Liver, Gallbladder, Exocrine
Pancreas
KNH 411
Pathophysiology of the Liver
 Alcoholism
 Chronic consumption of > 80 g of ethanol/day
 250cc (1 cup) hard liquor (80 proof) per day
 Alcoholic liver disease (ALD)
 Fatty liver, hepatitis, hardening of the liver
 Only 2%-10% leaves the system
 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 (liver increases by 5%)
 If alcohol not present – NASH (non-alcoholic)
 NAFLD (non-alcoholic fatty liver disease) 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
 Secondary malnutrition of vitamins A, D, E, and K
 Maldigestion or malabsorption of nutrients d/t GI
complications
 Bloated and disoriented
Pathophysiology of the Liver
 Malnutrition in the Alcoholic - GI Complications
 Esophagus – heartburn, reduced LES pressure, esophagitis,
stricture, tears from vomiting, change in saliva
 Stomach - gastritis, duodenitis, atrophy of gastric mucosal
barrier, hemorrage, PUD, pernicious anemia, stomach
cancer, B12 deficiencies
 Long term- 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 (dumping syndrome), bacterial
overgrowth
Pathophysiology of the Liver
 Alcoholism - Nutrition Implications
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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
 A, D, E, and K malabsorption
 Have slick gut
 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 (alcohol
interferes with absorption)
 Folate
 Thiamin
 Wet and dry beriberi (thiamin deficiency)
 Decreased nerve function
 Wernicke-Korsakoff syndrome
 Dementia
 Low plasma pyridoxine
 Vitamin C
 Vitamin D – impairs osteoblastic activity (building of bones
Pathophysiology of the Liver
 Alcoholism - vitamin and mineral deficiencies
 Vitamin K - clotting factors
 Can bleed out
 Vitamin A – night blindness
 Interaction between vitamin A and zinc
 Iron – altered response to infection
 Calcium – bone density and bone mass
 Potassium – hypokalemia (because of vomiting and diahhrea)
 Recommend multivitamin 2X RDA
 High protein, high calorie
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
 Supplement with magnesium and B-complex 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 (increase prothrombin time)
 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
 Can lead to cirrhosis or long term liver damage
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
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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- accumulation of fat in the liver
Pathophysiology of the Liver
 Cirrhosis – etiology
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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 (sulfobromophthalein) 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
 Salt is water loving, so body holds on to water
 Restricting fluid to 1500 cc (5-6 cups)
 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
 3-15 (3 is the worst)
 “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 (gamma amino buteric acid)
Pathophysiology of the Liver
 Cirrhosis – hepatic encephalopathy
 Treatment depends on type, extent of neurological damage,
presence of precipitating factors
 Psychological profile
 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
 1 year survival rate after transplant
Pathophysiology of the Liver
 Liver Transplant – Nutrition Therapy
 Individualized
 Pretransplant
 Kcal 34-45 kcal/kg; protein 1-1.5 g/kg (high calorie intake)
 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 every 6 months
 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
 Worsens with age
 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
 Diet, exercise, limit sweets and alcohol, add fruits,
vegetables, and whole grains
 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)
 Sudden weight loss can result in more gallstones
 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
 Bowel rest
 Severe attacks – oral feedings withheld
 Less severe - clear liquid diet, progress as tolerated; low
fat
 Small, frequent meals (6 small meals)
 Limit fat
The Pancreas
 Pancreatitis - Nutrition Support for Acute
 Provide adequate kcal & protein, minimize nitrogen losses,
manage imbalances
 Manage glucose
 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
 70% of fat should be medium chain
 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
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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
Want to prevent further damage
May need to supplement vitamins