from amino acids and glycerol Glucose and CHO Metabolism Insulin increases transport of glucose into –skeletal muscle –adipose tissue –fibroblasts (immature connective tissue) But not –liver --intestinal cells –renal tubules --blood vessels –lens of eye --cells of nervous system CHO and Insulin Insulin Enhances Glucose Utilization in insulin sensitive tissues by enhancing activity of enzymes –Without insulin, glucose isn’t used as well •Glycolytic enzymes are slow: decreased glycolysis •TCA cycle enzymes are slowed: decreased energy available •Glycogen synthesis slowed down •Glycogen breakdown increased CHO and Insulin Insulin slows gluconeogenesis: less glucose made from amino acids –Without insulin, increased gluconeogenesis: Amino acids are converted to glucose Fat and Insulin Insulin slows breakdown of fat and increases formation of fat –Without insulin: fat breakdown increases –fat formation decreases Protein and Insulin Protein synthesis high and degradation of protein low with insulin –Without insulin protein synthesis low, breakdown high –results in high ureagenesis Protein and Insulin Amino acid uptake in muscle and adipose tissue is high with insulin –Without insulin: slow amino acid uptake and increase protein breakdown •Muscle wasting Insulin and Urea and Ketones Insulin slows ureagenesis(slow breakdown of proteins) –without insulin: increased ureagenesis Insulin slows ketone production(fat breakdown without use of CHO intermediates) –without insulin: increased ketones Pathogenesis of Clinical Signs Hyperglycemia due to lack of insulin –When blood exceeds renal threshold(160-200 mg/dl): Glucose excreted in urine •Glucose attracts water: POLYURIA •Causes fluid loss: induces thirst: POLYDIPSIA •Weight loss and tissue wasting induces hunger: POLYPHAGIA –Type 1 vs Type 2: Type2 may not experience polyphagia Complications: Acute Hypoglycemia: Insulin Shock due to:
    • –Failure to eat prescribed diet –delayed meals following insulin –illness: vomiting, diarrhea –sudden increase in exercise –error in insulin dosage –weight loss without decrease in insulin dose –renal insufficiency: kidney doesn’t clear insulin Insulin Shock: Symptoms Hunger, weakness, mental confusion perspiration, cold, clammy skin blurred vision, loss of coordination paralysis, unconsciousness, convulsions death Insulin Shock Treatment Quick source of glucose –By mouth if awake: fruit juice, corn syrup, sugar, candy –Injected glucagon: induces breakdown of glycogen to glucose Rebound hyperglycemia( Somogyi Effect) –glycogen release coupled with increased glucose intake: induces hyperglycemia Acute: Ketoacidosis: Diabetic Coma Accounts for 1 to 3 % of deaths of all diabetics Caused by hyperglycemia due to: –omission of insulin dose –failure to follow diet: overeating –sudden withdrawal of insulin with start of oral hypoglycemic agents –stress: infections, trauma: insulin resistance Symptoms: Diabetic Coma Children: onset pretty quick Tired, weakness, vomiting fruity odor of breath Kussmaul respiration, coma in 12-24 hours Adult onset often slower If untreated: coma, brain damage, death Ketosis and Ketoacidosis Bicarbonate: pH buffer in blood H+ +HCO3- <----->H2CO3<----->H20+CO2 bicarb carbonic ion acid If H+ continues to be loaded from ketone bodies, body has net loss of carbon dioxide and bicarbonate ion. pH can’t be maintained Ketosis and Ketoacidosis Without insulin, ketosis can occur releasing H+’s which eventually overcome body’s ability to buffer pH and keep it at 7.4 or so. Phase 3: (ketosis) bicarbonate normal, pH 7.4, Acidosis is not present Phase 2: (ketoacidosis) bicarbonate lost, pH drops (7.4 to 7.2), moderate acidosis Phase 1: (diabetic coma) pH 7.2, severe acidosis Diabetic coma treatment Diabetes/blood glucose regulated with regular insulin. As control occurs, shifted to longer acting insulin and diet is adjusted to match insulin. If pt is confused or comatose,should not be given food or drink
    • IV fluids and electrolytes are added: IV glucose when BG is controlled Hyperosmolar non-ketotic coma Type 2 diabetics: BG is 900 to 3000 mg/dl –ketosis is mild or absent; no acidosis –often undiagnosed older pt –often another problem precipitates the problem and coma ensues. •E.g.: MI, CVA, Renal Failure, other physical stressing problems •Stress increases resistance to insulin •Increases BG dramatically Non-ketotic coma: Type 2 pt Very high BG induces glucose loss in urine –Increased urine loss –increased hyperosmolar condition in blood –not much ketosis because insulin is present and fat is not broken down –dehydration and high BG causes coma –40-70 % mortality Non-ketotic Coma Treatment Insulin administration K+ replacement due to urine loss through leaching gradual fluid replacement: guard against cerebral edema Chronic Complications General Mechanisms 1. Alternate insulin insensitive pathways Glucose -----> sorbitol ------> fructose Glucose gets into non-insulin dependent cells and sorbitol and fructose are formed –accum & interfere with normal cell function –e.g.: in erythrocytes: sorbitol decreases O2 carrying capacity; tissues become anoxic Chronic Mechanisms: 2. Glycoprotein formation: –With high glucose levels, increased formation of glycoproteins(proteins with CHO attached) –e.g.: Glucose attached to Hb: called glycosylated Hb •HbA1C or HbA1: Indication of long term elevated BG –e.g.: increased glycoprotein makeup of blood vessel basement membranes Basement membrane thickening Glycoproteins thicken basement membrane Makes diffusion of nutrients and waste products more difficult –Results in anoxic, poorly nourished cells especially in peripheral areas •Nutrients can’t get in, wastes can’t get out •Circulation problems that result in wound healing problems. Mechanisms vs Anatomical lesions Angiopathies: accounts for 80% of deaths in diabetics –Micro: small blood vessels –Macro: large blood vessels •especially Type 1: increased serum lipids common –with decreased insulin: increased lipolysis –decreased lipoprotein lipase activity •Basement membrane thickening, poor exchange of nutrients and waste
    • Major areas of concern for Angiopathies Kidney: Nephropathy Nervous tissue: Neuropathy Eyes: Retinopathy Nephropathy 10% of all deaths but 50 + % of all Type 1 Db deaths progresses asymptomatically until renal failure is advanced –Renal Failure discussed later Results from thickening of basement membrane, sclerosis of blood vessels Neuropathy Less life threatening poorly controlled Db results in nerve damage –loss of fine motor control, pain –mechanism probably includes sorbitol and fructose buildup in nervous tissue Retinopathy Common cause of blindness in diabetics Mechanism: basement thickening & sorbitol pathway –poor nutrient, waste exchange –buildup of fructose and sorbitol Diagnosis of Db It has become more simple to Dx Db New standards include –FPG of > 126 mg/dl = Dx Db repeated •no Cal intake for over 8 hours or –Casual PG of > 200 mg/dl plus symptoms or –Two-hour PG of > 200 mg/dl following OGTT •This is not now recommended as routine method Other Db related labs Cortisone GTT –inject cortisone which mimics the the effect of stress –monitor BG for two hours Blood Insulin Radioimmunoassay –Estimate Blood Insulin C peptide chain assay –measure of endogenous insulin production Treatment of Db No current cure Improve quality of life/ prolong life Treatment directed toward –relieving symptoms –decreasing the severity of the disease by enabling body to use glucose –prevent or correct complications –assure adequate nutrition Four Facets of Db Care Control diet Insulin injections and hypoglycemic drugs Exercise Education
    • Hygiene and emotional well-being of the person Insulin About 25% of Db pt use insulin subcutaneous injections Types: –rapid acting: regular insulin: 30 minute onset •Lispro : 5 to 15 minute onset –Intermediate acting: NPH 2 to 4 hour onset –Long acting: Ultralente 5 to 8 hours –Combinations cocktails: some of each of these Oral Hypoglycemic Agents Type 2 diabetics: –Most frequently used: Diabinese (chloropropamide): this attaches to a receptor on the Beta Cells of pancreas and stimulate release of pre-formed insulin –Troglitazone: Approved for use 1997; Directly decreases insulin resistance. Potential liver toxicity. Check serum transaminase 1st 1-2 months;then 3 mo Diet Intervention Steps: 1. Nutrition Assessment 2. Distribute Calories among energy nutrients 3. Distribute CHO between meals 4. Use CHO counting –three levels CHO Counting: Level 1 Goal: CHO Consistency & flexible food choices Intended Audience –Type 1, Type 2, GDM Primary Distribution –MD offices, hospitals, clinics, HMO with RD on staff CHO Counting: Level 2 Goal: Adjust meds/food/ activities based on patterns from client daily records Intended audience: any DB pt who has mastered the techniques of carbohydrate counting Primary Distribution: Settings with RD who has Db training/experience CHO Counting: Level 3 Goal: Adjust insulin dose using ratio of carbohydrate/insulin dosage Intended audience: people on intensive insulin therapy; people who have mastered insulin adjustment and supplementation Primary distribution: Settings with health care team trained in intensive therapy How to count CHO? Food labels Exchanges lists –One CHO = 15 grams CHO –one starch, one milk, one fruit Nutrient reference books Computerized pre-programmed food scales CHO Counting Advantages? Single-nutrient focus More precise matching of food and insulin Flexible food choices Potential for improved blood glucose
