Acute and chronic cholecystitis......Ca Gall bladder

1. Gall bladder
Dr. Snehil Agrawal

2. Introduction
 Pear-shaped organ
 9 cm in length
 1 L of bile is secreted by the liver per day.
 Between meals, bile is stored in the gallbladder, where it is concentrated.
 Capacity of approximately 50 ml.

4. HISTOLOGY
 Lacks the muscularis mucosae and submucosa.
 Mucosal layer
 Smooth muscle layer
 Perimuscular layer
 Serosal layer

6. Congenital Anomalies:
 Congenitally absent
 Gallbladder duplication with conjoined or independent cystic ducts.
 A longitudinal or transverse septum may create a bilobed gallbladder.
 Aberrant locations of the gallbladder, most commonly partial or complete
embedding in the liver substance.
 A folded fundus is the most common anomaly, creating a phrygian cap.
 Agenesis of all or any portion of the hepatic or common bile ducts and
hypoplastic narrowing of biliary channels (true “biliary atresia”).
 Choledochal cysts

8. Cholelithiasis: gallstones
 Gallstones afflict 10% of the population
 80% of stones are cholesterol stones
 Remainder: bilirubin calcium salts [pigment stones]

9. Risk factors:
 Demography [Europe, N & S America, Mexico]
 Advancing age
 Female sex
 Obesity
 Rapid weight reduction
 Gallbladder stasis
 Hyerlipidaemia
 Chronic haemolytic syndromes
 Biliary infection
 Gastrointestinal disorders: [CD, CF, pancreatic insufficiency]
 Acquired disorders. Gallbladder stasis, either neurogenic or hormonal.
 Hereditary factors. Genes encoding hepatocyte proteins that transport biliary lipids,
known as ATP-binding cassette (ABC) transporters have associations with gallstone
formation

11. Pathogenesis of Cholesterol Stones:
 Cholesterol is rendered soluble in bile by aggregation with water-soluble bile salts
and water-insoluble lecithins, both of which act as detergents.
 When cholesterol concentrations exceed the solubilizing capacity of bile
(supersaturation), cholesterol can no longer remain dispersed and nucleates into
solid cholesterol monohydrate crystals.

14. Pathogenesis of Pigment Stones
 Complex mixtures of insoluble calcium salts of unconjugated bilirubin
along with inorganic calcium salts.
 Hemolytic anaemias and infections of the biliary tract
 → increased unconjugated bilirubin in the biliary tree
 → form precipitates : insoluble calcium bilirubinate salts.

19. Cholecystitis
 Def: Inflammation of the gall bladder
 Can be divided into
– Acute cholecystitis
– Chronic cholecystitis
– Acute superimposed on chronic

20. Acute cholecystitis
 Can be divided into :
 – Acute Calculous CS: 85-90% of the cases. Most common complication of gall
stones and emergency cholecystectomy
 – Acute Acalculous CS (10-15% of cases), Iscemia

21. Acute calculous cholecystitis

22. Acute acalculous cholecystitis
 Risk factors : sepsis with hypotension and multisystem organ failure,
immunosuppression, major trauma, diabetes mellitus, infections
 Impaired blood flow to cystic artery (end artery)→ compromised blood flow
→ ischaemia of gall bladder
 Inflammation and edema of gall bladder wall compromising blood flow,
accumulation of microcrystals of cholesterol ( biliary sludge), viscous bile,
and gall bladder mucous →cystic duct obstruction

23. Pathology
Gross :
 Enlarged, tense, edematous, red or violaceous colour (subserosal
haemorrhage)
 Fibrinous /fibrinopurulent exudate covering the serosa
 +- stones obstructing the neck or
 cystic duct– Lumen contains blood and pus(empyema)
 Green black necrotic- gangrenous
Microscopic :
 acute inflammation in the wall
 mucosal ulceration.
 May be associated with abscess
 formation or gangrenous necrosis

27. Chronic cholecystitis
 Chronic cholecystitis may be a sequel to repeated bouts of mild to severe
acute cholecystitis, but in many instances it develops in the apparent
absence of antecedent attacks.
 Associated with cholelithiasis > 90% of cases
 • Pathogenesis : supersaturation of bile predisposes to both chronic inflammation and
stone formation.
 • 1/3 of cases : E.coli and enterococci can be isolated from the bile

28. Clinical features :
 recurrent attacks of epigastric or right upper quadrant pain
 Nausea, vomiting and intolerance to fatty foods.

29. Pathology
Gross :
 smooth and glistening to dull
serosa (subserosal fibrosis)
thickened wall, opaque gray-white
appearance
 Uncomplicated cases, lumen
contains clear, green,mucoid bile
and stones with normal mucosa

30. Microscopic
 Reactive proliferation of mucosa
 Inflammation (lymphocytes, plasma cells, and macrophages in the mucosa and
in the subserosal fibrous tissue). May be minimal.
 Prominent outpouching of the mucosal epithelium through the wall (Rokitansky
Aschoff sinuses)
 Marked subepithelial and subserosal fibrosis
 +-Superimposed acute inflammation
 +-Extensive calcification within the wall →porcelain gall bladder →increase risk of
cancer

31. Variants of chronic cholecystitis
 Cholecystitis glandularis, when the mucosal folds fuse together due to
inflammation and result in formation of crypts of epithelium buried in the
gallbladder wall.
 Porcelain gallbladder is the pattern when the gallbladder wall is calcified
and cracks like an egg-shell.
 Acute on chronic cholecystitis is the term used for the morphologic changes
of acute cholecystitis superimposed on changes of chronic cholecystitis.

