Liver Gallbladder Exocrine Pancreas KNH 411 Pathophysiology of
Liver, Gallbladder, Exocrine Pancreas KNH 411
Pathophysiology of the Liver Alcoholism Chronic consumption of > 80 g of ethanol/day--comprable to 250 cc’s (1 cup 80 proof liquor; liter of wine; 6 12 oz 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 Liver Fatty 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/reduction NAFLD(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 Liver Malnutrition in the Alcoholic Malnutrition caused by displacement of nutrients Maldigestion or malabsorption of nutrients d/t GI complications-- may be bloated, diarrhea, anorexic decrease alcohol increased energy content
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 motility of GI can be damaged decreased HCl secretion and loss of intrinsic factor due to alcohol--can cause decreased B 12 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 Liver Alcoholism - Nutrition Implications hepatitis, cirrhosis Significant caloric contributions – obesity Irregular eating habits Decreased appetite – eventually lead to 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(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 Liver Alcoholism - vitamin and mineral deficiencies Folate Thiamin--alcohol effects uptake and utilization Wet and dry beri--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 Liver Alcoholism - 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 2 X RDA high protein high calorie very malnourished individuals
Pathophysiology of the Liver Alcoholism – 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 vitamins want to supplement magnesium and B vitamin
© 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 (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)
Pathophysiology of the Liver 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
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 – B 12, 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--accumulation of fat in liver
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--comprised function of liver due to increased blood pressure Esophageal varices--streaks of bleeds in esophagus due to portal hypertension Rupture with hemorrhage
Pathophysiology of the Liver Cirrhosis – clinical manifestations Enlarged liver from necrosis Ascites and edema--entire body fluid build up SGOT elevated, BSP clearing time reduced BSP- sulfobromophthalein; can cause increased BP Vitamin deficiencies, depressed hgb, hct--vitamin A, D, and B vitamins need to get checked Jaundice, lack of appetite, delirium tremens Fever, gallstones, ulcers, GERD, gastritis, diarrhea Looking at long term IV nutrition
Pathophysiology of the Liver Cirrhosis – 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 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 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 Liver Cirrhosis – 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 Liver Cirrhosis – 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
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 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 for liver transplant
Pathophysiology of the 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
Pathophysiology of the 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 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--decreases fat malabsorption 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 – 24 X DRI, but avoid hypervitaminosis Vitamin E – protection of lungs from oxidative stress 15 -25 IU/d Vitamin D – 2 -4 µg/d. L/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 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--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 Acute Enteral support below ligament of Treitz(tissue connecting duodenum to diaphragm) via nasogastric tube--help to give more kcals Initiate feeding 25 m. L/hour, advance to 25 kcal/kg over 24 -48 hrs. small amount at first to avoid dumping syndrome Nearly fat-free elemental formulas Advance to oral diet when amylase and lipase decrease towards normal
The Pancreas Pancreatitis - Nutrition Support for Acute bowel 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 - 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--body wouldn’t have to produce enzymes needed to break down LCT Maintain weight Monitor fat and water-soluble vitamins Medical management of p. H Treat with insulin if indicated
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