Identification of Nutrition Problem(s) Diabetes is in poor control

– hypoglycemic episodes

– weight loss

– little knowledge of Db and dietSetting Objectives Formulate 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 briefObjectives Which of the following offers a pt centered, quantifiable, concise, brief, and realistic statement? A. I will teach the pt how to select a 1500 kcal diet from the hospital menu B. Pt will be able to select a 1500 kcal diet from the hospital menu after 3, 1/2 hour education sessions.Realistic Objectives Important to take into account

– Education level of pt

– limitations, physical, mental, emotional

– resources

– family supportRelationship: Nutrition Problems & Objectives At least one objective for each problem, in some cases more than one objective Example: Problem--- Hypoglycemia Objectives:

– 1. Find out when Hypoglycemic attacks occur

• Diagnostic(Dx)

– 2. Pt will modify diet following education to reduce incidence of hypoglycemia

• Prescriptive(Rx)

Objectives Pt will demonstrate an understanding of hypoglycemia following a 1/2 hr education session

– Education(Ed)Problem 2: Weight loss Pt 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 Objective: 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 This 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 Objective 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 gInterventions: Intervention 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 If 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 If 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 negativeCalorie Count As meals are served, RD can’t always be present, so nursing staff records the amounts eaten of the foods served Based 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 problemNutrition Care Record Documentation 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 interventionNutrition Care Record All these work toward helping the pt understand the nutrition care and to be an active participantFactors Describing Contents of Medical Records All entries should be labeled: “Nutrition Note”, or what is accepted for your institution Sign Entry; If hand written, use black ink

Factors to consider in Records Clearly state, don’t imply.

Describe accurately, and concisely State relevant info to pt problem Use appropriate technical language Correct spelling, grammar: complete sentences are not always necessary Use objective style: Pt vs he or sheRecords Write legibly Use of correct abbreviations

– Medical terminologyTypes of Medical Records 2 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 NotesData Base Established at the time care is initiated Includes:

– Pt profile

• description of pt with environmental, social & family factors• Med Hx• family Med Hx• review of systems concerning problems• existing nutrition assessmentProblem List Established by Physician Based on Data Defines Problems

– Anything that requires

• Dx• or management

– Known allergies and intollerances should also be listedInitial Care Plans Plans for dealing with each problem listed are written by the Physician Orders made by the physician These may include nutrition intervention These are most commonly written in SOAP format

– Sometimes in DAP formatSOAP An emulsifiying agent which helps to cleanse and degrease or A format to record relevant data and plans about the pt being considered S: Subjective: info from pt, family or other difficult to measure source

– e.g.: Pt states, “I hate milk” SOAP O: Objective

– Data from tests, blood values,

– ht, wt, age, desired wt

– current diet order

– medicationsSOAP A: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 complianceSOAP P: 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 EdSOAP Physician 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 formatSOAP Once 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 formatSOAP = DAP More correctly stated:

– SO = D

– in some medical records, the S and O material is all recorded as Data (D)Assessment: Calorie Needs Harris Benedict Equation: Males: 66.47+(13.75xwt)+(5xht)--(6.76xa) Females:655.1+(9.56xwt)+(1.85xht)--(4.68xage) ht in cm; wt in kg; age in years This results in BEE TEE=BEE x activity factor x injury factorActivity and Injury Factors In bed: 1.2 Ambulatory: 1.3 Injury: Surgery: Minor 1.1; Major 1.2 Infection: Mild 1.2; Mod 1.4; Severe 1.6 Burns: 40% of body: 1.5; 100% 1.9 Trauma: Skeletal 1.35; Head 1.6; Blunt 1.35

Energy Needs: Another Method Maintenance: 25-30 kcal/kg Maintenance w/ activity: 30-35 Elective surgery: 28-30 Anabolism: 35-40 Trauma: 35-40

Severe Trauma, burns: 45-55 Sepsis: 45-55Children: Calorie needs Age(yrs) REE per kg per day 0-0.5 320 108 650 0.5-1 500 98 850 1-3 740 102 1300 4-6 950 90 1800 7-10 1130 70 2000

Adolescence: Calorie Needs Age REE per kg per day males 11-14 1440 55 2500 15-18 1760 45 3000 females 11-14 1310 47 2200 15-18 1370 40 2200Medical TerminologyTypes of TerminologyRoot WordsModifiersGeneral AbbreviationsUnit AbbreviationsRoot WordsExamples of Words MeaningsArterio- ArteryLith- StonePoly- Many or muchCardi- HeartSclero- HardArterio-Sclerosis hard arteriesModifiers: Prefixes and SuffixesTachy- 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 failureA-V ArteriovenousCBC complete blood countSOB shortness of breathTIA transcient ischemic attackWNL Within normal limits

Frequency Designations q.h. every hour q.d. Every day b.i.d. Twice daily q.id 4 x dayqod every other dayprn as required

ad lib as desiredUnit Abbreviations ml milliliter mcg microgramcc cubic centimeterhs hour of sleepmEq milliequivalent

DiabetesDefinition of DiabetesA group of diseases of endocrine system with similar symptoms

– Hyperglycemia

– premature vascular disease

– kidney disease

– retinal damageIncidence of Diabetes3 % of middle aged adults6.4 % of 65-75 yo: many are unaware0.4% of young adultsAcute care hospitals:

– Diabetic patients most common therapeutic dietPublic Health Significance:

– Blindness, CVD, renal failure, amputations, reduced life expectancyTypes of DiabetesD. Insipidus: large urine outputD. 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 diabeticsDiabetes: TypesType 2: also called adult onset, NIDDMabout 90% of DM ptsdecreased sensitivity of insulin or inability to secrete: But insulin is presentOnset is gradualTreatment: diet, exercise, hypoglycemic meds (diabenese), sometimes insulinSecondary DiabetesOther conditions cause diabetes to occurExamples:

– Pancreatitis: inflamed pancreas due to alcoholism, or infection decreases insulin production

– When pancreatitis is reduced, insulin production returnsSecondary DiabetesGestational Diabetes:

– During pregnancy, interaction between hormones and glucose metabolism

• Human Placental Lactogen and Human Growth Hormone are insulin antagonistsPrimary DiabetesGenetic Related Disease

– Predisposition vs a trait or disease

– Dependent on environmental factorsType 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 1Type 1 genetic vs environmentCertain viral agents are Beta cyto-toxic

– Rubella, mumps, Epstein-Barr(mononucleosis)

– Chemical agents: rodentocide VacorCoupled with genetic factor:

– Human Leukocyte Antigen (HLA)

– Factors carried on 6th Chromosome

– Combination of agent and certain HLA results in Beta Cell DestructionDestruction of Beta CellsHLA + agent = production of antibodies that destroy Beta cells on pancreasmany 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 GeneticsMonozygotic twins: If one gets type 2, almost all of the other twins will get it.75% of Type 2 are obeseIn other countries where obesity is low, so is incidence of Type 2 diabetesType 2: Mechanism?Probably several

– May include poor Beta Cell response to elevated BG

– Insulin receptor down regulationInsulin receptors: insulin fills and this opens transport of glucose into insulin dependent cellsInsulin Receptor Down RegulationWith 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 glycerolGlucose and CHO MetabolismInsulin 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 systemCHO and InsulinInsulin 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 increasedCHO and InsulinInsulin slows gluconeogenesis: less glucose made from amino acids

– Without insulin, increased gluconeogenesis: Amino acids are converted to glucose Fat and InsulinInsulin slows breakdown of fat and increases formation of fat

– Without insulin: fat breakdown increases

– fat formation decreasesProtein and InsulinProtein synthesis high and degradation of protein low with insulin