    • Clients feel more in charge CHO Counting Challenges? Weighing and measuring food Keeping foor records initially and periodically Recording blood glucose before and after eating Handling numbers and calculations Maintaining healthy eating/Wt management The Gastrointestinal Tract Diseases and Other Problems Diagnostic Tests Motility –radiographic tests Secretions –collections –biopsy Motility Test Barium Swallow –a substance that is radio-opaque –1. Overnight fast –2. Barium swallow: malted milk with barium sulfate –3. Follow movement with fluoroscopy –4. Analysis may reveal filling defects, gastric atony, hyperperistalsis, blockage, etc. Measurement of Gastric Acids Steps: –1. Basal Acid Secretion collected and measured after overnight fast –2. Histamine administered: stimulate gastric secretion –3. Collection of gastric juices again –4. Expressed as maximal acid output or peak acid output Acid Conditions Defined Hyperchlorhydria: Excess acid secretion –Often accompanies peptic ulcers, cholecystitis (inflamed gall bladder), Hypochlorhydria: Low acid secretion –often accompanies pernicious anemia (pt lack of B12 Intrinsic Factor), celiac sprue (malabsorption syndrome), chronic gastritis, pellagra(niacin deficiency) Acid Conditions Defined Hypochlorhydria (con’t) –Occasionally seen in cancer, nephritis, cholecystitis, diabetes. Achlorhydria: no free acid but other peptic activity may be present –pernicious anemia: Often caused by a genetic inability to produce Intrinsic Factor: Helps B12 Absorption General Dietary Considerations Secretory activity of stomach, small intestine, gall bladder, pancreas and liver Motility of tract Bacterial flora Comfort and ease of digestion maintenance and repair of mucosa structure Diseases of the Esophagus Esophagitis Hiatal Hernia Surgery of the Mouth or Esophagus Tonsillectomy Cancer of Mouth, Pharynx and Esophagus Esophagitis Function of Esophagus:
    • –Esophagus moves food from mouth to the stomach through diaphragm and through lower esophageal sphincter –Peristaltic wave motion –Difficulty in swallowing: sDue to neurological problem: part of rehab from stroke, MVA, etc Esophagitis Usually occurs in lower esophagus –Following gastric reflux which irritates esophageal mucosa: often called heartburn Acute esophagitis: –due to irritating food, viral inflammation or intubation Chronic or Reflux E. –Due to repeated reflux from stomach –hiatal hernia, vomiting, reduced LES pressure Lower Esophageal Sphincter Many factors affect competency of LES –Decreases with: –Pregnancy –oral contraception –late menstrual period Esophagitis: Nutrition Care Objectives: –1. Prevent irritation of inflammed tissue –2. Prevent esophageal reflux –3. Decrease the irritating capacity or acidity of gastric juice Nutrition Care Liquid diet may decrease abrasive nature of foods on the inflamed tissue –OJ, tomato juice, etc are acidic and might cause irritation –Chili peppers, black pepper may be irritating Some foods decrease LES pressure and should be limited –alcohol, peppermint, chocolate, caffeine Nutrition Care Timing of the meal: Restrict food before bedtime or lying down –less gastric content to push against LES Obesity increases pressure on LES –Wt loss may improve Esophagitis: Drug Treatment LES Pressure increased with –Bethanocal(cholinergic drug) –metoclopramide (dopamine antagonist) –some antacids, which also lower gastric acidity Gastric Acid decreased with –cimetidine(histamine receptor blocker) Barrier for inflamed tissue –Alginates(Gaviscon) Hiatal Hernia Common cause of gastroesophageal reflux and esaphagitis Diet Therapy: –No eating 3 hours before reclining or sleep –Avoid foods that are know to cause heartburn: scaffeine, chili powder, black pepper, peppermint, chocolate Surgery of Mouth and Esophagus If oral intake is possible –liquid formulas; pureed foods If oral intake is not possible
    • –gastrostomy of jejunostomy tube to provide enteral feedings sThese can be formulas or blenderized table foods Tonsillectomy Removal of inflamed or infected lymphoid tissue in the throat –First 24 hours, cold liquids and soft foods such as milk shakes, juices. –By day 2 warm fluids and soft foods –By day 3 to 5: Normal diet Cancer of the Oral Cavity, Pharynx, Esophagus Treatment: resection of tumor, chemotherapy, radiation –May interrupt or cause problems with chewing and swallowing Nutrition Support: If GI tract functional: Enteral feeding If GI tract not functional: parenteral nutrition When Oral intake is possible: –soft, moist foods easy to chew and swallow –small frequent meals of high-caloric density The Stomach Indigestion Acute and Chronic Gastritis Gastric Surgery Carcinoma of the Stomach Gastric and Duodenal Ulcers Indigestion: Dyspepsia Causes are many: Discomfort in GI tract May be symptom of gallbladder disease, ulcer, chronic appendicitis –Further intervention may be required Cause may be unknown and associated with stress, overindulgence, rapid eating –Note eating patterns , and suggest changes Acute Gastritis Similar symptoms to esophagitis Causes may be overeating, overuse of EtOH, tobacco, over use of aspirin Trauma, surgery, shock, renal failure, fever, radiation therapy, Helicobacter pylori infection Nutrition: rest stomach for 24-48 hours: no food; Then add liquids and advance as tolerated Chronic Gastritis Cause unknown: often precedes cancer or ulcer Infection of Helicobacter pylori ? Nutrition care: General good nutrition –adequate calories; avoid gastric irritants and stimulants –Avoid large meals that distend the stomach and induces pain Atophic gastritis Loss of parietal cells –inability to produce HCl (achlorhydria) and intrinsic factor Reduced B12 status Requires B12 injections Gastric Surgery Treatment for damage that is not reparable –Ulceration –Tumor Billroth 1 –Dumping Syndrome: not much absorptive surface Intact nutrients to lower bowel with water influx Gastric Surgery Billroth 2 –Less dumping because of conservation of more absorptive surface Pyloroplasty
    • –Enlarge the Pyloric valve to increase rate of chyme passage to duodenum Helps relieve gastric pressure in esophagitis May result in duodenal reflux Vagotomy Vagus nerve severed to reduce rate of gastric emptying and HCl secretion –May result in dumping syndrome Dumping syndrome: –When food is dumped into the Jejunum instead of gradual movement without total digestion –Results in hypertonic contents drawing in water from surrounding tissue Dumping Syndrome Results in diarrhea, cramping plus Decrease in blood volume: –low cardiac output, sweating, tachycardia, electocardiographic changes, weakness Treatment: Use of fiber to slow rate of glucose absorption may be useful Laying down following eating to slow gastric emptying Dumping Syndrome: Nutritional Management High Pro, moderate fat, high calorie –1.5 - 2 g/kg PRO –35-45 Cal/kg –use of MCT –Lie down after eating –Avoid liquids with meals –Avoid foods not well tolerated –Eat small meals Alimentary Hypoglycemia Post-meal hypoglycemia: weakness, perspiration, hunger, nausea, anxiety, tremors Caused by rapid absorption of glucose and resultant over-secretion of insulin –BG drops quickly Treatment: eat small meals; avoid concentrated sweets Stomach Surgery: Malabsorption Billroth 2: bypassing duodenum –Results in steattorhea, dumping syndrome –secretion of secretin and pancreozymin by duodenum mucosa Normally these stimulate duodenum to secrete enzymes and bicarbonate Foods aren’t as well digested Pancreas atrophies Anemia: Post-gastric surgery Caused by iron deficiency due to poor iron absorption or bleeding –HCL in stomach changes Iron to Ferrous form (Fe+2) –With reduced time in stomach, less exposure to acid and less change to ferrous iron –Less absorption of iron results B12 deficiency because of IF reduced production Anemia May require supplementation of iron, B12, folate May require B12, iron parenteral administration Gastric and Duodenal Ulcers Peptic Ulcer: Erosion of gastric or duodenal mucosa Etiology: Helicobacter pylori infection –Gastric: acid production normal or low –duodenal reflux into stomach –Intake of NSAID’s such as aspirin –Duodenal: 2/3 have normal acid production –increased gastric emptying; inability of duodenum to handle acid; low bicarbonate Ulcer Management Medical:
