LFT Interpretation PDF

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LFT Interpretation & explanation...

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LFT Interpretation Resource: GP Resource, geeky medics, a guide to lab Ix, GP tutorial, https://labtestsonline.org.uk/tests/liver-function-tests (Good resource), medical masterclass page 18, LFTs include: 

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Transaminases o AST & ALT o Both ↑ in hepatocellular damage, o ↑↑ in drug toxicity, acute viral hepatitis, liver ischaemia o ↑ in alcohol-related, ALT o Source: liver specific o Isolated elevation: o Elevation with__: AST o Source: liver, heart, skeletal muscle, kidney, RBC ALP o Source: liver, bone, (gall stone? Biliary tract?) GGT (gamma-glutamyl transferase) o Albumin o Measure of liver function Total bilirubin o Prothrombin (PT) time o Indirect measure of liver function Coagulation screen o Measure of liver function ALT, AST, ALP and GGT: distinguish between hepatocellular damage and cholestasis Bilirubin, albumin and PT: assess the liver’s synthetic function

AST Source Significance of elevated level Causes

ALT

MI or cardiac pathology,

ALP

Hyperthyroidism Bone disease, liver disease, hyper/hypoPTH Consider stopping statins if ALT more than x3

GGT

of upper range

Geeky medics – Interpreting LFTs Step 1: Assess ALT & ALP  

If ALT raised: more than x10 rise (↑↑) or less than x10 (↑) If ALP raised: more than x10 (↑↑) or less than x10 (↑)

Step 2: Compare ALT & ALP  

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ALT: hi conc. In hepatocytes, released w/hepatocellular injury (marker for liver cell injury) ALP: in liver, bile duct, bone tissue o Raised in liver pathology due to ↑ synthesis in response to cholestasis (reduction or stoppage of bile flow) o Indirect marker of cholestasis o Isolated ALP ↑: bone (Paget’s disease of bone) Comparison (ALT x10 ↑ vs ALP x3 ↑) o ↑ALT > ↑ALP  predominant hepatocellular injury o ↑ALP > ↑ALT  suggest cholestasis o Can have mix of both GGT o Check with ↑ALP o ↑GGT  biliary epithelial damage & bile flow obstruction, alcohol, drugs (phenytoin) o ↑↑ GGT  cholestasis Isolated ↑ALP o w/o GGT  non-hepatobiliary pathology o anything leading to ↑bone breakdown o Causes:  Bony mets, primary bone tumours (sarcom), vitD deficiency, recent bone fractures, renal osteodystrophy Jaundiced but normal ALT & ALP o Isolated ↑ bilirubin o Think pre-hepatic causes of jaundice o Causes:  Gilbert’s syndrome (most common cause), haemolysis (check blood film, FBC, reticulocyte count, haptoglobin, LDH levels to confirm)

Step 3: Assess hepatic function 

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Liver’s synthetic f(x): o Conjugations & elimination of bilirubin o Albumin synthesis o Clotting factor synthesis o Gluconeogenesis Thus measure

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o Serum bilirubin o Serum albumin o PT time o Serum blood glucose Bilirubin o Haem breakdown product o Unconjugated = non-water soluble, taken to liver to excrete (made soluble) o S&S can differentiate conjugated & unconjugated hyperbilirubinaemia o Colour of urine  Unconjugated – not excreted in urine, not affect colour of pt. urine  Conjugated – pass in urine, makes it darker o Colour of stool  If bile & pancreatic lipase are unable to reach bowel (due to blockage, posthepatic) fat is not absorbed  steatorrhoea (sign of biliary/pancreatic issue) o Colour of urine + stools  indication to jaundice cause:  Normal urine + normal stools = pre-hepatic cause (nothing affected)  Dark urine + normal stools = hepatic cause (conjugated)  Dark urine + pale stools = post-hepatic cause (obstructive) o Causes of unconjugated hyperbilirubinaemia include (pre-hepatic):  Haemolysis (e.g. haemolytic anaemia)  Impaired hepatic uptake (drugs, congestive cardiac failure)  Impaired conjugation (Gilbert’s syndrome) o Causes of conjugated hyperbilirubinaemia include:  Hepatocellular injury  Cholestasis  Liver disease, pancreatic disease, Dublin-Johnson syndrome Albumin o Helps to bind water, cations, FA and bilirubin; role in oncotic pressure o ↓ in:  Liver disease (cirrhosis - ↓ production), inflammation (acute, temporary ↓ in liver production), excess loss (protein-losing enteropathy or nephrotic syndrome) PT time o Measures extrinsic pathway o In absence of other 2o causes (anticoagulant use, vitK deficiency), PTT can indicate liver dysf(x) ALT/AST ratio o ALT > AST  CLD o AST > ALT  cirrhosis, acute alcoholic hepatitis Gluconeogenesis o Serum blood glucose  indirect measurement of liver synthetic function o One of last functions lost in liver failure

Step 4: Common patterns of derangement

Step 5: What to do next  

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Determine potential causes Common causes of acute hepatocellular injury include: o Poisoning (paracetamol overdose) o Infection (Hepatitis A and B) o Liver ischaemia Common causes of chronic hepatocellular injury include: o Alcoholic fatty liver disease o Non-alcoholic fatty liver disease o Chronic infection (Hepatitis B or C) o Primary biliary cirrhosis Less common causes of chronic hepatocellular injury include: o alpha-1 antitrypsin deficiency o Wilson’s disease o Haemochromatosis

Liver screen               

LFTs Coagulation screen Hepatitis serology (A/B/C) Epstein-Barr Virus (EBV) Cytomegalovirus (CMV) Anti-mitochondrial antibody (AMA) Anti-smooth muscle antibody (ASMA) Anti-liver/kidney microsomal antibodies (Anti-LKM) Anti-nuclear antibody (ANA) p-ANCA Immunoglobulins – IgM/IgG Alpha-1 Antitrypsin – Alpha-1 Antitrypsin deficiency Serum Copper – Wilson’s disease Ceruloplasmin – Wilson’s disease Ferritin – Haemochromatosis

Urinary bile 

Bile  duodenum

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+ bacteria  urobilinogen Excreted in faeces, some in urine V sensitive urine test for liver damage, haemolytic disease and severe infections Normally has a little bit in urine If no pass into bowels (obstruction), detect in urine...