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Diseases of GB and BD (revised)

lecture for students

Chang Min Cho

on 10 September 2017

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Transcript of Diseases of GB and BD (revised)

Kyungpook National University Chilgok Hospital

Center for of Pancreatobiliary cancer

Diseases of the Gallbladder and Bile ducts
Chang-Min Cho, MD, PhD
Anatomy of biliary system
Physiology of Bile production and flow

Pathophysiology and clinical manifestation
Obstructive jaundice
Secondary biliary cirrhosis
Diagnosis and treatment
Ischemia or gangrene of GB wall
Infection by gas-producing organisms
C. welchii, C. perfringens
E. coli
Elderly and diabetes
Gas within GB lumen in simple film
Antibiotics + surgical intervention
IV fluid and antibiotics
Urgent cholecystectomy due to complication
Percutaneous cholecystostomy
Postcholecystectomy complication and wound infection
due to underlying multisystemic problems
Overall mortality; 5-20%
Serious trauma or burns
postpartum period following prolonged labor
postoperative period of orthopedic or nonbiliary major surgery
Prolonged parenteral hyperalimentation
Obstructing adenocarcinoma of GB
Tortion of GB
Unusual bacterial infection
Parasite infestation
Systemic disease
Inflammation of GB without stone
5-10% of acute cholecystitis patients
Ischemia, infections, and chemical injury by biliary contents
Obstruction of cystic duct
Acute cholecystitis with unexplained fever, RUQ pain
US; distended GB with thin wall, pericholecystic fluid
Sphincter of Oddi
Prevent reflux of duodenal content into duct
Promote bile filling of the GB
Powerful contraction of GB
Decreased resistance of SO
Increased hepatic secretion of bile
Enhanced flow of biliary contents into duodenum
Disordered GB motility with recurrent biliary pain without GB stone
CCK cholescintigraphy
Abnormal GB ejection fraction (<40% at 45min)
Surgical findings
Chronic cholecystitis
Gallbladder muscle hypertrophy
Markedly narrowed cystic duct
Diagnostic criteria
Recurrent episodes of biliary pain
Abnormal CCK cholescintigraphy
Reproduction of pain after CCK infusion
Final storage reservoir for bile
Concentrate bile by removing water
Lipid concentration from 3g/dL in hepatic bile to 10g/dL in GB
Mucin secretion for epithelial protection
Secretion of hydrogen ion
Prevent calcium salt deposition
Duodenal-gallbladder enteric nervous stimulation
10-20% in resting state
70% contraction in postprandial duodenal lipid
Na+/taurocholic cotransporter (NTCP)
Organic anion transporting protein
ATP-dependent canalicular transport systems
Bile salt export pump (BSEP)
Conjugate export pump (MRP2)
Multidrug export pump (MDR1)
Phospholipid export pump (MDR3)
Canalicular cholesterol transporter
Maintain bile flow and volume
Secretion of chloride, bicarbonate, and water
CFTR defect in cystic fibrosis
Reduced choleresis
Formation of mucus plugs
Focal biliary cirrhosis and gallstone
Bile acids (80%)
Lecithin and phospholipids (16%)
Cholesterol (4%)
Lithogenic bile; 8-10%
Drugs and metabolites
Intrahepatic biliary canaliculus
Intrahepatic bile duct(small, medium, and large)
Common hepatic duct
Cystic duct
Common bile duct
Ampulla of Vater
Active transport of bile acids from hepatocytes into bile canaliculi
Active transport of other organic anions
Cholangiocellular secretion
Secretin mediated
Biliary colic
Anatomy of biliary system
Anatomy of biliary system
Anatomy of pancreatobiliary system
Secretion and storage of bile salt
Solubilize intestinal lipid
Excretion of cholesterol
Maintain cholesterol homeostasis
Excretion of excess bilirubin
Excretion of organic ions and drug metabolites
Primary function of biliary system
Bile flow regulation
Major solute components of bile
Bile acids
Transport systems of bile salts
Enterohepatic circulation
Congenital anomalies
Biliary atresia and hypoplasia
Choledochal cysts
Congenital biliary ectasia
Trauma, Stricture, and Hemobilia
Extrinsic compression of the bile ducts
Hepatobiliary parasitism
Sclerosing cholangitis
Diseases of the Bile Ducts
Congenital anomalies
Acute and chronic cholecystitis
Cacluous cholecystitis
Acalculous cholecystitis
Emphysematous cholecystitis
Acalculous cholecystopathy
Complications of cholecystitis
Empyema and hydrops
Gangrene and perforation
Fistula formation and gallstone ileus
Limey (milk of calcium) bile and Porcelain gallbladder
Hyperplastic cholecystoses
Cholesterol polyp
Hyperplastic cholecystoses
Inflammatory polyp
Adenomatous polyp

