Liver, Gallbladder, Pancreas Clinical Nutrition Assessment And Intervention Fall 2024 PDF

11/17/24 Liver, Gallbladder, Pancreas LEC TU RE 12 C LINIC AL NU TRITIO N ASSESSMENT AND INTERV ENTIO N FAL L 2024 1 1 Liver Structure v Located in upper-right quadrant...

11/17/24 Liver, Gallbladder, Pancreas LEC TU RE 12 C LINIC AL NU TRITIO N ASSESSMENT AND INTERV ENTIO N FAL L 2024 1 1 Liver Structure v Located in upper-right quadrant v Healthy liver is brownish-red § Dark, yellowish-brown when infiltrated with fat v Has four anatomical lobes: right, quadrate, caudate, left lobe o Two functional lobes: right & left v Supplied with blood from two sources: hepatic artery & portal vein o Hepatic artery supplies ~1/3 of blood (from the aorta) o Portal vein supplies ~2/3 of blood (from GI tract) v ~1500mL blood/minute circulates through the liver o Exits via R and L hepatic veins → inferior vena cava 2 2 1  11/17/24 3 3 4 4 2  11/17/24 Physiology & Functions v 10-20% required to sustain life v Performs > 500 tasks v Main functions o Metabolism of carbohydrate, protein and fat o Storage and activation of vitamins and minerals o Synthesis and excretion of bile § Bile is formed in liver; exits liver through a series of bile ducts → common bile duct; stored in gallbladder; released into duodenum § Emulsifies fat in the intestine and forms compounds with fatty acids to facilitate their absorption o Conversion of ammonia to urea o Drug, alcohol metabolism (detoxification) o Filtering 5 5 Physiology & Functions v Carbohydrate metabolism o Conversion of galactose & fructose → glucose o Storage of glucose as glycogen (glycogenesis) o Breakdown of glycogen to glucose (glycogenolysis) o Gluconeogenesis from precursors § Lactic acid § Glycogenic amino acids § Intermediates of Krebs cycle 6 6 3  11/17/24 Physiology & Functions v Protein metabolism o Transamination (transfer of amino group from one compound to another) & deamination (removal of an amino group) o Convert amino acids to substrates that are used in energy and glucose production & synthesis of non-essential amino acids v Synthesis of o Blood clotting factors § fibrinogen § PT o Serum proteins § Albumin § Transferrin o Lipoproteins 7 7 Physiology & Functions v Lipid metabolism o β-Oxidation § Fatty acids converted to acetyl-coenzyme A to produce energy § Fatty acids → energy production § Ketone bodies o Synthesis and hydrolysis § Triglycerides § Phospholipids § Cholesterol § Lipoproteins 8 8 4  11/17/24 Physiology & Functions v Involved in storage, activation, transport of many vitamins & minerals o Storage § Fat-soluble vitamins § B12 § Zinc, iron, copper o Synthesizes proteins that transport: § Vitamin A § Iron § Zinc § Copper o Activation § Carotene converted to Vitamin A § Folate converted to 5-methyl THF (tetrahydrofolic acid) § Vitamin D converted to 25-hydroxycholecalciferol 9 9 Common Laboratory Tests: Liver Function Hepatic Excretion Total Bilirubin (serum) ↑ Bilirubin overproduction Defect in hepatic uptake Urine Bilirubin ↑ More sensitive than total bilirubin Cholestasis Serum alkaline ↑ Flow of bile blocked in the liver phosphatase (ALP) (bone, kidney, intestine) Ƴ-Glutamyl ↑ Flow of bile blocked in the liver transpeptidase (GGT) (kidney, heart, pancreas, brain) 10 10 5  11/17/24 Common Laboratory Tests: Liver Function v Bilirubin o Breakdown product of heme o Liver is responsible for clearing the blood of bilirubin o Bilirubin is taken up by hepatocytes o Secreted in the bile; one of many constituents of bile § Secreted into the intestine v Normal values o Total: 0.3-1.0 mg/dl o Prehepatic: Possibly due to hemolytic anemia and o Indirect: 0.2-0.8 mg/dl internal hemorrhage o Direct: 0.1-0.3 mg/dl o Hepatic: Deficiencies in bilirubin metabolism - problems with the liver (cirrhosis and viral hepatitis) v Increased total bilirubin o Posthepatic: Obstruction of the bile ducts, reflected o Jaundice as deficiencies in bilirubin excretion 11 11 Common Laboratory Tests: Liver Function Hepatic Enzymes Alanine aminotransferase (ALT, ↑ Liver cell damage formerly SGPT) Highest levels in liver Aspartate aminotransferase ↑ Liver cell damage (AST, formerly SGOT) Also present in cardiac and skeletal muscle AST:ALT > 1.0 Alcoholic cirrhosis, liver congestion, metastatic liver tumor AST:ALT < 1.0 Acute hepatitis, viral hepatitis 12 12 6  11/17/24 Common Laboratory Tests: Liver Function Serum Proteins PT ↑ Decreased synthesis of clotting factors with liver dysfunction Albumin ↓ Synthesis decreases with liver dysfunction Cannot use as a marker of nutrition status in liver disease Others Ammonia ↑ Decreased conversion to urea with increasing liver dysfunction 13 13 Diseases of the Liver v Acute, chronic, inherited, acquired o Hepatitis § Acute viral hepatitis § Fulminant hepatitis § Chronic hepatitis § Alcoholic hepatitis