Liver, Gallbladder, Exocrine Pancreas KNH 411

Liver, Gallbladder, Exocrine Pancreas

KNH 411

Pathophysiology of the LiverAlcoholism

Chronic consumption of > 80 g of ethanol/day--comprable to 250 cc’s (1 cup 80 proof liquor; liter of wine; 6 12oz beers; 6 1.5 oz shots) per day

Alcoholic liver disease (ALD)--hepatitis(inflammation of liver) or cirrhosis(hardening of liver)

Dependency may be evident as tolerance or withdrawal

Ethanol rapidly and completely absorbed even with malabsorption--only 2-10% is eliminated from the system

Cannot be stored - oxidized/metabolized is absorbed from GI tract directly

Pathophysiology of the LiverFatty Liver - Etiology in latter stages of disease

liver increases in size/weight by 5%Steatohepatitis - inflammation; usually related to

ALD If alcohol not present – NASH treatment is weight control/reductionNAFLD(nonalcoholic fatty liver disease) progresses to

cirrhosis and hepatic carcinoma Strong association with obesity, diabetes, metabolic

syndrome Most common type among adolescents

Pathophysiology of the LiverMalnutrition in the Alcoholic

Malnutrition caused by displacement of nutrientsMaldigestion or malabsorption of nutrients d/t GI

complications-- may be bloated, diarrhea, anorexicdecrease alcohol increased energy content

Pathophysiology of the LiverMalnutrition in the Alcoholic - GI Complications

Esophagus – heartburn, reduced LES pressure, esophagitis, stricture, tears from vomiting

Stomach - gastritis, duodenitis, atrophy of gastric mucosal barrier, hemorrage, PUD, pernicious anemia, stomach cancer

motility of GI can be damageddecreased HCl secretion and loss of intrinsic factor

due to alcohol--can cause decreased B12 absorption long term concern--esophageal cancer

Pathophysiology of the Liver

Malnutrition in the Alcoholic - GI Complications Intestine – structural and morphological changes,

hemorrhagic lesions of villi tips, decreased motility, increased digestion time, bacterial overgrowth(constantly adding in alcohol instead of the nutrition necessary)

Pathophysiology of the LiverAlcoholism - Nutrition Implications

hepatitis, cirrhosisSignificant caloric contributions – obesity Irregular eating habitsDecreased appetite – eventually lead to weight lossKcal derived from ethanol

0.8 X proof X ounces = kcal

Pathophysiology of the LiverAlcoholism – Malnutrition

PEM Poor dietary intake, malabsorption, hypercatabolic state,

altered energy storage, biochemical changes(look at albumin status, total bilirubin)

Vitamin deficiency--look at KADE levels/malabsorption

Major cause of liver damage and resulting dysfunction trying to alter their behavior

Pathophysiology of the LiverAlcoholism - vitamin and mineral deficiencies

Folate Thiamin--alcohol effects uptake and utilization

Wet and dry beriberi--may show signs in nerve function and decreased sensation in nervous system

Wernicke-Korsakoff syndrome--altered mental status--dimensia

Low plasma pyridoxine--due to inadequate intake Vitamin C--175-500 mg a day to try to replace what has

been lost Vitamin D – impairs osteoblastic activity--building of the

bones

Pathophysiology of the LiverAlcoholism - vitamin and mineral deficiencies

Vitamin K - clotting factors--pancreatic insufficiency Vitamin A – night blindness Interaction between vitamin A and zinc--decreased intake

and absorption of vit A can lead to night blindness Iron – altered response to infection, can start bleeding out Calcium – bone density and bone mass Potassium – hypokalemia--poor intake, but also because of

vomiting and diarrhea, may need to IV hydrate with potassium in it

Recommend multivitamin 2X RDAhigh proteinhigh calorievery malnourished individuals

Pathophysiology of the LiverAlcoholism – nutritional effects

Imbalanced diet and/or anorexia

Maldigestion and malabsorption--inflammation of stomach, pancreas and intestines causes this

Increased catabolism of visceral protein and skeletal muscle--wasting of the body

Increased excretion of vitaminswant to supplement magnesium and B vitamin

© 2007 Thomson - Wadsworth

Pathophysiology of the LiverHepatitis – inflammation of the liver

caused by virus, bacteria, toxins, obstruction, parasites or drugsHAV – via oral-fecal routeHBV – blood transfusions, blood-derived

fluids, or improperly sterilized medical equipment

HCV – exposure of blood or body fluids from infected person; no vaccine

HDV, HEV


Hepatitis – clinical manifestations

Jaundice, dark urine, anorexia, fatigue, headache, nausea, vomiting, fever

Hepatomegaly and splenomegaly

Bilirubin, alkaline phosphatase, serum AST elevated


Hepatitis – Nutrition Therapy

Spare liver and provide nutrients for regenerationAdequate rest, fluids, good nutrition, avoidance of

further damage (IV hydration) Increase dietary intake

30-35 kcal/kg body weight (≥ 3000 kcal)