    • –1. Neutralization of acid –2. Reduction of acid secretion in stomach –3. Preservation of epithelial tissue –4. Eradication of H. pylori Ulcer Management 1. Neutralization: Antacids –Aluminum hydroxide: good acid neutralization but binds phosphorus and inhibits absorption –Calcium carbonate: good acid neutralization but stimulates gastrin secretion but probably better than Al hydroxide 2. Reduce acid secretion: Cimetidine (Tagamet)Blocks histidine receptors Ulcer Management 3. Cytoprotection: such as arachidonic acid –Helps to form a protective mucosal layer over ulcer 4. Antibiotics: tetracycline –fights off H. pylori –combined with antiacid, even better results Nutrition and Ulcers 1. Reduce acid secretion 2. Maintain acid resistance 3. Limit Pt discomfort 4. Restore good nutritional status Nutrition Eat three small meals a day Avoid caffeine and alcohol and cigarettes Avoid aspirin and other NSAID’s Avoid known irritant foods Eat in a relaxed atmosphere Take antiacids 1 to 3 hours after meals and before bedtime Intestinal Disease Principles of nutrition care: –Highly individualized based on pt care –Fiber content and residue are important considerations Residue: the portion of diet that contribute to the content of the feces Some disease states require restriction of residue e.g.: acute inflammatory bowel disease: (IBD) Reduced fecal output is part of treatment Minimum Residue Diet Avoid whole-grain breads, cereals, brans, seeds, peanuts, popcorn, legumes, potatoes, coconut Avoid fruits and vegetables: use juices instead Avoid connective tissue in meat Limit milk and milk products to 2 cups per day Minimum Residue Diet Use of elemental formulas may be helpful –Vivonex from Novartis Nutrition Symptoms of Intestinal Dysfunction Flatulence Constipation Diarrhea Steattorhea Diseases of the Small Intestine Celiac Disease Tropical Sprue Intestinal Brush Border Enzyme Deficiencies such as Lactase Def. Celiac Disease(Gluten-Sensitive Enteropathy) Caused by a reaction to gliadin, EtOH-soluble portion of gluten
    • –Mechanism unknown –Environmental and genetic components –Gliadin may sensitize T lymphocytes to release lymphokine that damages the intestinal cells –Usually affects cells of jejunum or ileum causing malabsorption Celiac disease: Symptoms Onset may be early: children when they initiate foods with gliadin or middle age Kids: diarrhea, failure to thrive, projectile vomiting, 10 + stools/day Adults: weight loss, weakness, steattorhea, with or without diarrhea Celiac Nutritional Care Removing gliadin from diet –wheat, barley, buckwheat, rye and oats –sub with corn, potatoes, rice, soybean, tapioca, and arrowroot Supplementing vitamins, minerals, protein, electrolyte replacement Secondary problems such as lactose intolerance requires lactose restriction Tropical Sprue Unknown origin: found in tropical areas, perhaps associated with exposure to coliform bacteria –increased risk with nutritional deficiency Symptoms: D, Anorexia, abdominal distention, night blindness, glossitis, stomatitis, cheilosis, pallor, edema Treatment: –tetracycline, with folate and B12 supplements Enzymes Deficiencies Three types of occurrence: –1. Rare congenital, appears in infancy –2. Secondary to other diseases: Crohn’s disease, celiac disease –3. Genetically acquired form: appears after childhood Examples: Lactase deficiency most common Lactase Deficiency 70 % of world’s adults are unable to digest Lactose, especially in blacks, Asians and South Americans Even those who retain Lactase, activity is reduced in adulthood to about 10% of neonatal value Dx: Lactose tolerance test: 50 g lactose given; less than 25 mg/dl glucose in blood Lactase Deficiency: Nutrition Care Reduce or remove lactose from diet Some milk products with reduced lactose can be tolerated –aged-cheeses Lactaid-treated milk: pre-digests lactose Diseases / Problems of Large Intestine Inflammatory Bowel Disease (IBD) –Crohn’s disease –Ulcerative colitis Irritable Bowel Syndrome(IBS) Diverticular Disease Colon Cancer Surgeries Inflammatory Bowel Disease Onset 15 to 25 years in both sexes Crohn’s: may start in small intestine and spread even after partial resection Course varies: may become benign and disappear, may cause blockage or fistula Symptoms: fatigue, anorexia, weight loss, watery to loose stools (ileal involvement); incontinence, rectal bleeding(colon involvement) Ulcerative Colitis Chronic inflammation & ulceration of large intestine mucosa: always initiates in rectum Most common in 20 to 40 yos or 50 to 60 yos Symptoms: rectal bleeding, D, dehydration, electrolyte imbalance, anemia,
    • Treatment for IBD Surgical resection –effective in Ulcerative colitis: ends threat of colon cancer and recurrence in most cases –may not be effective in Crohn’s Disease Nutrition: Enteral nutrition to prepare for surgery appears to work IBD: Nutrition Care Fairly Complicated and individualized based on the current state of disease. Usually leads to malnutrition, food sensitivities and intolerances Objective is to find a means to supply nutrients which don’t induce intestinal distress IBD: Nutrition High energy: 40 to 50 kcal/kg High Protein: 1 to 1.5 g/kg Frequent feedings Steattorhea induces loss of Ca, Zn and Mg –assessed and supplemented –Fat 25% of kcal; use of MCT oil IV EPA may be helpful IBD: Nutrition Lactose avoidance due to secondary lactase deficiency High fiber diet as a norm, but may be limited during acute flare-ups Anemia: iron, B12, and folate supplements TPN may be necessary if needs are not met by GI tract Irritable Bowel Syndrome(IBS) Abnormal stooling pattern lasting longer then 3 months D, Constipation, excessive flatulence, rectal pain, blood in stools Cause unknown Diet: normal with high fiber(20 to 30 grams) if this fails then Antidiarrheal agents, stress reduction Diverticulosis, -itis Outpocketing of colonic wall due to herniation May result from low fiber diet 10 to 15% develop diverticulitis: ulceration and perforation causing blood loss and infection –10 % of those requiring surgery die Diet: High fiber; low residue during flareup Surgery:Resection Effect depends on where and how much is removed –If ileocecal valve is intact: regulates flow of material from small to large intestine –If removed: uncontrolled movement and diarrhea Ileostomy/Colostomy Ileostomy:When entire Colon is removed –New opening for waste removal Colostomy: When rectum removed Nutrition: depending on the GI tract removed, specific recommendations –eg: if terminal ileum is removed: B12 supplementation or injection required THE GASTROINTESTINAL TRACT Diseases and Other Problems Diagnostic Tests Motility – radiographic tests Secretions – collections – biopsy Motility Test Barium Swallow
    • – a substance that is radio-opaque – 1. Overnight fast – 2. Barium swallow: malted milk with barium sulfate – 3. Follow movement with fluoroscopy – 4. Analysis may reveal filling defects, gastric atony, hyperperistalsis, blockage, etc. Measurement of Gastric Acids Steps: – 1. Basal Acid Secretion collected and measured after overnight fast – 2. Histamine administered: stimulate gastric secretion – 3. Collection of gastric juices again – 4. Expressed as maximal acid output or peak acid output Acid Conditions Defined Hyperchlorhydria: Excess acid secretion – Often accompanies peptic ulcers, cholecystitis (inflamed gall bladder), Hypochlorhydria: Low acid secretion – often accompanies pernicious anemia (pt lack of B12 Intrinsic Factor), celiac sprue (malabsorption syndrome), chronic gastritis, pellagra(niacin deficiency) Acid Conditions Defined Hypochlorhydria (con’t) – Occasionally seen in cancer, nephritis, cholecystitis, diabetes. Achlorhydria: no free acid but other peptic activity may be present – pernicious anemia: Often caused by a genetic inability to produce Intrinsic Factor: Helps B12 Absorption General Dietary Considerations Secretory activity of stomach, small intestine, gall bladder, pancreas and liver Motility of tract Bacterial flora Comfort and ease of digestion maintenance and repair of mucosa structure Diseases of the Esophagus Esophagitis Cardiovascular Disease Definitions: CVD Coronary Heart Disease (CHD) also known as coronary artery disease (CAD) or ischemic heart disease (IHD) Costs $138 billion/yr in 59 million in US have some form of the disease –CHD, stroke, HTN, rheumatic heart disease Mortality CHD is the leading cause of death in men and women in the US; 480,000 people died in 1992 from CHD 1960: 286 per 100,000 died of CHD 1990: 152 per 100,000 died of CHD Why the drop? Etiology of CHD Lack of blood flow to the blood vessels surrounding the heart andserving the myocardium Major cause is atherosclerosis –Slow progressive disease that is multifactorial –Plaque or atheromas: build up of intimal layer lipids, calcium, fibrin; after arterial wall injury
    • –Increased risk with injury due to HTN, elevated cholesterol, smoking, Db, obesity, high sat fat Pathology of Atherosclerosis Progression from fatty streaks to –intermediate lesions to –fibrous plaques to –complicated lesions •These contain a core of lipid surrounded by a cap of smooth muscle cells, macrophages, and collagen Dx: invasive angiography (cardiac catheterization) –Dye is injected and x-rays are taken Catheterization X-rays reveal narrowing and blockages due to atherosclerosis Other indications of CHD: –Hx of MI and myocardial ischemia –Hx of coronary artery surgery –High white blood cell count •Each Standard Deviation increase in WBC: 42% increase in CHD incidence Thrombosis: Clot Thrombus can contribute to the formation of the plaque and to blockage –Increased risk with cigarette smoking, epinephrine levels due to stress and hypercholesterolemia Results in Myocardial Infarction –death of tissue Risk Factors for CHD Male sex > 45 yo or Female > 55 yo Fam Hx CHD (MI or sudden death before 55 yo) cig smoking HTN (> 140/90) Low HDL (< 35 mg/dl) Db Hx cerebro- or peripheral vascular disease National Cholesterol Ed Prog Primary Prevention based on Total Cholesterol, HDL-c, and LDL plus risk factors Secondary Prevention: in adults with evidence of CHD Types of Classifications Phenotype classification –lipoprotein abnormality is described but the etiology is not given Genetic Problem –Etiology of problem is given –This explains the reason for the lipoprotein abnormality Phenotype Classification Phenotype Lipoprotein Abn Lipids Type I high chylomicrons hi Tri &Chol Type II a hi LDL hiChol
