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GALLBLADDER Fe A. Bartolome, MD, FPASMAP Department of Pathology

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Presentation on theme: "GALLBLADDER Fe A. Bartolome, MD, FPASMAP Department of Pathology"— Presentation transcript:

1 GALLBLADDER Fe A. Bartolome, MD, FPASMAP Department of Pathology
Our Lady of Fatima University

2 Common Locations of Stones

3 Cholelithiasis (Gallstones)
BILIARY TRACT Cholelithiasis (Gallstones) Cholesterol Stones More prevalent in: Industrialized countries Advancing age 20 to cholesterol Caucasian women hypersecretion Pregnancy & oral contraceptive use Estrogenic influence  inc. expression of hepatic lipoprotein receptors + inc. hepatic HMG-CoA reductase activity  inc. cholesterol uptake & biosynthesis Gallbladder stasis (neurogenic and hormonal)

4 Cholelithiasis (Gallstones)
BILIARY TRACT Cholelithiasis (Gallstones) Cholesterol Stones More prevalent in: Inborn error of metabolism a. Impaired bile salt secretion and synthesis b. Defects in lipoprotein receptors – hyperlipidemia syndromes Obesity and rapid weight loss  increased biliary cholesterol secretion

Hepatocellular hypersecretion of cholesterol Cholesterol conc. > solubilizing capacity of bile SUPERSATURATION Inc. free cholesterol penetrate GB wall Dec. ability of mucosa to detoxify by esterification Dec. responsiveness to cholecystokinin GALLBLADDER HYPOMOTILITY Stasis ACCELERATED CHOLESTEROL CRYSTAL NUCLEATION PROMOTE MUCUS HYPERSECRETION & MICROPRECIPITATION OF CALCIUM SALTS STONE

6 BILIARY TRACT Morphology: Cholesterol monohydrate + calcium salts
Pale yellow, round to ovoid, finely granular Pure cholesterol stones  radiolucent If with calcium carbonate  radio-opaque Incidental finding of cholesterolosis  accumulation of cholesterol enters within lamina propia of GB  mucosal surface with minute yellow flecks  “strawberry” gallbladder

7 Cholesterolosis Cholesterol deposits

8 BILIARY TRACT Cholesterol stones

9 BILIARY TRACT Pigment Stones Increased incidence in: Asians
Rural areas Chronic hemolytic syndromes Bacterial contamination of biliary tract GI diseases – ileal disease (e.g. Crohn’s) or bypass Cystic fibrosis with pancreatic insufficiency

10 BILIARY TRACT Pathogenesis:
Infection of biliary tract (E. coli, A. lumbricoides, Opistorchis sinensis)  release of microbial -glucuronidase  hydrolysis of B2  increased B1 Intravascular hemolysis  hepatic secretion of B2  (+) deconjugation in biliary tree  increased B1

11 BILIARY TRACT Morphology:
Mixture of abnormal insoluble calcium salts of B1 + inorganic calcium salts Two types: Black pigment stones Found in sterile GB bile Oxidized polymers of calcium salts of B1, calcium carbonate, calcium phosphate, mucin glycoprotein and little amount of cholesterol monohydrate crystals Rarely > 1.5 cm diameter

12 BILIARY TRACT Morphology: Two types: Black pigment stones
Present in greater number; 50% - 75% radio- opaque; crumble to touch Brown stones Found in infected intra- and extrahepatic ducts Pure calcium salts of B1, mucin glycoprotein, substantial cholesterol fraction, calcium salts of palmitate and stearate Laminated and soft with soap-like or greasy consistency Radiolucent

13 BILIARY TRACT Black Pigment Stones

14 BILIARY TRACT Clinical Features of Gallstones 70% - 80% asymptomatic
May present with biliary pain – excruciating and constant, colicky  most prominent Complications: Cholecystitis 6. Obstructive cholestasis Empyema 7. Pancreatitis Perforation 8. Erode into adjacent small bowel Fistula formation loop  gallstone ileus Cholangitis 9. Increased risk for CA

