Hepatobiliary and Pancreas PDF

MNT FOR HEPATOBILIARY AND PANCREATIC DISORDERS Allison Charny, MS, RD, CDE, CDN Krause’s Food & the Nutrition Care Process Ch 30 Overview  Hepatitis  Alcoholic Liver Disease  Gallbladder Disease  Pancreatic Disease Liver  Largest organ  Great...

MNT FOR HEPATOBILIARY AND PANCREATIC DISORDERS Allison Charny, MS, RD, CDE, CDN Krause’s Food & the Nutrition Care Process Ch 30 Overview  Hepatitis  Alcoholic Liver Disease  Gallbladder Disease  Pancreatic Disease Liver  Largest organ  Greatest, most varied functions  Many functions of nutritional metabolism  Diseased liver  in size and can be palpated Functions of the Liver  Bile  Detoxification  CHO metabolism  Protein metabolism  Fat metabolism  Vitamin and mineral storage  Filters bacteria Hepatitis  Inflammation of the liver  Many etiologies  Infections ◼ viral hepatitis ◼ HAV, HBV, HCV, HDV, HEV  Accumulation of fat ◼ NAFLD, NASH  Toxins ◼ alcohol Symptoms of Hepatitis Primary Secondary  anorexia  icterus  malaise  jaundice  headache  hyperbilirubinemia  n/v  dark  hepatomegaly  splenomegaly Alcoholic Liver Disease  ~ 10% of the population  Acetaldehyde  Toxic by-product of ETOH metabolism Excessive Alcohol Consumption  Alcoholic Liver Disease 3 Stages: Hepatic steatosis, alcoholic hepatitis, cirrhosis Stage 1 Hepatic Steatosis  Fatty liver ◼ Reversible with abstinence ◼ H from ETOH replaces H from fat for energy ◼ Fat accumulates in the liver ◼ Labs ◼  lipids Alcoholic Liver Disease Stage 2 Alcoholic Hepatitis  Resolution with abstinence  Hepatomegaly  Abdominal pain and wt loss  Labs (see table 28-1) ◼ transaminase levels (LFTs: AST, ALT) ◼ Bilirubin ◼ Albumin ◼ Anemia Alcoholic Liver Disease Stage 3 Cirrhosis  Repeated necrosis and regeneration → scar tissue   Pressure in the liver due to scar tissue  Cirrhosis due to ETOH = Laennec’s cirrhosis*  Symptoms similar to Stage 2 with ammonia, depending on condition  Cirrhosis develops in ~ 15% of heavy drinkers  *Cirrhosis also caused by: CHF, viral hepatitis, autoimmune hepatitis, biliary atresia (closure of bile duct), long term drug use, metabolic disorders (hemochromatosis, glycogen storage dz, Wilson’s dz) Alcoholic Liver Disease Consequences of cirrhosis: Portal Hypertension – due to  blood flow into the obstructed liver  Varices – dilation of the vessels leading to the liver as pressure increases → GI bleed (esophagus, stomach, intestine)  Ascites – fluid in the peritoneal cavity, due to portal hypertension forcing plasma from liver’s blood vessels, and  albumin Jaundice may be absent or present Portal Circulation Varices Clinical Manifestations of Cirrhosis Clinical Manifestations of Cirrhosis ESLD/Hepatic Failure  Failure – function at  25% due to severe cell loss  Acute – fulminant – viral, toxic overdose  Chronic – Progressive Portal Systemic Encephalopathy (aka Hepatic Encephalopathy) Liver failure w/ alterations in neuromuscular function and behavior (see Box 28-1) due to: 1. liver’s inability to detoxify ammonia, a brain toxin -main source of ammonia is blood from GI bleed and intestinal bacteria 2.  in BCAA (used for energy)  in AAA ( muscle proteolysis) 3. other metabolic abnormalities -hypoxia, hypovolemia, hypotension, azotemia, hypoalbuminemia, hypoglycemia, electrolyte imbalances To Decrease Ammonia  Lactulose – non-digestible disaccharide, causing osmotic diarrhea and excretion of ammonia  neomycin – destroys bacteria producing ammonia  BCAA, AAA – veg, meat protein   dietary protein not supported Assessment of Nutritional Status Difficult!  