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Pathology of Gall BladderPathology of Gall Bladder
Gallstones (cholelithiasis)Gallstones (cholelithiasis)
Gallstones are the most common biliary pathology.Gallstones are the most common biliary pathology.
 Gallstones are classified according to their chemical compositionGallstones are classified according to their chemical composition
intointo
1.Cholesterol stones,1.Cholesterol stones,
 SolitarySolitary( cholesterol( cholesterol solitairesolitaire) upto 2-3cm or) upto 2-3cm or Mulberry shapedMulberry shaped
stonesstones
 Pale or yellow, round to ovalPale or yellow, round to oval
2. Pigment stones.2. Pigment stones.
 Black (sterile) or brown (infected)Black (sterile) or brown (infected)
 Composed of calcium salts of unconjugated bilirubin.Composed of calcium salts of unconjugated bilirubin.
 They are mostly small (<1cm) and multiple.They are mostly small (<1cm) and multiple.
3.Mixed stones and3.Mixed stones and
 Mixed stones account for 75-90 per cent of gallstones.Mixed stones account for 75-90 per cent of gallstones.
 Cholesterol is the major component.Cholesterol is the major component.
 Other components include calcium bilirubinate, calcium phosphate,Other components include calcium bilirubinate, calcium phosphate,
calcium carbonate, calcium palmitate and proteins.calcium carbonate, calcium palmitate and proteins.
 Usually they are multiple, and they are often faceted.Usually they are multiple, and they are often faceted.
Pigment gallstones. from a patient with a mechanical mitral valve
prosthesis, leading to chronic hemolysis
Risk Factors for cholesterol stone (4F)Risk Factors for cholesterol stone (4F)
 FFemale genderemale gender
 Obesity (Obesity (FFatty)atty)
 Pregnancy (Pregnancy (FFertile)ertile)
 Oral contraceptives and hormone replacement therapy (HRT)Oral contraceptives and hormone replacement therapy (HRT)
 Bile StasisBile Stasis
 Incidence increases with age (Incidence increases with age (FForty)orty)
Risk factors for pigment stoneRisk factors for pigment stone
 Chronic hemolytic anemiasChronic hemolytic anemias
 CirrhosisCirrhosis
 Biliary infectionBiliary infection
AetiologyAetiology (Cholesterol)(Cholesterol)
The aetiology is probably multifactorial. Factors implicated areThe aetiology is probably multifactorial. Factors implicated are
 Metabolic (increased cholesterol level)Metabolic (increased cholesterol level)
 InfectiveInfective
 Bile stasis.Bile stasis.
PathogenesisPathogenesis
Factors helping formation of cholesterol Gall stonesFactors helping formation of cholesterol Gall stones
 Supersaturation of bile with cholesterolSupersaturation of bile with cholesterol
 Nucleation calcium salts may be the nucleation sites for cholesterolNucleation calcium salts may be the nucleation sites for cholesterol
stonesstones
 GB hypomotility /StasisGB hypomotility /Stasis
 Accretion - They must remain in the GB long enough choelsterolAccretion - They must remain in the GB long enough choelsterol
crystals to agglomerate into stonescrystals to agglomerate into stones
PathogenesisPathogenesis
Factors helping formation of cholesterol Gall stonesFactors helping formation of cholesterol Gall stones
 Supersaturation of bile with cholesterolSupersaturation of bile with cholesterol
 Nucleation - calcium salts promotes nucleationNucleation - calcium salts promotes nucleation
 GB hypomotility – accelerates nucleationGB hypomotility – accelerates nucleation
 Hyper secretion of GB mucous traps the crystals permitting theirHyper secretion of GB mucous traps the crystals permitting their
