1. The gallbladder can be divided into three parts and lacks two layers. It may also have congenital anomalies. 2. Common gallbladder disorders include cholelithiasis and cholecystitis. 3. Extrahepatic bile duct disorders include stones, infections, and atresia in infants. 4. Tumors of the biliary tract include both benign and malignant types such as adenomas and adenocarcinomas.

1. Title: Gall bladder and biliary tract
Objectives: to
1. Identify anatomy and histology of gall bladder
and 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.

2. Anatomy and histology:
 Gallbladder is divided into: fundus, body, and neck.
 Lacks muscularis mucosa and submucosa and
consists only of:
(1) mucosal lining: single layer of columnar cells.
(2) fibromuscular layer.
(3) adventitia( serosa).
 Gallbladder mucosa may penetrate deep into
muscle wall (Rokitansky-Aschoff sinuses).

4.  Confluence of biliary tree is common bile duct
which discharge its contents through
ampulla of Vater into duodenal lumen.
 In 60% to 70% of individuals main pancreatic duct
joins common bile duct to drain through
common channel.

5. Congenital Anomalies:
 Gallbladder may be congenitally absent.
 Gallbladder duplication with conjoined or
independent cystic ducts.
 Longitudinal or transverse septum (bilobed gallbladder).
 Aberrant locations of gallbladder occur in 5% to 10%
of population, most commonly is partial or complete
embedding in liver .

6. 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,and
hyperlipidemia.
o Pigment stones: chronic hemolytic syndromes, biliary
infection, gastrointestinal disorders (crohn’s disease).

7. Pathogenesis of gall stones:
 Cholesterol stone:
o bile supersaturated with cholesterol.
o gallbladder hypomotility promotes nucleation of cholesterol.
o mucus hypersecretion in gallbladder traps cholesterol
crystals permitting their aggregation into stones.
 Pigment Stone:
o It’s mixture of unconjugated bilirubin with inorganic
calcium salts.
o unconjugated bilirubin increased with:
 infection of biliary tract (E.coli).
 intravascular hemolysis.

8. 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 stone
may fill the fundus.
 Stones composed largely of cholesterol are radiolucent;
sufficient calcium carbonate render them radio-opaque.

9. Pigment gall stones:
classified as "black" and "brown“
 black stones: found in sterile gallbladder (no infection).
 brown stones: found in infected intrahepatic or
extrahepatic ducts.
 black stones are multiple and may crumble on touch,
because of calcium carbonates and phosphates are
radio-opaque.
 brown stones are soft and have soaplike or greasy in
consistency, those which contain calcium soaps are
radiolucent.

10. Clinical Features:
 Gallstones may be present for decades before
symptoms develop.
 70% to 80% of patients remain asymptomatic.
 Prominent symptom is biliary pain, which tends to be
sever and constant , or "colicky" (spasmodic).
 Complications : empyema, perforation, fistulae, inflammation
of biliary tree (cholangitis), and obstructive cholestasis or
pancreatitis .

11. Cholecystitis:
Acute Cholecystitis:
Acute calculous cholecystitis :
 90% precipitated by obstruction of
neck of gall bladder or cystic duct.
 It’s primary complication of gallstones.
 It’s most common reason for emergency cholecystectomy.

12. 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.

13. Pathogenesis:
Acute calculous cholecystitis :
 Mucosal phospholipases hydrolyzes luminal lecithins
to toxic lysolecithins.
 Protective mucus layer is disrupted, exposing mucosal
epithelium to direct action of bile salts.
 Prostaglandins released from distended gallbladder
contribute to mucosal and mural inflammation.
 Gallbladder distention and increased intraluminal
pressure compromise blood flow to mucosa.

14. 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 , viscous
bile causing cystic duct obstruction in absence of
stone formation.
 Edema of wall compromising blood flow.