15 BILIARY TRACT CHOLECYSTITIS Acute Calculous Cholecystitis Primary complication of gallstones Most common reason for emergency cholecystectomy Precipitated by obstruction of neck or cystic duct

16 Acute Calculous Cholecystitis: Pathogenesis
BILIARY TRACT Acute Calculous Cholecystitis: Pathogenesis OBSTRUCTION Hydrolysis of luminal lecithins by mucosal phospholipases Production of toxic lysolecithins Disruption of glycoprotein mucus layer Exposure of epithelium to direct detergent action of bile salts (+) GB dysmotility (+) GB distention & inc. intraluminal pressure Compromised mucosal blood flow INFLAMMATION

17 Acute Calculous Cholecystitis: Morphology
BILIARY TRACT Acute Calculous Cholecystitis: Morphology Gross: GB enlarged and tense Bright red or blotchy; violaceous to green-black (if with necrosis, called gangrenous cholecystitis Subserosal hemorrhages Cloudy or turbid bile  fibrin, frank pus, hemorrhage If pure pus, called empyema of gallbladder Microscopic: acute inflammation

18 Acute Cholecystitis

19 Histological section of severe acute cholecystitis showing extensive ulceration of the mucosa, haemorrhage, oedema and a dense transmural infiltrate of neutrophils and mononuclear inflammatory cells.

20 Acute Acalculous Cholecystitis
BILIARY TRACT Acute Acalculous Cholecystitis Occurs in the absence of gallstones Seen in severely ill patients Usually occurs in the following circumstances: Post-operative state (major, non-biliary surgery) Severe trauma Severe burns Multi-system organ failure Sepsis Prolonged IV hyperalimentation Postpartum state

21 Acute Acalculous Cholecystitis: Pathogenesis
BILIARY TRACT Acute Acalculous Cholecystitis: Pathogenesis Result from ischemia Contributing factors: Dehydration & multiple blood transfusion  inc. pigment load Hyperalimentation & assisted ventilation  GB stasis Accumulation of microcrystals of cholesterol, viscous bile and GB mucus  cystic duct obstruction without stone formation Inflammation and edema of wall  compromise blood flow Bacterial contamination and generation of lysolecithins


23 This intraoperative photograph shows a subserosal perforation of an acute, emphysematous, acalculous cholecystitis in a 58-year-old diabetic man. He presented with features suggestive of ileus.

24 Clinical Features of Acute Cholecystitis
BILIARY TRACT Clinical Features of Acute Cholecystitis Acute calculous – sudden onset Acute acalculous – insidious onset Symptoms include: Progressive RUQ or epigastric pain Mild fever Anorexia Tachycardia Sweating Nausea and vomiting

25 Chronic Cholecystitis
BILIARY TRACT Chronic Cholecystitis Associated with cholelithiasis (90%) Calculous or acalculous Organisms: E. coli and Enterococci Symptoms of chronic calculous cholecystitis similar to the acute form Morphology: variable Subserosal fibrosis Thickened wall and opaque gray-white appearance

26 Chronic Cholecystitis
BILIARY TRACT Chronic Cholecystitis Microscopic: Mild cases – lymphocytes, plasma cells, macrophages Severe cases – subepithelial and subserosal fibrosis with mononuclear infiltration Rokitansky-Aschoff sinuses

27 Chronic Cholecystitis
BILIARY TRACT Chronic Cholecystitis RA sinuses Normal gallbladder

28 Chronic Cholecystitis
BILIARY TRACT Chronic Cholecystitis Other forms (rare): Porcelain GB Extensive dystrophic calcification within GB Inc. association with GB carcinoma Xanthogranulomatous cholecystitis Shrunken, nodular and chronically inflamed GB with foci of necrosis and hemorrhage; gallstones usually present Hydrops of GB Atrophic, chronically obstructed GB containing only clear secretions

29 Xanthogranulomatous cholecystitis: fibrotic thickening of the gallbladder wall and narrowing of the gallbladder lumen.