aggregation into stonesaggregation into stones
AetiopathogeneisAetiopathogeneis PigmentPigment
 Increased concentration of pigments – HaemolysisIncreased concentration of pigments – Haemolysis
 Precipitation of calcium salts of unconjugated bilirubinPrecipitation of calcium salts of unconjugated bilirubin
 Infection – E. Coli, ascaris lumbricoids, liver flukesInfection – E. Coli, ascaris lumbricoids, liver flukes
Effects and complications of gallstonesEffects and complications of gallstones
In the gall bladder:In the gall bladder:
 Silent stonesSilent stones
 Acute cholecystitis –Acute cholecystitis –
Empyema, Gangrene, Perforation,Empyema, Gangrene, Perforation,
 Chronic cholecystitisChronic cholecystitis
 MucoceleMucocele
 CarcinomaCarcinoma
In the bile ducts:In the bile ducts:
 Obstructive jaundiceObstructive jaundice
 CholangitisCholangitis
 Acute pancreatitisAcute pancreatitis
In the intestine:In the intestine:
 Acute intestinalAcute intestinal
obstructionobstruction
(gallstone ileus)(gallstone ileus)
CholecystitisCholecystitis
 AcuteAcute
 ChronicChronic
Acute cholecystitisAcute cholecystitis
1. Acute calculous cholecystitis1. Acute calculous cholecystitis
 It is an acute inflammation of the gallbladder, usually caused byIt is an acute inflammation of the gallbladder, usually caused by
obstruction of neck or cystic duct by gallstones. (90%)obstruction of neck or cystic duct by gallstones. (90%)
2. Acute acalculous cholecystitis - 10 %2. Acute acalculous cholecystitis - 10 %
PathogenesisPathogenesis
 ACC is initially the result of chemical irritation and inflammationACC is initially the result of chemical irritation and inflammation
 The action of phospholipases derived from the mucosa hydrolyzesThe action of phospholipases derived from the mucosa hydrolyzes
biliary lecithin to lysolecithin, which is toxic to the mucosa.biliary lecithin to lysolecithin, which is toxic to the mucosa.
 Distention and increased intraluminal pressure may alsoDistention and increased intraluminal pressure may also
compromise blood flow to the mucosa.compromise blood flow to the mucosa.
 These events occur in the absence of bacterial infection; only laterThese events occur in the absence of bacterial infection; only later
may bacterial contamination develop.may bacterial contamination develop.
MorphologyMorphology
 GB is enlarged ,tensed, redGB is enlarged ,tensed, red
 Shows evidence of acute inflammation- congestion, edema, and Fibrinous orShows evidence of acute inflammation- congestion, edema, and Fibrinous or
suppurative exudate on serosasuppurative exudate on serosa
On being openedOn being opened
 Obstructive stone in neck or cystic ductObstructive stone in neck or cystic duct
 The lumen is filled with cloudy fluid, may contain several stoneThe lumen is filled with cloudy fluid, may contain several stone
 Empyema of GB – when it contains frank pusEmpyema of GB – when it contains frank pus
Wall of GBWall of GB
 ThickenedThickened
 Gangrenous cholecystitis – may be necrosis of mucosa with small to largeGangrenous cholecystitis – may be necrosis of mucosa with small to large
ulcersulcers
 It may perforate or ruptureIt may perforate or rupture
HistologyicallyHistologyically
 The microscopic features are classical for acute inflammation andThe microscopic features are classical for acute inflammation and
include hyperemia, polymorphonuclear leukocyte infiltration, edemainclude hyperemia, polymorphonuclear leukocyte infiltration, edema
and in severe cases, necrosis of the wall of the gall bladder.and in severe cases, necrosis of the wall of the gall bladder.