– Without insulin protein synthesis low, breakdown high

– results in high ureagenesis

Protein and InsulinAmino acid uptake in muscle and adipose tissue is high with insulin

– Without insulin: slow amino acid uptake and increase protein breakdown

• Muscle wastingInsulin and Urea and KetonesInsulin slows ureagenesis(slow breakdown of proteins)

– without insulin: increased ureagenesisInsulin slows ketone production(fat breakdown without use of CHO intermediates)

– without insulin: increased ketonesPathogenesis of Clinical SignsHyperglycemia 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 polyphagiaComplications: AcuteHypoglycemia: 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 insulinInsulin Shock: SymptomsHunger, weakness, mental confusionperspiration, cold, clammy skinblurred vision, loss of coordinationparalysis, unconsciousness, convulsionsdeathInsulin Shock TreatmentQuick source of glucose

– By mouth if awake: fruit juice, corn syrup, sugar, candy

– Injected glucagon: induces breakdown of glycogen to glucoseRebound hyperglycemia( Somogyi Effect)

– glycogen release coupled with increased glucose intake: induces hyperglycemiaAcute: Ketoacidosis: Diabetic ComaAccounts for 1 to 3 % of deaths of all diabeticsCaused 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 resistanceSymptoms: Diabetic ComaChildren: onset pretty quickTired, weakness, vomitingfruity odor of breathKussmaul respiration, coma in 12-24 hoursAdult onset often slowerIf untreated: coma, brain damage, deathKetosis and KetoacidosisBicarbonate: pH buffer in bloodH+ +HCO3

- <----->H2CO3<----->H20+CO2

bicarb carbonic ion acidIf H+ continues to be loaded from ketone bodies, body has net loss of carbon dioxide and bicarbonate ion. pH can’t be maintainedKetosis and KetoacidosisWithout 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 presentPhase 2: (ketoacidosis) bicarbonate lost, pH drops (7.4 to 7.2), moderate acidosisPhase 1: (diabetic coma) pH 7.2, severe acidosisDiabetic 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 drinkIV fluids and electrolytes are added: IV glucose when BG is controlledHyperosmolar non-ketotic comaType 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 dramaticallyNon-ketotic coma: Type 2 ptVery 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 % mortalityNon-ketotic Coma TreatmentInsulin administrationK+ replacement due to urine loss through leachinggradual fluid replacement: guard against cerebral edemaChronic ComplicationsGeneral Mechanisms1. Alternate insulin insensitive pathwaysGlucose -----> sorbitol ------> fructoseGlucose 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 anoxicChronic 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 thickeningGlycoproteins thicken basement membraneMakes 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 lesionsAngiopathies: 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 wasteMajor areas of concern for AngiopathiesKidney: NephropathyNervous tissue: NeuropathyEyes: RetinopathyNephropathy10% of all deaths but50 + % of all Type 1 Db deathsprogresses asymptomatically until renal failure is advanced

– Renal Failure discussed laterResults from thickening of basement membrane, sclerosis of blood vesselsNeuropathyLess life threateningpoorly controlled Db results in nerve damage

– loss of fine motor control, pain

– mechanism probably includes sorbitol and fructose buildup in nervous tissueRetinopathyCommon cause of blindness in diabeticsMechanism: basement thickening & sorbitol pathway

– poor nutrient, waste exchange

– buildup of fructose and sorbitolDiagnosis of DbIt has become more simple to Dx DbNew 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 methodOther Db related labsCortisone GTT

– inject cortisone which mimics the the effect of stress

– monitor BG for two hoursBlood Insulin Radioimmunoassay

– Estimate Blood InsulinC peptide chain assay

– measure of endogenous insulin productionTreatment of DbNo current cureImprove quality of life/ prolong lifeTreatment directed toward

– relieving symptoms

– decreasing the severity of the disease by enabling body to use glucose

– prevent or correct complications

– assure adequate nutritionFour Facets of Db CareControl diet

Insulin injections and hypoglycemic drugsExerciseEducationHygiene and emotional well-being of the personInsulinAbout 25% of Db pt use insulinsubcutaneous injectionsTypes:

– 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 theseOral Hypoglycemic AgentsType 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 InterventionSteps:1. Nutrition Assessment2. Distribute Calories among energy nutrients3. Distribute CHO between meals4. Use CHO counting

– three levelsCHO Counting: Level 1Goal: CHO Consistency & flexible food choicesIntended Audience

– Type 1, Type 2, GDMPrimary Distribution

– MD offices, hospitals, clinics, HMO with RD on staff

CHO Counting: Level 2Goal: Adjust meds/food/ activities based on patterns from client daily recordsIntended audience: any DB pt who has mastered the techniques of carbohydrate countingPrimary Distribution: Settings with RD who has Db training/experienceCHO Counting: Level 3Goal: Adjust insulin dose using ratio of carbohydrate/insulin dosageIntended audience: people on intensive insulin therapy; people who have mastered insulin adjustment and supplementationPrimary distribution: Settings with health care team trained in intensive therapy How to count CHO? Food labelsExchanges lists

– One CHO = 15 grams CHO

– one starch, one milk, one fruitNutrient reference booksComputerized pre-programmed food scalesCHO Counting Advantages?Single-nutrient focus

More precise matching of food and insulinFlexible food choicesPotential for improved blood glucoseClients feel more in chargeCHO Counting Challenges?Weighing and measuring foodKeeping foor records initially and periodicallyRecording blood glucose before and after eatingHandling numbers and calculationsMaintaining healthy eating/Wt management

The Gastrointestinal TractDiseases and Other ProblemsDiagnostic TestsMotility– radiographic testsSecretions– collections– biopsyMotility TestBarium 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 AcidsSteps:– 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 outputAcid Conditions DefinedHyperchlorhydria: 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 DefinedHypochlorhydria (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 AbsorptionGeneral Dietary ConsiderationsSecretory activity of stomach, small intestine, gall bladder, pancreas and liverMotility of tractBacterial floraComfort and ease of digestionmaintenance and repair of mucosa structureDiseases of the EsophagusEsophagitisHiatal HerniaSurgery of the Mouth or EsophagusTonsillectomy

Cancer of Mouth, Pharynx and EsophagusEsophagitisFunction of Esophagus:– Esophagus moves food from mouth to the stomach through diaphragm and through lower esophageal sphincter– Peristaltic wave motion– Difficulty in swallowing: Due to neurological problem: part of rehab from stroke, MVA, etcEsophagitisUsually occurs in lower esophagus– Following gastric reflux which irritates esophageal mucosa: often called heartburnAcute esophagitis:– due to irritating food, viral inflammation or intubationChronic or Reflux E.– Due to repeated reflux from stomach– hiatal hernia, vomiting, reduced LES pressureLower Esophageal SphincterMany factors affect competency of LES– Decreases with:– Pregnancy– oral contraception– late menstrual periodEsophagitis: Nutrition CareObjectives:– 1. Prevent irritation of inflammed tissue– 2. Prevent esophageal reflux– 3. Decrease the irritating capacity or acidity of gastric juiceNutrition CareLiquid 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 irritatingSome foods decrease LES pressure and should be limited– alcohol, peppermint, chocolate, caffeineNutrition CareTiming of the meal: Restrict food before bedtime or lying down– less gastric content to push against LESObesity increases pressure on LES– Wt loss may improve Esophagitis: Drug TreatmentLES Pressure increased with– Bethanocal(cholinergic drug)– metoclopramide (dopamine antagonist)– some antacids, which also lower gastric acidityGastric Acid decreased with– cimetidine(histamine receptor blocker)Barrier for inflamed tissue– Alginates(Gaviscon)Hiatal HerniaCommon cause of gastroesophageal reflux and esaphagitisDiet Therapy:– No eating 3 hours before reclining or sleep– Avoid foods that are know to cause heartburn: caffeine, chili powder, black pepper, peppermint, chocolateSurgery of Mouth and Esophagus

