liver function
metabolism of macronutrients , storage and activation of vitamins and minerals, formation and excretion of bile, conversion of ammonia to urea, metabolism of steroids, filter and flood chamber
what are 7 common lab tests used to test for liver function?
1. hepatic excretion
2. cholestasis tests
3. hepatic enzymes
4. serum proteins
5. markers of specific liver diseases
6. specific tests for viral hepatitis
7. miscellaneous tests
hepatic excretion
lab tests for serum bilirubin, urine bilirubin, serum bile acids
cholestasis tests
lab tests for serum alkaline phosphatase, 5'NT,LAP,GGT
hepatic enzymes
lab tests for ALT, AST, serum lactic dehydrogenase
serum proteins
lab tests for PT, PTT, serum albumin, serum globulin, mitrochondrial antibody, antinuclear and smooth-muscle antibodies
markers of specific liver diseases
lab tests for serum ferritin, ceruloplasmin, alpha-fetro protein, alpha1-antitrypsin
specific tests for viral hepatitis
lab tests for IgM anti-HAV, IgG anti-HAV, HBsAg, HBeAg, IgM or IgG anti-HBc, anti-HBe, anti-HBs, anti-HCV, HCV-RNA, IgM or IgG anti-hdv, IgM anti-HEV, IgG anti-HEV
miscellaneous tests
lab tests for ammonia
8 diseases of the liver
1. acute viral hepatitis
2. fulminant hepatitis
3. chronic hepatitis
4. non-alcoholic steatohepatitis (NASH)
5. alcoholic liver disease
6. cholestatic liver diseases
7. inherited disorders
8. other liver diseases
NASh
non-alcoholic steatohepatitis
acute viral hepatitis
A, B, C, D, E, G/GB
alcoholic liver disease
hepatic steatosis, alcoholic hepatitis, alcoholic cirrhosis
3 cholestatic liver disease
1. primary biliary cirrhosis
2. sclerosing cholangitis
3. hepatic osteodystrophy
inherited disorders
wilson's disease
what happens with acute viral hepatitis?
widespread inflammation of the liver that is caused by Hep A, B, C, D, and E
four phases of acute viral hepatitis
1. prodromal phase
2. preicteric phase
3. icteric phase
4. convalescent phase
fulminant hepatitis
syndrome in which severe liver dysfunction is accompanied by hepatic encephalopathy
chronic hepatitis
at least 6-month course of hepatitis or biochemical and clinical evidence of liver disease with confirmatory biopsy findings of unresolving hepatic inflammation
alcoholic liver disease is caused by
excess alcohol ingestiong characterized by fatty liver (hepatic steatosis), hepatitis, or cirrhosis
what are the 3 stages of alcoholic liver disease
1. hepatic steatosis
2. alcoholic hepatitis
3. cirrhosis
what may alcoholic cirrhosis lead to?
GI bleeding, hepatic encephalopathy, portal hypertension, ascites
ingested alcohol converst to what?
1. hydrogen: replaces fat as a fuel source and it acculuates, makes fatty liver which causes hepatitis, which creates cirrhosis
2. acetaldehyde: hepatoxicity, decreases viatmina activation, inflammation and necrosis to hepatitis and cirrhosis
PBC
primary biliary cirrhosis
- any chronic cholesttatic disease caused by progressive destruction of small and intermediate-sized intrahepatic bile ducts, -immune-mediated disease
do men or females have PBC majority?
90% of patients are women
sclerosing cholangitis
fibrosing inflammation of segments of extrahepatic bile ducts, with or without involvement of intrahepatic ducts
- hepatic osteodystrophy may occur from vit D and calcium malabsorption
alcoholic liver disease is a result of what
excessive alcohol ingestion characterized by fatty liver, hepatitis, or cirrhosis
fatty liver
hepatic steatosis
what are the 3 stages of alcohol liver disease
1. hepatic steatosis
2. alcoholic hepatitis
3. cirrhosis
what type of alcoholic liver disease leads to GI bleeding, hepatic encephalopathy, portal hypertension, and ascites?
alcoholic cirrhosis
alcohol splits into what when digested?
