Hepatic

1
Hepatic

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

2
Hepatic

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

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Normal Structure

• Biliary ducts Fig. 18-9, Gould next

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Liver and gallbladder with ducts
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Normal liver in situ
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Blood Supply to Liver

• Liver circulation Fig. 22-1 next

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Liver circulation
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Sinusoids

• Sinusoids Fig. 13-1 next
• Also see Fig. 18-11 in Gould

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Cut surface normal liver with vessels bile ducts
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Liver sinusoids
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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

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Kupffer cells

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

13
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

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Pressure in Liver

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

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Metabolic

• What are the metabolic functions of the liver?

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Detoxification

• Kupffer cells
• Toxins detoxified
• Removal of ammonia make urea

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Digestion

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

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• What happens to all of these functions in liver
  disease?

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Progression of Liver Disease

• Fatty liver
• Hepatitis
• Cirrhosis
• ESLD

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Fatty liver
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Hepatitis

• Infectious mononucleosis
• Toxic chemicals
• Viral infection
• Excessive use of alcohol

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Viral Hepatitis

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

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Viral Hepatitis

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

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Hepatitis

• Symptoms
• jaundice can occur
• pale stools
• easily fatigued

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Hepatitis

• Symptoms
• nausea anorexia
• fever
• liver tenderness
• liver enlarged

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Hepatitis

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

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Prehepatic Jaundice

• Fig. 18-12 in Gould
• Hemolytic jaundice
• Excessive rbc break down
• Unconjuaged bilirubin high
• Stool dark/normal color

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Intrahepatic Jaundice

• If unconjugated bilirubin high means liver cell
  damage
• If conjugated bilirubin high, means blockage

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Posthepatic Jaundice

• Conjugated bilirubin high
• Light colored stool

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Cirrhosis

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

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Cirrhotic liver, external surface macronodular
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Cirrhotic liver, macronodular
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Cirrohtic and fatty liver, micronodular
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Hepatoxic Drugs

• Alcohol
• Acetaminophen
• Androgenic steroids
• Cyclosporine
• Erythromycin
• Glucocorticoids

• Isoniazid
• Methotrexate
• Methyldopa
• NSAIDs

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Damage Liver

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

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Portal HTN

• Due to damaged liver
• Pressure too high on which end?

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Esophageal varices with portal HTN
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Portal HTN Ascites

• Forces plasma out of vessels
• Is Alb high or low in the blood?
• Na restricted diet
• Fluid restricted diet

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End-stage Liver Disease

• Less than 25 of liver functions
• Portal systemic encephalopathy (PSE)

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ESLD Stages

• Stage 1
• apathy
• restlessness
• reversal of sleep rhythm

• Stage 1
• slowed intellect
• impaired computational ability
• impaired handwriting

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ESLD Stages

• Stage 2
• lethargy
• drowsiness
• disorientation
• asterixis

• Stage 3
• stupor (arousable)
• hyperactive reflexes
• extensor plantar responses

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ESLD Stages

• Stage 4
• coma
• response to painful stimuli only

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ESLD

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

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ESLD

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

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ESLD

• False neurotransmitter hypothesis by Fischer
• phe tyr - precursor of epinephrine
  norepinephrine
• trypothan - precurson of serotonin

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ESLD

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

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ESLD

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

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Subjective Global Assessment

• Four elements of pt. Hx
• Recent loss of body wt
• Changes in usual diet
• Presence of significant gastrointestinal symptoms
• Patients functional capacity

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SGA

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

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SGA

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

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SGA

• Significant wt loss
• gt1 to 2 in 1 week
• gt5 in 1 month
• gt7.5 in 3 months
• gt10 in 6 months
• gt40 life threatening

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SGA

• Significant wt loss
• unplanned or recent loss of gt10
• gt20 in surgical pt

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Labs Clinical Signs

• Serum ammonia
• HH
• Aklaline phosphostase
• BUN
• AST
• ALT
• Bilirubin

• K
• Blood glucose
• TG FFA
• Prolonged prothrombin time
• Alb
• LDH
• Ascites edema

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Medications

• Lactulose
• Neomycin
• Steriods

• Insulin
• Diuretics
• IV albumin
• Avoid excessive fat soluble vitamins

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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

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MNT

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

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MNT

• Uncomplicated hepatitis stable cirrhosis
• high protein
• 1.2 g/kg or 1.5 g/kg

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MNT in ESLD

• Before coma
• high protein
• keep protein high until see problems on next
  slide
• then restrict protein

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MNT in ESLD

• Coma
• start 40 g protein
• BCAA formulas
• increase protein 10 g until see
• increase total bilirubin
• increase prothrombin time
• coma

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MNT in ESLD

• Try to not restrict fluid intake
• Case study 32 - 1, 2, 3, 4, 5, 6, 7, 12
• If time 14