HPB Flashcards
What type of jaundice is this from the blood results?
Obstructive jaundice
Why is the clotting deranged in this patient?
-The liver produces the majority of clotting factors
-In severe liver damage and biliary obstruction there will be reduced intraluminal bile salts
-Therfore reduced absorption of vitamin K as vitamin K is a fat soluble vitamin
-Vitamin K is required to absorb clotting factors 2, 7, 9, 10
In what form does bilirubin circulate within the plasma?
As free bilirubin and conjugated to glucuronic acid
Which clotting studies will be abnormal?
This will lead to derangement in PT and INR
How could you correct a coagulation abnormality in this patient?
-Vit K
-FFP
-PCC
How are fats digested?
What is ALP?
-Enzyme present in bile canaliculi
-Present also in bone and placental tissue
-Increases in cholestasis to greater extent than ALT/AST
-ALT/AST present in hepatocytes and their presence suggests liver damage rather than obstructive jaundice
-ALT > AST in liver pathology
What other investigation would you want to do?
-Abdominal ultrasound
What finding on abdominal ultrasound will confirm presence of obstructive jaundice?
-Dilatation of intra and extrahepatic bile ducts
What would you do if CBD stone demonstrated on US?
ERCP
What is the function of bile?
-Emulsification of fat into micelles thus increasing the surface area for the action of pancreatic lipase
How do bile salts help in the emulsification of fat?
-Bile salt anions are hydrophilic on one side and hydrophobic on the other
-Therefore they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophilic end facing towards the fat and the hydrophobic end facing outwards
-Hydrophilic sides are negatively charged; this prevents fat droplets surrounded by bile from re-aggregating into larger fat particles
What are the constituents of bile?
-Water
-Salt
-Lecithin
-Bile pigments (biliverdin, bilirubin
-Bile salts and bile acids (sodium glycocholate and sodium taurocholate)
-Small amounts copper/other excreted metals
What is bilirubin conjugated to?
In the liver conjugates with glucuronic acid by the enzyme glucuronyl transferase
Describe the bilirubin metabolism and elimination
- Bilirubin is derived primarily from the breakdown of senescent red blood cells
- Extrahepatic bilirubin is bound to serum albumin and delivered to the liver
- Hepatocellular uptake
- Glucuronidation by glucuronosyltransferase in the hepatocytes generate bilirubin monoglucuronides and diglucuronides, which are water soluble and readily excreted into bile
- Gut bacteria deconjugate the bilirubin and degrade it to colorless urobilinogens.
- Urobilinogen can be oxidised to stercobilin, which gives stool its brown colour
- 10% of urobilinogen is reabsorbed into the enterohepatic circulation to be re-excreted in the bile: some of this is instead processed by the kidneys, colouring the urine yellow
What is urobilinogen? How is it formed? How does it circulate?
-Biproduct of bilirubin metabolism formed in the intestine by gut flora
-Some is excreted in faeces after oxidation (stercobilinogen), some is reabsorbed into the portal circulation
-Some of the reabsorbed urobilinogen is again excreted by the liver but small amounts enter the systemic circulation and are excreted in urine
Describe the enterohepatic circulation
-Reabsorbs bile salts from the small intestine (95%) and returns them back to the liver
Why in this case is urobilinogen not detectable in the urine?
Because there is an obstruction to the flow of bile and bilirubin does not reach the gut
What are the complications of the reduction of bile salts in the small intestine with obstructive jaundice?
-Steatorrhea due to malabsorption of fat
-Poor absorption of fat soluble vitamins (ADEK)
What would be the diagnosis if the patient had RUQ pain, fever, chills?
Ascending cholangitis
What are the differentials in this case?
Acute relapsing pancreatitis
Acute cholecystitis
Ascending cholangitis
Pancreatic pseudocyst
The patient is tachypnoeic, why?
-Abdominal pain
-Pressure from pancreatic pseudocyst
-ARDS
Describe the glasgow score
note neutrophils = WCC
What is the pathogenesis of acute pancreatitis?
-Duct obstruction–> reflux of bile into the pancreatic ducts causing injury–> increase in intraductal pressure may lead to damage to pancreatic acini, leading to leakage of pancreatic enzymes with further damage to pancras
-Direct acinar damage: due to viruses, bacteria, drugs or trauma
-Protease release causes widespread destruction of the pancreas which causes further enzyme release
-Lipase release causes fat necrosis, causing characteristic whitish flecks on pancreas, mesentery and omentum, often with calcium deposition
-Elastase destroys blood vessels, causing haemorrhage and haemorrhagic exudate into the peritoneum
-Haemorrhage may lead to acute haemorrhagic pancreatitis
Identify liver, spleen, pancreas, vertebrae, aorta, stomach and pancreatic pseudocyst
What are the complications of a pancreatic pseudocyst?