Diseases of the Gallbladder
A group of disorders of the GB
characterized by excessive proliferation of normal tissue components
benign proliferation of GB surface epithelium
glandlike formations
extramural sinuses
transverse strictures
fundal nodule (adenoma or adenomyoma) formation
abnormal deposition of lipid (cholesterol ester) within macrophages
lamina propria of the GB wall
diffuse or localized form
cholesterol stone in 50%

Indication of cholecystectomy
adenomyomatosis and cholesterolosis with symptomatic or cholelithiasis
Hyperplastic cholecystoses
Prevalence in adult population: 5%
Few significant change in asymptomatic patients
polyps < 10 mm in diameter during 5 year period
Recommendation of cholecystectomy
symptomatic patients
asymptomatic patients > 50 years of age
polyps > 10 mm in diameter
associated with gallstones or polyp growth on serial USG
Gallbladder polyps
Medical therapy
Inhospital stabilization before cholecystectomy
NPO and / or Nasogastric suction
Replacement of ECF volume depletion and electrolyte abnormalities
Analgesia: meperidine or NSAIDs
Intravenous antibiotics
E. coli, Klebsiella spp. and Streptococcus spp.
anaerobe coverage in gangrenous or emphysematous cholecystitis
reduced postop. complication
Treatment of acute cholecystitis
Surgical therapy
mainstay of therapy
urgent (emergency) cholecystectomy or cholecystostomy
complication of acute cholecystitis
emyema, emphysematous cholecystitis, or perforation
mortality rate: 3%
early elective (laparoscopic) cholecystectomy
within 72 hours of diagnosis
mortality rate: 0.5%
delayed surgical intervention
> 6 weeks after diagnosis
unacceptable medical condition for early surgery
diagnosis in doubt
Treatment of acute cholecystitis
Abnormalities in number, size and shape
Phrygian cap
partial or complete septum that sepeates the fundus from the body
Anomalies of position or suspension
left-sided GB
intrahepatic GB
floating GB
Congenital anomalies
Pathophysiology of gallstone
Colicky pain
Pattern of biliary colic
Laparoscopic cholecystectomy
Procedure of choice
Minimal access approach

Consideration before surgical therapy
1) Presence of symptoms
2) Presence of prior complication
History of acute cholecystitis, pancreatitis, gallstone fistula
3) Presence of underlying condition predisposing to increased risk of complications
Calcified or porcelain GB and/or previous attack of acute cholecystitis

Prophylactic cholecystectomy
Large stone > 3 cm in diameter
Congenitally anomalous gallbladder
Young age with asymptomatic gallstone
Treatment: Gallstones - surgical therapy
Gallstone dilution
Ursodeoxycholic acid (UDCA)
decreasing cholesterol saturation of bile
retarding cholesterol crystal nucleation
10-15 mg/kg per day
radiolucent stone < 5 mm in diameter
higher recurrent rate (30-50% over 3-5 years)
recurrent cholelithiasis after cholecystectomy
Treatment: Gallstones - Medical therapy
Acute inflammation of GB due to impacted stone in cystic duct
Factors of inflammatory response
mechanical: increased pressure and distention
chemical: release of lysolecithin and other local tissue factors
bacterial (50-85%)