Small, frequent meals--good amount of proteins carbs and fats to get caloric needs(could do a PO calorie intake and an IV calorie intake)


Hepatitis – Nutrition Therapy

Adequate protein 1-1.2 g/kg body weight (higher than the noraml .8) promotes rejuvenation of the liver

30-40% of kcal from fat May not be well tolerated if bile is compromised, may need to lower its to 20%

Supplemental vitamin K--will increase prothrombin time

Potassium and sodium if vomiting and diarrhea


Alcoholic hepatitis - toxic liver injury associated with chronic ethanol consumption

Increased susceptibility to infections

Fatigue, weakness, anorexia, fever, hepatomegaly


Alcoholic Hepatitis - Treatment/ Nutrition TherapyAbstention from alcoholTreatment of withdrawal symptomsCorrection of nutritional deficienciesMultivitamin – B12, folate, thiamin,

pyridoxine, vitamins A & DMultimineral – zinc, magnesium, calcium,

phosphorusAdequate kcal and protein


Cirrhosis - chronic liver disease in which healthy tissue is replaced by scar tissue, blocking the flow of blood, resulting in loss of liver function

Most common causes – chronic alcoholism and HCV

Steatosis is first stage--accumulation of fat in liver


Cirrhosis – etiologyAssociated with alcoholismScar tissue formsConversion of fat to lipoprotein impairedAccumulation of fat in the liverPortal hypertension may develop--comprised

function of liver due to increased blood pressureEsophageal varices--streaks of bleeds in esophagus

due to portal hypertensionRupture with hemorrhage

Pathophysiology of the LiverCirrhosis – clinical manifestations

Enlarged liver from necrosis Ascites and edema--entire body fluid build upSGOT elevated, BSP clearing time reduced

BSP- sulfobromophthalein; can cause increased BPVitamin deficiencies, depressed hgb, hct--vitamin A, D,

and B vitamins need to get checked Jaundice, lack of appetite, delirium tremensFever, gallstones, ulcers, GERD, gastritis, diarrheaLooking at long term IV nutrition

Pathophysiology of the LiverCirrhosis – complications

Portal hypertension--abnormal pressure thats present in the portal venus system

Ascites--fluid build up

Hepatic encephalopathy--central nervous system dysfunction; causes you to not be coherent

Pathophysiology of the LiverCirrhosis – portal hypertension

Always present with ascites

Decrease in hepatic vascular bed; obstruction, increased resistance, arteriovenous anastomoses

Pathophysiology of the LiverCirrhosis – ascites

Accumulation of fluid in peritoneal cavity; most common complication

1.5-2 liters is taken off; causes you to lose 1 g of protein per 100 cc’s and are losing 1000-2000 cc’s

Hepatic fibrosis, reduced osmotic pressure, increased retention of sodium

Pathophysiology of the LiverCirrhosis – ascites: nutrition therapy

Encourage oral proteins/ supplements

Restricting salt to 2 g/d--more salt causes fluid to build up faster

Restricting fluid to 1500 cc--5 to 6 cups of fluid a day

Adequate kcal--25-35 kcals per kilo

Diuretics--when these are used what nutrients are they wasting, need to replace these nutrients in IV line

Pathophysiology of the LiverCirrhosis – hepatic encephalopathy

Syndrome of impaired mental status and abnormal neuromuscular function

2 types graded onto 4 clinical scales; Child-Pugh score--scale of 1-4, 4 being the worst

The Glasgow coma scale--for patients not coherent; scale from 3-5, 3 being the worst

“Flap” - asterixis


Pathogenesis unknown; inability to eliminate products toxic to brain

4 major hypotheses: Ammonia Synergistic neurotoxin False neurotransmitter GABA benzodiazepine


Treatment depends on type, extent of neurological damage, presence of precipitating factors

Treatments Dietary protein restriction (minimum 50 g/d), plant

sources, increased fiber, milk and cheese, BCAAs Monitor serum potassium level Correct hypoglycemia, vitamin deficiencies


Liver transplant – considered in cases where effects of disease have higher potential mortality than transplant