SequelaeSequelae
 SubsideSubside
 Chronic CholecystitisChronic Cholecystitis
 Sub acute cholecystitisSub acute cholecystitis
 Porcelain (calcified) GBPorcelain (calcified) GB
 Carcinoma of GBCarcinoma of GB
ComplicationsComplications
 Gangrene of the gallbladderGangrene of the gallbladder
 Perforation and peritonitisPerforation and peritonitis
 Fistula formation and gallstone ileusFistula formation and gallstone ileus
 Ascending cholangitisAscending cholangitis
 Liver abscess, sub hepatic or subdiaphragmatic abscessLiver abscess, sub hepatic or subdiaphragmatic abscess
 SepticaemiaSepticaemia
Mucocele of GBMucocele of GB
 Distention of GB filled by clear, watery, mucinous secretionDistention of GB filled by clear, watery, mucinous secretion
PathogenesisPathogenesis
 Total obstruction of cystic ductTotal obstruction of cystic duct
 Trapped bile is absorbedTrapped bile is absorbed
 GB becomes filled with clear, mucinous secretions from mucosal cellsGB becomes filled with clear, mucinous secretions from mucosal cells
AppearanceAppearance
 Enlarged, tense & translucentEnlarged, tense & translucent
 Wall becomes thinWall becomes thin
Chronic cholecystitisChronic cholecystitis
It is the continuous chronic inflammation of the gallbladder usuallyIt is the continuous chronic inflammation of the gallbladder usually
caused by gallstonescaused by gallstones
Aetiology – Probable actorsAetiology – Probable actors
 Sequelae to acute cholecystitisSequelae to acute cholecystitis
 Always associated with gall stonesAlways associated with gall stones
 Supersaturation of bile – (Chemical injury)Supersaturation of bile – (Chemical injury)
 Infection – enteric bacteriaInfection – enteric bacteria
MacroscopicMacroscopic
 GB – contracted, normal or enlargedGB – contracted, normal or enlarged
 Wall is hypertrophic or atrophicWall is hypertrophic or atrophic
 Flattening of mucosal folds, thinning & atrophy of mucosaFlattening of mucosal folds, thinning & atrophy of mucosa
Micro:Micro:
 Chronic inflammation and Rokitansky-Aschoff sinuses (OutpouchingsChronic inflammation and Rokitansky-Aschoff sinuses (Outpouchings
of the mucosa through the wall)of the mucosa through the wall)
Late complication:Late complication:
 Calcification of the gallbladder ("porcelain gallbladder")Calcification of the gallbladder ("porcelain gallbladder")
 Carcinoma of gall bladder.Carcinoma of gall bladder.
Carcinoma of GallbladderCarcinoma of Gallbladder
 Malignant epithelial tumor of the gallbladder, commonly of theMalignant epithelial tumor of the gallbladder, commonly of the
adenocarcinoma type.adenocarcinoma type.
 Squamous cell carcinoma or adenosquamous carcinoma may ariseSquamous cell carcinoma or adenosquamous carcinoma may arise
from squamous metaplasisafrom squamous metaplasisa
EtiologyEtiology
 Cancer of the gallbladder is strongly associated with stone disease.Cancer of the gallbladder is strongly associated with stone disease.
 Even in patients with gallstones, the risk of carcinoma is low.Even in patients with gallstones, the risk of carcinoma is low.
PathogenesisPathogenesis
 Unknown,Unknown,
Gross PathologyGross Pathology
Mass that may be:Mass that may be:
 diffuse (70%)diffuse (70%)
 polypoid (30%)polypoid (30%)
growing in diffuse fashion in the wall of the
gallbladder, associated with extensive
involvement of the liver.
Adenocarcinoma of the gallbladder having
a predominantly papillary configuration.
9.gall bladder
9.gall bladder

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9.gall bladder

  • 1. Pathology of Gall BladderPathology of Gall Bladder
  • 2. Gallstones (cholelithiasis)Gallstones (cholelithiasis) Gallstones are the most common biliary pathology.Gallstones are the most common biliary pathology.  Gallstones are classified according to their chemical compositionGallstones are classified according to their chemical composition intointo 1.Cholesterol stones,1.Cholesterol stones,  SolitarySolitary( cholesterol( cholesterol solitairesolitaire) upto 2-3cm or) upto 2-3cm or Mulberry shapedMulberry shaped stonesstones  Pale or yellow, round to ovalPale or yellow, round to oval
  • 3. 2. Pigment stones.2. Pigment stones.  Black (sterile) or brown (infected)Black (sterile) or brown (infected)  Composed of calcium salts of unconjugated bilirubin.Composed of calcium salts of unconjugated bilirubin.  They are mostly small (<1cm) and multiple.They are mostly small (<1cm) and multiple. 3.Mixed stones and3.Mixed stones and  Mixed stones account for 75-90 per cent of gallstones.Mixed stones account for 75-90 per cent of gallstones.  Cholesterol is the major component.Cholesterol is the major component.  Other components include calcium bilirubinate, calcium phosphate,Other components include calcium bilirubinate, calcium phosphate, calcium carbonate, calcium palmitate and proteins.calcium carbonate, calcium palmitate and proteins.  Usually they are multiple, and they are often faceted.Usually they are multiple, and they are often faceted.
