Liver, Gallbladder, Exocrine
Pancreas
KNH 411
Pathophysiology of the Liver
 Alcoholism
Chronic consumption of > 80 g of ethanol/day
Alcoholic liver disease (ALD)
Dependency may be evident as tolerance or withdrawal
Ethanol rapidly and completely absorbed even with
malabsorption
 Cannot be stored - oxidized




Pathophysiology of the Liver
 Fatty Liver - Etiology
 Steatohepatitis - inflammation
 If alcohol not present – NASH
 NAFLD progresses to cirrhosis and hepatic carcinoma
 Strong association with obesity, diabetes, metabolic syndrome
 Most common type among adolescents
Pathophysiology of the Liver
 Malnutrition in the Alcoholic
 Malnutrition caused by displacement of nutrients
 Maldigestion or malabsorption of nutrients d/t GI
complications
Pathophysiology of the Liver
 Malnutrition 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
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
Pathophysiology of the Liver
 Alcoholism - Nutrition Implications




Significant caloric contributions – obesity
Irregular eating habits
Decreased appetite – weight loss
Kcal derived from ethanol
 0.8 X proof X ounces = kcal
Pathophysiology of the Liver
 Alcoholism – Malnutrition
 PEM
 Poor dietary intake, malabsorption, hypercatabolic state,
altered energy storage, biochemical changes
 Vitamin deficiency
 Major cause of liver damage and resulting dysfunction
Pathophysiology of the Liver
 Alcoholism - vitamin and mineral deficiencies
 Folate
 Thiamin
 Wet and dry beriberi
 Wernicke-Korsakoff syndrome
 Low plasma pyridoxine
 Vitamin C
 Vitamin D – impairs osteoblastic activity
Pathophysiology of the Liver
 Alcoholism - vitamin and mineral deficiencies
 Vitamin K - clotting factors
 Vitamin A – night blindness
 Interaction between vitamin A and zinc
 Iron – altered response to infection
 Calcium – bone density and bone mass
 Potassium – hypokalemia
 Recommend multivitamin 2X RDA
Pathophysiology of the Liver
 Alcoholism – nutritional effects
 Imbalanced diet and/or anorexia
 Maldigestion and malabsorption
 Increased catabolism of visceral protein and skeletal muscle
 Increased excretion of vitamins
© 2007 Thomson - Wadsworth
Pathophysiology of the Liver
 Hepatitis – inflammation of the liver caused
by virus, bacteria, toxins, obstruction,
parasites or drugs
 HAV – via oral-fecal route
 HBV – blood transfusions, blood-derived fluids, or
improperly sterilized medical equipment
 HCV – exposure of blood or body fluids from
infected person; no vaccine
 HDV, HEV
Pathophysiology of the Liver
 Hepatitis – clinical manifestations
 Jaundice, dark urine, anorexia, fatigue, headache, nausea,
vomiting, fever
 Hepatomegaly and splenomegaly
 Bilirubin, alkaline phosphatase, serum AST elevated
Pathophysiology of the Liver
 Hepatitis – Nutrition Therapy
 Spare liver and provide nutrients for regeneration
 Adequate rest, fluids, good nutrition, avoidance of further
damage
 Increase dietary intake
 30-35 kcal/kg body weight (≥ 3000 kcal)
 Small, frequent meals
Pathophysiology of the Liver
 Hepatitis – Nutrition Therapy
 Adequate protein
 1-1.2 g/kg body weight
 30-40% of kcal from fat
 May not be well tolerated
 Supplemental vitamin K
 Potassium and sodium if vomiting and diarrhea
Pathophysiology of the Liver
 Alcoholic hepatitis - toxic liver injury associated with
chronic ethanol consumption
 Increased susceptibility to infections
 Fatigue, weakness, anorexia, fever, hepatomegaly
Pathophysiology of the Liver
 Alcoholic Hepatitis - Treatment/ Nutrition
Therapy
Abstention from alcohol
Treatment of withdrawal symptoms
Correction of nutritional deficiencies
Multivitamin – B12, folate, thiamin, pyridoxine,
vitamins A & D
 Multimineral – zinc, magnesium, calcium,
phosphorus
 Adequate kcal and protein




Pathophysiology of the Liver
 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
Pathophysiology of the Liver
 Cirrhosis – etiology







