liver disease Flashcards
Causes of high BR
gallstones - obstructive
haemolysis
hepatitis
alcoholic liver
anatomy of liver
o Centre of liver lobule – portal tracts (hepatic artery, bile duct, portal vein) at corner of hexagon, centre have central vein -> hepatic vein
o Hepatocytes – brick like cell – blood flow through sinusoid from the portal tract – exit through the central vein
divide the hepatocytes into 3 groups - 1 around portal tract, 2 midzone, 3 around central vein
endothelial cells lining the sinusoid have big spaces - blood can go to the hepatocytes
between the endothelial cells and the hepatocytes have the space of Disse - where stellate cells sit
how does the hepatic portal vein tie up with the function of the liver
o Hepatic portal vein come from gut – liver clear up gunky blood – 1st pass metabolism, clean blood through central vein to the heart
causes of high BR and investigations to determine them
Prehepatic – haemolysis = making more BR – FBC and film
Hepatic – repeat LFT
Post-hepatic – obstructive jaundice - AlkPhos usually goes up in obstructive
what is the van den Bergh reaction
measures serum bilirubin via fractionation A direct reaction measures conjugated bilirubin. The addition of methanol causes a complete reaction, which measures total bilirubin (conjugated plus unconjugated); the difference measures unconjugated bilirubin (an indirect reaction).
describe paediatric jaundice
might be normal - usually is, but should be unconjugated and due to liver immaturity, coupled with a fall in Hb early in life
• If it doesn’t settle, other rare causes should be
looked for including hypothyroidism, other
causes of haemolysis (including a Coombes
test or DAT), and the unconjugated bilirubin
will be useful.
describe phototherapy
Converts bilirubin into two other compounds,
lumirubin and photobilirubin which are
isomers that do not need conjugation for
excretion.
helps clear BR in normal paediatric jaundice
describe Gilberts disease
common dont need to worry autosomal recessive 50% carry the gene BR rise with fasting all LFTs normal shouldn’t biopsy people because cant be other things and there are risks
gilberts: •50% of us carry the gene •What will the population prevalence (as a percentage (%) of the full syndrome be given that half of us carry the gene?
probability both parents carry the gene: 25%
therefore probabilty of child having disease is 6%
•5-6% of the population have the disease
•1 in 20
•(15 in 300)
diagnostic test for Gilberts - not done anymore
induce liver enzymes - give phenobarbitone and BR levels fall
mechanism of Gilberts
UDP glucuronyl transferase activity reduced to 30% = slow down clearance of BR = higher level of BR, especially when fast Unconjugated bilirubin tightly albumin bound and does NOT enter urine
what do you look at to assess liver function
Liver makes clotting factors and albumin – so PT, PTTK, BR and albumin quite representative, albumin slow to change
But prothrombin time changes rapidly – so best for liver function
what do you look at liver enzymes for
ALT and AST – enzymes leak out, nothing to do with function. In different hepatocytes in different zones – pattern recognition
ALT – responsible for gluconeogenesis
Alk Phos high in post-hep – affect tracts – so assume more alk phos in this area
LFTs and paracetamol OD
damage liver = large ALT and AST leak out – sky high but diesnt correlate. PT correlates – goes up, if PT is sec goes up by >1sec every hr – need to be thinking of ringing liver unit, might need transplant. If PT stay the same can keep in normal hospital
ddx: •Aged 35 •Chronic alcohol intake •Often appeared drunk to A + E •Nausea, abdo pain and jaundice. •LFTs abnormal: Bilirubin 90
•Pre hepatic (Gilberts, haemolysis) - exclude early
•Viral hepatitis
•Alcoholic hepatitis (hurts)
•Cirrhosis
alcoholic fatty liver
•Post hepatic: Gallstones (painful), pancreatic
ca. (painless)
what is suggested: Aged 35 •Chronic alcohol intake •Often appeared drunk to A + E •Nausea, abdo pain and jaundice. •LFTs abnormal: Bilirubin 90 •Alk Phos 200 (NR <130) •AST 1500 (<50); ALT 750 (<50)
AST and ALT very high •Suggest hepatocyte damage •Alk Phos marginal: •Excludes obstructive jaundice. therefore ddx: o Viral hepatitis – check viral tures – more likely to have viral if you drink alcohol, common o Autoimmune hepatitis o Alcoholic hepatitis
describe hepititis A
o Faecoorally transmitted
o Eat bad food
o Don’t feel ill
o Excrete virus in faeces at 3-4wks and become ill
o Then recover with IgM – jaundice but recover
o No carrier form – either die (not fatal, but if malnourished – die), or cure – cant have again, have IgG
describe Hepititis B
o Not spread by mouth – blood transfusion, sharing needles
o If inject self with Hep B – virus replicate
o Incubation for a month, then start to make virus replicate
o Surface ag and core (e Ag) – they multiply in blood
o Immune system makes Ab to different parts of virus
o Against e Ag – e decline
o Still infective – making surface ag
o Then pt will have e Ab – if find e Ab – means been exposed to live virus, never vaccinate with this
o Then make surface Ab
o Vaccine has pure surface Ag – engineered/purified – all have anti-HBs (if just s – likely vaccinated, if both – exposed)
o A lot of people never clear the virus – make Ab to E, but always chronic ag – infectious forever, unless they have treatment
o Illness often subclinical – don’t know they’re carriers – individuals still infective
defining histological features of alcoholic hepatitis
- liver cell damage, swollen hepatocytes (mallory hyaline is pink uniform substance due to hepatocyte damage)
- inflammation - neutrophils and lymphocytes
- fibrosis, collagen around the hepatocytes