60-70%: experience of prior attack
biliary colic with radiation to shoulder area
low-grade fever
enlarged, tense palpable GB in 25-50%
Murphy's sign: increased pain and inspiration arrest during deep inspiration or cough with subcostal palpation of RUQ
Acute cholecystitis
Characteristic history and PE
sudden onset of RUQ tenderness
mildly elevated bilirubin (<50%)
modest elevation in AST/ALT (< x5 UNL) in < 25%

Image studies
Ultrasonography: stone, thickening of wall, pericholecystic fluid, and dilation of bile duct
radionuclide biliary scan
Acute cholecystitis - diagnosis
GB stones with acute cholecystitis
Clinical courses of acute cholecystitis
Impacted stone in cystic duct or neck of GB causing compression of CBD
CBD obstruction and jaundice

Surgical treatment
removing cystic duct, GB and impacted stone
Mirizzi's syndrome
Remission of symptom within 2-7 days
Recurrent cholecystitis
25% within 1 year
60% within 6 year
early surgery whenever possible: best treatment
Acalculous cholecystitis
Precipitating factors
Emphysematous cholecystitis
Acaculous cholecystopathy
Repeated bouts of subacute or acute cholecystitis
Persistent mechanical irritation by gallstone
Bacteria in bile in > 25%

Clinical features
asymptomatic for years
progress to symptomatic GB disease
present with complications
Chronic cholecystitis
Empyema and hydrops
Gangrene and perforation
Fistula formation and gallstone ileus
Lime (milk of calicum) bile and Procelain GB
Complications of cholecystitis
Early complications

Persistent postcholecystectomy symptom
overlooked symptomatic nonbiliary disorder
reflux esophagitis, peptic ulceration, pancreatitis, IBS

Postcholecystectomy syndrome; disorder of extrahepatic bile duct
biliary stricture
retained biliary calculi
cystic duct stump syndrome
stenosis or dyskinesia of SOD
bile salt-induced diarrhea or gastritis
Postcholecystectomy complications
Congenital anomalies
most common biliary anomalies in infancy
severe obstructive jaundice during first month of life
pale stool
possible in 10%
Roux-en-Y choledochojejunostomy
Kasai procedure (hepatic portoenterostomy)

late complication
chronic cholangitis, hepatic fibrosis, portal hypertension
Biliary atresia and hypoplasia
Cystic dilation of CBD
Onset of symptom
after age 10 in 50%
abdominal pain, jaundice and abdominal mass (1/3)
Increased risk for cholagiocarcinoma
surgical excision of cyst and biliary-enteric anastomosis
Choledochal cysts
Dilation of intrahepatic bile duct
Caroli's disease: major intrahepatic radicles
Congenital hepatic fibrosis: inter-and intralobular ducts
Clinical manifestation
recurrent cholangitis
abscess formation
gallstone formation
ultrasound, MRC and CT
Progression to
secondary biliary cirrhosis with portal hypertension
extrahepatic biliary obstruction
recurrent sepsis with hepatic abscess
Congenital biliary ectasia
10-15% of patients with cholelithiasis: passage of stone into CBD
increased incidence with increasing age

majority of CBD stone;
secondary stone in cholesterol stone of GB

primary calculi arising de novo in the ducts
usually pigment stone
hepatic parasitism or chronic, recurrent cholangitis
congenital anomalies of the bile duct (Caroli's disease)
dilated, sclerosed, or strictured ducts
MDR3 (ABCB4) gene defect
Pathophysiology and clinical manifestation
GB stone with CBD stone
Clinical course of CBD stones
Asymptomatic for years
Spontaneously passing into duodenum
Obstructive jaundice
Secondary biliary cirrhosis
Gallstone pancreatitis
Biliary colic with
increased level of AST/ALT, ALP and bilirubin
CBD stone: elective ERCP
GB stone: cholecystectomy
Benign stricture
Dilated CBD
Free movement in CBD
Small stone
Impacted at distal CBD
Acute or chronic inflammation of bile duct
Caused by partial obstruction to bile flow
75% of patients with acute cholangitis
positive bacterial culture on bile (75%)
Charcot's triad
biliary pain, jaundice and spiking fevers with chill