    • Type II b hi LDL,IDL, VLDL hiChol hi Tri Type III hi IDL, VLDL-rem ditto Phenotype Classification Phenotype Lipoprotein Abn Lipids Type IV hi VLDL hiChol hiTrig Type V hi Chylo, hi VLDL hi Tri hiChol Genetic Hyperlipidemias Familial Hypercholesterolemia –similar to Type II a with hi LDL-c –LDL receptor dysfunction •Absent or non-functional •Heterozygotes have one abnormal and one normal gene –1 in 500 people –serum cholesterol averages 360 mg/dl from birth –requires aggressive medical intervention to delay or prevent CHD FH: Homozygotes More severe hypercholesterolemia and atherosclerosis –MI or death in first or second decade of life –Heterozygotes often have CHD onset at 45 in males & 55 in females –Tx for Homozygotes: plasmapheresis to remove LDL’s biweekly –Tx for hetero: Step II diet with drugs Polygenic Familial Hyperchol Multiple gene defects: not all have been documented –Dx LDL above the 90th percentile –apo E-4 allele is common in polygenic FH –Tx: Step II diet with medications Familial Combined Hyperlidemia LDL-C and Triglycerides above 90th %tile Overproduction of apo B-100 –Too much VLDL produced Several lipoprotein patterns seen –1. hyperLDL with normal TG Type II a –2. HyperLDL with Hyper TG Type II b –3. Hyper VLDL Type IV Tx: Step II diet, wt reduction, Db control increased activity, Medication Familial Dyslipdemia High TG and low HDL-C Dx: at least two members of family have over 90th %tile and less than 10th %tile respectively Other associated problems: android obesity, insulin resistance, type 2 Db, HTN Tx: lifestyle intervention similar to other hyperlipidemias Familial Dysbetalipoproteinemia
    • Type III; relatively uncommon –1 in 5000 persons in US –Catabolism of VLDL and Chylomicrons are slow due to abnormal apolipoprotein E •E-2 instead of E-3 or E-4 Dx: determining the isoforms of apo E presents with: age, hypothyroidism, obesity, Db, and other dyslipidemias Tx: like others: Step II diet, wt loss, Db Tx Pharmacologic Tx of CHD % classes of agents used 1. Bile acid sequestrants –Tie-up bile and cholesterol in gut –Decrease absorption of Ca, fat, fat-sol vitamins, folate, MCT and glucose –Cause nausea and vomiting Pharm. agents 2. Nicotinic acid (niacin) –reduces formation of cholesteol –side effects: N/V/D; liver dysfunction; peptic ulcer, flatulence, flushing 3. HMG-CoA Reductase Inhibitors –Lovastain: inactivates rate limiting enzyme in Chol production –Side effects: N, abdominal pain, change in bowel function Pharm. Agents 4. Fibrates: –Gemfibrozil: Abdominal pain, dyspepsia, D, Constipation, flatulence 5. Probucol: –changes in bowel function, N Medical Intervention Coronary Angioplasty –Percutaneous transluminal coronary angioplasty (PCTA) –Use of a balloon to breakup the plaque deposit –local anesthetic –about 400,000 performed/yr –Most common problem is recurrence of blockage –Diet: Step II diet or more severe for motivated pt Medical Intervention Coronary Artery Bypass Surgery (CABG) Vein from the leg or artery from the chest is used to bypass the occluded vessel in the heart 468,000 surgeries performed/yr Diet includes Step II when pt can tolerate solid food Hypertension Definition: –Systolic BP of 140 or higher and/or –Diastolic BP of 90 or higher –50 million in US
    • –95% have primary or essential HTN •Cause cannot be determined –Primary prevention includes: wt loss, increased physical activity (30 min 3x/wk), sodium restriction(1800 mg/d) and limit EtOH < 2 drinks/d Pharmacologic Treatment of HTN Most Common are: –1. Diuretics: increase loss of fluid and reduce total volume of blood: Thiazide •Reduction of pressure •Also increase K loss in urine •Requires increase in K in food/ or supplements –2. Beta-blockers: Block nerves that cause reduction in arterial lumen which increases pressure •Propranolol Congestive Heart Failure CHF is a result of process where heart gradually loses the ability to provide blood flow to the rest of the body –CHD, HTN, Renal disease can all lead to CHF –About 3 million in US –92 % of deaths from CHF over 65 yo –Risk factors: Db, HTN, left ventriculare hypertrophy, heart disease CHF Nutritional Care Cardiac Cachexia: lean body and fat store loss due to reduced intake of food but also elevated tumor necrosis factor in circulation Wt loss may be masked by fluid retention Tx: sodium restriction; individualize from moderate(4 g: NAS) to severe(250 mg: extreme diet rarely used) Renal Disease Kidney Function: to maintain normal composition and volume of the blood Anatomy of Kidney l1 million Nephrons: Consists of qGlomerulus connected to a series of tubules which can be broken into functional segments •proximal convoluted tubule •loop of Henle •distal tubule •collecting duct qGlomerulus surrounded by Bowman’s capsule •mass of capillaries: blood is filtered to produce ultrafiltrate Kidney Function lUltrafiltrate contains blood material that is less than 6500 molecular weight lNo blood cells lNo protein lNo other large molecules Kidney Function lWater and electrolyte conservation qAntidiuretic Hormone (ADH) secreted by posterior pituitary when osmolality of blood rises •Shuts off when osmolality falls
    • qKidney can concentrate urine as much as 1200 mOsm or as dilute as 50 mOsm qUrinary volumes vary based on need to excrete extra fluid Kidney Function lADH: Diseased kidney doesn’t respond to ADH as well and tends to allow water retention qReduced urine output in Renal patients qoliguria:less than 500 ml/day Kidney Function lOther Waste Products accumulate with renal failure lAzotemia: Build up of urea, uric acid, creatinine and ammonia Kidney Function: Blood Pressure lRenin-Angiotensin System: qDecreased blood pressure induces glomerular cells to secrete renin •Acts in plasma to form angiotensin I •converted to angiotensin II –vasoconstrictor: elevates BP –stimulates aldosterone secretion by adrenal glands »Causes kidneys to retain water and sodium qIn diseased kidney, this mecahism may be less functional: high or low blood pressure/water retention Kidney Function: RBC Formation lErythropoietin: kidney produces this hormone qActs on bone marrow to produce RBC’s qIndiseased kidney, lack of Erythropoietin: •results in severe anemia qRenal patients are given injections of erthyropoietin to stimulate RBC rpduction Kidney Function: Ca, P lVitamin D activation happens in kidney lWith diseased kidney, this is slowed down lLess active vitamin D qResults in less absorption of Ca in gut qmore bone release of Ca and weak bones •Poor bone status Diseases of the Kidney lGlomerular Diseases qNephrotic syndrome qNephritic syndrome lTubule and interstitium diseases qAcute renal failure (ARF) qOther tubular diseases qPyelonephritis Nephrotic Syndrome lGroup of diseases cause qProteinloss through glomeruli qhypoalbuminemia with edema •concentrates blood qhypercholesterolemia qhypercoagulability qabnormal bone metabolism Nephrotic Syndrome lMost often caused by: qDiabetes qsystemic lupus eryththematosus(SLE)
    • •connective tissue disorder of immune origin •causes damage to many systems and noted by skin eruptions, arthritis, neurological problems qamyloidosis:abnormal deposits of amyloid in tissues •a starch-like glycoprotein primary cause unknown •secondary due to TB and rheumatoid arthritis Nephrotic Syndrome: Nut Care lObjective: replace lost protein in urine lHigh Biological Value Protein from 0.6 to 1.5 g/kg/d lEnergy 35 to 50 kcal/kg/d for adults; 100 to 150 kcal/kd/d for kids qto spare protein lEdema: mild sodium restriction lHypercholesterolemia: lipid lowering drugs with chronic Nephrotic Syndrome Nephritic Syndrome lInflammation of capillary loops of glomerulus caused by several disease states qacute glomerulonephritides: often caused by streptococcal infection damaging glomerular barrier to blood cells •Blood in urine •Sudden onset/short duration •May proceed to complete recovery, chronic nephrotic syndrome, End Stage Renal Disease(ESRD) Nephritic Syndrome: Nut Care lObjectives: maintain good nutritional status lOften focus is on treating underlying cause lUsually no need to restrict protein, or K unless uremia or hyperkalemia exists lSodium restriction with HTN Diseases of Tubules & Interstitium lAcute Renal Failure: Sudden reduction in Glomerular Filtration Rate (GFR) lGFR: the quantity of glomerular filtrate formed per unit of time by the kidneys lResults in the inability to filter wastes from the blood lCauses are many ARF : Causes 3 Categories lPrerenal lIntrinsic lPostrenal Obstructive lTreatment: remove underlying problem lCourse of the problem depends on underlying cause ARF: Intrinsic Problems lPossible causes: qtoxicdrugs qallergyto drugs qprogressive glomerulonephritis qischemia leading to acute tubular necrosis •infections, severe trauma, surgical accidents •mortality about 70 % •treated with hemodialysis to reduce acidosis •Diuretic phase then return of waste elmination ARF: Nut Care