33. Complications of cholecystitis
 Bacterial superinfection with cholangitis or sepsis
 Gall bladder perforation and local abscess formation
 Gall bladder rupture with diffuse peritonitis
 Biliary enteric (cholecystenteric) fistula, with drainage of bile into adjacent
organs, entry of air and bacteria into biliary tree and potentially gallstone-
induced intestinal obstruction (ileus)
 Aggravating of pre-existing medical illness, with cardiac, pulmonary, renal or
liver decompensation
 Porcelain gall bladder with increased risk of cancer

36. TUMOURS OF BILIARY TRACT

37. BENIGN TUMOURS
 Papilloma
 Adenoma
 Adenomyoma
 Fibroma
 Lipoma
 Myxoma
 Haemangioma

38. MALIGNANT TUMOURS
 Carcinoma of the gallbladder
 Carcinoma of the bile ducts
 Ca ampulla of Vater

39. Carcinoma of the Gallbladder
 Primary carcinoma of the gallbladder is more prevalent.
 Women > men
 7th decade
 Remain undetected until the time it is widely spread and rendered
inoperable.

42. Pathogenesis:
 Cholelithiasis and cholecystitis
 Chronic bacterial or parasitic infections
 Oncoprotein ERBB2 (Her-2/neu) overexpression,PBRM1 and MLL3
 Chemical carcinogens structurally similar to naturally-occurring
bile acids. Eg.methyl cholanthrene.
 Primary sclerosing cholangitis, ulcerative colitis, liver flukes,
chronic Salmonella typhi and paratyphi infections, and
Helicobacter infection.

43. Gross
 infiltrating and exophytic.
 The infiltrating pattern –
• more common
• poorly defined area of diffuse mural thickening and induration.
• Deep ulceration can cause direct penetration into the liver or fistula formation to
adjacent viscera.
• Scirrhous and have a very firm consistency.
 The exophytic pattern-
• grows into the lumen as an irregular, cauliflower mass
• Invades the underlying wall
• Luminal portion may be necrotic, hemorrhagic and ulcerated.
• Most common sites: fundus & neck; 20% involve lateral walls.

45. Histology
 Most are adenocarcinomas – may be papillary or poorly differentiated.
 About 5% are squamous cell carcinomas.
 Neuroendocrine tumors- rare
 By the time this cancer is discovered, most have invaded the liver or spread
to the bile ducts or portal hepatic lymph nodes.

48. Clinical features
 • Insidious onset
 • Similar to cholelithiasis (Abd pain, jaundice, anorexia, nausea and vomiting)
 • Accidental finding during cholecystectomy for symptomatic gall stone
 • Tx :
– surgical resection (including adjacent liver)
– +- chemotherapy.

49. PROGNOSIS
 Outlook by stage
 Sadly, for most people cancer of the gallbladder does not have a very good
outlook.
 By the time it is diagnosed, it is often in the later stages and treatment is
unlikely to cure it.
 1 out of 10 (10%) will live for more than 5 years.

50. Carcinoma of Ampulla of Vater and
Extrahepatic Bile Ducts
 Ampullary carcinoma - adenocarcinoma located in the ampulla of Vater.
 In advance cases, it is indistinguishable from 3 other cancers in the vicinity:
i) cancer of adjacent duodenal mucosa with secondary involvement of ampulla;
ii) cancer of terminal third of bile duct infiltrating in the ampulla;
iii) carcinoma of the head of pancreas merging into the ampulla.
 Advanced cancer involving the ampulla - periampullary carcinoma

51.  Ampullary carcinoma
pre-existing polyp in the ampulla
Part of familial adenomatous polyposis or neurofibromatosis type 1.
 Bile duct cancers
associated with ulcerative colitis, sclerosing cholangitis, parasitic infestations
of the bile ducts with Fasciola hepatica (liver fluke), Ascaris lumbricoides and
Clonorchis sinensis.
No association between carcinoma of common bile duct and gallstones.

52. MORPHOLOGIC FEATURES
 Ampullary carcinoma
Centered on the ampulla bulging into the duodenum(intraampullary carcinoma)
Form circumferential growth around the ampulla (periampullary carcinoma).
 Grossly
ampullary carcinoma projects into the duodenal lumen and has a papillary surface.
Bile duct carcinoma- small, extending for 1-2 cm along the duct, producing thickening
of the affected duct.
 Histologically
Usually adenocarcinoma
Varying from well-differentiated to poorly differentiated
May or may not be mucin-secreting.
Perineural invasion is frequently present.

54. Clinical Features:
 Obstructive jaundice is the usual presenting feature which is characterised by
intense pruritus.
 Pain, steatorrhea, weight loss and weakness may be present.
 The tumour usually metastasises to the regional lymph nodes.
 Prognosis of ampullary carcinoma is better than pancreatic cancer and bile duct
carcinoma.