If oral intake is possible– liquid formulas; pureed foodsIf oral intake is not possible– gastrostomy of jejunostomy tube to provide enteral feedings These can be formulas or blenderized table foodsTonsillectomyRemoval 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 dietCancer of the Oral Cavity, Pharynx, EsophagusTreatment: resection of tumor, chemotherapy, radiation– May interrupt or cause problems with chewing and swallowing

Nutrition Support: If GI tract functional: Enteral feedingIf GI tract not functional: parenteral nutritionWhen Oral intake is possible:

– soft, moist foods easy to chew and swallow– small frequent meals of high-caloric densityThe StomachIndigestionAcute and Chronic GastritisGastric SurgeryCarcinoma of the StomachGastric and Duodenal UlcersIndigestion: DyspepsiaCauses are many: Discomfort in GI tractMay be symptom of gallbladder disease, ulcer, chronic appendicitis– Further intervention may be requiredCause may be unknown and associated with stress, overindulgence, rapid eating– Note eating patterns , and suggest changesAcute GastritisSimilar symptoms to esophagitisCauses may be overeating, overuse of EtOH, tobacco, over use of aspirinTrauma, surgery, shock, renal failure, fever, radiation therapy, Helicobacter pylori infectionNutrition: rest stomach for 24-48 hours: no food; Then add liquids and advance as toleratedChronic GastritisCause unknown: often precedes cancer or ulcerInfection of Helicobacter pylori ?Nutrition care: General good nutrition– adequate calories; avoid gastric irritants and stimulants– Avoid large meals that distend the stomach and induces painAtophic gastritisLoss of parietal cells– inability to produce HCl (achlorhydria) and intrinsic factor

Reduced B12 statusRequires B12 injections

Gastric SurgeryTreatment for damage that is not reparable – Ulceration– TumorBillroth 1– Dumping Syndrome: not much absorptive surface

Intact nutrients to lower bowel with water influxGastric Surgery

Billroth 2– Less dumping because of conservation of more absorptive surfacePyloroplasty– Enlarge the Pyloric valve to increase rate of chyme passage to duodenum

Helps relieve gastric pressure in esophagitisMay result in duodenal reflux

VagotomyVagus nerve severed to reduce rate of gastric emptying and HCl secretion– May result in dumping syndromeDumping syndrome:– When food is dumped into the Jejunum instead of gradual movement without total digestion– Results in hypertonic contents drawing in water from surrounding tissueDumping SyndromeResults in diarrhea, cramping plusDecrease in blood volume:– low cardiac output, sweating, tachycardia, electocardiographic changes, weaknessTreatment: Use of fiber to slow rate of glucose absorption may be usefulLaying down following eating to slow gastric emptyingDumping Syndrome: Nutritional ManagementHigh 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 mealsAlimentary HypoglycemiaPost-meal hypoglycemia: weakness, perspiration, hunger, nausea, anxiety, tremorsCaused by rapid absorption of glucose and resultant over-secretion of insulin– BG drops quicklyTreatment: eat small meals; avoid concentrated sweetsStomach Surgery: MalabsorptionBillroth 2: bypassing duodenum– Results in steattorhea, dumping syndrome– secretion of secretin and pancreozymin by duodenum mucosa

Normally these stimulate duodenum to secrete enzymes and bicarbonateFoods aren’t as well digestedPancreas atrophies

Anemia: Post-gastric surgeryCaused 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 resultsB12 deficiency because of IF reduced productionAnemiaMay require supplementation of iron, B12, folateMay require B12, iron parenteral administrationGastric and Duodenal UlcersPeptic Ulcer: Erosion of gastric or duodenal mucosaEtiology: 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 bicarbonateUlcer ManagementMedical: – 1. Neutralization of acid– 2. Reduction of acid secretion in stomach– 3. Preservation of epithelial tissue– 4. Eradication of H. pyloriUlcer Management1. 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 hydroxide2. Reduce acid secretion: Cimetidine (Tagamet)Blocks histidine receptorsUlcer Management3. Cytoprotection: such as arachidonic acid– Helps to form a protective mucosal layer over ulcer4. Antibiotics: tetracycline– fights off H. pylori– combined with antiacid, even better resultsNutrition and Ulcers1. Reduce acid secretion2. Maintain acid resistance3. Limit Pt discomfort4. Restore good nutritional statusNutritionEat three small meals a dayAvoid caffeine and alcohol and cigarettesAvoid aspirin and other NSAID’sAvoid known irritant foodsEat in a relaxed atmosphereTake antiacids 1 to 3 hours after meals and before bedtimeIntestinal DiseasePrinciples 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 fecesSome disease states require restriction of residuee.g.: acute inflammatory bowel disease: (IBD) Reduced fecal output is part of treatment

Minimum Residue DietAvoid whole-grain breads, cereals, brans, seeds, peanuts, popcorn, legumes, potatoes, coconutAvoid fruits and vegetables: use juices insteadAvoid connective tissue in meatLimit milk and milk products to 2 cups per dayMinimum Residue DietUse of elemental formulas may be helpful– Vivonex from Novartis NutritionSymptoms of Intestinal DysfunctionFlatulenceConstipationDiarrheaSteattorhea

Diseases of the Small IntestineCeliac DiseaseTropical 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 malabsorptionCeliac disease: SymptomsOnset may be early: children when they initiate foods with gliadin or middle ageKids: diarrhea, failure to thrive, projectile vomiting, 10 + stools/dayAdults: weight loss, weakness, steattorhea, with or without diarrheaCeliac Nutritional CareRemoving gliadin from diet– wheat, barley, buckwheat, rye and oats– sub with corn, potatoes, rice, soybean, tapioca, and arrowroot Supplementing vitamins, minerals, protein, electrolyte replacementSecondary problems such as lactose intolerance requires lactose restrictionTropical SprueUnknown origin: found in tropical areas, perhaps associated with exposure to coliform bacteria– increased risk with nutritional deficiencySymptoms: D, Anorexia, abdominal distention, night blindness, glossitis, stomatitis, cheilosis, pallor, edemaTreatment:– tetracycline, with folate and B12 supplementsEnzymes DeficienciesThree 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 childhoodExamples: Lactase deficiency most commonLactase Deficiency70 % of world’s adults are unable to digest Lactose, especially in blacks, Asians and South AmericansEven those who retain Lactase, activity is reduced in adulthood to about 10% of neonatal valueDx: Lactose tolerance test: 50 g lactose given; less than 25 mg/dl glucose in bloodLactase Deficiency: Nutrition CareReduce or remove lactose from dietSome milk products with reduced lactose can be tolerated– aged-cheesesLactaid-treated milk: pre-digests lactoseDiseases / Problems of Large IntestineInflammatory Bowel Disease (IBD)– Crohn’s disease– Ulcerative colitisIrritable Bowel Syndrome(IBS)Diverticular DiseaseColon CancerSurgeries