    • lEarly: TPN may be used to maintain nutritional status lHemodialysis, peritoneal dialysis or continuous arteriovenous filtration (CAVH) qCAVH uses small ultra filtration membranes to produce an ultrafiltrate •this is replaced with parenteral nutrition fluids to prevent fluid overload ARF: Nut Care lProtein:Early, TPN with Glucose and some protein in form of essential A.A.s such as Aminosyn- RF(Abbot Labs) lAmount of Protein dependent on pt q0.3 g/kg and progress toward 0.8 to 1 as pt improves lEnergy needs are high: 50 kcal/kg most from CHO and lipids via TPN or enterally with addition of formulas (Polycose, Ross) Pyelonephritis: UTI lNo specific nutritional management lChronic cases: cranberry juice qReduced adherence of E.coli to epithelial walls of urinary tract Nephrolithiasis: Kidney Stones l10 % of men and 3 % of women have a stone during adulthood lFormed in kidney when substances in urine reach levels that cause crystallization lMay be made from calcium salts, uric acid, cystine, struvite (ammonium, magnesium, and phosphate) Kidney Stones: treatment lIn all cases: High fluid intake (1.5 to 2 liter/day) to keep urine dilute lOther intervention depends on the cause l80% of stones composed of Ca oxalate or Ca phosphate lCauses are multiple: qhyperparathyroid ism, hyperuricosuria, renal tubule acidosis (RTA) Kidney Stones: Treatment lRemove underlying cause: qe.g.: remove parathyroid adenoma if Hyperparathyroid qTreatRTA with medications to reduce acidity qHypercalciuria seldom treated with low Ca diet lNutrition: Reduce Oxalate in diet, add additional Ca to diet to tie up oxalate in gut Kidney Stones: Uric Acid lAssociated with gout, an acid urine lTreatment with raising urine pH to 6 to 6.5 through high alkaline-ash diet qmilk,nuts, vegetables except corn and lentils, all fruits except cranberries, prunes, plums, molassess qavoid breads, meats, cheese, pnut butter, and vegies and fruits above Glomerular Filtration Rate (GFR) lDefn: total plasma volume filtered by the kidney per unit of time lNormal is 120 ml/min lGFR = Urine X Urine volume inulin l _____________________ l Plasma inulin lCan also be done with creatinine Normal Kidney Function lHow long does it take to filter all of a person’s blood? HINT: 6 L of blood Other Labs Used to Determine Kidney Function lBlood Urea Nitrogen(BUN): How well urea is cleared by the kidney
    • qNormal is 8 to 23 mg/dl qHigh is indication of poor fxn lCreatinine: end product of creatine metabolism in muscle; cleared in urine qNormal is 0.6 to 1.6 mg/dl qHigh is indication of poor function Progressive Nature of Renal Disease lSlow, steady, decline in renal function lNutrition intervention depends on Renal Function determined by GFR lProtein Intake: major concern lProtein GFR l0.8 g/kg(60%HBV) >55 ml/min l0.6g/kg(60% HBV) 25-55 ml/min Progressive Renal Disease lProtein restriction: individualized qMust be weighed against possible protein malnutrition qIfelected, careful monitoring of protein status must be made with anthropometric and lab values End-Stage Renal Disease lCan be caused by several disease states l90 % have Db, glomerulonephritis, or HTN lProblems include: qinability to remove wastes qmaintenance of fluid and electrolyte balance qproblems with hormone production lUremia: high BUN, a major problem Uremia: Symptoms lWith BUN at 100 and Creatinine at 10-12 symptoms usually show up lGenerally: weakness, nausea, cramping, itching, metallic taste lFurther intervention required ESRD: Treatment lTransplantation lDialysis qHemo qPeritoneal •intermittent peritoneal dialysis (IPD) •Continuous ambulatory PD(CAPD) Transplantation: Nut Care lBased on metabolic effects of immunosuppressive meds: corticosteroids and cyclosporine lCorticosteroids: qincrease PRO metabolism, hyperlipidemia, Na retention, wt gain, glucose intolerance, reduced Ca and Vit D metabolism lCyclosporine: hyperkalemia, HTN, ^ lipids Transplant Nutrition Care lFirst month Post-transplant: qPRO: 1.5 to 2 g/kg qEnergy:30 to 35 kcal/kg qmoderate Na restriction to prevent fluid retention (80-100 mEq/d); monitor K and P lAfter one month: qPRO: 1 g/kg
    • qAdjust Kcal to maintain/achieve Ideal weight Hemodialysis lMost common form of dialysis lFistula created by surgery connects an artery and a vein usually on the forearm qmay require an artificial vessel to enlarge the vessel qLarge needles are temporarily inserted to allow blood to exit the body and circulate through the dialysis machine qUsually required 3 x / week for 3 to 5 hours Hemodialysis: Nut Care lEnergy: 35 kcal/kg IBW lPRO: 1 to 1.2 g/kg; 1.2 to 1.5 if needed lFluid: 800 ml/d + urine output lNa: 2-3 grams/day lK: 2-3 grams/day lP: 1 to 1.2 g/d Peritoneal Dialysis lMakes use of the semi permeable membrane of the tissues in the peritoneal cavity lCatheter surgically implanted in the abdomen lDextrose containing dialysate is instilled into abdomen qwastes diffuse into dialysate Peritoneal Dialysis lFluid is withdrawn and discarded; new fluid is then instilled lLess efficient then hemo l10 to 12 hrs, 3 x week lPRO: 1.2 to 1.5 g/kg due to larger Pro loss lEnergy: 30 kcal/kg (40-50 for repletion) lFluid, Na, K, and P same as hemo Continuous Ambulatory Peritoneal Dialysis(CAPD) lSimilar to peritoneal but the dialysate is exchanged manually without the help of a machine lExchanged 4 to 5 x /day for 24-hour treatment lIncreased loss of Protein, increased absorption of Dextrose, up to 800 kcal/d CAPD Nut Care lPRO: 1.2 to 1.5 g/kg lEnergy: 25 kcal/kg lFluid: ad lib lNa: 6 - 8 grams / d lK: 3-4 g/d lP: 1.5 to 3 g/d lWeight gain is the norm for CAPD patients ESRD: Other concerns lPsychological Support: large life changes qDepression: lack desire to eat qThirst, lack of taste and taste changes due to uremia lVitamin D status: activation of Vit D happens in the kidney qloss of function results in low status qVit D supplements
    • Complications lLow Vit D results in low Ca in blood qTriggers release of PTH; this removes Ca from bone qResultsin osteitis fibrosa cystica: a demineralized bone disease causing dull bone pain qSerum P remains high because it is not cleared by kidney qCalcium intake should be high, P should be low Complications of Renal Disease lCalcium supplements help bind P in the gut qCa carbonate, acetate, lactate or gluconate qCa citrate is avoided because it helps absorb Al lVit D orally or intravenous helps with hypocalcemia lFluoride serum levels often high in dialysis pt: contributes to decalcification of bone qDeionized Fl containing water before used in dialysis Iron/Hemoglobin status lKidney produces erythropoietin which induces bone to produce RBCs qSynthetic EPO injections are used to treat lVitamin deficiencies may occur qReduced intake with P restriction: many P rich foods are also vitamin rich, e.g.: fruits and vegetables qWater soluble vitamins are dialyzed off Complications lVitamin supplements given: some specially formulated for dialysis pts qNephrocaps: Fleming and Co. lCarbohydrate: glucose intolerance due to tissue resistance to insulin qmay require control of glucose in diet in hyper qmay require addition of dextrose to dialysate in hypoglycemic Complications lAtherosclerosis: most frequent cause of death in hemodialysis qCaused by underlying disease: HTN, diabetes, nephrotic disease qPlus abnormal lipid metabolism in ESRD qIncreased synthesis of VLDL and decreased clearance qdiet restriction of fat; and use of lipid lowering drugs may be used with high risk ESRD pts Use of Parenteral Nutrition lWhen pt is too sick to eat, TPN may be required lMore on TPN later Renal Assignment lPage 801 Hemodialysis case study #1 lDo a nutrition assessment on pt lWrite in up in SOAP format that includes Problem list in ‘A’ and solutions in ‘P’ lInclude in the solution list a one day diet based on appropriate intake of Kcal, fluid, Pro, K, P, and Na lUse exchange list on p 792 to help lIn addition, answer questions presented Physiological Stress Stress Happens: Infections Fever Surgery Burns Trauma Metabolic Need with Stress
    • Increased Kcal need Often unable to meet need nutritionally Results in decrease in nutritional status Increases risk of infection This stress response differs from starvation In starvation: Uses up glycogen Then amino acids from skeletal muscle and circulating proteins are used –Gluconeogenesis –Negative N balance -12 g/day of Nitrogen loss Represents 75 g/day of protein loss or about 3 ounces After several days, body conserves N and uses FA’s Fatty Acid Utilization Serum insulin decrease therefore allowing FA’s to be mobilized Fatty acids are beta oxidized to 2C units in liver –converted to ketones when no CHO is present –N losses drop to 4 grams/day –Body starts using ketones for energy –Metabolic rate drops Metabolic Stress Response Differs: Causes increase in metabolic rate When metabolic stress and starvation are coupled: –Body needs more energy –Starts breakdown of lean tissue Hormonal and Endogenous Mediators of Stress Adrenocorticotropic Hormone (ACTH) Catecholamines (Epinephrine, Norepinephrine from the adrenal medulla) Aldosterone Antidiuretic Hormone (ADH) Phagocytic Cells Net Result: MORE ENERGY SUBSTRATES AND MORE OXYGEN Hormones ACTH –Result of nervous stimulation of hypothalamus –Acts on Adrenal Cortex to release cortisol –Causes mobilization of amino acids from skeletal muscles Catecholamines (epinephrine and nor-ep.) –Released by Adrenal Medulla with shock and high glucagon/insulin ratio –increased glycogenolysis, gluconeogenesis, lipolysis Mediators of Stress Aldosterone: Released with stress –Na retention in kidney Antidiuretic Hormone (ADH) –Retains water in kidney Phagocytic Cells in Stress Release cytokines and tumor necrosis factor –induce greater uptake of amino acids by liver –induce greater production of proteins
