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35 Cards in this Set
- Front
- Back
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Liver "function" tests
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hepatobiliary disease:Aminotransferases
AST* ALT* Lactate dehydrogenase Alkaline phosphatase* GGT 5’ Nucleotidase Hepatic Function:Protein Synthesis Albumin PT / INR Total protein SPEP/Globulins T-bilirubin* Cholesterol |
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3 fxns of the liver
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1-power (energy), also makes bile.
2-manufacturing of proteins for transport and coagulation cascade. like albumin and vit k II VII IX and X 3- waste management |
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What blood test help you distinguish leiver funtion?
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Protein Synthesis
Albumin PT / INR Total protein SPEP/Globulins T-bilirubin Cholesterol |
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Aminotransferases
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AST and ALT
Intracellular aminotransferring enzymes in the process of gluconeogenesis Aspartate Aminotransferase (AST) Aspartic acid Oxaloacetic acid Alanine Aminotransferase (ALT) Alanine Pyruvic acid Present in large quantities in hepatocytes AST is both cytosolic and a mitochondrial isoenzyme ALT is a cytosolic enzyme “Leak” in serum 2o to hepatocyte injury / death Elevation in many forms of liver disease Highest in those with severe hepatocyte necrosis |
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Aminotrsnsferases Sensitivity
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Both abnormal in most cases of significant liver disease
Often normal in advanced cirrhosis. ALT more specific to liver |
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Aminotransferase specificity
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AST less specific- liver, muscle (skeletal and cardiac)
ALT more specific hepatocyte necrosis |
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DIagnostic value for livr damage: Amintotransferases
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Level of Elevation:
Correlates poorly with extent of necrosis on biopsy and not predictive of prognosis But serial measurements can be of value Fulminant hepatitis: Rapid AST & ALT fall with rising bilirubin and PT ->Poor prognosis < 500 IU -> many disorders >2000 IU -> limited differential |
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Aminotransferases at very hi levels: >2000IU/L
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Acute drug- or toxin-induced hepatitis
acetaminophen Halothane Amanita mushrooms CCl4 Hepatic ischemia (shock liver) Acute viral hepatitis |
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Time course of ALT elevation
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can have recovery in a few days to weeks. from viruses usu weeks tomonths to recover.
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Alcoholic Hepatitis Aminotransferases
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AST/ALT ratio > 2:1
Suggestive of alcoholic liver disease >3:1 is even more specific Mainly reflects low ALT level Alcohol-related deficiency of pyridoxine AST & ALT should be < 300 IU/L If AST > 500 IU/L, rule out co-existing cause Acetaminophen toxicity Viral hepatitis |
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Alcoholic Liver Disease
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The history is the key – 60 g/dayusu a drink is ab 10 grams
Alcoholic cirrhosis Gynecomastia, parotids, Dupuytren’s Alcoholic hepatitis: RUQ pain, anorexia, fever, jaundice, RUQ tender hepatomegaly, abnormal LFTs, leukocytosis Treatment: Abstinence Nutrition Consider prednisolone or pentoxifylline |
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Lactate Dehydrogenase
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Very non-specific
Rarely useful in addition to aminotransferases Occasionally helpful Ischemic hepatitis: massive elevation Malignant infiltration: sustained elevation |
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LDH elevation
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Liver, acute & chronic
Muscle injury Skeletal Cardiac Hemolysis CVA Kidney infarction |
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Alkaline Phosphatase Tissue source
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Group of enzymes that function best at pH 9
Levels are age dependent Bone disease: Bone cell production (osteoblastic) Liver disease: Biliary tract obstruction Liver Bone Placenta Kidney Intestines Leukocytes Tumor |
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Hepatic Alkaline Phosphatase
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Location:
Hepatocyte canalicular membrane Bile duct epithelium luminal membrane Serum elevation Increased synthesis Increased release Serum ½ life: 1 week Levels may take days to normalize after resolution of obstruction any disease that atacks or obstructs bile ducts will cause incr. |
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g-Glutamyl Transpeptidase (GGT)
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Not found in bone
Helpful confirming elevated alk phos to be of liver origin Microsomal enzyme Inducible by EtOH & drugs 5' Nucleotidase Similar sensitivity to alkaline phos for obstructive and infiltrative processes Like GGT, can be used to confirm elevated alk phos to be of liver origin |