Inflammatory Bowel DiseaseOnset 15 to 25 years in both sexesCrohn’s: may start in small intestine and spread even after partial resectionCourse varies: may become benign and disappear, may cause blockage or fistulaSymptoms: 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 rectumMost common in 20 to 40 yos or 50 to 60 yosSymptoms: rectal bleeding, D, dehydration, electrolyte imbalance, anemia, Treatment for IBDSurgical resection– effective in Ulcerative colitis: ends threat of colon cancer and recurrence in most cases– may not be effective in Crohn’s DiseaseNutrition: Enteral nutrition to prepare for surgery appears to work IBD: Nutrition CareFairly Complicated and individualized based on the current state of disease.Usually leads to malnutrition, food sensitivities and intolerancesObjective is to find a means to supply nutrients which don’t induce intestinal distressIBD: NutritionHigh energy: 40 to 50 kcal/kgHigh Protein: 1 to 1.5 g/kgFrequent feedingsSteattorhea induces loss of Ca, Zn and Mg– assessed and supplemented– Fat 25% of kcal; use of MCT oilIV EPA may be helpfulIBD: NutritionLactose avoidance due to secondary lactase deficiencyHigh fiber diet as a norm, but may be limited during acute flare-upsAnemia: iron, B12, and folate supplementsTPN may be necessary if needs are not met by GI tractIrritable Bowel Syndrome(IBS)Abnormal stooling pattern lasting longer then 3 monthsD, Constipation, excessive flatulence, rectal pain, blood in stoolsCause unknownDiet: normal with high fiber(20 to 30 grams) if this fails thenAntidiarrheal agents, stress reduction

Diverticulosis, -itisOutpocketing of colonic wall due to herniationMay result from low fiber diet10 to 15% develop diverticulitis: ulceration and perforation causing blood loss and infection– 10 % of those requiring surgery dieDiet: High fiber; low residue during flareupSurgery:ResectionEffect 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 diarrheaIleostomy/ColostomyIleostomy:When entire Colon is removed– New opening for waste removalColostomy: When rectum removedNutrition: depending on the GI tract removed, specific recommendations– eg: if terminal ileum is removed: B12 supplementation or injection requiredTHE 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 DiseaseDefinitions: 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 diseaseMortality

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 fatPathology 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 takenCatheterization

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 incidenceThrombosis: 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 tissueRisk 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 diseaseNational 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 abnormalityPhenotype 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 dittoPhenotype Classification

Phenotype Lipoprotein Abn Lipids

Type IV hi VLDL hiChol

hiTrig

Type V hi Chylo, hi VLDL hi Tri

hiCholGenetic 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 CHDFH: 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 drugsPolygenic 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 medicationsFamilial 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, MedicationFamilial 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 hyperlipidemiasFamilial 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 TxPharmacologic 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 vomitingPharm. 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 functionPharm. Agents

4. Fibrates:

– Gemfibrozil: Abdominal pain, dyspepsia, D, Constipation, flatulence

5. Probucol:

– changes in bowel function, NMedical 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 ptMedical 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 foodHypertension

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/dPharmacologic 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

• PropranololCongestive 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 diseaseCHF 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

1 million Nephrons: Consists of Glomerulus connected to a series of tubules which can be broken into functional segments• proximal convoluted tubule• loop of Henle• distal tubule• collecting duct Glomerulus surrounded by Bowman’s capsule• mass of capillaries: blood is filtered to produce ultrafiltrate Kidney Function

Ultrafiltrate contains blood material that is less than 6500 molecular weight

No blood cells

No protein

No other large moleculesKidney Function

Water and electrolyte conservation Antidiuretic Hormone (ADH) secreted by posterior pituitary when osmolality of blood rises• Shuts off when osmolality falls Kidney can concentrate urine as much as 1200 mOsm or as dilute as 50 mOsm Urinary volumes vary based on need to excrete extra fluidKidney Function

ADH: Diseased kidney doesn’t respond to ADH as well and tends to allow water retention Reduced urine output in Renal patients oliguria: less than 500 ml/dayKidney Function

Other Waste Products accumulate with renal failure

Azotemia: Build up of urea, uric acid, creatinine and ammoniaKidney Function: Blood Pressure

Renin-Angiotensin System: Decreased 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 In diseased kidney, this mecahism may be less functional: high or low blood pressure/water retentionKidney Function: RBC Formation

Erythropoietin: kidney produces this hormone Acts on bone marrow to produce RBC’s In diseased kidney, lack of Erythropoietin:• results in severe anemia Renal patients are given injections of erthyropoietin to stimulate RBC rpductionKidney Function: Ca, P

Vitamin D activation happens in kidney

With diseased kidney, this is slowed down

Less active vitamin D Results in less absorption of Ca in gut more bone release of Ca and weak bones• Poor bone statusDiseases of the Kidney

Glomerular Diseases Nephrotic syndrome Nephritic syndrome

Tubule and interstitium diseases Acute renal failure (ARF) Other tubular diseases PyelonephritisNephrotic Syndrome

Group of diseases cause Protein loss through glomeruli hypoalbuminemia with edema• concentrates blood hypercholesterolemia hypercoagulability abnormal bone metabolismNephrotic Syndrome

Most often caused by: Diabetes systemic lupus eryththematosus(SLE)• connective tissue disorder of immune origin• causes damage to many systems and noted by skin eruptions, arthritis, neurological problems amyloidosis:abnormal deposits of amyloid in tissues• a starch-like glycoprotein primary cause unknown• secondary due to TB and rheumatoid arthritisNephrotic Syndrome: Nut Care

Objective: replace lost protein in urine

High Biological Value Protein from 0.6 to 1.5 g/kg/d

Energy 35 to 50 kcal/kg/d for adults; 100 to 150 kcal/kd/d for kids to spare protein

Edema: mild sodium restriction

Hypercholesterolemia: lipid lowering drugs with chronic Nephrotic SyndromeNephritic Syndrome

Inflammation of capillary loops of glomerulus caused by several disease states acute 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

Objectives: maintain good nutritional status

Often focus is on treating underlying cause

Usually no need to restrict protein, or K unless uremia or hyperkalemia exists

Sodium restriction with HTNDiseases of Tubules & Interstitium

Acute Renal Failure: Sudden reduction in Glomerular Filtration Rate (GFR)

GFR: the quantity of glomerular filtrate formed per unit of time by the kidneys

Results in the inability to filter wastes from the blood

Causes are manyARF : Causes 3 Categories

Prerenal

Intrinsic

Postrenal Obstructive

Treatment: remove underlying problem

Course of the problem depends on underlying causeARF: Intrinsic Problems

Possible causes: toxic drugs allergy to drugs progressive glomerulonephritis ischemia 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 elminationARF: Nut Care

Early: TPN may be used to maintain nutritional status

Hemodialysis, peritoneal dialysis or continuous arteriovenous filtration (CAVH) CAVH uses small ultra filtration membranes to produce an ultrafiltrate• this is replaced with parenteral nutrition fluids to prevent fluid overloadARF: Nut Care

Protein:Early, TPN with Glucose and some protein in form of essential A.A.s such as Aminosyn-RF(Abbot Labs)

Amount of Protein dependent on pt 0.3 g/kg and progress toward 0.8 to 1 as pt improves

Energy needs are high: 50 kcal/kg most from CHO and lipids via TPN or enterally with addition of formulas (Polycose, Ross)Pyelonephritis: UTI

No specific nutritional management

Chronic cases: cranberry juice Reduced adherence of E.coli to epithelial walls of urinary tractNephrolithiasis: Kidney Stones

10 % of men and 3 % of women have a stone during adulthood

Formed in kidney when substances in urine reach levels that cause crystallization

May be made from calcium salts, uric acid, cystine, struvite (ammonium, magnesium, and phosphate)Kidney Stones: treatment

In all cases: High fluid intake (1.5 to 2 liter/day) to keep urine dilute

Other intervention depends on the cause

80% of stones composed of Ca oxalate or Ca phosphate

Causes are multiple: hyperparathyroid ism, hyperuricosuria, renal tubule acidosis (RTA)Kidney Stones: Treatment

Remove underlying cause: e.g.: remove parathyroid adenoma if Hyperparathyroid Treat RTA with medications to reduce acidity Hypercalciuria seldom treated with low Ca diet

