MEDI7302 Study Guide - Final Guide: Sickle-Cell Disease, Ileocecal Valve, Cirrhosis
Biliary
Learning
objectives
Produce a differential diagnosis for a patient with obstructive jaundice and explain the
approach to investigation for the underlying causes
Understand why gallstones develop
Document the complications of gallstones and the options for management
Understand the difference in pathophysiology and management of cholecystitis and
cholangitis
Gallbladder
anatomy
Anatomical relations
Intraperitoneal organ, direct relation to visceral surface of liver, sits between
true R and L lobes of liver in gallbladder fossa at Cantlie's line
Anterior and superior border - inferior liver border, anterior abdominal wall
Posterior border - transverse colon, proximal duodenum
Inferior border - biliary tree, remaining duodenum
Gallbladder structure
30-50mL storage capacity, thin walled, contractile
Fundus - rounded distal portion
Body - largest part
Neck - continuous with cystic duct, Hartmann pouch (mucosal fold, common
location for gallstone lodgement)
Biliary tree structure
Liver secretes bile into canaliculi -> intralobular ducts -> collecting ducts -> R
and L hepatic ducts -> common hepatic duct
Gallbladder releases bile into cystic duct (containing spiral valves of Heister)
Common hepatic duct + cystic duct combine to form common bile duct
Common bile duct + pancreatic duct combine to form hepatopancreatic
ampulla/ Ampulla of Vater
Ampulla of Vater is regulated by Sphincter of Oddi (muscular valve) to
release bile into duodenum via major duodenal papilla
Vascular supply
Cystic artery (coeliac trunk -> common hepatic artery -> right hepatic artery ->
cystic artery)
Neck - cystic veins (cystic veins -> portal vein)
Fundus + body - hepatic sinusoids directly
Neuro supply
Coeliac plexus (SNS, sensory)
CN X (PSNS) - contraction of gallbladder, secretion of bile (however both
processes usually occur via CCK in gustatory response
Anomalies
o40% patients have arterial anomaly
oMost common is replaced R hepatic artery arising from SMA (R
hepatic runs posterior to portal vein)
oAlso have replaced L hepatic artery arising from gastric artery
Lymph drainage
Cystic lymph nodes at gallbladder neck -> hepatic lymph nodes -> coeliac
lymph nodes
Cystohepatic triangle/ Triangle of Calot
Surgical triangle - cystic duct (lateral), inferior/ visceral liver surface (superior)
& common hepatic duct (medial)
Cystic artery runs through middle of Calot's
Critical view of safety
oImportant landmark for cholecystectomy
oCalot's triangle is dissected free of all tissue except cystic duct and
cystic artery + exposure base of liver
oOnce achieving this view, the two structures entering gallbladder can
only be cystic artery & cystic duct
find more resources at oneclass.com
find more resources at oneclass.com
Portal vein (posterior)
Common hepatic artery -> R hepatic
(gives off cystic artery to GB) + L hepatic
(goes to L liver lobe)
Diagrams
Obstructive
jaundice
Differentials
oLuminal obstruction - gallstones
oWall pathology - atresia of CBD, stricture, sclerosing cholangitis,
find more resources at oneclass.com
find more resources at oneclass.com
cholangiocarcinoma
oExternal compression - pancreatitis, tumour of pancreas head, tumour of AoV
oCholestasis associated with pregnancy
Approach to investigation
oBilirubin, urobilinogen
oAST, ALT, ALP, GGT
oPT, INR
oUSS or CT scan
Gallstones Epidemiology
o10-15% adults have gallstones
oW > M, older > younger
Risk factors (4 F's)
oFemale (estrogen increases cholesterol stone formation via hormones,
supplements, OCP)
oFat (obesity increased cholesterol levels)
oFertile (pregnancy/ multiparity)
oForty (age 40)
oRapid weight loss (decrease lipids, imbalance bile composition)
oFamilial (Native Americans)
oConcomitant disease (haemolysis, small bowel disease or resection, CD)
oTotal parenteral nutrition
Admirand's triangle
oDescribes the relationship
between 3 solutes - cholesterol, lecithin, bile
salts - and the formation of gallstones
oBelow solid line (solutes
remain in solution)
oAbove solid line (gallstone
formation via supersaturation, nucleation and
stone growth/ crystal deposition)
oChange in relative
concentrations causes bile to become less
soluble & prone to stone formation
Cholesterol
most soluble in mixture containing
at least 50% bile salts + smaller
amounts of lecithin
oA - normal bile
concentrations
oB - cholesterol
crystals and micelles form
oC - cholesterol
crystals, micelles and vesicles form
oD/E - micelles and
vesicles form
Types of gallstones
Pure cholesterol o75-90% gallstones
oComposition - precipitated cholesterol
oStrong correlation with OCP use, pregnancy, elderly
age, obesity, low dietary fibre, fam hx
oPathogenesis
Bile becomes supersaturated by cholesterol
('lithogenic bile') -> bile salts/ acids or phospholipids cannot hold
anymore in solution -> cholesterol precipitates out of solution as
solid
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Produce a differential diagnosis for a patient with obstructive jaundice and explain the approach to investigation for the underlying causes. Document the complications of gallstones and the options for management. Understand the difference in pathophysiology and management of cholecystitis and cholangitis. Intraperitoneal organ, direct relation to visceral surface of liver, sits between true r and l lobes of liver in gallbladder fossa at cantlie"s line. Anterior and superior border - inferior liver border, anterior abdominal wall. Neck - continuous with cystic duct, hartmann pouch (mucosal fold, common location for gallstone lodgement) Liver secretes bile into canaliculi -> intralobular ducts -> collecting ducts -> r and l hepatic ducts -> common hepatic duct. Gallbladder releases bile into cystic duct (containing spiral valves of heister) Common hepatic duct + cystic duct combine to form common bile duct. Common bile duct + pancreatic duct combine to form hepatopancreatic ampulla/ ampulla of vater.
