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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 – 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
� 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