1. acetaldehyde
2. hydrogen
where does the hydrogen go that was split off of hydrogen?
it replaces fat as a fuel source and that fat accumulates which causes fatty liver (hepatic steatosis)
what happens to the acetaldehyde that was split from alcohol digestion?
it causes a toxicity in the liver called hepatoxicity
what are the problems with hepatoxicity from acetaldehyde from alcohol?
1. decreases vitamin activation
what does decreased vitamin activation cause from hepatoxicity?
1. inflammation and necrosis
2. hypovitaminemia
the fatty liver and hepatoxicity from alcohol causes inflammation and necrosis from the acetaldehyde causes what?
hepatitis
hepatitis can lead to
cirrhosis
hepatitis is caused by
fatty liver from hydrogen and inflammation and necrosis from decreased vitamin activation
PBC
primary biliary cirrhosis , chronic cholestatic disease caused by progressive destruction of small and intermediate-sized intrahepatic bild ducts, whereas the extrahepatic biliary tree and larger intrahepatic ducts are normal
what is destroyed in primary biliary cirrhosis?
small and intermediate-sized intrahepatic bile ducts
what is normal in PBC?
extrahepatic biliary tree and larger intrahepatic ducts
PBC is what type of disease?
immune-mediated disease
do more men or women get PBC?
women, 90% of patients are women
sclerosing cholangitis
fibrosing inflammation of segments of extrahepatic bile ducts, with or without involvement of intrahepatic ducts
-may cause vit D and calcium malabsorption that causes hepatic osteodystrophy
- IBD may be associated
what is different between primary biliary cirrhosis and sclerosing cholangitis?
sclerosing cholangitis involves the extrahepatic biliary tree, where as PBC does not
what are 3 inherited disorders?
1. hemochromatosis
2. wilson's disase
3. alpha1-antitrypsoin deficiency
hemochromatosis
inherited disease of iron overload
wilson's disease
autosomal recessive disorder associated with impaired biliary copper excretion
what is not excreted with wilson's disease?
wilson's disease
alpha-antitrypsin defiency
causes cholestasis or cirrhosis and can cause liver and lung cancer
what is the disease inherited by iron overload?
hemochromatosis
what disorder causes cholestasis or cirrhosis and may cause liver or lung cancer?
alpha1-antitrypsin deficiency
what are some other causes of liver disease?
1. liver tumors
2. systemic diseases (rheumatoid arthritis, systemic lupus erythematosus)
3. acute ischemic and chronic congestive hepatopathy
4. parasitic, bacterial, fungal, and granulomatous liver disease
ascites
enlarged stomach
is there muscle wasting it cirrhosis?
yes
testicular atrophy is caused by
cirrhosis
what is the color of urine for people with cirrhosis
tea colored
what color is the stool with people with cirrhosis
clay colored
what nutrition assessment parameters for end stage liver disease may influence interpretation?
1. body weight
2. anthropometric measurements
3. creatinine-height index
4. nitrogen balance studies
5. 3-mathylhistidine excretion
6. visceral protein levels
7. immune function tests
8. bioelectrical impedance
what 4 general topics does SGA parameters for nutritional evaluation of liver transplant candidates look for?
1. history
2. physical
3. existing conditions
4. nutritional rating (based on results of above parameters)
what does SGA look for in evaluating history for liver transplant candidates?
1. weight change (consider ascites and edema)
2. appetite
3. taste changes and early satiety
4. dietary recall
5. persistent GI problems
what physical things does SGA look for when considering liver transplant cadidates?
1. muscle wasting
2. fat stores
3. ascites
4. edema
what are the existing conditions that SGA looks at for liver transplant candidates
1. other diseases
2. GI bleeding
3. renal insufficiency
4. infection
based on existing conditions what do nutritional rating do they look for for liver transplant candidates?
1. well nourished
2. moderately/severely malnourished
what directly causes malnutrition in liver disease?