    • –Other interactions Interactions between Nutrition and Infections Decreased Nutrition lowers resistance to Infection Infection aggravates existing malnutrition Therefore: people with chronic undernutrition –Succumb to infections or –Take longer to recover Nutrient needs Increase During Infection Stress reaction induces catabolic effect with increased losses of nitrogen, Mg, K, P and Zn Increased energy need with severe infections or fever Anorexia decreases food intake Increased losses due to V/D Malabsorption in enteric infections may decrease nutrient utilization Estimating Stress Level Traditional methods not always useful Urine Urea Nitrogen (UUN) measure of Metabolic Stress –0-5 grams N/d normometabolism –5-10 g N/d mild hypermetabolism (Level 1 stress) –10-15 g N/d Mod hypermetabolism (Level 2 stress) –over 15 severe(Level 3 stress) Estimating Energy Needs Indirect Calorimetry: -A good method of estimating energy expenditure in critically ill patient –Not always available Use of Harris-Benedict: BEE times stress factor –1.35 Skeletal trauma –1.6 major stress –2.0 severe thermal injury Energy Nutrients 25 to 30 nonprotein kcal/kg per day CHO 60 to 70 % of Kcals –5 to 7 mg/kg/minute or about 7.2 g/kg/day Fat: remainder of nonprotein kcals –15 to 40 % of Kcal PRO: 1.5 to 2 g/kg/day –nonprotein cal to gram Nitrogen ratio 100:1 –More protein doesn’t add any advantage Protein Branch-chained amino acids (BCAA) have been shown to be low in sepsis and severe injured pt blood –Adding BCAA-enriched solutions may help with improved nitrogen retention improved hepatic protein synthesis decreased protein degradation achievement of N equilibrium in less time Estimating Energy and Protein 1. H-B: BEE eg 1500 (67kg)
    • 2. BEE x injury factor(eg: surgery 1.5) –Total Kcals needed = 1500x1.5= 2250 3. Protein requirements 1.5-2g/kg –1.5 x 67 = 100 grams protein x 4 = 400 kcal –100 g protein/6.25 g Pro/g N = 16 g N –2250-400= 1850 nonprotein kcal –nprotein/gram N =1850/16=115 PRO and NonProtein Kcals Alternate Method (assume 67 kg person) 30 to 35 kcal/kg = 2010 to 2345 kcal/day 1.5 to 2.0 g protein/kg = 67 kg x 1.5 = 100 to 134 grams Pro/day 100/6.25 = 16134/6.25gPro/gN=21 134 x 4 kcal/g=536 nonpro kcal= 1474 to 1809/21=70 to86 1474/16=92 to 1809/16=113 Nutrition Support Selecting a method If the gut works, use it When a person is unable to ingest enough food to meet their nutritional needs –nutrition support is needed –could be enteral if the gut works –could be parenteral if the gut doesn’t work Enteral Nutrition By way of the GI tract Could be –Oral Supplements –Tube Feedings •Nasogastric •Nasoduodenal or nasojejunal •Enterostomies –Gastrostomies Percutaneous Endoscopic Gast.(PEG) –Jejunostomies Multiple Lumen tubes Selecting an Oral Supplement 1. Degree of inability to meet needs 2. Presence or absence of disphagia 3. Taste preference or sensitivity 4. Availability of labor and resources for preparation 5. Tolerance to lactose or other components 6. Tolerance of osmotic load Supplement Components Kcals: 250 kcal/ 240 ml portion is the norm Fat: –Usually Long Chain Triglycerides •Could be MCT if pt doesn’t tolerate fats Protein: –8 to 14 grams of intact protein CHO –Form varies: Simple adds sweetness and osmotic load
    • Tube Feedings: Route of Access Several Factors: –1. Length of time required •Short term: usually through nasopharynx •Longer term through enterostomal routes –2. Risk of aspiration –3. Degree of digestion available –4. If there is a planned surgical intervention Nasogastric Route Nasogastric Tube: simplest access Pt requires functional GI tract and normal gag reflex Can be large bore tube (French #12+) –Used for food, medications and gastric suctioning or Small bore, pliable tube –Greater comfort, but more easily clogged Nasoduodenal or Nasojejunal Tube threads through stomach to duodenum or jejunum Migration from stomach to duodenum via peristaltic waves may take a few days Radiologic verification is required Small bowel feedings require careful selection of enteral formula Enterostomies Surgical Gastrostomy –Catheter is placed through the abdominal wall into the stomach •A balloon is inflated to hold the catheter in place in stomach •Requires good gastric functioning •Can be associated with skin erosion, leakage of gastric contents leading to peritonitis Surgical Jejunostomy Needle jejunostomy(temporary) Catheter jejunostomy(more permanent) –both reduce risk of pulmonary aspiration –small lumen size of tube difficult to maintain so not often performed Fluid requirements 1ml of water per kcal 35 ml/kg usual body weight Formulas contain 80 to 85% water may need to add water as an additional flush Osmolality Intact formulas fall between 300 to 500 mOsmol/kg , approx the same as body fluids –No real concerns with fluid shifts Hydrolyzed formulas are often higher –up to 900 mOsmol/kg –contributes to extra fluid and electrolyte loss –diarrhea –Proper administration is key Administration of Enterals Continuous drip Intermittent drip Bolus feeding
    • Continuous Drip Estimated total kcal needs are made Rate per hour determined based on the kcal content of formula –2000 kcals needed per day –Formula has 1kcal/cc –2000kcal/1kcal/cc= 2000 cc’s needed –2000cc/24 hrs=83cc’s/hr is set as the goal volume Administration of Continuous Drip Caution when initiating tube feeding If the gut has not been used lately If the formula is hyperosmolar Feedings are typically started at 30 to 50 cc’s/hr –Then advanced 25 to 30 cc’s/hr every 8 to 12 hours until the target rate is obtained –Feedings of 300 to 500 mOsmol/kg can be started at full strength; hyper dilute in half Admin of Tube Feeding If intolerance: decrease to previous increment and advance as tolerated Don’t hang a bag for more than 4 to 8 hours –Food born illness Don’t add new formula on top of old formula Bag should be changed daily Administration of Tube Feedings If fed into stomach, stomach contents checked every 4 to 8 hours –if volume exceeds 100 to 500 ml, stomach isn’t emptying quickly and volume admin should be reduced •Risk of pulmonary aspiration Intermittent or Bolus Feedings Quality of Life: A more normal lifestyle with intermittent feedings –Frees pt to be mobile Figuring intermittent or bolus feedings similar to continuous Total Kcals determined Divided by number of hours feeding General: 4 to 6 feedings @ 20 to 60 min Administration of Bolus or Intermittent Feeding Residuals checked more frequently: every 2 to 4 hours Few pts can tolerate more than 450 ml per feeding Pt needs to be monitored for several potential problems Monitoring Tube Fed Pt Weight 3 x wk Signs of Edema daily Signs of dehydration daily Fluid In/Out daily Cal, Pro, fat, CHO, vit & min 2+/wk N balance (24-hour UUN) weekly Gastric residuals (2 to 4 hrs) Monitoring Tube Fed pt Stool output and consistency (daily) Urine Glucose (every 6 hours until rate is established then daily for Db pt) Serum electrolytes, BUN, creatinine, blood count (2-3 x wk) Blood chemistry: total protein, albumin, pre-albumin, Ca, Mg, P, Liver Fxn weekly
    • Tube Feeding Problem Pulmonary Pt with 1800 kcal need -No renal problems or fluid restrictions –gastrostomy in place Tube feeder with Pulmocare –Pro: casein; CHO: cornstarch and sucrose; Fat: mixed triglycerides –1.5 kcal/ml; 55.2 % kcal from Fat; 28.1 % kcal from CHO rest from Pro; 80% water –? How much Pulmocare?; how much fluid;Pro? Pulmocare Problem Osmolality is 465 mOsmol/kg –How would you administer this? –What would you monitor to determine tolerance? –What would you monitor to determine if needs were met? Parenteral Nutrition If pt is unable to receive nutrients via the GI tract –Then Parenteral Nutrition is Appropriate Parenteral Access Peripheral Access: –Arm (or leg) –900 mOsm/kg upper limit of acceptable –Higher concentrations cause vein to become inflamed and collapse. –PICC(Peripherally Inserted Central Catheter) •Higher concentration is possible •End of lumen is threaded to a larger vessel with greater dilution capacity Parenteral Access Short Term Central Catheter –Subclavian vein central catheter •line inserted into Subclavian and threaded to the superior vena cava •Provides maximum dilution of parenteral solution and no damage to the vein lumen •Risk of infection Parenteral Access Long-term Access –When access is required for many months or longer, a permanent catheter is surgically placed –A port is imbedded under the skin which is accessible Terminology with Parenteral Solutions D Dextrose W Water NS Normal Saline (0.9%) NaCl solution 0.9 g NaCl/ 100 ml D5W 5% Dextrose solution in water (5 g Dextrose in water) D51/2 NS 5% Dexrose in 1/2 Normal Saline (0.45 g NaCl in 100 ml Water) Nutrients in Parenteral Soln Protein –Combination of essential and non-essential aa’s –Generally 15 to 20 % of total Kcal needs in most solutions –Often a 10% amino acid solution is used –10 g / 100 ml which represents 100 grams/liter