Nutrition: Reduce Oxalate in diet, add additional Ca to diet to tie up oxalate in gutKidney Stones: Uric Acid

Associated with gout, an acid urine

Treatment with raising urine pH to 6 to 6.5 through high alkaline-ash diet milk, nuts, vegetables except corn and lentils, all fruits except cranberries, prunes, plums, molassess avoid breads, meats, cheese, pnut butter, and vegies and fruits aboveGlomerular Filtration Rate (GFR)

Defn: total plasma volume filtered by the kidney per unit of time

Normal is 120 ml/min

GFR = Urineinulin X Urine volume

_____________________

Plasmainulin

Can also be done with creatinineNormal Kidney Function

How long does it take to filter all of a person’s blood? HINT: 6 L of bloodOther Labs Used to Determine Kidney Function

Blood Urea Nitrogen(BUN): How well urea is cleared by the kidney Normal is 8 to 23 mg/dl High is indication of poor fxn

Creatinine: end product of creatine metabolism in muscle; cleared in urine Normal is 0.6 to 1.6 mg/dl High is indication of poor functionProgressive Nature of Renal Disease

Slow, steady, decline in renal function

Nutrition intervention depends on Renal Function determined by GFR

Protein Intake: major concern

Protein GFR

0.8 g/kg(60%HBV) >55 ml/min

0.6g/kg(60% HBV) 25-55 ml/minProgressive Renal Disease

Protein restriction: individualized Must be weighed against possible protein malnutrition If elected, careful monitoring of protein status must be made with anthropometric and lab valuesEnd-Stage Renal Disease

Can be caused by several disease states

90 % have Db, glomerulonephritis, or HTN

Problems include: inability to remove wastes maintenance of fluid and electrolyte balance problems with hormone production

Uremia: high BUN, a major problemUremia: Symptoms

With BUN at 100 and Creatinine at 10-12 symptoms usually show up

Generally: weakness, nausea, cramping, itching, metallic taste

Further intervention requiredESRD: Treatment

Transplantation

Dialysis Hemo Peritoneal• intermittent peritoneal dialysis (IPD)• Continuous ambulatory PD(CAPD)Transplantation: Nut Care

Based on metabolic effects of immunosuppressive meds: corticosteroids and cyclosporine

Corticosteroids: increase PRO metabolism, hyperlipidemia, Na retention, wt gain, glucose intolerance, reduced Ca and Vit D metabolism

Cyclosporine: hyperkalemia, HTN, ^ lipidsTransplant Nutrition Care

First month Post-transplant: PRO: 1.5 to 2 g/kg Energy: 30 to 35 kcal/kg moderate Na restriction to prevent fluid retention (80-100 mEq/d); monitor K and P

After one month: PRO: 1 g/kg Adjust Kcal to maintain/achieve Ideal weightHemodialysis

Most common form of dialysis

Fistula created by surgery connects an artery and a vein usually on the forearm may require an artificial vessel to enlarge the vessel Large needles are temporarily inserted to allow blood to exit the body and circulate through the dialysis machine Usually required 3 x / week for 3 to 5 hoursHemodialysis: Nut Care

Energy: 35 kcal/kg IBW

PRO: 1 to 1.2 g/kg; 1.2 to 1.5 if needed

Fluid: 800 ml/d + urine output

Na: 2-3 grams/day

K: 2-3 grams/day

P: 1 to 1.2 g/dPeritoneal Dialysis

Makes use of the semi permeable membrane of the tissues in the peritoneal cavity

Catheter surgically implanted in the abdomen

Dextrose containing dialysate is instilled into abdomen wastes diffuse into dialysatePeritoneal Dialysis

Fluid is withdrawn and discarded; new fluid is then instilled

Less efficient then hemo

10 to 12 hrs, 3 x week

PRO: 1.2 to 1.5 g/kg due to larger Pro loss

Energy: 30 kcal/kg (40-50 for repletion)

Fluid, Na, K, and P same as hemoContinuous Ambulatory Peritoneal Dialysis(CAPD)

Similar to peritoneal but the dialysate is exchanged manually without the help of a machine

Exchanged 4 to 5 x /day for 24-hour treatment

Increased loss of Protein, increased absorption of Dextrose, up to 800 kcal/dCAPD Nut Care

PRO: 1.2 to 1.5 g/kg

Energy: 25 kcal/kg

Fluid: ad lib

Na: 6 - 8 grams / d

K: 3-4 g/d

P: 1.5 to 3 g/d

Weight gain is the norm for CAPD patientsESRD: Other concerns

Psychological Support: large life changes Depression: lack desire to eat Thirst, lack of taste and taste changes due to uremia

Vitamin D status: activation of Vit D happens in the kidney loss of function results in low status Vit D supplementsComplications

Low Vit D results in low Ca in blood Triggers release of PTH; this removes Ca from bone Results in osteitis fibrosa cystica: a demineralized bone disease causing dull bone pain Serum P remains high because it is not cleared by kidney Calcium intake should be high, P should be lowComplications of Renal Disease

Calcium supplements help bind P in the gut Ca carbonate, acetate, lactate or gluconate Ca citrate is avoided because it helps absorb Al

Vit D orally or intravenous helps with hypocalcemia

Fluoride serum levels often high in dialysis pt: contributes to decalcification of bone Deionized Fl containing water before used in dialysisIron/Hemoglobin status

Kidney produces erythropoietin which induces bone to produce RBCs Synthetic EPO injections are used to treat

Vitamin deficiencies may occur Reduced intake with P restriction: many P rich foods are also vitamin rich, e.g.: fruits and vegetables Water soluble vitamins are dialyzed offComplications

Vitamin supplements given: some specially formulated for dialysis pts Nephrocaps: Fleming and Co.

Carbohydrate: glucose intolerance due to tissue resistance to insulin

may require control of glucose in diet in hyper may require addition of dextrose to dialysate in hypoglycemicComplications

Atherosclerosis: most frequent cause of death in hemodialysis Caused by underlying disease: HTN, diabetes, nephrotic disease Plus abnormal lipid metabolism in ESRD Increased synthesis of VLDL and decreased clearance diet restriction of fat; and use of lipid lowering drugs may be used with high risk ESRD ptsUse of Parenteral Nutrition

When pt is too sick to eat, TPN may be required

More on TPN laterRenal Assignment

Page 801 Hemodialysis case study #1

Do a nutrition assessment on pt

Write in up in SOAP format that includes Problem list in ‘A’ and solutions in ‘P’

Include in the solution list a one day diet based on appropriate intake of Kcal, fluid, Pro, K, P, and Na

Use exchange list on p 792 to help

In addition, answer questions presented

Physiological StressStress Happens:InfectionsFeverSurgeryBurnsTraumaMetabolic Need with StressIncreased Kcal needOften unable to meet need nutritionallyResults in decrease in nutritional statusIncreases risk of infectionThis stress response differs from starvationIn starvation:Uses up glycogenThen amino acids from skeletal muscle and circulating proteins are used

– Gluconeogenesis

– Negative N balance-12 g/day of Nitrogen lossRepresents 75 g/day of protein loss or about 3 ouncesAfter several days, body conserves N and uses FA’s

Fatty Acid UtilizationSerum insulin decrease therefore allowing FA’s to be mobilizedFatty 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 dropsMetabolic Stress Response Differs:

Causes increase in metabolic rateWhen metabolic stress and starvation are coupled:

– Body needs more energy

– Starts breakdown of lean tissueHormonal and Endogenous Mediators of StressAdrenocorticotropic Hormone (ACTH)Catecholamines (Epinephrine, Norepinephrine from the adrenal medulla)AldosteroneAntidiuretic Hormone (ADH)Phagocytic CellsNet Result: MORE ENERGY SUBSTRATES AND MORE OXYGENHormonesACTH

– Result of nervous stimulation of hypothalamus

– Acts on Adrenal Cortex to release cortisol

– Causes mobilization of amino acids from skeletal musclesCatecholamines (epinephrine and nor-ep.)