1. maldigestion or malabsorption
2. anorexia (inadequate oral intake)
what indirectly causes malnutrition from liver diseases?
1. early satiety or dysgeusia
2. nausea and vomiting
3. altered metabolism
4. restricted diets
what are the clinical findings for malnutrition?
1. abnormal liver function tests
2. jaundice
3. ascites and edema
4. hepatic encehalopathy
5. portal hypertension and varices
6. altered amino acid levels
7. vitamin/mineral deficits
8. glucose intolerance or fasting hypoglycemia
what should nutrition assessment be for liver disease?
1. serial monitoring of body weight and anthropometry
2. dietary intake
3. subjective global assessment
4. laboratory tests for nutritional deficiency as vit D, folic acid, B12, thiamin, and others
after clinical findings and nutrition assessment what is the medical management for liver disease?
1, diuretic therapy
2. medication for encephalopathy (lactulose, neomycin)
3. management of portal hypertensive bleeding (pharmacologic therapy, shunts, banding)
4. monitoring of blood glucose
after clinical findings and nutrition assessment what is the nutrition management for liver disease?
1. increased energy intake via small, frequent meals
2. sodium restriction for fluid retention
3. fluid restriction for hypnatermia
4. carbohydrate-controlled diets for hyperglycemia
5. vitamin and mineral supplements
6. oral liquid supplements or enteral
what vit and mineral deficits are seen in severe hepatic failure?
1. vit A
2. vit D
3. vit E
4. vit K
5. vit B6
6. vit B12
7. folate
8. niacin
9. thiamin
10. zinc
11. magnesium
12. iron
13. potassium
14. phosphorus
cirrhosis causes portal hypertension, what should you do?
PN for at least 5 days
cirrhosis causes ascites, what should you do?
sodium restriction diet
cirrhosis causes hyponatremia, what should you do?
fluid restriction, moderate sodium intake
how many stages are there for hepatic encephalotpathy?
4
symptoms of stage 1 of hepatic encephalopathy
1. mild confusion
2. agitation
3. irritability
4. sleep disturbance
5. decreased attention
symptoms of stage 2 of hepatic encephalopathy
1. lethargy
2. disorientation
3. innapproriate behavior
4. drowsiness
symptoms of stage 3 of hepatic encephalopathy?
1. somnolence but arousable
2. incomprehensible speech
3. confusion
4. aggression when awake
stage 4 symptoms of hepatic encephalopathy
coma
end-stage liver disease causes what
hepatic encephalopathy
what are the major causes of hepatic encephalopathy?
1. GI bleeding
2. fluid and electrolyte abnormalities
3. uremia
4. use of sedatives
5. hypo-hyperglycemia
6. alcohol withdrawal
7. constipation
8. acidosis
what are the four things we should do for end-stage liver disease?
1. consider major causes of encephalopathy
2. treat underlying cause
3. treat with medications
4. ensure adequate diet is consumed
what are two medications for end-stage liver disease hepatic encephalopathy
1. lactulose
2. neomycin
what should we do before we use medications for end-stage disease, hepatic encephalophathy?
treat underlying cause of encephalopathy
should there be protein restriction for end-stage liver disease?
try to avoid it
are BCAA formulas used for end-stage liver disese?
yes
what are the glucose alterations?
treat as diabetes
for fat malabsorption what should you use?
use MCT's, and low-fat diets
medium chain triglycerides
if pt has osteopenia how should we treat?
1. weight maintenance
2. well-balanced diet
3. adequate protein
4. high calcium
5. aqequate vit D
6. avoid alcohol
what are some common meds used after liver transplantation?
1. azathioprine
2. antithymocyte globulin
3. basiliximab
4. cyclosporine
5. aclizumab
6. glucocorticoids
7. muromonab CD-3
8. mycophenolate mofetil
9. sirolimus
10. tacrolimus
11. 15-deoxysperagualin
when should nutrition care be given to liver transplants?
pre, immediate, and long term post
long-term preventive nutrition to optimize health and to avoid or minimize...
