Download kkkkkkk

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