Serum protein indicators altered  Hydration affects labs  Urine, 24-hour N excretion do not reflect pt status  Wt unreliable – ascites, edema  Vit/min nutriture – difficult to assess, considering the role of the liver Assessment of Nutritional Status  Use Subjective global Assessment (SGA) see Box 28-2: (broad perspective)  Physical signs, symptoms  Physiologic stress  Med/surg histories  GI symptoms and complaints  Hx of wt loss and functional capacity  Clinical signs/symptoms  of protein, energy and fluid status  of specific vit/min deficiencies related to liver disease  Labs  See Table 28-1 Objectives of MNT  Maintain/improve nutritional status  Individualize based on effects of liver disease  portal HTN, ascites, hyponatremia, hepatic encephalopathy, glucose alterations, fat malabsorption, hepatorenal syndrome  Remember:  alcoholics – usually poor nutritional status to begin with; ETOH often replaces food  inadequate oral intake – anorexia  malabsorption, steatorrhea, ETOH affects mucosa  altered metabolism (effects of  liver fxn) MNT Energy  Adequate kcal for protein sparing and anabolism  25-35 kcal/kg (ABW) or dry weight  20 kcal / kg obese; 40 kcal / kg underweight  1.2-1.4 stress factor REE (use 1.5-1.75 w/ infection, steatorrhea) MNT Protein  In general: 1-1.5 g/kg IBW w/without encephalopathy  Liver dz without encephalopathy:.8-1.0 g / kg dry wt; 1.2-1.3 for +N balance.  If  stress: sepsis, GI bleed, severe ascites then 1.5g / kg protein  Low protein diet orders for encephalopathy may still be seen in practice but are not supported in the research literature MNT Carbohydrate  Hypoglycemia  ETOH blocks gluconeogenesis  Liver failure causes decreased gluconeogenesis  Hyperglycemia  MNT for DM MNT Lipid  Avoid overfeeding in general as altered fat metabolism can cause fatty liver  25-40% of kcal - average 30% of kcal as fat to provide adequate energy.  Steatorrhea may occur in pts due to  bile salts, meds (neomycin)   40g low fat diet  Difficult to get adequate kcal on low-fat  MCT 15 ml 3x / day MNT Vitamins  Thiamin - Wiernicke’s syndrome  ETOH interferes w/ thiamin absorption  w/o thiamin no conversion of pyruvate to acetyl CoA – increased lactate – lactic acidosis.  S&S: peripheral neuropathy, tachycardia, anorexia, HA  Folate  May be decreased in diet and poorly absorbed  B12 is cofactor in conversion of folate to its active form MNT Vitamins  B12  Required for myelin formation  ETOH interferes w/ intrinsic factor production  S&S: peripheral neuropathy, parasthesia, loss of position sense, impaired deep tendon reflexes, depression, irritability, and memory loss  Megaloblastic anemia  Due to folate and B12 deficiency  Supplement both (folate can mask a B12 deficiency)  B12 injection if ETOH abuse continues MNT Fat Soluble Vitamins  Supplement, with water soluble forms, if steatorrhea  Signs of Vit K deficiency  Liver synthesizes vit K dependent clotting factors  Increased prothrombin time (PT) with liver dz MNT Minerals  Provide when recognized as deficient   Fe storage – Hemochromatosis   Cu storage – Wilson’s disease  Also in liver dz, esp due to ETOH: Zn, Mg, Ca (steatorrhea) MNT Electrolytes  K+ restriction if impaired renal function; K+ supplement may be needed if pt on a K+ wasting diuretic  Na+ restriction with fluid retention  ascites, edema Fluid  Restriction may be necessary w/ ascites, edema  Hyponaetremia  1-1.5 L / day, depending on severity MNT  Small frequent meals  Ascites,  kcal, N balance, hypoglycemia  Enteral supplements  Kcal, some w/ BCAA  Tube