1. excessive weight gain
2. hyperlipidemia
3. hyperglycemia
4. hypertension
5. osteopenia
hyperlipidemia
high fat levels, cholesterol levels, increase in an amount of fat in the blood
hyperglycemia
high blood sugar
hypertension
high blood pressure in cardiovascular arteries and veins
osteopenia
lower than normal bone mineral density, not as severe as osteoperosis
cirrhosis
replacement of liver tissue by fibrosis, scar tissue, and regenerative nodules
what two ducts meet and go into the duodenum?
bile duct from liver and pancreatic duct from pancreas
gallbladder diseases
1. cholelithiasis
2. acute cholecystitis
3. chronic cholescystitis
4. acute cholangitis
5. sclerosing cholangitis
6. cholestasis
cholelithiasis
avoid obesity and fasting; follow low-fat diet
acute cholecystitis
hold feedings or PN, then low-fat diet
chronic cholecystitis
low-fat diet
cholestasis
occurs when not enteral feedings
what are 3 tests for pancreatic functions?
1. secretin stimulation test
2. glucose tolerance test
3. 72-hour stool fat test
secretin stimulation test
measures pancreatic secetion, particaularly bicarbonate, in response to secretin stimulation
glucose tolerance test
assesses endocrine function of the pancreas by measuring insulin response to a glucose load
72-hour stool fat test
assesses exocrine function of the pancreas by measuring fat absorption that reflects pancreatic lipase secretion
what causes pancreatitis?
1. chronic alcoholism
2. biliary tract disease
3. hypertriglyceridemia hypercalcemia
4. gallstones
5. trauma
6. certain drugs some viral infections
what is the diganosis for pancreatitis?
1. apply ranson's criteria
2. tests of pancreatic function such as
a. secretin stimulation test
b. glucose tolerance test
c. 72-hour stool fat test
clinical findings for pancreatitis
1. abdominal pain and distention
2. nausea
3. vomiting
4. steatorrhea
severe pancreatitis has what clinical findings
1. hypotension
2. oliguria
3 hyspnea
what is the medical management for acute pancreatitis after diagnosis and clinical findings?
1. withhold oral feeding
2. give IV fluids
3. administer H2-receptor antagonists, somatostatin
what is the medical management for chronic pancreatitis after diagnosis and clinical findings
1. manage intestinal pH
2. administer insulin for glucose intolerance
how do we manage intestinal pH for chronic pancreatitis?
1. antacids
2. H2-receptor antagonists
3. proton pump inhibitors
what is the nutrition management for acute pancreatitis
1. withhold oral and enteral feeding
2. support with IV fluids
3. if oral can't start within 5-7 days, start nutrition supoprt
4. polymeric formula through TF beyond the ligament of treitz for less severe cases of prolonged pancreatitis
5. PN intiated for
PN should be initiated for severe acute pancreatitis if..
1. if TG's are less than 400 mg/dl before PN iitiation, use a 3-in1 solution and monitor TG levels
2. if TG's are elevated above 400 mg/dl, use a dextrose-based solution, monitor serum glucose frequently, and treat as needed with insulin
once oral nutrition is started in acute pancreatitis, what should you provide?
1. easily digested foods
2. low-fat diet
3. 6 small meals
4. adequate protein intake
5. increased calories
what is the nutrition management for chronic pancreatitis?
1. provide oral diet as in acute phase
2. TF can be used when oral diet is inadequate
3. supplement pancreatic enzymes
4. supplement fat-soluble vitamins and vitamin B12
what is the MNT for acute pancreatitis?
1. withhold oral feeding; maintain hydration intravenously
2. progress diet as tolerated; low-fat diet, six small meals
3. nutrition support as needed
what is the MNT for chronic pancreatitis?
1. high risk for PEM
2. antioxidants, pancreatic enzymes, MCT
3. glucose intolerance
what are teh goals of nutrition care in liver, biliary system, and exocrine pancreas disease?
1. improve nutritional status
2. support the patient during acute phases of illness