Found primarily in liver, heart, kidney, pancreas, and muscles. Elevated with significant tissue damage
AST (7-40)
Increased levels primarily in hepatocellular necrosis, liver damage, myocardial infarction, and to a lesser extent kidney infection.
ALT (5-36)
Increases are usually found in cellular death and/or leakage from cell. Can confirm myocardial or pulmonary infarction. By itself usually means hemolysis.
LDH (5-150)
Increases in biliary obstruction. Also present in blastic bone disease, pregnancy, or skeletal growth.
Alkaline phosphatase (30-120)
May be elevated in liver disease, particularly alcohol abuse, occult bile duct obstruction, cholangitis, and drug abuse.
Gama-Glutamyl Transpeptidase (GGT) (0-30)
Elevated in liver disease, hemolytic anemia, and toxic effects to some drugs
total bilibrubin (.2-1.5)
unconjugated bilirubin is transported with
ligandin or z protein
unconjugated bilirubin is conjugated to
glucouronic acid
conjugated bilirubin in the SI is converted to urobilinogen by
bacterial proteases
90% of urobilinogen is excreted in
feces
major cause of prehepatic jaundice
RBC hemolysis
major cause of hepatic jaundice
Viral hep, drugs, cirrhosis, and tumors
major cause of posthepatic jaundice
Gallstones or cancer of bile ducts
weakness, dark urine, anemia, icterus, and splenomegaly
hemolytic jaundice
- Increased UB without bilirubinuria
- increased fecal and urine urobilinogen
- hemolytic anemia
- hemoglobinuria
- increased reticulocytes
hemolytic jaundice
hemoglobinuria seen in
acute intravascular hemolysis
urinary changes in hemolytic jaundice
absent bilirubin and increased/normal urobilinogen
fecal changes in hemolytic jaundice
normal stercobilinogen
due to intra/extra hepatic obstruction of bile ducts
obstructive jaundice
Hepatitis, PBC, and drugs can cause
intrahepatic jaundice
Stones, stricture, inflammation, and tumors can cause
extra hepatic biliary obstruction
examples of impaire/absent hepatic conjugation of bilirubin leading to hepatic jaundice
- decreased GT activity (Gilberts) can cause
- hereditary absence/def of UDPGT (Grigler-Najjar synd)
hereditary absence/def of UDPGT
Grigler-Najjar synd
decreased GT activity
Gilberts
familial or hereditary disorders causing hepatic jaundice
- Dubin-Johnson synd
- rotor synd
acquired disorders that cause hepatic jaundice
- hepatocellular necrosis
- intrahepatic cholestasis
intrahepatic-liver cell damage/blockage of bile canaliculi will cause
obstructive jaundice
examples of intrahepatic-liver cell damage/blockage of bile canaliculi
- drugs/toxins
- Dubin-Johnson synd
- E or preg
- hep/virus
- tumors
- intrahepatic biliary hypo
- primary biliary cirrhosis
weakness, low appetite, hepatomegaly, palmar erythema, spider angioma
symptoms of hepatic jaundice
- normal liver function
- elevated CB and UCB
- elevated bilirubinuria
lab findings of hepatic juandice
examples of extrahepatic/obstructive bile ducts causing obstructive jaundice
- tumor compression/obstruction
- choledochal cyst
- extrahepatic biliary atresia
- intraluminal stones
- stenosis/postop
- pain
- fever from ascending cholangitis
- palpabe/tender gallbladder
- enlarged/smooth liver
cholestasis
- increased serum bilirubin, bilirubinuria, ALP, and cholesterol
- decreased or absent feceal urobilinogen
obstructive jaundice
increased bilirubin and reduced/absent urobilinogen
urinary changes from extrahepatic obsructive jaundice
reduced/absent faecal
faecal changes from extrahepatic obsructive jaundice
proportion of conj bilirubin to the total raised bilirubin that is more suggestive of hepatic than posthepatic jaundice
20-40% of total
proportion of conj bilirubin to the total raised bilirubin that is more suggestive of posthepatic than hepatic jaundice
over 50% of total
proportion of conj bilirubin to the total raised bilirubin that is more suggestive of juandice secondary to haemolysis or constitutional (Gilberts, Crigler-Najjar)
less than 20%