With alcoholism - six months abstinence

Psychological and nutritional evaluations1 year survival rate for liver transplant


Liver Transplant – Nutrition Therapy lessen effects of malnutrition because of disease

state lessen effects of disease itself

Individualized

Pretransplant Kcal 34-45 kcal/kg; protein 1-1.5 g/kg Normalize macro- and micronutrients Normalize blood sugar, nitrogen balance, relevant labs


Liver Transplant – Nutrition Therapy

Posttransplant Regualr diet – slightly lower kcal and pro. Other nutrients individualized based on

immunosuppressant drug regimen May cause hyperglycemia, sodium retention,

potassium retention Provide DRI for vitamins

hyperglycemia-decrease simple sugars, make them more complex

2000-4000 mg of sodium look at potassium levels

Pathophysiology of the LiverCystic fibrosis-associated liver disease (CFALD) -

inherited disorder of epithelial transport

Mutated gene codes for defective protein

Cl is prevented from leaving cell and water cannot exit

Mucus thickens, cilia cannot function, bacteria collect on the cells

infections

Pathophysiology of the LiverCF – Nutrition Therapy

Counseling on risks associated with alcohol and herbal therapies

Kcal needs increase 20-40%May need MCT--decreases fat malabsorptionDo not restrict proteinAssess status of fat-soluble vitaminsPancreatic enzyme supplements with meals and

supplements

Pathophysiology of the LiverCF – Nutrition Therapy

Vitamin A - risk for night blindness and conjunctival xerosis – 2-4X DRI, but avoid hypervitaminosis

Vitamin E – protection of lungs from oxidative stress 15-25 IU/d

Vitamin D – 2-4 µg/dL/day--(deficiencies not normally found in kids because they are outside more)

Vitamin K – 2.5-10 mg/daily

EFA supplementation

The Gallbladder

Stores, concentrates and secretes bile

Removal of water and electrolytes – increasing concentration

Storage

Control of delivery of bile salts to duodenum

The Gallbladder

Cholelithiasis – Nutrition Therapy

Assess alcohol intake Increase complex CHO and insoluble fiberAssess vitamin C intake ? Low-fat dietCounsel on lifestyle habitsPlain, simple foods best tolerated

The Gallbladder


Acute attack

NPO and complete bowel rest Parenteral nutrition as needed Advance as tolerated to liquids, low fat Limited amounts of fats and solid foods added Progress to regular diet

The Gallbladder


Chronic condition

Low fat (25% kcal) Weight reduction (gradual) Adjust pro and CHO for weight Water-soluble forms of fat-soluble vitamins

The Gallbladder


Postoperative Cholecystectomy

Oral feedings resumed once bowel sounds return Advance as tolerated to regular diet Increased fiber to manage diarrhea Manage digestive symptoms: fatty food intolerances,

heartburn, nausea

The Pancreas

Pancreatitis - nutrition therapy

Provide minimal stimulation of affected systems--bowel rest

Severe attacks – oral feedings withheld

Less severe - clear liquid diet, progress as tolerated; low fat

Small, frequent meals

The Pancreas

Pancreatitis - Nutrition Support for Acute

Provide adequate kcal & protein, minimize nitrogen losses, manage imbalances

Enteral preferred method

Maintain gut integrity Reduce septic and metabolic complications Less costly around 40 kcals per kilo proteins increased by 8% trying to preserve lean muscle mass

The Pancreas

Pancreatitis - Nutrition Support for AcuteEnteral support below ligament of Treitz(tissue

connecting duodenum to diaphragm) via nasogastric tube--help to give more kcals

Initiate feeding 25 mL/hour, advance to 25 kcal/kg over 24-48 hrs. small amount at first to avoid dumping syndrome

Nearly fat-free elemental formulasAdvance to oral diet when amylase and lipase

decrease towards normal

The Pancreas

Pancreatitis - Nutrition Support for Acutebowel rest

Parenteral – only considered in pts. for whom enteral access not possible or not tolerated

Mixed fuel, volume increased slowly to 25 kcal/kg

Intralipid les than 15-30% of kcal, protein individualized

The Pancreas

Pancreatitis - InsufficiencyFrequent, small meals moderate to low in

fatPancreatic enzymes taken with foodAlcohol, coffee, tea, spices, irritant

condiments avoidedMCT may be added--body wouldn’t have to

produce enzymes needed to break down LCT

Maintain weightMonitor fat and water-soluble vitaminsMedical management of pHTreat with insulin if indicated

Documents

Liver, Gallbladder, Exocrine Pancreas KNH 411