    • –Final concentration often expressed as the con in the final volume after mix with CHO and Fat Fat in Parenteral Soln Usually comes in 10% or 20% solutions 10 % represents 1.1 kcal/ml 20 % represents 2.0 kcal/ml Usually composed of safflower, soy oils with egg yolk as an emulsifier to hold in solution Generally 20 to 30 % of Kcal Don’t exceed 60% (2.5 g/kg/d) CHO in Parenteral Solution Dextrose monohydrate –D Glucose –Concentrations range from 5% to 70% –Shouldn’t exceed 5 mg/kg/min –Used to spare protein and provide kcals Calculation of Osmolality Dextrose grams/l x 5 Protein grams x 10 Fat is isotonic so no osmotic force electrolytes further add to osmolarity 50 g of dextrose plus 30 grams of protein (50 x 5) + (30 x 10) = 550 mOsm/l Indications for Peripheral Vein Feedings 1. Short term: enteral feeding again in 7 d 2. Transition with enteral feeding 3. Mild to mod malnutrition:supplemental nutrition needed 4. Normal or mild elevation of metabolic rate 5. No organ failure or fluid restriction Indications for Central Vein Feeding 1.Unable to enteral feed for 7 + days 2. Mod to severely elevated metabolic rate 3. Moderate to sever malnutrition 4. Cardiac, renal, or hepatic failure or other conditions limiting fluid 5. Limited access to peripheral veins 6. Able to access central vein Compounding Methods Two methods of prescription compounding: 1. All components except fat 2. All components including fat May be batch mixed to save money or may be individually prescribed and mixed Is done by pharmacist in aseptic conditions Administration of TPN Continuous Infusion –Initiate at 42 cc/hr or 1000 L/d –increase incrementally until goal rate is reached over next two to three days –If TPN is interrupted, infuse D10W or D20W until TPN can be restarted Guard against hypoglycemia Cyclic Infusion To free individuals who are capable of mobility TPN for 12 to 18 hour infusion periods are possible. Allows pt to be mobile for 6 to 12 hours Cyclic administration is established incrementally Monitoring and Problem Solving
    • Actual intake of TPN is monitored Monitor Growth, weight Metabolic parameters Table 20-10 p442 –serum lytes, BG, Hb, etc General –Volume of infusate, oral intake, urinary output Infection –Clin Observations: temp., WBC, cultures Refeeding syndrome With intro of energy substrates following a period of no intake, may cause Refeeding Syndrome –Shift of phosphorus, potassium from serum to intracellular sits for ATP production •causes hypophosphatemia, hypokalemia •Can be severe and life threatening •Needs to be monitored and may require additional IV replacement of P and K Transitional Feeding Parenteral to Enteral –begin at 30 cc/hr –increase 25-30 cc/hr every 8 to 24 hours –Parenteral solution is reduced accordingly Parenteral to Oral –Monitor oral intake; less predictable than above –Reduce Parenteral accordingly Enteral to Oral –Adjust to intermittent feeding first Nutrition Support in Other Settings Long-term Care –More happening in nursing facilities Home Care –People are at home receiving nutrition support –Concerns: •motivation •family’s ability to handle •benefit of receiving nut support •limitations such as phyical Ethical Issues End of life decisions –Based on advance directives from patient –What is the patient’s desire about end fo life life support? Standards and Guidelines –American Society of Parenteral and Enteral Nutrition –Guidelines for use of nutrition support Problems 3 liters of D5W was given via peripheral IV over a 24 hour period. How many kcals did it provide? (1 gram Dextrose monohydrate= 3.4 grams) (5 g/100ml) (1000ml/l)(3 l)(3.4 kcal/g)=510 kcal Problem
    • 2.5 l of 3.5% Dextrose (3.5 g/100ml)(1000ml/l)(2.5 l)(3.4 kcal/g)= 297.5 kcal Problem 3 l of 25% Dextrose and 3.5% Amino Acids How many kcals and % kcal from each? (25g/100ml)(1000ml/l)(3 l)(3.4kcal/g)= 2550kcal from CHO (3.5g/100ml)(1000ml/l)(3 l)(4kcal/g)= 420 kcal from PRO Total = 2550 + 420 = 2970; 2550/2970=86% from CHO and 14% PRO Problem 500 ml of 10% fat emulsion distributed in 2.5 l of TPN solution which has a final concentration of 20% Dextrose and 3.5 % Amino acids. How many total kcals and what % from each energy nutrient? (20 g/100ml)(1000ml/l)(2.5 l)(3.4 kcal/g) = 1700 from CHO (3.5 g/100ml)(1000ml/l)(2.5 l)(4 kcal/g) = 350 from PRO Problem (cont) 10% fat emulsion = (1.1 kcal/ml) (500 ml)= 550 kcal from Fat Total = 1700 + 350 + 550 = 2600 kcal 1700/2600 = 65% from CHO 350/2600 = 13.4% from Pro 550/2600 = 21 % from Fat Nut Assessment Pt requires 2200 kcal 60% kcal from CHO 25% kcal from fat 15% kcal from PRO How would you formulate this? Fat first: you need 2200 x .25 = 550 kcal 10 % fat emulsion @ 1.1 kcal/ml 550 kcal/ 1.1 kcal/ml = 500 ml 10% soln Nut assessment Final volume of 2000 ml Fat contributes 500 ml 1500 ml for PRO and CHO 2200 kcal x .6 = 1320 kcal/3.4 kcal/g= 388 g CHO/1500 ml = 25 % Dextrose solution 2200 kcal x .15 = 330 kcal/4kcal/g = 82.5 g PRO/1500 = 5.5 % aa solution final concentration Nutrition and Cancer Diet and Cancer 80 % of cancers are related to environmental causes 35% of all cancers are diet related In Japan, low rate of breast and colon cancer After 2 to 3 generations in the US, Japanese Americans have similar rate of breast and colon cancer ‚Due to changes in diet and lifestyle Two Concerns Regarding Cancer and Diet Diet to prevent Cancer some controversy about fat vs total kcal intake related to certain cancers. ‚Obesity related to estrogen sensitive cancers of the breast, and endometrial cancers. Energy restriction during growth reduces the risk of cancer in rats Antioxidants and cancer: Vit A, E, C, Selenium, beta Carotene, Zn may have some relationships. Nitrates, Nitrites and Nitroso compounds Nitrates in foods can easily be converted to Nitrites Nitrites interact with food components to form nitroso-compounds ‚nitrosamines which may be involved in gastric and other cancers
    • ‚Nitrates are found in vegetables and subject to conversion in GI tract especially in infants with low acid stomach Cancer and Substrate Metabolism Tumor exerts calorie drain Anorexia usually turns down metabolism But not with Cancer: Metabolism is turned up CHO: constant drain of CHO Kcal in anaerobic metabolism Production of lactic acid May increase gluconeogenesis of lactate via Cori cycle in some cancer patients Protein Metabolism Most changes include emaciation due to tissue protein breakdown to supply amino acids required to build cancer cells hypoalbuminemia visceral organ atrophy muscle wasting Lipid metabolism Cancer promotes lipolysis Subsequent reduction in total body fat Decreased lipid clearance from the serum and elevated plasma free fatty acids Other Metabolic Abnormalities Electrolyte imbalance hypercalcemia especially in bone metastasizing tumors or breast, lung and pancreas Fluid imbalances diarrhea causing tumors: secretion of serotonin vomiting with intestinal obstruction Alterations in taste and smell contributes to anorexia Cancer Therapy Chemotherapy kills rapidly reproducing tissues nausea and vomiting, taste abnormalities Radiation Therapy: whole body or regional Radiation enteritis: inflamation GI tract, head and neck ‚short-lived or long lasting Surgery: depending on site of removal Nutrition Care of Cancer Pt Goals: 1. Prevent or correct nutritional deficiencies 2. Minimize weight loss Early intervention is important Timing of Food presentation early in the morning foods that are liked avoid food aversions use of ‘scapegoat’ foods prior to chemo Diet and Cancer Nutritional Effects of Cancer Cancer Cachexia ‚Wt loss ‚anorexia ‚asthenia(tiredness, weakness) ‚abnormalities of protein, CHO and Fat metabolism Cause unknown but probably related to cytokine production ‚tumor necrosis factor, interleukin 1 and 6 Inflammatory cytokines
    • Produced by tissues undergoing damage or cancer growth My induce growth in cancer cells May impair metabolism in non-cancerous tissue ‚Induce nausea ‚Affect energy metabolism Liver & HIV/AIDS Functions of the Liver Carbohydrate Metabolism Formation and storage of glycogen (glycogenesis) Conversion of galactose and fructose to glucose Produces glucose from lactic acid, glycogenic AA’s, and intermediates of the TCA cycle (gluconeogenesis) Functions of the Liver Fat Metabolism Oxidation of FA’s to acetyl-CoA for use in the TCA cycle (beta-oxidation) Synthesis of TG’s, cholesterol, bile salts, and phospholipids Conversion of carbohydrate and protein intermediates to fat (lipogenesis) Ketone bodies produced Functions of the Liver Protein Metabolism Transamination & oxidative deamination –Convert AA’s to substrates that are utilized in energy and glucose production –Synthesis of non-essential AA’s Synthesis of plasma proteins Urea formation for removal of ammonia from body fluids Functions of the Liver Other Activates vitamin D Converts carotene to vitamin A Storage of iron as ferritin Storage of fat-soluble vitamins, vit B12, Zn, Fe, Mg Drug metabolism (including alcohol) Deactivation of hormones Hepatitis Inflammation of the liver Viral –A, B, C, D, E Alcohol Drug-induced Alcoholic Liver Disease (ALD) 3 Stages Fatty liver (hepatic steatosis) –Caused by:
