Lecture 10- Liver Function Tests

Pt/INR and bilirubin=

liver functions

AST and ALT=

liver injury/inflammation

indications to check liver fuction

• GI: epigastric or RUQ pain, nausea, ascites, edema

• General: fatigue

• skin: generalized pruritic, jaundice

• eyes: scleral icterus

• dark colored urine

• routine screening

• monitoring (cirrhosis, hepatitis)

• monitoring effects of medications

ALT

• hepatocellular damage

• most specific → only found in liver (AA metabolism)

AST

• hepatocellular damage

• if only value increased→ something outside (ex. heart)

alanine aminotransferase (ALT)

• enzyme predominately found in liver

  • smaller amnts in kidney, heart, skeletal muscle

• elevations: liver injury or dysfunction

  • specific for hepatocellular disease

• drugs- acetaminophen, allpurinol, codeine, OCP, salicylate, tetracyclines

aspartate aminotranferase (AST)

• enzyem found highly concentrated inthe liver, heart, and skeletal muscle

  • smaller amnts in pancreas, kidney, RBC

• elevation trends:

  • acute hepatitis - 20x normal

  • gallstone obstruction- 10x normal, then quick fall

  • cirrhosis- AST =amnt of active infalmmation

alkaline phosphate (ALP)

• enzyme found mostly in liver, biliary tract epithelium, and bone

• useful in detecting liver and bone diseases

• elevations- cholestatic process adn impaired bile flow

• isolated increased ALP- confirm liver by checking GGT

• most sensitive test for tumor metastasis to liver

markers of synthetic function

• albumin

• PT/INR

• bilirubin

synthetic function: albumin

• 20 day half life

• synthesized in liver

• maintains osmotic pressure

• transports drugs, hormones, and enzymes

• measure of hepatic function adn nutrition

• decreased= chronic liver disease or malnutrition

synthetic function: PT/INR

• reflects synthetic function (CF V, VII, IX, X)

synthetic function: bilirubin

• total= indirect + direct

• metabolism and excretion

A/G ratio

protein help maintain osmotic pressure within vascular space

• total protein= albumin (60%) + globulin

• normally A/G>1

• decrease albumin, increase globulin → A/G<1

• can differentiate btwn GI protein loss, liver disease, and autoimmune disease

A/G ratio- globulin

• synthesized in the liver

• carrier proteins, complement, enzymes, immunoglobulin, some=measure nutrition

• heal after infection

indirect bilirubin

• unconjugated

• fat soluble

• bound to albumin to travel to liver

direct bilirubin

• conjugated

• water soluble

• stored as bile in gallbladder or excreted in feces or urine

hepatic injury

• hepatocellular pattern: very increased ALT/AST >ALP

• disproportionate elevation of AST adn ALT compared to ALP

• AST:ALT suggests etiology

AST:ALT <1

• drug induced liver injury

• alcoholic liver disease

• nonalcoholic fatty liver disease

• acute viral hepatitis

• chronic hepatitis C infection

AST: ALT >2

alcoholic fatty liver disease

cholestasis

cholestatic pattern: very increased ALP> ALT/AST

• ALP is disproportionately elevated

• extrahepatic- choledocholithiasis, cholangiocarcinoma

• intrahepatic- primary biliary cholangitis, drug- induced cholestasis, sepsis

• gamma-glutamyl transferase (GGT)

  • confirm hepatic source of ALP if GGT also elevated

  • if GGT normal- consider boen dz; can occur in pregnancy

gamma-glutamyl tranaferase (GGT)

• high concentrations in liver and biliary tract

  • smaller amnts in kidney, spleen, heart, intestinem brainm prostate glanf

• very sensitive in detecting biliary disease

• can detect chronic alcohol ingestion

• elevation trends:

  • GGT usually parallels ALP

  • increase ALP with normal GGT= skeletal disease

  • increase ALP and GGT= hepatobiliary disease

isolated hyperbilirubinemia

• very increased bilirubin> ALT/AST and ALP

• fracionate bilirubin

• unconjugated- hemolysism gilbert syndrome

• conjugated- continue eval for hepatobiliary dz- damage or obstruction

• use hepatic functional panel» CMP to differentiate cause of hyperbilirubinemia

indirect bilirubinemia

• stems from hepatocellular dysfunction (eg hepatitis); inability to convert from unconjugated to conjugated bilirubin in liver

direct ilirubinemia

• ostruction of bile duct with gallstone or tumor (cholestasis); inability to be excreted properly

trends- amylase

• levels increase within 12 hours on disease onset

• levels normalize within 48-72 hrs

trends- lipase

• more sensitive than amylase

• levels rise 4-8 hrs of symptom onset, peak at 24hrs

• elevation lasts 8-14 days

• if 3x upper limit of normal= 80% sensitive adn 93% specific fro acute pancreatitis