LFTs Flashcards
Pattern:
ALT/AST in 1000s, ALP mildly raised
Acute hepatitic picture
Pattern:
AST/ALT in 100s
Chronic hepatitic picture
Pattern:
ALP significantly raised, ALT/AST mildly raised, raised bilirubin
Cholestatic (obstructive) picture
Pattern:
Raised gammaGT, increased mean corpuscular volume, AST/ALT mildly elevated (AST>ALT)
Alcoholic picture
Pattern:
Raised gammaGT, increased mean corpuscular volume, AST/ALT mildly elevated (AST>ALT), raised bilirubin
Acute alcoholic hepatitis
Pattern:
Liver enzymes may be normal, reduced albumin, raised coagulation tests
Cirrhosis/chronic liver disease
ALT sources
Specific to liver
AST sources
- Liver
- Heart
- Skeletal muscle
- Kidneys
- Pancreas
What would cause a marked increase (>1000) in ALT and AST?
- Toxin/drug induced hepatitis eg paracetamol
- Acute viral hepatitis (Hope A/B/E, EBV, CMV)
- Liver ischaemia
What would cause a modest increase (300-500) in ALT and AST?
- Chronic viral/alcoholic/autoimmune hepatitis
- Biliary obstruction
What would cause a mild increase (<300) in ALT and AST?
- Cirrhosis
- Non-alcoholic fatty liver disease
- Hepatocellular carcinoma
- Haemachromatosis/Wilson’s disease
ALP sources
Main sources:
biliary ducts, bone (Paget’s disease, bony metastasis, fractures, osteomalacia, renal bone disease)
Lesser sources:
placenta, small intestine (fatty meals), kidneys (chronic kidney disease)
How can you determine if ALP is of hepatic origin?
GammaGT mirrors ALP so can be used to determine if ALP is of hepatic origin.
What would cause a marked increase (>4x normal) in ALP?
Cholestasis (eg gallstones, primary biliary cholangitis, primary sclerosing cholangitis, pancreatic cancer, drugs)
What would cause gammaGT to be raised?
- Alcohol abuse
- Enzyme inducing drugs
What would cause an increase in unconjugated bilirubin?
- Increased red blood cell break down
- Impaired hepatic uptake (drugs, heart failure)
- Imparied coagulation (Gilbert’s syndrome, physiological neonatal jaundice)
Causes of increased conjugated bilirubin
- Hepatocellular dysfunction (liver disease)
- Impaired hepatic secretion (cholestasis)
Functional liver tests
- Albumin (albumin is synthesised in the liver and has a half life of around 20 days)
- Prothromin time / INR (depends on clotting factors and fibrinogen which are synthesised by the liver)
What would cause a raised PT / INR?
- Liver disease (with imparied function)
- Vitamin K deficiency
- Consumptive coagulopathy (eg disseminated intravascular coagulation)
What could macrocytic anaemia in the context of deranged LFTs indicate?
Alcohol
What could thrombocytopenia in the context of deranged LFTs indicate?
Effect of alcohol on bone marrow, hypersplenism, liver cirrhosis, or disseminated intravascular coagulation
Further investigations to find cause of deranged LFTs
- Viral
- Viral hepatides: hepatitis A IgM, hepatitis B surface antigen, hepatitis C IgG, hepatitis E IgM
- CMV serology
- EBV serology
- Autoimmune liver screen
- Anti-smooth muscle (autoimmune hepatitis type 1)
- Anti-mitochondrial (primary biliary cholangitis)
- Anti-nuclear (autoimmune hepatitis type 1, SLE)
- Tumour markers - if cirrhosis/weight loss
- alpha-fetoprotein (hepatocellular carcinoma)
- Infiltrative
- Ferritin and transferrin saturation (haemachromatosis)
- Serum copper and caeruloplasmin + 24 hour urinary copper
- Fasting glucose and lipids (fatty liver disease)
- Metabolic
- alpha1-antitrypsin
- Immunoglobulins and protein electrophoresis (IgM raised in primary biliary cholangitis, IgA raised in alcoholic liver disease, IgG raised in autoimmune hepatitis)
- TTG antibody (Coeliac disease)
- Toxins
- Paracetamol level (paracetamol overdose)
Non-hepatic causes of deranged LFTs
- Drugs:
- Hepatitis: sodium valproate, methotrexate, paracetamol, tuberculosis antibiotics
- Cholestasis: co-amoxiclav, clarithromycin, carbamazepine, chlorpromazine
- Right heart failure
- Sepsis
- Coeliac disease
- Haemolysis
- Hyperthyroidism
- Right lower lobe pneumonia