feedings of PN  BCAA, AAA Biliary and Pancreatic Disorders Anatomy/Physiology Gallbladder  Concentrate, store, excrete bile produced by liver  Bile  Contains ◼ Cholesterol ◼ Bilirubin ◼ Bile ◼ Cu, Mn  Excreted into small intestine  Reabsorbed via portal circulation Gallbladder Disease Biliary dyskinesia  Spasm of sphincter of Oddi  doesn’t open properly   pressure in G.B. as bile accumulates Gallbladder Disease Definitions  Cholelithiasis  Gallstones within gall bladder  Cholecystitis  Inflammation / infection of the gall bladder  Choledocholithiasis  Gallstone→bile duct→obstruction→cramps; no bile into duodenum  Choledochotomy  Surgical incision of the common bile duct  Cholecystectomy  Surgical gall bladder removal; ducts enlarge somewhat to form a “pouch”; bile secreted to intestine directly Gallbladder Disease Definitions  Cholangitis  Inflammation of bile ducts  Cholestasis  “Sludge” build up in gallbladder due to lack of release of bile ie prolonged TPN; use some enteral feeding  Cholecystitis – infection / inflammation of gall bladder  Lipid malabsorption  Bile back-up → liver damage and/or pancreatitis → return to circulation - jaundice MNT  Cholecystitis  Low fat ~ 40 g / day; 25-30% of kcal to provide GI stimulation  Monitor water soluble and fat soluble vits  Cholelithiasis  Prevent obesity, severe fasting  Cholesytectomy  Low-fat not needed Gallbladder Disease Definitions: Treatment and Evaluation  Litholytic therapy  dissolving stones w/ bile salts  ESWL – electrocorporeal shock wave lithotripsy  ERCP – endoscopic retrograde cholangeopancretography  radiologic exam of bile and pancreatic ducts Pancreas  Endocrine  glucagon, insulin, somatostatin (inhibits insulin, gastrin, growth hormone) → blood stream  Exocrine  enzymes – lipase, trypsin, amylase and  bicarbonate → intestinal lumen via pancreatic duct; for CHO, pro, fat digestion  Pancreatic duct merges with common bile duct Pancreatic Disease Pancreatitis – inflammation of pancreas  Acute  ETOH  Chronic  Biliary tract dz  Gallladder dz  Drugs  Trauma  Virus   Triglycerides Pancreatic Disease  Severe pancreatitis can lead to hemorrhage or death  If the cause leads to blockage of ducts: activation of pancreatic enzymes → auto-digestion of the gland →  serum amylase and lipase  If cells are extensively damaged, serum amylase and lipase may be normal (production is )  With extensive pancreatic destruction – glucose intolerance → damage now affecting endocrine function of pancreas MNT Acute Pancreatitis  Pain with secretion of pancreatic enzymes (autodigestion)  Goal: Minimal stimulation of enzyme secretion  No oral feeding / IV hydration or clear liquids / negligible fat (fat free) / advance to low fat → regular, 6 small feedings  If severe TPN or TF to the jejunum; standard or possibly elemental lowfat formula  Hypermetabolic  Adequate kcal and protein   Ca+   alb →  Ca+  “SOAP” of f.a.’s and Ca+ MNT Chronic Pancreatitis  Treat wt  due to malabsorption, N/V, diarrhea  Small meals, low fat  No ETOH  Pancreatic enzyme replacement orally if malabsorption of protein and fat (pancreatic function decreased by ~ 90%)  B12, fat soluble vitamin def – improves w/ enzyme replacement  Adequate kcal  As much fat as can tolerate; usually a “lower” fat diet  Meds to promote intestinal pH (antacids) often needed when bicarbonate secretion is affected Medical Management  Surgery  Whipple procedure – pancreaticoduodenectomy ◼ Pancreatic duct is reanastomosed to the jejunum ◼ Pancreatic insufficiency can result  MNT ~ to chronic pancreatitis