Title: Gall bladder and biliary tractObjectives: to1. Identify anatomy and histology of gall bladderand biliary passage.2. Describe congenital anomalies of gall bladder.3. Outline disorders of gall bladder.4. Explain disorders of extrahepatic bile ducts.5. Study tumors of biliary tract.
Anatomy and histology: Gallbladder is divided into: fundus, body, and neck. Lacks muscularis mucosa and submucosa andconsists only of:(1) mucosal lining: single layer of columnar cells.(2) fibromuscular layer.(3) adventitia( serosa). Gallbladder mucosa may penetrate deep intomuscle wall (Rokitansky-Aschoff sinuses).
Confluence of biliary tree is common bile ductwhich discharge its contents throughampulla of Vater into duodenal lumen. In 60% to 70% of individuals main pancreatic ductjoins common bile duct to drain throughcommon channel.
Congenital Anomalies: Gallbladder may be congenitally absent. Gallbladder duplication with conjoined orindependent cystic ducts. Longitudinal or transverse septum (bilobed gallbladder). Aberrant locations of gallbladder occur in 5% to 10%of population, most commonly is partial or completeembedding in liver .
Disorders of gallbladder:Cholelithiasis (gallstones): Two main types of gallstones:o 80% are cholesterol stones.o 20% are pigment stones. Risk factors for gallstones:-o cholesterol stones: advancing age, female gender,obesity, rapid weight reduction, gallbladder stasis,andhyperlipidemia.o Pigment stones: chronic hemolytic syndromes, biliaryinfection, gastrointestinal disorders (crohn’s disease).
Pathogenesis of gall stones: Cholesterol stone:o bile supersaturated with cholesterol.o gallbladder hypomotility promotes nucleation of cholesterol.o mucus hypersecretion in gallbladder traps cholesterolcrystals permitting their aggregation into stones. Pigment Stone:o It’s mixture of unconjugated bilirubin with inorganiccalcium salts.o unconjugated bilirubin increased with: infection of biliary tract (E.coli). intravascular hemolysis.
Morphology :Cholesterol stones: Pure cholesterol stones are pale yellow, round to ovoid. With calcium carbonate, phosphates, and bilirubin,Stone become gray-white to black on transection. Most often are multiple stones, rarely single large stonemay fill the fundus. Stones composed largely of cholesterol are radiolucent;sufficient calcium carbonate render them radio-opaque.
Pigment gall stones:classified as "black" and "brown“ black stones: found in sterile gallbladder (no infection). brown stones: found in infected intrahepatic orextrahepatic ducts. black stones are multiple and may crumble on touch,because of calcium carbonates and phosphates areradio-opaque. brown stones are soft and have soaplike or greasy inconsistency, those which contain calcium soaps areradiolucent.
Clinical Features: Gallstones may be present for decades beforesymptoms develop. 70% to 80% of patients remain asymptomatic. Prominent symptom is biliary pain, which tends to besever and constant , or "colicky" (spasmodic). Complications : empyema, perforation, fistulae, inflammationof biliary tree (cholangitis), and obstructive cholestasis orpancreatitis .
Cholecystitis:Acute Cholecystitis:Acute calculous cholecystitis : 90% precipitated by obstruction ofneck of gall bladder or cystic duct. It’s primary complication of gallstones. It’s most common reason for emergency cholecystectomy.
Acute acalculous cholecystitis : occurs in severely ill patient in absence of gallstones . Most cases occur in following circumstances:(1) postoperative state.(2) severe trauma ( car accidents, war injuries) .(3) severe burns.(4) multisystem organ failure .(5) sepsis.(6) prolonged intravenous hyperalimentation.(7) postpartum state.
Pathogenesis:Acute calculous cholecystitis : Mucosal phospholipases hydrolyzes luminal lecithinsto toxic lysolecithins. Protective mucus layer is disrupted, exposing mucosalepithelium to direct action of bile salts. Prostaglandins released from distended gallbladdercontribute to mucosal and mural inflammation. Gallbladder distention and increased intraluminalpressure compromise blood flow to mucosa.
Acute acalculous cholecystitis: Result from ischemia. Cystic artery is an end artery with no collateral circulation. Contributing (assisting) factors include:- Dehydration and multiple blood transfusions. Gallbladder stasis as with hyperalimentation. Accumulation of microcrystals of cholesterol , viscousbile causing cystic duct obstruction in absence ofstone formation. Edema of wall compromising blood flow.
Morphology:Grossly: Gall bladder is enlarged and tense, withbright red to green-black discoloration. The serosal covering layered by fibrin, andin severe cases by suppurative exudate. No specific morphologic differences betweenacute calculous and acalculous cholecystitis,except for absence of stones in latter. Gall bladder lumen is filled with turbid bile.
Microscopically: Usual pattern of acute inflammation:edema, leukocytic infiltration, vascular congestion,frank abscess formation, or gangrenous necrosis. When the contained exudate is pure pus,the condition is referred to empyema of gallbladder.