– Released by Adrenal Medulla with shock and high glucagon/insulin ratio

– increased glycogenolysis, gluconeogenesis, lipolysisMediators of StressAldosterone: Released with stress

– Na retention in kidneyAntidiuretic Hormone (ADH)

– Retains water in kidneyPhagocytic Cells in StressRelease cytokines and tumor necrosis factor

– induce greater uptake of amino acids by liver

– induce greater production of proteins

– Other interactionsInteractions between Nutrition and InfectionsDecreased Nutrition lowers resistance to InfectionInfection aggravates existing malnutritionTherefore: people with chronic undernutrition

– Succumb to infections or

– Take longer to recoverNutrient needs Increase During InfectionStress reaction induces catabolic effect with increased losses of nitrogen, Mg, K, P and ZnIncreased energy need with severe infections or feverAnorexia decreases food intakeIncreased losses due to V/DMalabsorption in enteric infections may decrease nutrient utilizationEstimating Stress LevelTraditional methods not always usefulUrine 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 NeedsIndirect Calorimetry:

-A good method of estimating energy expenditure in critically ill patient

– Not always availableUse of Harris-Benedict: BEEtimes stress factor

– 1.35 Skeletal trauma

– 1.6 major stress

– 2.0 severe thermal injuryEnergy Nutrients25 to 30 nonprotein kcal/kg per dayCHO 60 to 70 % of Kcals

– 5 to 7 mg/kg/minute or about 7.2 g/kg/dayFat: remainder of nonprotein kcals

– 15 to 40 % of KcalPRO: 1.5 to 2 g/kg/day

– nonprotein cal to gram Nitrogen ratio 100:1

– More protein doesn’t add any advantageProteinBranch-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 retentionimproved hepatic protein synthesisdecreased protein degradationachievement of N equilibrium in less time

Estimating Energy and Protein1. H-B: BEE eg 1500 (67kg)2. BEE x injury factor(eg: surgery 1.5)

– Total Kcals needed = 1500x1.5= 22503. 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=115PRO and NonProtein KcalsAlternate Method (assume 67 kg person)30 to 35 kcal/kg = 2010 to 2345 kcal/day1.5 to 2.0 g protein/kg = 67 kg x 1.5 = 100 to 134 grams Pro/day100/6.25 = 16134/6.25gPro/gN=21134 x 4 kcal/g=536nonpro kcal= 1474 to 1809/21=70 to861474/16=92 to 1809/16=113

Nutrition SupportSelecting a methodIf the gut works, use itWhen 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 NutritionBy way of the GI tractCould be

– Oral Supplements

– Tube Feedings

• Nasogastric

• Nasoduodenal or nasojejunal

• Enterostomies– Gastrostomies Percutaneous Endoscopic Gast.(PEG)– Jejunostomies Multiple Lumen tubesSelecting an Oral Supplement1. Degree of inability to meet needs2. Presence or absence of disphagia3. Taste preference or sensitivity4. Availability of labor and resources for preparation 5. Tolerance to lactose or other components6. Tolerance of osmotic loadSupplement ComponentsKcals: 250 kcal/ 240 ml portion is the normFat:

– Usually Long Chain Triglycerides

• Could be MCT if pt doesn’t tolerate fatsProtein:

– 8 to 14 grams of intact proteinCHO

– Form varies: Simple adds sweetness and osmotic loadTube Feedings: Route of AccessSeveral 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 interventionNasogastric RouteNasogastric Tube: simplest accessPt requires functional GI tract and normal gag reflexCan be large bore tube (French #12+)

– Used for food, medications and gastric suctioning orSmall bore, pliable tube

– Greater comfort, but more easily cloggedNasoduodenal or NasojejunalTube threads through stomach to duodenum or jejunumMigration from stomach to duodenum via peristaltic waves may take a few daysRadiologic verification is requiredSmall bowel feedings require careful selection of enteral formulaEnterostomies

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 peritonitisSurgical JejunostomyNeedle jejunostomy(temporary)Catheter jejunostomy(more permanent)

– both reduce risk of pulmonary aspiration

– small lumen size of tube difficult to maintain so not often performedFluid requirements1ml of water per kcal35 ml/kg usual body weightFormulas contain 80 to 85% watermay need to add water as an additional flushOsmolalityIntact formulas fall between 300 to 500 mOsmol/kg , approx the same as body fluids

– No real concerns with fluid shiftsHydrolyzed formulas are often higher

– up to 900 mOsmol/kg

– contributes to extra fluid and electrolyte loss

– diarrhea

– Proper administration is keyAdministration of EnteralsContinuous dripIntermittent dripBolus feedingContinuous DripEstimated total kcal needs are madeRate 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 DripCaution when initiating tube feedingIf the gut has not been used latelyIf the formula is hyperosmolarFeedings 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 halfAdmin of Tube FeedingIf intolerance: decrease to previous increment and advance as toleratedDon’t hang a bag for more than 4 to 8 hours

– Food born illnessDon’t add new formula on top of old formulaBag should be changed dailyAdministration 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 aspirationIntermittent or Bolus FeedingsQuality of Life: A more normal lifestyle with intermittent feedings

– Frees pt to be mobileFiguring intermittent or bolus feedings similar to continuousTotal Kcals determinedDivided by number of hours feedingGeneral: 4 to 6 feedings @ 20 to 60 minAdministration of Bolus or Intermittent FeedingResiduals checked more frequently: every 2 to 4 hoursFew pts can tolerate more than 450 ml per feedingPt needs to be monitored for several potential problemsMonitoring Tube Fed PtWeight 3 x wkSigns of Edema dailySigns of dehydration dailyFluid In/Out dailyCal, Pro, fat, CHO, vit & min 2+/wkN balance (24-hour UUN) weeklyGastric residuals (2 to 4 hrs)

Monitoring Tube Fed ptStool 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 weeklyTube Feeding ProblemPulmonary Pt with 1800 kcal need

-No renal problems or fluid restrictions

– gastrostomy in placeTube 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 ProblemOsmolality 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 NutritionIf pt is unable to receive nutrients via the GI tract

– Then Parenteral Nutrition is AppropriateParenteral AccessPeripheral 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 capacityParenteral AccessShort 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 infectionParenteral AccessLong-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 SolutionsD DextroseW WaterNS Normal Saline (0.9%) NaCl solution 0.9 g NaCl/ 100 mlD5W 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 SolnProtein

– 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 FatFat in Parenteral SolnUsually comes in 10% or 20% solutions10 % represents 1.1 kcal/ml20 % represents 2.0 kcal/mlUsually composed of safflower, soy oils with egg yolk as an emulsifier to hold in solutionGenerally 20 to 30 % of KcalDon’t exceed 60% (2.5 g/kg/d)CHO in Parenteral SolutionDextrose monohydrate

– D Glucose

– Concentrations range from 5% to 70%

– Shouldn’t exceed 5 mg/kg/min

– Used to spare protein and provide kcalsCalculation of OsmolalityDextrose grams/l x 5Protein grams x 10Fat is isotonic so no osmotic forceelectrolytes further add to osmolarity50 g of dextrose plus 30 grams of protein(50 x 5) + (30 x 10) = 550 mOsm/lIndications for Peripheral Vein Feedings1. Short term: enteral feeding again in 7 d2. Transition with enteral feeding