Nonsupurative acute cholangitis
most common
rapid response to antibiotics
Suppurative acute cholangitis
presence of pus in bile duct
mental confusion, bacteremia, septic shock
poor response to antibiotics
multiple hepatic abscess
prompt drainage of infected bile
endoscopic sphincterotomy
Gradual obstruction of CBD over weeks or months
Obstruction secondary to choledocholithiasis
associated with chronic calculous cholecystitis
Painless jaundice
malignancy of pancreatic head mass, bile ducts, or ampull of Vater
palpably enlarge GB without tenderness

Clinical feature
dark urine (bilirubinuria)
light colored (acholic) stool
abnormality of LFT
CBD stone: > 5 mg/dl
malignancy: > 20mg/dl
elevation of ALP, AST/ALT
Obstructive jaundice
Gallstone pancreatitis
acute cholecystitis (15%)
choledocholithiasis (>30%)

Clinical suggestion of pancreatitis in patient with acute cholecystitis
back pain or pain to the left abdomen of midline
prolonged vomiting with paralytic ileum
pleural effusion, left side
Diagnosis and Treatment
complication of prolonged or intermittent duct obstruction
with or without recurrent cholangitis
stricture or neoplasm
progressive even after correction of obstructing process
portal HTN, heaptic failure and death
deficiencies of fat-soluble vitamins (A, D, E, and K)
Secondary biliary cirrhosis
ERCP with papillotomy and stone extraction
preoperative or postoperative
suspected CBD stone in GB stone
history of jaundice or pancreatitis
abnormal LFT
imaging evidence of stone (USG, MRCP)
Trauam, strictures, and hemobilia
Extrinsic compression of the bile duct
Hepatobiliary parasitism
Sclerosing cholangitis
Other disorders
surgical trauma (cholecystectomy)
bile leak or abscess formation
biliary obstruction or cholangitis
percutaneous or endoscopic cholangiography
bile cytology

traumatic or operative injury to liver or bile duct
intraductal rupture of hepatic abscess or aneurysm of hepatic artery
biliary or hepatic tumor hemorrhage
mechanical complications of choledocholithiasis or hepatobiliary parasitism
diagnostic procedure
clinical manifestation
biliary pain, obstructive jaundice, and melena
endoscopy or angiography
Trauma, stricture, and hemobilia
partial or complete obstruction of bile duct
pancreatic head tumor
complications of pancreatitis
LN involvement of porta hepatis by lymphoma or metastatic carcinoma
Extrinsic compression of the bile duct
Hepatobiliary parasitism
biliary infestation by adult helminth or ova
chronic, recurrent pyogenic cholangitis
with or without abscess, stone, or obstruction
trematodes or flukes
Clonorchiasis sinensis
Opisthorchis viverrrini
O. felineus
Fasciola hepatica
Ascaris lumbricoides: intraductal migration from duodenum
Echinococcus spp.: intrabiliary rupture of hydatid cyst
Progressive, inflammatory, sclerosing, and obliterative process
affecting extrahepatic and/or intrahepatic bile duct
associated condition
IBD, esp UC in 75%
autoimmune pancreatitis
IgG4-associated cholangitis
unknown etiology
elevated serum IgG4
infiltration of IgG4 (+) plasma cell in bile duct and liver
not associated with IBD
glucocorticoid: treatment of choice and/or azathioprine
relapse: common
Sclerosing cholangitis
Biliary atreasia and hypoplasia
Choledochal cysts
Congenital biliary ectasia
Chronic or intermittent biliary obstruction
RUQ abdominal pain, pruritus, jaundice, or acute cholangitis
Late course
biliary cirrhosis, hepatic failure, or portal HTN
multifocal, diffusely strictures
intervening segments of normal or dilated ducts
beaded appearance on cholangiography
Primary sclerosing cholangitis
Sclerosing cholangitis: treatment
to control symptom of pruritus
Antibiotics in cholangitis
Vitamin D and calcium replacement
Glucocorticoid, MTx, and cyclospotine: no effective
UDCA (20 mg/kg)
improvement of LFT
no survival effect
Endoscopic management
balloon dilation or stenting
Surgical management
biliary-enteric anastomosis
liver transplantation
Natural courses of gallstone
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