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WEEK 3:

Liver function tests:

QuestionAnswer
what can cause liver damage infection, adverse drug reaction, alcohol abuse, obesity, and cancer
types of liver damage acute or chronic
acute liver damage swollen and oedamtous
chronic liver damage fibrotic
what type of infection can lead to liver damage viral hepatitis (about 25% liver failure)
what adverse drug reactions can cause liver damage (6) paracetamol overdose, clavulanic acid in augmentin (co-amoxiclav), valproate, amiodarone, and herbal preparations
symptoms and signs of liver disease jaundice and pruritus (itching) , nausea and vomiting, hepatomegaly (big liver), ascites, dark urine and pale stools in cholestasis (blocked bile movement), and spider naevi in alcoholic liver disease
spider naevi in femalles normal in small amount
features of cirrhosis jaundice, itching, coagulation defects, tendency to bleed and be hypercoagulable, hypoalbuminaemia (low level albumin), pitting oedema and ascites, hepatic encephalopathy
port systemic shunts blood shunting to spleen causes hypersplenism so is treated with surgical shunts to bypass
hepatic encephalopathy reversible metabolic disorder leading to alterations in mental status and potentially coma and death
hepatic encephalopathy causes increase in aromatic amino acids (eg phenylalanine) converted into false neurotransmitters, and increase in serum ammonia
precipitating factors for hepatic encephalopathy high protein diet and sedation
ammonia derives from metabolism of amino acids and from release of ammonia from amino acids by bacterial ureases in bowel
ammonium NH4+ absorption not reabsorbed in bowel and is excreted in stool
reducing ammonia in colon includes restriction of protein intake and oral neomycin, oral administration of lactulose (making NH4+ convert into NH3 excreted into faeces)
LFTs test for (6) ALP (alkaline phosphatase), ALT (alanine aminotransferase), AST (aspartate aminotransferase), Albumin, GGT (y-glytamyl transpeptidase/transferase) and Bilirubin
ALT
AST
ALP
GGT
albumin
coagulation
hepatocellular
obstruction
synthetic function
bilirubin
bilirubin increased in
journey of haem made of iron and globin, haem -> biliverdin -> insoluble bilirubin -> liver converts it into -> water soluble bilirubin -> biliary excretion
what happens after biliary excretion gut bacteria either enterohepatic cycle it back into bilirubin/ urobilinogen back into liver or bacteria make 5-10% into stercobilinogen in stools
serum albumin often reduced in who
plasma half life
ALT & AST intracellular enzymes whose presence in blood indicates hepatocyte damage and death
AST is found in hepatocyte mitochondria
ALP mainly made in liver and bone where levels rise with intrahepatic and extrahepatic biliary obstruction and with sinusoidal obstruction
GGGTs microsomal enzyme found in many cells + tissues with highest concs in liver made by hepatocytes and by epithelial lining of small bile ducts
modest increase in aminotransferase and large increases in ALP and GGT suggests biliary obstruction (cholestatic or obstructive)
isolated elevation of serum GGT relatively common and may occur during ingestion of microsomal enzyme inducing drugs including alcohol
drugs toxic to hepatocytes
types of cholestasis intrahepatic and extrahepatic
intrahepatic cholestasis blockage of intrahepatic bile ducts
causes of intrahepatic cholestasis
extrahepatic cholestasis blockage of common bile duct (CBD)
causes of extrahepatic cholestasis
gross and microscopic findings in cholestatic liver disease enlarged, greenish liver and bile ducts distended with bile and bile lakes and bile infarcts
clinical features in cholestasis (reduced bile flow) (hepatic or post hepatic)
lab findings in cholestasis (reduced bile flow)
icteric jaundice
Created by: 22tango
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