30 Chronic Cholecystitis: Clinical Features
BILIARY TRACT Chronic Cholecystitis: Clinical Features Recurrent attacks of steady or colicky epigastric or RUQ pain Nausea and vomiting Intolerance for fatty foods

31 Chronic Cholecystitis: Complications
BILIARY TRACT Chronic Cholecystitis: Complications Bacterial superinfection  cholangitis or sepsis GB perforation and local abscess formation GB rupture with peritonitis Biliary enteric (cholecystenteric) fistula Aggravation of pre-existing medical illness

32 BILIARY TRACT Tumors of Gallbladder Adenomas
Benign epithelial  localized neoplastic growth of lining epithelium Tubular, papillary or tubulopapillary Inflammatory polyps Sessile mucosal projections Chronic inflammatory cells & lipid-laden macrophages Adenomyosis Hyperplasia of muscularis with intraluminal hyperplastic glands

33 BILIARY TRACT Cancer of Gallbladder Women > males; 7th decade
(+) gallstones in 60% - 90% of cases  chronic irritation and inflammation Majority adenocarcinoma; 5% SSCA Two forms: Infiltrative More common; poorly-defined Scirrhous with firm consistency Can cause direct penetration of GB wall or fistula formation to adjacent viscera

34 BILIARY TRACT Cancer of Gallbladder Exophytic Grows into the lumen
Irregular, cauliflower mass with invasion of underlying wall Most common site of involvement: fundus and neck; lateral wall (20%) With centrifugal invasion of liver at time of discovery Common site of seeding: lungs, peritoneum, GIT

35 Histologic & Molecular Sequence in the Pathogenesis of Gallbladder Carcinoma

36 Moderately-differentiated GB Carcinoma
Normal GB Moderately-differentiated GB Carcinoma Well-differentiated GB Carcinoma

37 BILIARY TRACT Cancer of Gallbladder Clinical:
Indistinguishable from cholelithiasis  abdominal pain, jaundice, anorexia, nausea and vomiting Palpable GB Features of acute cholecystitis

Choledocholithiasis Stones within the bile ducts of the biliary tree Higher incidence in Asia  pigmented stones Clinical: usually asymptomatic but may manifest with: Obstruction Pancreatitis Cholangitis Hepatic abscess Secondary biliary cirrhosis Acute calculous cholecystitis


Cholangitis Bacterial infection of the bile ducts Secondary to obstruction to bile flow due to stones Other causes: In-dwelling stents or catheters Tumors Acute pancreatitis Benign strictures Infection (viruses, fungi, parasites)


Cholangitis Pathogenesis: obstruction  stasis  secondary bacterial infection  enter biliary tract via sphincter of Oddi Organisms: enteric gram (-) aerobes (E. coli), Klebsiella, Clostridium, Bacteroides, Enterobacter, group D Streptococci Clinical: fever and chills, abdominal pain, jaundice

Ascending Cholangitis Infection of intrahepatic biliary radicals Suppurative Cholangitis Bile ducts distended and filled with purulent bile Most severe form  lead to sepsis

Biliary Atresia Complete obstruction of lumen of extrahepatic biliary tree within the first three months of life Pathogenesis: two forms Fetal form (20% of cases) 20 to failure of establishment of laterality of thoracic and abdominal organ development  aberrant intrauterine development of extrahepatic biliary tree Associated with: malrotation of viscera, interrupted IVC, polysplenia, congenital heart disease

Biliary Atresia Pathogenesis: two forms Perinatal form More common; normally developed biliary tree destroyed following birth Causes: a. Possible viral infection (Reovirus & Rotavirus) b. Genetic predisposition

Biliary Atresia Morphology: Inflammation and fibrosing stricture of hepatic or common bile ducts Periductal inflammation of intrahepatic ducts Obstruction of intrahepatic biliary tree