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Albumin
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not good measure of liver fxn
Liver synthesizes 10 g/day Liver disease: decreased synthesis Serum ½ life 20 day No change in acute liver injury Not useful to follow progress Other factors effecting albumin levels: Nutritional status Volume status Vascular integrity Increased catabolism Urinary losses |
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Prothrombin Time
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can be good measure of liver fxn
Hemostasis Coagulation factors synthesized in the liver Not factor VIII (vascular endo / reticuloendo) PT prolongation: Vitamin K deficiency (malabsorption, malnutrition, antibiotics) Warfarin (Coumadin) DIC Liver disease: --Synthetic: Acute or chronic liver failure -- Cholestatic: Biliary obstruction to detremine the issue you can inject vit k and watch for improvement |
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tools for prognosticating ppl with liver disease
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MELD score and Child Pugh
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Sources of bilirubin
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hemoglobin from red blood cells. heme from hepatic enzymes and other proteins.
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fate of Bilirubin
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u-bili to c-bili to urobilinogens or stercobilin
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Breakdown of bilirubin
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heme is unconjugated, liver conjugates it into non polar substance that can be excreted in bile or urine.
Albumin delivers bili to membrane, taken to ER and meets with UDP and conjugates it, then transported and exrected into bile canaliculus and then excreted into duodenum. |
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Premature babies and jaundice
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Lack of UDP transferace so inability to conjuate bili and baby beomes jaundice.
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Breast milk jaundice
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delay in UDP devt, breast milk has beta glucuronidase, deconjugates bilirubin and causes jaundice
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Gilberts Syndrome
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Auto dominant, up to 10% of caucasians, low level of activity of UDP enzyme. Exacerbated by fasting or illness like a cold. Normal aminotransferase, alkaline phos and urine
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Crigler najjar
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auto recesive- cant live with type one, type two u can induce enzyme with phenobarbitol.
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dubin johnson syndrome
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excretion problem
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LFTS for Bilirubin Metabolism Disorders
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x
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LFTS in Hepatocellular Disorders
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x
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LFTS in choestatic disorders
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x
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Disorders of bilirubin metabolism
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Increased bilirubin production
Hemolysis, ineffective erythropoesis, massive transfusion, hematoma resorption Decreased bilirubin conjugation Physiologic jaundice of the newborn, Gilbert’s syndrome, Crigler-Najjar syndrome Decreased bilirubin secretion Dubin-Johnson syndrome, Rotor’s syndrome |
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Hepatocellular disorders
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Primarily AST and ALT elevations:
Viral hepatitis (A,B,C,D,E) Alcohol Medication-induced liver disease Ischemic liver injury Nonalcoholic Steatohepatitis (NASH) Autoimmune hepatitis Hemochromatosis Wilson’s disease Alpha-1 Antitrypsin Deficiency Acute Fatty Liver of Pregnancy |
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Choleostatic Disorders
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primarily alk phos elevation
Extrahepatic bile duct obstruction Choledocholithiasis Pancreas cancer, cholangiocarcinoma Primary sclerosing cholangitis Primary biliary cirrhosis Intrahepatic cholestasis Medication-induced, TPN, sepsis, post-op Intrahepatic cholestasis of pregnancy Infiltrative disorders Sarcoid, amyloid, infection, neoplasm |
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Hx in eval of Abn liver tests
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Associated fever or weight loss
Use of alcohol Risk factors for viral hepatitis (S/D/R&R) History of jaundiced illness Prior biliary tract surgery Medications Family history of liver disease |
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Physical exam in eval of abn liver tests
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Jaundice
Spider angiomata Confusion/asterixis Gynecomastia Palpable left lobe of liver Splenomegaly Ascites |