Chronic Cholecystitis: May follow repeated bouts of acute cholecystitis,but mostly develops in absence of acute attacks. Associated with cholelithiasis in over 90% of cases. Chronic acalculous cholecystitis exhibits symptoms andhistology similar to calculous form. Supersaturation of bile predisposes to both chronicinflammation and stone formation Microorganisms (E.coli and enterococci) can becultured from bile in one third of cases.
Morphology:Grossly: The serosa is smooth and glistening, but may bedulled by subserosal fibrosis. On sectioning the wall is thickened, rarely to more thanthree times than normal. The wall has gray-white appearance and less flexiblethan normal. In uncomplicated case the lumen contains cleargreen-yellow mucoid bile and stones . The mucosa itself is generally preserved.
Microscopically: In mild cases: scattered lymphocytes, plasma cells, andmacrophages in both mucosa and subserosal fibrous tissue. In sever cases: marked subepithelial and subserosal fibrosis,with mononuclear inflammatory cells infiltration. Outpouchings of mucosal epithelium through the wall(Rokitansky-Aschoff sinuses). Rarely extensive dystrophic calcification withingallbladder wall (porcelain gallbladder) which increasethe incidence of cancer.
Disorders of extrahepatic bile ducts:1. Choledocholithiasis : Presence of stones within bile ducts, as opposed tocholelithiasis (stones in gallbladder). Both cholesterol and pigmented stones . Asymptomatic or cause:(1) obstruction (2) pancreatitis (3) cholangitis(4) hepatic abscess (5) secondary biliary cirrhosis(6) acute calculous cholecystitis.
2. Cholangitis: Bacterial infection of bile ducts. Result from : choledocholithiasis, indwelling catheter,tumors, acute pancreatitis, and benign strictures. Infection of intrahepatic biliary radicals is termedAscending cholangitis. The bacteria are usually enteric Gram-negativeaerobes such as E. coli, and Klebsiella.
3. Biliary atresia: It’s most frequent cause of death from liver diseasein early childhood, owing to rapidly progressingsecondary biliary cirrhosis.Pathogenesis:Two major forms , based on timing of obliteration:- Fetal form:o 20% of cases, it is due to aberrant intrauterinedevelopment of extrahepatic biliary tree. Perinatal form:o 80% of cases, in which normally developedbiliary tree is destroyed following birth.
o Although the cause is unknown, viral infectionand genetic inheritance suspected.Morphology: Features of extrahepatic biliary obstruction in2/3rd of cases:- marked bile ductular proliferation,portal tract edema and fibrosis, and parenchymalcholestasis. In remainder(1/3rd):- inflammatory destruction ofintrahepatic ducts leads to paucity of bile ducts.
Tumors of biliary tract:Benign tumors:• Adenomas :benign epithelial tumors, classified as tubular, papillary,and tubulopapillary.• Inflammatory polyps:sessile mucosal projections with stroma infiltratedwith chronic inflammatory cells and lipid-ladenmacrophages.• Adenomyosis of gallbladder:hyperplasia of muscularis externa ,containing intramuralhyperplastic glands.
Carcinoma of gallbladder: Slightly more common in women. Occurs mainly in seventh decade of life. 5-year survival rate is 1% . Gallstones are present in 60% to 90% of cases. Conditions associated with increased risk: cholecysto-enteric fistula. porcelain gallbladder. ulcerative colitis. Adenomyomatosis. polyposis coli. anomalous connection between common bile ductand pancreatic duct.
Clinical Features: Symptoms are insidious and indistinguishable fromthose of cholelithiasis : abdominal pain, jaundice,anorexia, and nausea and vomiting. The patient may develop a palpable gallbladderand acute cholecystitis ; or have incidental finding ofcarcinoma at time of cholecystectomy for gallstones. The most common abnormal lab. finding iselevated alkaline phosphatase level.
Morphology:Grossly :Infiltrating pattern: More common. Appears as diffuse thickening and induration ofgallbladder wall. Scirrhous tumors and have very firm consistency.Exophytic pattern: Grows into lumen of gall bladder as a cauliflower mass. At the same time invades the underlying wall. Luminal portion of tumor may be necrotic, hemorrhagic,and ulcerated .
Microscopically : Most are adenocarcinomas:o mainly tubular , some are papillary.o well to moderately differentiated.o others are poorly differentiated to undifferentiated . 5% are squamous cell ca. or have adenosquamousdifferentiation. A minority exhibit:carcinoid, or a varietyof mesenchymal features.Well diff. adenocarcinoma of G.bladder
Summary:1. Gallbladder is divided into fundus, body, and neck.It lacks muscularis mucosa and submucosa.2. Gallbladder may be congenitally absent, duplicated,having longitudinal or transverse septum, oraberrant locations.3. Disorders of gallbladder: Cholelithiasis, acute andchronic cholecystitis.4. Disorders of extrahepatic bile ducts:Choledocholithiasis, cholangitis, and biliary atresia.5. Tumors of biliary tract: Benign tumors like adenoma,and malignant tumors like adenocarcinoma.
Questions:1. Mention conditions associated with increasedrisk of gall bladder carcinoma?2. Discuss briefly disorders of extrahepatic bile ducts?Thank you