Biliary Atresia Classification: Type I – limited to CBD Type II – CBD + hepatic duct with patent proximal branches Type III – 90%; with obstruction of bile ducts at or above the porta hepatis Types I and II – surgically correctable Type III – not correctable; liver transplant

48 Diagram depicting types of extrahepatic biliary atresia, based on a classification established by Kasai: Type I: occlusion of common bile duct Type IIa: obliteration of common hepatic duct Type IIb: obliteration of common bile duct and hepatic and cystic ducts, with uninvolved gallbladder and cystically dilated ducts at porta hepatis Type III: obliteration of common, hepatic, and cystic ducts without anastomosable ducts at porta hepatis. (Redrawn from Desmet and Callea.)

Biliary Atresia Clinical: Female preponderance Neonatal cholestasis Normal birth weight and post-natal weight gain Initially normal stools  acholic stools Serum bilirubin = 6 – 12 mg/dL Mod. Increased aminotransferase & ALP levels

50 This 3 month old child died with extrahepatic biliary atresia, a disease in which there is inflammation with stricture of hepatic or common bile ducts. This leads to marked cholestasis with intrahepatic bile duct proliferation, fibrosis, and cirrhosis. This liver was rock hard. The dark green color comes from formalin acting on bile pigments in the liver from marked cholestasis, turning bilirubin to biliverdin.

Tumors: Choledochal Cysts Congenital dilations of CBD Children < 10 y/o Jaundice + symptoms of biliary colic If with cystic dilation of intrahepatic biliary tree  Caroli disease Predispose to: stone formation, stenosis & stricture, pancreatitis In older patients, inc. risk of bile duct CA

52 Type I cysts represent approximately 85% of most series
Type I cysts represent approximately 85% of most series. They are fusiform in shape.

53 Type II cysts represents less than 2% of cases, and are often called common bile duct diverticulum.

54 Type III cysts also called choledochoceles represents approximately 2% of cases. Here the dilatation is localized to the terminal portion of the biliary tract

55 Type IV cysts represent the remaining approximately 10% of cases
Type IV cysts represent the remaining approximately 10% of cases. Here the dilatation affects both intrahepatic and extrahepatic bile ducts

56 Type V cysts are Caroli's disease
Type V cysts are Caroli's disease .They are purely intrahepatic in nature, and the association with cancer though present is weak than the rest of the group. They are frequently associated with portal hypertension and congenital hepatic fibrosis

57 The choledochal cyst was mobilized and fixed with holding sutures
The choledochal cyst was mobilized and fixed with holding sutures. Clips are seen in the cyst, which closed the right and left hepatic ducts. Resected specimen: The gallbladder (left) and the deflated bile duct cyst were removed (right). Waidner et al. Journal of Medical Case Reports :5   doi: /

Tumors: Cancer of Extrahepatic Ducts Insidious; painless, progressively deepening jaundice Elderly; men > women Risk factors: Primary sclerosing cholangitis Ulcerative colitis Cystic liver disease (Caroli’s dse and choledochal cyst) Fluke infection (Clonorchis sinensis)

Tumors: Klatskin Tumors Tumors arising from the part of the CBD between the cystic duct junction and the confluence of the R and L hepatic ducts Characteristic features: Slow growth Marked sclerosis Rare distant metastases

60 Type I tumor involves the main hepatic duct below the bifurcation
Type II tumor affects the main hepatic duct bifurcation Type III tumor involves segmental ducts beyond the primary hepatic duct bifurcation in one liver lobe (type IIIa: right lobe, type IIIb: left lobe) Type IV tumors involve segmental ducts in both liver lobes

61 Klatskin Tumor

Tumors: Clinical Features Jaundice secondary to obstruction Decolorization of stools Nausea and vomiting Weight loss Hepatomegaly (50%) Palpable gallbladder (25%) Inc. serum ALP and aminotransferases Bile-stained urine

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