15. Morphology:
Grossly:
 Gall bladder is enlarged and tense, with
bright red to green-black discoloration.
 The serosal covering layered by fibrin, and
in severe cases by suppurative exudate.
 No specific morphologic differences between
acute calculous and acalculous cholecystitis,
except for absence of stones in latter.
 Gall bladder lumen is filled with turbid bile.

16. 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.

17. 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 and
histology similar to calculous form.
 Supersaturation of bile predisposes to both chronic
inflammation and stone formation
 Microorganisms (E.coli and enterococci) can be
cultured from bile in one third of cases.

18. Morphology:
Grossly:
 The serosa is smooth and glistening, but may be
dulled by subserosal fibrosis.
 On sectioning the wall is thickened, rarely to more than
three times than normal.
 The wall has gray-white appearance and less flexible
than normal.
 In uncomplicated case the lumen contains clear
green-yellow mucoid bile and stones .
 The mucosa itself is generally preserved.

19. Microscopically:
 In mild cases: scattered lymphocytes, plasma cells, and
macrophages 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 within
gallbladder wall (porcelain gallbladder) which increase
the incidence of cancer.

20. Chronic cholecystitis

21. Disorders of extrahepatic bile ducts:
1. Choledocholithiasis :
 Presence of stones within bile ducts, as opposed to
cholelithiasis (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.

22. 2. Cholangitis:
 Bacterial infection of bile ducts.
 Result from : choledocholithiasis, indwelling catheter,
tumors, acute pancreatitis, and benign strictures.
 Infection of intrahepatic biliary radicals is termed
Ascending cholangitis.
 The bacteria are usually enteric Gram-negative
aerobes such as E. coli, and Klebsiella.

23. 3. Biliary atresia:
 It’s most frequent cause of death from liver disease
in early childhood, owing to rapidly progressing
secondary biliary cirrhosis.
Pathogenesis:
Two major forms , based on timing of obliteration:-
 Fetal form:
o 20% of cases, it is due to aberrant intrauterine
development of extrahepatic biliary tree.
 Perinatal form:
o 80% of cases, in which normally developed
biliary tree is destroyed following birth.

24. o Although the cause is unknown, viral infection
and genetic inheritance suspected.
Morphology:
 Features of extrahepatic biliary obstruction in
2/3rd of cases:- marked bile ductular proliferation,
portal tract edema and fibrosis, and parenchymal
cholestasis.
 In remainder(1/3rd):- inflammatory destruction of
intrahepatic ducts leads to paucity of bile ducts.

25. Tumors of biliary tract:
Benign tumors:
• Adenomas :
benign epithelial tumors, classified as tubular, papillary,
and tubulopapillary.
• Inflammatory polyps:
sessile mucosal projections with stroma infiltrated
with chronic inflammatory cells and lipid-laden
macrophages.
• Adenomyosis of gallbladder:
hyperplasia of muscularis externa ,containing intramural
hyperplastic glands.

26. 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 duct
and pancreatic duct.

27. Clinical Features:
 Symptoms are insidious and indistinguishable from
those of cholelithiasis : abdominal pain, jaundice,
anorexia, and nausea and vomiting.
 The patient may develop a palpable gallbladder
and acute cholecystitis ; or have incidental finding of
carcinoma at time of cholecystectomy for gallstones.
 The most common abnormal lab. finding is
elevated alkaline phosphatase level.

28. Morphology:
Grossly :
Infiltrating pattern:
 More common.
 Appears as diffuse thickening and induration of
gallbladder 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 .

29. Infiltrating pattern Exophytic pattern

30. 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 adenosquamous
differentiation.
 A minority exhibit:
carcinoid, or a variety
of mesenchymal features.
Well diff. adenocarcinoma of G.bladder

31. 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, or
aberrant locations.
3. Disorders of gallbladder: Cholelithiasis, acute and
chronic 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.

32. Questions:
1. Mention conditions associated with increased
risk of gall bladder carcinoma?
2. Discuss briefly disorders of extrahepatic bile ducts?
Thank you