CHEMPATH: LFTs and cases Flashcards
What is the normal liver function?
What is intermediary metabolism?
enzyme-catalysed processes
What does xenobiotic metabolism invovle?
What percentage of proteins in the body are expressed in the liver?
59%
What hormones are metabolised in the liver?
What are the components of bile? What is its function?
How is bilirubin metabolised and excreted?
Globin is turned over and reused
Iron is recycled
Heme binds albumin ,is glucoronytades to make it soluble (unconj is insoluble), conjugated bilirubin is then excreted
What cells are invovled in the reticuloendothelial system of the liver?
What are ALT, AST, ALP, GGT a marker of?
Serum markers of liver cell damage - because hepatocytes are filled with these
What are better indicators of liver function in LFTs?
Albumin
PT
What LFT is a tumour marker?
AFP
Describe hepatocyte anatomy.
Central vein ….
–> sinusoids –> hepatocytes –> excreted into bile canalliculi –> bile ducts –> gall bladder
What are ALT and AST?
Enzymes contained in hepatocyte cytoplasm
Elevated when hepatocytes die
Where else are ALT/AST found?
muscle, kidney, brain, pancreas
When is the ALT:AST useful?
Advanced fibrosis ALT:AST >1
Chronic alcoholism ALT:AST >2
What is GGT raised in characteristically? Where else is GGT found outside the liver?
What are the other sources of ALP? What physiological states is ALP raised in?
Give 3 causes of a low albumin.
Low production (CLD, malnut)
Loss (gut, kidney)
Sepsis (3rd spacing)
How much albumin is synthesised each day? What is its function?
8-14 g/day
20 day half-life
Contributed to onscotic pressure and binds many things
What is the function of AFP?
No known function in adults (low concentration)
In fetal life made by yolk sac, GI epithelium and liver
Used in HCC diagnosis
Hepatic damage/regeneration
Testicular cancer
Pregnancy
Summarise the causes of jaundice. Which type of bilirubin is raised in each?
What is the use of USS in jaundice diagnosis?
If jaundiced and….
- ALT/AST raised then hepatocellular damage
- ALP raised then dilated or undilated ducts –> diagnose
- everything else is normal in LFTs then Gilbert’s, haemolysis etc.
Should bilirubin be found in urine? What other product may be found?
Bilirubin should NOT be found. Only conjugated.
Urobilinogen is usually circulating in the plasma and so is usually found in urine (in obstructive jaundice urobilinogen disappears and bilirubin appears in urine)
What are the other investigations which may be used in a liver panel?
- Lipids, fasting glucose
- Coeliac
- Hepatitis screen (HBV sAg, HCV Ab)
- Alpha-1-1ntitrypsin
- Caeruloplasmin - low suggests Wilson’s disease
- Liver AAbs (LMK, aSMA, AMA)
- Igs
- Ferritin
- ANCA screen
Other:
- Tumour markers
- Fibroscan
- Liver biopsy
- Iron studied and HH genetics
- Viral DNA/RNA
- 24hr urinary copper
- Alpha-1-1antitrypsin phenotype
- CT
- MRCP
- MRI/MRI iron load
- EUS
- More complicated tests shown below
Guidelines for referral when there is an isolated ALT (not all need referral)
- Preserved synthetic function
- Non fasting and fasting uncojugated bilirub were measured
- Elevation in fasting bilirubin was then seen which was unconjugated
= Gilbert’s syndrome (this is harmless)
Bilirubin in urine means it is conjugated
Suggests diorder of bile ducts
But USS shows no obstruction
Diagnosis was drug induced cholestasis - intrahepatic, secondary to Augmentin (classically gives obstructive jaundice)
Looks obstructive,
O/E has Courvoisier’s Sign = in the presence of a painless palpable gallbladder, jaundice is unlikely to be caused by gallstones (i.e. with gallstones you get pain, malignant obstruction is usually no pain)
Predominantly obstructive picture with some alcoholic liver disease
USS shows dilated CBD and possible pancreatic mass so the diagnosis is pancreatic adenocarcinoma. You would do a CT scan and biopsy and look at local spread. Tx is to stent the CBD although this is a palliative measure.
- Liver is severely inflamed
- USS shows no dilated bile ducts. So this is likely hepatocyte damage alone
- Serum IgM and anti-HAV positive
Diagnosis is acute hepatitis A (commonest form of acute hepatitis)
Chronic liver disease with deterioration in synthetic function
USS shows coarse liver texture
Hep C confirmed by serology and PCR
Admitted to using heroin once in the seventies (very common risk factor as 70-80% of those with IVDU will have HCV)
Tx: antivirals + USS/AFP every 6 months to screen for HCC
High resp because compensating for acidosis.
INR is 2.8 so running out of hepatocytes to make clotting factors
Tx: N-acetyl cysteine
Transferred to transplant centre