    • ↑ mobilization of FA’s from adipose tissue ↑ hepatic synthesis of FA’s ↓ FA oxidation ↑ TG production Trapping of TG’s in the liver –Reversible with abstinence from alcohol Alcoholic Liver Disease (ALD) 3 Stages (continued) Alcoholic Hepatitis Cirrhosis Scar tissue formation Change in the normal architecture Irreversible ↑ portal hypertension…results in: Varices Ascites Hepatic Encephalopathy Grade I: Mild confusion and impaired coordination Grade II: Flapping tremors (asterixis) and slurred speech Grade IV: Loss of consciousness and coma Hepatic Encephalopathy Theories Behind the Cause Ammonia build-up Bacterial degradation Blood from GI bleed Dietary protein Altered neurotransmitter theory ↓ BCAA’s ↑ AAA’s, met, glu, asp, his Nutrition Assessment Degree of malnutrition Lab values Weight Triceps skinfold Subjective global assessment Nutrient Requirements Energy: 1.2-1.5 x BEE Dry weight Lipid: 25-40% of total kcals Protein: Controversial Vitamins and minerals HIV/AIDS Virus invades CD4+ (T-helper) lymphocyte cells
    • Transmitted via Blood and semen Shared contaminated needles Contaminated blood products Across the placenta from mother to baby Clinical Categories Acute phase Clinical categories A: Asymptomatic B: Symptomatic C: AIDS-indicator condition Common Problems Opportunistic infections Malignancies HIV encephalopathy Protein-energy malabsorption Diarrhea, steatorrhea Nutrition Assessment Lab values Problems pt is currently experiencing Weight history Dietary intake Subjective global assessment Nutrient Requirements Energy: 1.3-1.5 x BEE Protein: 1.0-1.4 gm/kg/day Fat Vitamins and minerals Acute and Chronic Pancreatitis Nutrition Management Functions of the Pancreas Upper Abdomen Exocrine and Endocrine Function Glucagon, Insulin, somatostatin(endocrine) Amylase, lipase, trypsin(exocrine) Common Bile Duct Food ingestion triggers pancreatic secretions Pancreatitis Inflammation of the pancreas Attacked by its own enzymes Mild to severe
    • Acute or chronic Mortality Rates: Acute: 10-25% Chronic: 5% Acute Pancratitis Causes: Gallstones Clogged Common bile duct: Autodigestion ETOH Abuse Pancreas sensitive to ETOH Abuse Other hypertriglyceridemia, drugs, mumps and other infections Chronic Pancreatitis No Cure Begins as acute; becomes chronic with scar tissue Years of ETOH abuse Affects digestion enzyme and insulin production Affects nutrition digestion and absorption Chronic Symptoms Wt loss N,V, D or Steatorhea Can be continuous or intermittent gradual or severe upper abdominal pain symptoms of DM Diagnostic Methods Serum Lipase and Amylase are elevated Peak 48-72 hrs after pancreas injury Phospholipase A2 elevated Decreased albumin and Ca Increased BG Increased TRIG Use of CT (computerized tomography)scan Nutritional Management Rest; Often NPO with IV hydration If mild: clear liquid diet Progress as tolerated to low fat diet Small meals; adequate protein If severe: TPN or Enteral with jejunostomy with elemental formulas Chronic Pancreatitis Treat acute attack Avoid large meals, high in fat and ETOH Low-fat diet; 40-60 g/day; MCT oil Supplemental pancreatic enzymes taken orally with meals Supplement fat soluble vitamins and B12 Insulin injections with glucose intolerance Cystic Fibrosis Pulmonary Disease with multisystem affect 1:2500 caucasian births Previous CF pt did not reach adulthood Current median age of death is 30 yrs CF pts secrete thick mucous that blocks tubes Affects Respiratory, sweat and saliva glands Cystic Fibrosis Affects Intestinal tract, pancreas, liver and reproductive tract Dx: positive sweat test; chronic lung disease, FTT, malabsorption test, family Hx
    • Cystic Fibrosis 85% have pancreatic insufficiency Mucous blocks ducts from secreting enzymes Results in malabsorption Thick mucous lining GI tract further decreases absorption Nutritional Status GI complications bulky stools; cramping; obstructions rectal prolapse Liver involvement High Risk for Malnutrition Nutritional needs difficult to meet due to malabsorption Nutritional Status Decrease PO dyspnea coughing/cough induced vomiting GI discomfort impaired smell and taste glucosuria Growth Retardation, FTT Difficulty achieving proper wt Nutritional Management Good nutritional status related to longer life Must coordinate nutrition with other therapies Goals: control malabsorption provide nutrition for growth prevent nutritional deficiencies Nutritional Management Pancreatic enzyme therapies oral administration with food fecal fat and nitrogen balance used to assess adequacy of enzyme supplementation Nutrition Management Energy: highly individualized Increased needs due to breathing efforts Requires high kcal, moderate fat indirect calorimetry useful Macronutrients/ Vitamins and Minerals Increased protein Fat 35-40% or more Fat-soluble vitamin supplementation Sodium losses in sweat Individual eval of mineral status How to Increase Energy Intake Nutritional Supplements Non-fat milk Powder Butter, margarine, gravies, dressings Concentrated sugars Fortified dishes Enteral or Parenteral Drug-Nutrient Interactions Drug Nutrient Interactions Can Occur When: Drugs are taken with food or nutritional supplements Drugs are taken with alcohol
    • Drugs are used to induce specific drug nutrient interactions Drugs are taken in multiple drug regimens Drugs that cause nutrient depletion are taken for a long time Responsibility to Monitor Drug-Nutrient Interactions Pharmacists Nurses Dietitians Drug Action: Three Stages 1. Pharmaceutical stage –Dissolution or disintegration of drug 2. Pharmacokinetic stage –absorption, distribution, metabolism, and elimination of the drug 3. Pharamacodynamic stage –body’s physiologic and/or psychologic response to the drug Risk For Interactions Occurs most commonly in long-term treatment for chronic disease Depends on the function of the Mixed-Function Oxidase System (MFOS) system that oxidizes a bunch of substances includes cytochrome P-450 NAOPH-cytochrome P-450 reductase, and phosphatidylcholine Is effected by nutrient deficiencies (Protein, vit C, E, and A) How Might Drugs Affect Nutritional Status? Drugs that Affect Intake Loss of Appetite or taste Drugs that Affect Nutrient Absorption Drugs that Affect Nutrient Metabolism Antivitamins Monoamine Oxidase Inhibitors(MAO) Excretion of Nutrients Drug-Induced Electrolyte Alterations Drugs that Affect Intake Appetite suppressants: Ritalin used with hyperactive children long-term use may result in growth-retardation catch-up growth may occur when discontinued Cisplatin: a cytotoxin agent used in cancer therapy causes nausea, vomiting, and reduced food intake Drugs That Affect Nutrient Absorption Luminal Effects: Influencing Transit Time Laxatives Bile Acid Activity Cholestyramine sequesters bile acids inhibits fat digestion Change of pH Antacids change pH and reduce absorption of Ca, Mg, Fe and Zn Drugs that Affect Nutrient Metabolism Inhibition of Synthesis of Certain Enzymes by Competing for vitamins or Vitamin Metabolites necessary for their structure Methotrexate used in treatment of leukemia and rheumatoid arthritis This breaksdown folate and induces a folate deficiency DNA synthesis is stopped
    • Monoamine Oxidase Inhibitors Common Interaction: MAOI and pressor amines in foods Two classes of biologically active amines psychoactive: neurotransmitters norepinephrine and dopamine vasoactive: pressor amines tyramine, serotonin, histamine these are found in many foods but are rarely a problem because they are quickly deaminated MAOI and foods(Cont) However, with drugs that inhibit amine removal, some foods containing these substances aren’t as well tolerated eg: tyramine containing foods eaten while on MAOI Increases blood pressure Antidepressant: Phenelzine sulfate Pt needs to avoid tyramine containing foods cheese, smoked fish, chianti wines meat extracts, beer, ale, Excretion of Nutrients Some drugs displace a nutrient from plasma binding site and make it available for kidney filtering D-penicillamine is used to treat heavy metal poisoning It chelates the intended metal and makes it available for kidney removal This also chelates other metals and removes them from the circulation and induces a deficiency eg: Zinc Electrolyte Alterations Thiazide: a loop diuretic that enhances Na loss also increases K loss K supplements may be required Drugs of Abuse Legal: caffeine, nicotine, alcohol Illegal: marijuana, cocaine Can induce nutritional deficiencies by decreasing nutrient intake Decrease appetite(or increase appetite) Caffeine: induce Calcium loss in urine Some Common Drug-Nutrient Interactions Anticonvulsants(ACDs) Phenytoin, phenobarbitol, etc induce deficiencies of folate, biotin, vitamin D reduces hydroxylation of calciferol to 25, OHD3 Oral Contraceptives Increased need for B6, folate Increased Vitamin A in circulation: may lead to decreased stores Increase serum Iron versus non users Anti-inflammatory Drugs Glucocorticoids: used to decrease inflammation, suppress the immune system development of osteoporosis in 50 % of long-term users HIV meds: AZT used to inhibit virus replication Induces megaloblastic anemia through reduced erythropoiesis Treat with recombinant human erythropoietin(EPO) Use of Alternative Therapy Herbal remedies are commonly thought to be less toxic than drugs This isn’t necessarily true: Examples: aloe: can increase diarrhea and intestinal loss ginseng: can cause diarrhea and intestinal loss ephedra: changes in blood pressure, dizziness Nutritional Status May Affect Drug Therapy
    • Drug absorption and transport Drug Metabolism Drug Excretion