Gall Bladder Flashcards
Biliary tree
Right + left hepatic ducts = common hepatic duct (CHD)
CHD + Cystic duct = Common Bile Duct (CBD)
CBD joins with pancreatic duct = hepatopancreatic ampulla of vater
Ampulla of Vater releases bile and pancreatic enzymes into duodenum through oddi of sphincter
Gall Bladder blood supply
Cystic artery (R. Hep. Artery -> Com. Hep. Artery) Cystic vein into portal vein
Gall bladder nerve innervations
Parasympathetic (contraction): Vagus Nerve
Sympathetic and Sensory: Coeliac Plexus
Cholelithiasis
Uncomplicated gall stones
Types of gall stones and RF
Cholesterol gall stones: most common (90%). RF: FHx, diet (obesity, metabolic syndrome, sudden weight reduction), age, and female sex hormones.
Brown pigmented gall stones: Result of stasis and infection. Unconjugated Bilirubin and calcium salts RF:Bile ducts strictures or parasitic infestation
Black pigmented: Polymerised calcium bilirubinate (5-10%). RF: age, chronic haemolytic anaemia, cirrhosis, cystic fibrosis, and ileal disease
Typical presentation of gall stones
Most asymptomatic.
Can present with RUQ pain, sometimes after food
Constant pain, increasing intensity. Pain duration <30 mins is not biliary colic. More than 5 hrs suggests complicationor cholecystitis
Key investigation for gall stones
US initial test
If unremarkable and symptoms persists CT scan or MRCP if query choledocholithiasis (common bile duct stones)
Management for gall stones
Asymptomatic: Observe
Symptomatic: Lap. Cholecystectomy
choledocholithiasis with/without symptoms: ERCP
Acute Cholecystitis
Acute gall bladder inflammation
Lasts 3-6 hours. Fever is common
RUQ tenderness with + murphy’s sign
Investigation for acute cholecystitis
US is the definitive test
If unclear then use hepatobiliary iminodiacetic acid HIDA
CT is not as good as US for diagnosing, but it is useful when obesity or gaseous distension limits ultrasound interpretation
Management of acute cholecystitis
Supportive care (fluids, analgaesia, obs)
Oral/IV Abx-cefuroxime or ciprofloxacin and metranidazole
Lap. Cholecystectomy
If poor surgical candidate:
Percutaneous cholecystectomy drainage tube
Primary Sclerosing Cholangitis (PSC)
Chronic progressive cholestatic liver disease
Inflammation and fibrosis of intrahepatic and/or extrahepatic bile ducts causing strictures
PSC more commonly associated with UC or CD
UC
2/3rd of people with PSC have associated IBD
Common risk factors of PSC
Male 2:1 ratio
Hx of IBD
Genetic: First degree relative has PSC
Common age of diagnosis is in 40s to 50s
Common signs and symptoms
Abdo pain (non specific RUQor epigastric) Pruritus Fatigue Weight Loss Fever (bacterial cholangitis) Jaundice
Key investigations for PSC
Raised ALP (bile duct injuiry or blockage) Raised serum gGT: supports liver origin of ALP not bone Serum aminotransferases, raised bili
May have reduced albumin if in severe liver disease stages
Abdo US
CT
MRCP or ERCP: MRCP is better diagnostically but if considering need for therapy (high suspicion of dominant stricture or cholangiocarninoma) consider ERCP
Management of PSC
Asymptomatic: Observation and lifestyle change
Pruritus relief: Colestyramine (bile acid sequesterant)
Autoimmune hepatitis: immunosuppressants (corticosteroids)
Hepatic Osteopenia: Calcium and Vit D supplements
Hepatic Osteoporosis: Bisphosphonates and HRT
ERCP if cant gain access via endoscopy do percutaneous transhepatic cholangiography (PTC) can allow for biliary drainage, stent placement, and/or stricture dilation
End stage liver disease: Liver transplant
Primary biliary cholangitis/cirrhosis (PBC)
Progressive chronic disease of the small intrahepatic ducts characterised by progressive bile duct damage.
Difference between PSC and PBC
PSC involves sclerosis of the hepatic biliary ducts resulting in back of bile in the liver causing cholestatic liver disease
PBC involves the small intrahepatic ducts and not the biliary ducts so no association with biliary duct sclerosis.
Cause of PBC
Believed to be autoimmune, mainly antimitochondrial antibodies found in 95% of patients. Common Ab is pyruvate dehydrogenase complex E2 subunit (PDC-E2) Can also be seen on ANA
Pathophysiology of PBC
damage to, and progressive destruction of, the biliary epithelial cells lining the small intrahepatic bile ducts
Bile duct loss is progressive and in the end stages of the disease there can be a complete loss of small intrahepatic ducts. Loss of bile duct cross-sectional area within the liver leads to cholestasis with variable and progressive bile acid retention.
Result is over time liver cirrhosis
Pathophysiology of PSC
inflammation and injury of the medium- and large-sized bile ducts leading to fibrosis and multi-focal stricturing of the ducts.
Common risk factors for PBC
Female 10:1 ratio
Peak incidence between 45-60 yrs old
Common signs ans symptoms for PBC
Hx/FHx of autoimmune disease
Hx of hypercholesterolaemia (cholestasis. H. HDL and lipoprotein X)
Pruritus
Dry eyes and mouth (sjogren’s syndrome-autoimmune)
In late stages (liver disease):
Jaundice
Metabolic changes
Portal hypertensive features (ascites, variceal bleeding, splenomegaly)
