CP 59 - Disease of Hepatobiliary & liver tumours and billary Flashcards
when will jaundice be visible to human eyes
when bilirubin >40 umol/l
what is pre-hepatic jaundice?
due to too much bilirubin produced - haemolytic anaemia
what is hepatic jaundice
due to too few functioning liver cells - acute diffuse liver cell injury, end stage chronic liver disease, inborn errors
what is post-hepatic jaundice
bile duct obstruction - stone, stricture, tumours of bile duct, pancreas
what is bilirubin?
broken down product of haemoglobin
how is bilirubin excreted out of the body
by hepatocyst through converting unconjugated bilirubin into conjugated bilirubin which is soluble in water and excreted in bile
what happens to conjugated bilirubin if bile duct is blocked
reabsorb by hepatocyst and excrete in urine instead
what happen to bilirubin once it passes into the intestine
it will be converted into by bacteria to faecal urobilinogen and makes up the brown colour of faeces
where is erythrocytes engulf and digested
in spleen by splenic macrophages
what is the explanation of pathogenesis for pre-hepatic jaundice?
unconjugated - then bound to albumin which is insoluble and so not excreted - ie yellow colour only
what is the explanation of pathogenesis for hepatic jaundice?
bilirubin mainly conjugated and so soluble - yellow colour and dark urine
what is the explanation of pathogenesis for post- hepatic jaundice?
bilirubin is conjugated and so soluble and excreted just can not get to the gut - yellow eyes, pale stool and dark urine
what are some examples of liver enzymes which can be used for testing for liver disease
liver enzymes -
Leak from hepatocytes – ALT, AST, (mild increase - chronic liver disease, v. high acute liver disease)
Leak from bile ducts – Alk phos (high in obstructive jaundice and chronic biliary disease)
bilirubin, albumin, clotting factors
what is the most important pathological features in liver with obstructive jaundice
bile in liver parenchyma
increase in time - portal tract expansion, oedema of the liver, accumulation of bile salts and copper (bile salts in skin - patients itchy)parenchyma
what is the most important histopathological features in liver with obstructive jaundice
bile plug in canaliculae between hepatocytes
Ductular reaction –
Portal tract enlarged by increase
In ductules and
oedematous fibrous tissue
how can suspected jaundice be investigated
USS for dilated ducts in obstruction - biopsy if nto dilated duct
what is the commonest cause to non-obstructive jaundice?
acute hepatitis
how long does chronic hepatitis has to be in order for it to be chronic?
over 6 months
causes of acute hepatitis
acute
- inflammatory - viral, drugs, autoimmune
- toxic/metabolic injury - alcohol, drugs etc
what are some of the presentation of acute hepatitis?
vary within a spectrum - Asymptomatic, malaise, jaundice, coagulopathy, encephalopathy, death
what are some of the histological changes i acute hepatitis?
Mild
apoptotic hepatocytes - acidophil body - spotty necrosis
presence of inflammatory cells
overall - lobular disarray
Severe
all hepatocytes have died - confluent panacinar necrosis
intermediate severe
bridging necrosis
what are the causes of chronic hepatitis
-Immunological injury –
virus, autoimmune, drugs
Toxic/metabolic injury – fatty liver disease, alcohol, non-alcoholic fatty liver disease (NAFLD), drugs
Genetic inborn errors – iron, copper, alpha1antitrypsin
Biliary disease – autoimmune, duct obstruction, drugs,
Vascular disease – clotting disorders, drugs
how does chronic liver disease process?
During any chronic liver disease,
scarring gradually increases and starts to link vascular structures (bridging)
eventually transforming the liver tissue into separate nodules – end stage = cirrhosis.
what cause Hep A?
Picorna RNA
what cause Hep B?
Hepadna DNA