Hepatic Working knowledge of physiological changes during disease process & effects on nutrition care.

Hepatic Translate nutrition needs into menus. Working knowledge of MNT for hepatic disease. Calculate and define diets for common conditions.

Normal Structure Biliary ducts Fig. 18-9, Gould next

Liver and gallbladder with ducts

Normal liver in situ

Blood Supply to Liver Liver circulation Fig next

Liver circulation

Sinusoids Sinusoids Fig next Also see Fig in Gould

Cut surface normal liver with vessels & bile ducts

Liver sinusoids

Sinusoids Capillary-like structures Blood from both the hepatic artery and portal vein flow in to the sinusoids Blood collects in central vein & then to hepatic vein

Kupffer cells Cells that line the sinusoids Phagocytic cells of the immune system

Pressure in Liver Normally very little resistance to blood flow in liver Hepatic vein pressure 0 mm Hg Portal vein pressure is 8 mm Hg

Pressure in Liver Portal hypertension Pressure in hepatic vein increases above 0 mm Hg

Metabolic What are the metabolic functions of the liver?

Detoxification Kupffer cells Toxins detoxified Removal of ammonia & make urea

Digestion Bile synthesis Bilirubin –product of breakdown of heme when rbc discarded –excreted in bile

What happens to all of these functions in liver disease?

Progression of Liver Disease Fatty liver Hepatitis Cirrhosis ESLD

Fatty liver

Hepatitis Infectious mononucleosis Toxic chemicals Viral infection Excessive use of alcohol

Viral Hepatitis Hepatitis A –fecal-oral route –rapid onset –2 - 6 weeks –acute type

Viral Hepatitis Hepatitis B and C –contaminated bodily fluids –slower onset –6 weeks to 6 months –can become chronic

Hepatitis Symptoms –jaundice can occur –pale stools –easily fatigued

Hepatitis Symptoms –nausea & anorexia –fever –liver tenderness –liver enlarged

Hepatitis Why do these clinical manifestations happen? –hypoglycemia –fluid imbalance –bleed more easily –elevated serum bilirubin > 20mg/dl

Prehepatic Jaundice Fig in Gould Hemolytic jaundice Excessive rbc break down Unconjuaged bilirubin high Stool dark/normal color

Intrahepatic Jaundice If unconjugated bilirubin high means liver cell damage If conjugated bilirubin high, means blockage

Posthepatic Jaundice Conjugated bilirubin high Light colored stool

Cirrhosis Repeated damage, necrosis to liver What will eventually happen to the liver?

Cirrhotic liver, external surface macronodular

Cirrhotic liver, macronodular

Cirrohtic and fatty liver, micronodular

Hepatoxic Drugs Alcohol Acetaminophen Androgenic steroids Cyclosporine Erythromycin Glucocorticoids Isoniazid Methotrexate Methyldopa NSAIDs

Damage Liver Hepatitis, especially if chronic Biliary disorders, obstruction Hemochromatosis Chronic use hepatotoxic drugs

Portal HTN Due to damaged liver Pressure too high on which end?

Esophageal varices with portal HTN

Portal HTN & Ascites Forces plasma out of vessels Is Alb high or low in the blood? Na restricted diet Fluid restricted diet

End-stage Liver Disease Less than 25% of liver functions Portal systemic encephalopathy (PSE)

ESLD Stages Stage 1 –apathy –restlessness –reversal of sleep rhythm Stage 1 –slowed intellect –impaired computational ability –impaired handwriting

ESLD Stages Stage 2 –lethargy –drowsiness –disorientation –asterixis Stage 3 –stupor (arousable) –hyperactive reflexes –extensor plantar responses

ESLD Stages Stage 4 –coma –response to painful stimuli only

ESLD Excessive ammonia in blood (NH3) Abnormal amino acid metabolism –BCAA lower –Aromatic AA higher

ESLD False neurotransmitter hypothesis by Fischer –too many Aromatic AA favored into brain –phe - hinder neuronal transmission

ESLD False neurotransmitter hypothesis by Fischer –phe & tyr - precursor of epinephrine & norepinephrine –trypothan - precurson of serotonin

ESLD False neurotransmitter hypothesis by Fischer –high level of phe result in false neurotransmitters & competes with normal neurotransmitters

ESLD Precepitating factors –GI bleed –increased dietary protein –constipation –infection –less hepatic function

Subjective Global Assessment Four elements of pt. Hx –Recent loss of body wt –Changes in usual diet –Presence of significant gastrointestinal symptoms –Patient’s functional capacity

SGA Three elements of physical exam –loss of subcutaneous fat –muscle wasting –presence of edema or ascites

SGA Deltoid muscle wasted Shoulders look squared off Muscle wasting at quadriceps femoris Anterior thigh

SGA Significant wt loss –>1 to 2% in 1 week –>5% in 1 month –>7.5% in 3 months –>10% in 6 months –>40% life threatening

SGA Significant wt loss –unplanned or recent loss of >10% –>20% in surgical pt

Labs & Clinical Signs Serum ammonia H&H Aklaline phosphostase BUN AST ALT Bilirubin K Blood glucose TG & FFA Prolonged prothrombin time Alb LDH Ascites & edema

Medications Lactulose Neomycin Steriods Insulin Diuretics IV albumin Avoid excessive fat soluble vitamins

MNT All liver diseases –high kcal –do not limit cho –moderate lipid –25% - 40% of kcal –if have to go low fat - 40 g/day

MNT All liver diseases –supplement vit & minerals –use water soluble forms –ascites - Na restrict –I & O –monitor blood K

MNT Uncomplicated hepatitis & stable cirrhosis –high protein –1.2 g/kg or 1.5 g/kg

MNT in ESLD Before coma –high protein –keep protein high until see problems on next slide –then restrict protein

MNT in ESLD Coma –start 40 g protein –BCAA formulas –increase protein 10 g until see increase total bilirubin increase prothrombin time coma

MNT in ESLD Try to not restrict fluid intake Case study , 2, 3, 4, 5, 6, 7, 12 If time 14