o Non-alcoholic fatty liver disease (NAFLD) § Steatosis (fatty liver) § Non-alcoholic steatohepatitis (NASH) o Cirrhosis o Cholestatic liver diseases o Inherited disorders (hemochromatosis) o Other 14 14 7  11/17/24 Hepatitis v Inflammation of the liver tissue o Causes: virus, bacteria, toxins, obstruction, parasites, chemicals o Clinical manifestations: jaundice, dark urine, anorexia, fatigue, nausea, vomiting, fever; enlarged liver (hepatomegaly); splenomegaly v Acute during for the first 6 months o Acute generally does not cause permanent damage o After 6 months → chronic hepatitis v Acute viral hepatitis: A, B, C, D and E o A and E (foodborne) § Infectious § Fecal-oral route o B, C and D § Blood and body fluids 15 15 Hepatitis v Hepatitis A (HAV) o Contracted through contaminated drinking water, food (seafood), sewage o Recovery usually complete; long-term consequences rare v Hepatitis B and C (HBV, HCV) o Transmitted via blood, blood products, semen, saliva o Chronic active hepatitis → cirrhosis and liver failure o HCV most common reason for needing liver transplant v Hepatitis D (HDV) o Co-infection or super-infection with HBV (requires HBV to replicate); rare in the US v Hepatitis E (HEV) o Transmitted via the oral-fecal route; rare in the US § Southern, eastern, central Asia; northern, eastern, western Africa; Mexico § Contaminated water appears to be source of infection o HEV is usually acute rather than chronic 16 16 8  11/17/24 Hepatitis v Normal Liver v Chronic Active Hepatitis 17 17 Liver Disease v Can be classified according to time of onset and duration o Fulminant liver disease o Acute liver disease (ALD) o Chronic Hepatitis 18 18 9  11/17/24 Liver Disease v Can be classified according to time of onset and duration o Fulminant liver disease, acute liver failure (ALF) § Absence of pre-existing liver disease and development of hepatic encephalopathy within 2-8 weeks of onset of disease causes include viral hepatitis (~75% of cases), chemical toxicity (eg acetaminophen, drug reactions), +other causes o Acute liver disease: Liver dysfunction that has been present for 1.5g/kg if malnourished (+good renal fx) § Avoid unnecessary protein restriction (with encephalopathy) o Many patients are malnourished o Outdated practice to restrict; >95% patients with cirrhosis can tolerate mixed-protein diet up to 1.5g/kg body weight o Can trial BCAA administration o Theory: Increased intake of vegetable protein § At least 50% HBV 41 41 Cirrhosis: MNT v Fluid Needs o Stable Cirrhosis § Fluid restrictions are not necessary o Non-stable: difficult to manage ascites or edema § Modest fluid restriction § Primary goal: mildly negative fluid balance o Hyponatremia § Serum Na level < 128 mEq/L, o 1,200 mL to 1,500 mL per day § Serum Na level < 125 mEq/L o 1,000 mL to 1,200 mL per day v Multivitamin and mineral supplementation o Use water-soluble forms for fat soluble vitamins o ↓ Thiamine → Wernicke’s encephalopathy 42 42 21  11/17/24 Nutrient Deficiencies 43 43 Cirrhosis: MNT v Consumption of small, frequent meals as tolerated o Early satiety common with ascites o Focus on high calorie, high protein foods to optimize intake v If patient has ascites: 2g sodium restriction v If patient has hyponatremia: fluid restriction v If patient has steatorrhea: avoidance of high-fat foods o Replace some LCT with MCTs o If significant stool fat losses, trial low fat diet (40g/d) o If diarrhea does not resolve, fat restriction should be discontinued v Monitor for glucose alterations, need for interventions v Oral supplements between meals (Ensure, Boost) o Trial Ensure Clear if fat not well tolerated v Enteral nutrition support when ongoing inadequate intake 44 44 22  11/17/24 Liver Transplant v Patients often malnourished before transplant v Encourage small, frequent, nutrient-dense meals v Increased kcal and protein needs: 30-35kcal/kg, 1.2-1.8g/kg protein v With Prograf (tacrolimus) or Gengraf (cyclosporine), avoidance of grapefruit and pomegranate, and their juices v Food safety very important post-transplant, especially first 6 months v EN may be indicated if oral intake is inadequate or contraindicated v PN is reserved for patients without adequate gut function o Caution! PN can adversely affect liver function v Long-term, preventive nutrition to optimize health o General healthy diet; avoid or minimize excessive weight gain, hyperglycemia, hypertension, hyperlipidemia, osteopenia 45 45 Liver Transplant: MNT Pretransplant Post transplant (Up Long-Term Post- to 8 wks postop) transplantation Calories é kcal é kcal Wt Maintenance (basal + ≥ 20%) (basal + 15-30%) (basal +10- 20%) PRO Moderate protein é Protein Moderate protein (1-1.5 g/kg) (1.2-1.75 g/kg) (1 g/kg) Fat 20-30% total kcal As Needed ≤30% total kcal CHO é CHO ↓ Simple CHO ↓ Simple CHO (simple/complex) Sodium