Associated with alcoholism
Scar tissue forms
Conversion of fat to lipoprotein impaired
Accumulation of fat in the liver
Portal hypertension may develop
Esophageal varices
Rupture with hemorrhage
Pathophysiology of the Liver
 Cirrhosis – clinical manifestations






Enlarged liver from necrosis
Ascites and edema
SGOT elevated, BSP clearing time reduced
Vitamin deficiencies, depressed hgb, hct
Jaundice, lack of appetite, delirium tremens
Fever, gallstones, ulcers, GERD, gastritis, diarrhea
Pathophysiology of the Liver
 Cirrhosis – complications
 Portal hypertension
 Ascites
 Hepatic encephalopathy
Pathophysiology of the Liver
 Cirrhosis – portal hypertension
 Always present with ascites
 Decrease in hepatic vascular bed; obstruction, increased
resistance, arteriovenous anastomoses
Pathophysiology of the Liver
 Cirrhosis – ascites
 Accumulation of fluid in peritoneal cavity; most common
complication
 Hepatic fibrosis, reduced osmotic pressure, increased
retention of sodium
Pathophysiology of the Liver
 Cirrhosis – ascites: nutrition therapy
 Encourage oral proteins/ supplements
 Restricting salt to 2 g/d
 Restricting fluid to 1500 cc
 Adequate kcal
 Diuretics
Pathophysiology of the Liver
 Cirrhosis – hepatic encephalopathy
 Syndrome of impaired mental status and abnormal
neuromuscular function
 2 types graded onto 4 clinical scales; Child-Pugh score
 The Glasgow coma scale
 “Flap” - asterixis
Pathophysiology of the Liver
 Cirrhosis – hepatic encephalopathy
 Pathogenesis unknown; inability to eliminate products toxic
to brain
 4 major hypotheses:
 Ammonia
 Synergistic neurotoxin
 False neurotransmitter
 GABA benzodiazepine
Pathophysiology of the Liver
 Cirrhosis – hepatic encephalopathy
 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
Pathophysiology of the Liver
 Liver transplant – considered in cases where effects of
disease have higher potential mortality than transplant
 With alcoholism - six months abstinence
 Psychological and nutritional evaluations
Pathophysiology of the Liver
 Liver Transplant – Nutrition Therapy
 Individualized
 Pretransplant
 Kcal 34-45 kcal/kg; protein 1-1.5 g/kg
 Normalize macro- and micronutrients
 Normalize blood sugar, nitrogen balance, relevant labs
Pathophysiology of the Liver
 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
Pathophysiology of the Liver
 Cystic 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 Liver
 CF – Nutrition Therapy
 Counseling on risks associated with alcohol and herbal
therapies
 Kcal needs increase 20-40%
 May need MCT
 Do not restrict protein
 Assess status of fat-soluble vitamins
 Pancreatic enzyme supplements with meals and supplements
Pathophysiology of the Liver
 CF – Nutrition Therapy
Vitamin A - risk for night blindness and conjunctival xerosis – 24X DRI, but avoid hypervitaminosis
 Vitamin E – protection of lungs from oxidative stress 15-25
IU/d
 Vitamin D – 2-4 µg/dL/day
 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 fiber
Assess vitamin C intake
? Low-fat diet
Counsel on lifestyle habits
Plain, simple foods best tolerated
The Gallbladder
 Cholelithiasis – Nutrition Therapy
 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
 Cholelithiasis – Nutrition Therapy
 Chronic condition
 Low fat (25% kcal)
 Weight reduction (gradual)
 Adjust pro and CHO for weight
 Water-soluble forms of fat-soluble vitamins
The Gallbladder
 Cholelithiasis – Nutrition Therapy
 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
 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
The Pancreas
 Pancreatitis - Nutrition Support for Acute
 Enteral support below ligament of Treitz via nasogastric
tube
 Initiate feeding 25 mL/hour, advance to 25 kcal/kg over
24-48 hrs.
 Nearly fat-free elemental formulas
 Advance to oral diet when amylase and lipase decrease
towards normal
The Pancreas
 Pancreatitis - Nutrition Support for Acute
 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 - Insufficiency
 Frequent, small meals moderate to low in fat
 Pancreatic enzymes taken with food
 Alcohol, coffee, tea, spices, irritant condiments
avoided
 MCT may be added
 Maintain weight
 Monitor fat and water-soluble vitamins
 Medical management of pH
 Treat with insulin if indicated