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

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. 22-1 next

Liver circulation

Sinusoids

• Sinusoids Fig. 13-1 next

• Also see Fig. 18-11 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. 18-12 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 32 - 1, 2, 3, 4, 5, 6, 7, 12

• If time 14