3. Mild to mod malnutrition:supplemental nutrition needed4. Normal or mild elevation of metabolic rate5. No organ failure or fluid restrictionIndications for Central Vein Feeding1.Unable to enteral feed for 7 + days2. Mod to severely elevated metabolic rate3. Moderate to sever malnutrition4. Cardiac, renal, or hepatic failure or other conditions limiting fluid5. Limited access to peripheral veins6. Able to access central veinCompounding MethodsTwo methods of prescription compounding:

1. All components except fat2. All components including fat

May be batch mixed to save moneyor may be individually prescribed and mixedIs done by pharmacist in aseptic conditionsAdministration of TPNContinuous 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 restartedGuard against hypoglycemia

Cyclic InfusionTo free individuals who are capable of mobilityTPN for 12 to 18 hour infusion periods are possible. Allows pt to be mobile for 6 to 12 hoursCyclic administration is established incrementallyMonitoring and Problem SolvingActual intake of TPN is monitoredMonitor Growth, weightMetabolic parameters Table 20-10 p442

– serum lytes, BG, Hb, etcGeneral

– Volume of infusate, oral intake, urinary outputInfection

– Clin Observations: temp., WBC, culturesRefeeding syndromeWith 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 KTransitional FeedingParenteral to Enteral

– begin at 30 cc/hr

– increase 25-30 cc/hr every 8 to 24 hours

– Parenteral solution is reduced accordinglyParenteral to Oral

– Monitor oral intake; less predictable than above

– Reduce Parenteral accordingly

Enteral to Oral

– Adjust to intermittent feeding firstNutrition Support in Other SettingsLong-term Care

– More happening in nursing facilitiesHome Care

– People are at home receiving nutrition support

– Concerns:

• motivation

• family’s ability to handle

• benefit of receiving nut support

• limitations such as phyicalEthical IssuesEnd 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 supportProblems3 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 kcalProblem2.5 l of 3.5% Dextrose(3.5 g/100ml)(1000ml/l)(2.5 l)(3.4 kcal/g)=297.5 kcalProblem3 l of 25% Dextrose and 3.5% Amino AcidsHow 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 PROTotal = 2550 + 420 = 2970; 2550/2970=86% from CHO and 14% PROProblem500 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 PROProblem (cont)10% fat emulsion = (1.1 kcal/ml) (500 ml)= 550 kcal from FatTotal = 1700 + 350 + 550 = 2600 kcal1700/2600 = 65% from CHO350/2600 = 13.4% from Pro550/2600 = 21 % from Fat Nut AssessmentPt requires 2200 kcal60% kcal from CHO25% kcal from fat15% kcal from PROHow would you formulate this?Fat first: you need 2200 x .25 = 550 kcal

10 % fat emulsion @ 1.1 kcal/ml550 kcal/ 1.1 kcal/ml = 500 ml 10% solnNut assessmentFinal volume of 2000 mlFat contributes 500 ml 1500 ml for PRO and CHO2200 kcal x .6 = 1320 kcal/3.4 kcal/g= 388 g CHO/1500 ml = 25 % Dextrose solution2200 kcal x .15 = 330 kcal/4kcal/g = 82.5 g PRO/1500 = 5.5 % aa solution final concentration

Nutrition and CancerDiet and Cancer80 % of cancers are related to environmental causes

35% of all cancers are diet relatedIn Japan, low rate of breast and colon cancerAfter 2 to 3 generations in the US, Japanese Americans have similar rate of breast and colon cancer

Due to changes in diet and lifestyleTwo Concerns Regarding Cancer and DietDiet 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 ratsAntioxidants and cancer: Vit A, E, C, Selenium, beta Carotene, Zn may have some relationships.

Nitrates, Nitrites and Nitroso compoundsNitrates 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 stomachCancer and Substrate MetabolismTumor exerts calorie drainAnorexia usually turns down metabolism

But not with Cancer: Metabolism is turned upCHO: constant drain of CHO Kcal in anaerobic metabolism

Production of lactic acidMay increase gluconeogenesis of lactate via Cori cycle in some cancer patients

Protein MetabolismMost changes include emaciation due to tissue protein breakdown to supply amino acids required to build cancer cells

hypoalbuminemiavisceral organ atrophymuscle wasting

Lipid metabolismCancer promotes lipolysisSubsequent reduction in total body fatDecreased lipid clearance from the serum and elevated plasma free fatty acidsOther Metabolic AbnormalitiesElectrolyte imbalance

hypercalcemia especially in bone metastasizing tumors or breast, lung and pancreasFluid imbalances

diarrhea causing tumors: secretion of serotoninvomiting with intestinal obstruction

Alterations in taste and smellcontributes to anorexia

Cancer Therapy

Chemotherapykills rapidly reproducing tissuesnausea and vomiting, taste abnormalities

Radiation Therapy: whole body or regionalRadiation enteritis: inflamation GI tract, head and neck

short-lived or long lastingSurgery: depending on site of removalNutrition Care of Cancer PtGoals:

1. Prevent or correct nutritional deficiencies2. Minimize weight loss

Early intervention is importantTiming of Food presentation

early in the morningfoods that are likedavoid food aversionsuse of ‘scapegoat’ foods prior to chemo

Diet and CancerNutritional 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 6Inflammatory cytokinesProduced by tissues undergoing damage or cancer growth

My induce growth in cancer cellsMay impair metabolism in non-cancerous tissue

Induce nausea Affect energy metabolism

Liver & HIV/AIDSFunctions of the LiverCarbohydrate MetabolismFormation 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 LiverFat MetabolismOxidation 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 producedFunctions of the LiverProtein MetabolismTransamination & 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 fluidsFunctions of the LiverOtherActivates vitamin DConverts carotene to vitamin AStorage of iron as ferritinStorage of fat-soluble vitamins, vit B12, Zn, Fe, MgDrug metabolism (including alcohol)Deactivation of hormonesHepatitisInflammation of the liver

Viral

– A, B, C, D, E

Alcohol

Drug-inducedAlcoholic Liver Disease (ALD)3 StagesFatty liver (hepatic steatosis)

– Caused by: mobilization of FA’s from adipose tissue hepatic synthesis of FA’s FA oxidation TG productionTrapping of TG’s in the liver

– Reversible with abstinence from alcoholAlcoholic Liver Disease (ALD)3 Stages (continued)Alcoholic Hepatitis

CirrhosisScar tissue formationChange in the normal architectureIrreversible portal hypertension…results in:

VaricesAscites

Hepatic EncephalopathyGrade I: Mild confusion and impaired coordination

Grade II: Flapping tremors (asterixis) and slurred speech

Grade IV: Loss of consciousness and comaHepatic EncephalopathyTheories Behind the CauseAmmonia build-up

Bacterial degradationBlood from GI bleedDietary protein

Altered neurotransmitter theory BCAA’s AAA’s, met, glu, asp, his

Nutrition AssessmentDegree of malnutrition

Lab values

Weight

Triceps skinfold

Subjective global assessmentNutrient RequirementsEnergy: 1.2-1.5 x BEE

Dry weight

Lipid: 25-40% of total kcals

Protein: Controversial

Vitamins and mineralsHIV/AIDSVirus invades CD4+ (T-helper) lymphocyte cells

Transmitted viaBlood and semenShared contaminated needlesContaminated blood productsAcross the placenta from mother to baby

Clinical CategoriesAcute phase

Clinical categoriesA: AsymptomaticB: SymptomaticC: AIDS-indicator condition

Common ProblemsOpportunistic infections

Malignancies

HIV encephalopathy

Protein-energy malabsorption

Diarrhea, steatorrheaNutrition AssessmentLab values

Problems pt is currently experiencing

Weight history

Dietary intake

Subjective global assessmentNutrient RequirementsEnergy: 1.3-1.5 x BEE

Protein: 1.0-1.4 gm/kg/day

Fat

Vitamins and minerals

Acute and Chronic PancreatitisNutrition ManagementFunctions of the PancreasUpper AbdomenExocrine and Endocrine Function

Glucagon, Insulin, somatostatin(endocrine)Amylase, lipase, trypsin(exocrine)

Common Bile DuctFood ingestion triggers pancreatic secretionsPancreatitisInflammation of the pancreasAttacked by its own enzymesMild to severeAcute or chronicMortality Rates:

Acute: 10-25%Chronic: 5%

Acute PancratitisCauses:

GallstonesClogged Common bile duct: Autodigestion

ETOH AbusePancreas sensitive to ETOH Abuse

Otherhypertriglyceridemia, drugs, mumps and other infections

Chronic PancreatitisNo CureBegins as acute; becomes chronic with scar tissueYears of ETOH abuseAffects digestion enzyme and insulin productionAffects nutrition digestion and absorptionChronic SymptomsWt lossN,V, D or SteatorheaCan be continuous or intermittentgradual or severe upper abdominal painsymptoms of DMDiagnostic MethodsSerum Lipase and Amylase are elevated

Peak 48-72 hrs after pancreas injuryPhospholipase A2 elevated

Decreased albumin and CaIncreased BGIncreased TRIGUse of CT (computerized tomography)scanNutritional ManagementRest; Often NPO with IV hydrationIf mild: clear liquid dietProgress as tolerated to low fat dietSmall meals; adequate proteinIf severe: TPN or Enteral with jejunostomy with elemental formulasChronic PancreatitisTreat acute attackAvoid large meals, high in fat and ETOHLow-fat diet; 40-60 g/day; MCT oilSupplemental pancreatic enzymes taken orally with mealsSupplement fat soluble vitamins and B12Insulin injections with glucose intoleranceCystic FibrosisPulmonary Disease with multisystem affect1:2500 caucasian birthsPrevious CF pt did not reach adulthoodCurrent median age of death is 30 yrsCF pts secrete thick mucous that blocks tubesAffects Respiratory, sweat and saliva glandsCystic FibrosisAffects Intestinal tract, pancreas, liver and reproductive tractDx:

positive sweat test; chronic lung disease, FTT, malabsorption test, family HxCystic Fibrosis85% have pancreatic insufficiencyMucous blocks ducts from secreting enzymesResults in malabsorptionThick mucous lining GI tract further decreases absorptionNutritional StatusGI complications

bulky stools; cramping; obstructionsrectal prolapseLiver involvement

High Risk for MalnutritionNutritional needs difficult to meet due to malabsorption

Nutritional StatusDecrease PO

dyspneacoughing/cough induced vomitingGI discomfortimpaired smell and tasteglucosuria

Growth Retardation, FTTDifficulty achieving proper wtNutritional ManagementGood nutritional status related to longer lifeMust coordinate nutrition with other therapiesGoals:

control malabsorptionprovide nutrition for growthprevent nutritional deficiencies

Nutritional ManagementPancreatic enzyme therapies

oral administration with foodfecal fat and nitrogen balance used to assess adequacy of enzyme supplementation

Nutrition ManagementEnergy: highly individualized

Increased needs due to breathing effortsRequires high kcal, moderate fatindirect calorimetry useful

Macronutrients/ Vitamins and MineralsIncreased proteinFat 35-40% or moreFat-soluble vitamin supplementationSodium losses in sweatIndividual eval of mineral statusHow to Increase Energy IntakeNutritional SupplementsNon-fat milk PowderButter, margarine, gravies, dressingsConcentrated sugarsFortified dishesEnteral or Parenteral

Drug-Nutrient InteractionsDrug Nutrient Interactions Can Occur When:Drugs are taken with food or nutritional supplementsDrugs are taken with alcoholDrugs are used to induce specific drug nutrient interactionsDrugs are taken in multiple drug regimensDrugs that cause nutrient depletion are taken for a long timeResponsibility to Monitor Drug-Nutrient InteractionsPharmacistsNursesDietitiansDrug Action: Three Stages1. Pharmaceutical stage

– Dissolution or disintegration of drug2. Pharmacokinetic stage

– absorption, distribution, metabolism, and elimination of the drug3. Pharamacodynamic stage

– body’s physiologic and/or psychologic response to the drug Risk For InteractionsOccurs most commonly in long-term treatment for chronic diseaseDepends on the function of the Mixed-Function Oxidase System (MFOS)

system that oxidizes a bunch of substancesincludes cytochrome P-450NAOPH-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 tasteDrugs that Affect Nutrient Absorption

Drugs that Affect Nutrient MetabolismAntivitaminsMonoamine Oxidase Inhibitors(MAO)Excretion of NutrientsDrug-Induced Electrolyte Alterations

Drugs that Affect IntakeAppetite suppressants:

Ritalin used with hyperactive childrenlong-term use may result in growth-retardationcatch-up growth may occur when discontinued

Cisplatin: a cytotoxin agent used in cancer therapycauses nausea, vomiting, and reduced food intake

Drugs That Affect Nutrient AbsorptionLuminal Effects:

Influencing Transit TimeLaxatives

Bile Acid ActivityCholestyramine sequesters bile acids

inhibits fat digestionChange of pH

Antacids change pH and reduce absorption of Ca, Mg, Fe and Zn

Drugs that Affect Nutrient MetabolismInhibition of Synthesis of Certain Enzymes by Competing for vitamins or Vitamin Metabolites necessary for their structure

Methotrexate used in treatment of leukemia and rheumatoid arthritisThis breaksdown folate and induces a folate deficiency

DNA synthesis is stoppedMonoamine Oxidase InhibitorsCommon Interaction: MAOI and pressor amines in foods

Two classes of biologically active aminespsychoactive: neurotransmitters

norepinephrine and dopaminevasoactive: pressor amines

tyramine, serotonin, histaminethese 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 MAOIIncreases blood pressure

Antidepressant: Phenelzine sulfatePt needs to avoid tyramine containing foods

cheese, smoked fish, chianti winesmeat extracts, beer, ale,

Excretion of NutrientsSome drugs displace a nutrient from plasma binding site and make it available for kidney filtering

D-penicillamine is used to treat heavy metal poisoningIt chelates the intended metal and makes it available for kidney removalThis also chelates other metals and removes them from the circulation and induces a deficiency

eg: ZincElectrolyte AlterationsThiazide: a loop diuretic that enhances Na loss

also increases K lossK supplements may be required

Drugs of Abuse

Legal: caffeine, nicotine, alcoholIllegal: marijuana, cocaineCan induce nutritional deficiencies by decreasing nutrient intake

Decrease appetite(or increase appetite)Caffeine: induce Calcium loss in urineSome Common Drug-Nutrient InteractionsAnticonvulsants(ACDs)

Phenytoin, phenobarbitol, etcinduce deficiencies of folate, biotin, vitamin D

reduces hydroxylation of calciferol to 25, OHD3Oral Contraceptives

Increased need for B6, folateIncreased Vitamin A in circulation: may lead to decreased storesIncrease serum Iron versus non users

Anti-inflammatory DrugsGlucocorticoids: used to decrease inflammation, suppress the immune system

development of osteoporosis in 50 % of long-term usersHIV meds: AZT used to inhibit virus replication

Induces megaloblastic anemia through reduced erythropoiesisTreat with recombinant human erythropoietin(EPO)

Use of Alternative TherapyHerbal remedies are commonly thought to be less toxic than drugsThis isn’t necessarily true: Examples:

aloe: can increase diarrhea and intestinal lossginseng: can cause diarrhea and intestinal lossephedra: changes in blood pressure, dizziness

Nutritional Status May Affect Drug TherapyDrug absorption and transportDrug MetabolismDrug Excretion