  • 4. Pigment gallstones. from a patient with a mechanical mitral valve prosthesis, leading to chronic hemolysis
  • 5. Risk Factors for cholesterol stone (4F)Risk Factors for cholesterol stone (4F)  FFemale genderemale gender  Obesity (Obesity (FFatty)atty)  Pregnancy (Pregnancy (FFertile)ertile)  Oral contraceptives and hormone replacement therapy (HRT)Oral contraceptives and hormone replacement therapy (HRT)  Bile StasisBile Stasis  Incidence increases with age (Incidence increases with age (FForty)orty) Risk factors for pigment stoneRisk factors for pigment stone  Chronic hemolytic anemiasChronic hemolytic anemias  CirrhosisCirrhosis  Biliary infectionBiliary infection
  • 6. AetiologyAetiology (Cholesterol)(Cholesterol) The aetiology is probably multifactorial. Factors implicated areThe aetiology is probably multifactorial. Factors implicated are  Metabolic (increased cholesterol level)Metabolic (increased cholesterol level)  InfectiveInfective  Bile stasis.Bile stasis. PathogenesisPathogenesis Factors helping formation of cholesterol Gall stonesFactors helping formation of cholesterol Gall stones  Supersaturation of bile with cholesterolSupersaturation of bile with cholesterol  Nucleation calcium salts may be the nucleation sites for cholesterolNucleation calcium salts may be the nucleation sites for cholesterol stonesstones  GB hypomotility /StasisGB hypomotility /Stasis  Accretion - They must remain in the GB long enough choelsterolAccretion - They must remain in the GB long enough choelsterol crystals to agglomerate into stonescrystals to agglomerate into stones
  • 7. PathogenesisPathogenesis Factors helping formation of cholesterol Gall stonesFactors helping formation of cholesterol Gall stones  Supersaturation of bile with cholesterolSupersaturation of bile with cholesterol  Nucleation - calcium salts promotes nucleationNucleation - calcium salts promotes nucleation  GB hypomotility – accelerates nucleationGB hypomotility – accelerates nucleation  Hyper secretion of GB mucous traps the crystals permitting theirHyper secretion of GB mucous traps the crystals permitting their aggregation into stonesaggregation into stones
  • 8. AetiopathogeneisAetiopathogeneis PigmentPigment  Increased concentration of pigments – HaemolysisIncreased concentration of pigments – Haemolysis  Precipitation of calcium salts of unconjugated bilirubinPrecipitation of calcium salts of unconjugated bilirubin  Infection – E. Coli, ascaris lumbricoids, liver flukesInfection – E. Coli, ascaris lumbricoids, liver flukes
  • 9. Effects and complications of gallstonesEffects and complications of gallstones In the gall bladder:In the gall bladder:  Silent stonesSilent stones  Acute cholecystitis –Acute cholecystitis – Empyema, Gangrene, Perforation,Empyema, Gangrene, Perforation,  Chronic cholecystitisChronic cholecystitis  MucoceleMucocele  CarcinomaCarcinoma In the bile ducts:In the bile ducts:  Obstructive jaundiceObstructive jaundice  CholangitisCholangitis  Acute pancreatitisAcute pancreatitis In the intestine:In the intestine:  Acute intestinalAcute intestinal obstructionobstruction (gallstone ileus)(gallstone ileus)
  • 10. CholecystitisCholecystitis  AcuteAcute  ChronicChronic Acute cholecystitisAcute cholecystitis 1. Acute calculous cholecystitis1. Acute calculous cholecystitis  It is an acute inflammation of the gallbladder, usually caused byIt is an acute inflammation of the gallbladder, usually caused by obstruction of neck or cystic duct by gallstones. (90%)obstruction of neck or cystic duct by gallstones. (90%) 2. Acute acalculous cholecystitis - 10 %2. Acute acalculous cholecystitis - 10 %
  • 11. PathogenesisPathogenesis  ACC is initially the result of chemical irritation and inflammationACC is initially the result of chemical irritation and inflammation  The action of phospholipases derived from the mucosa hydrolyzesThe action of phospholipases derived from the mucosa hydrolyzes biliary lecithin to lysolecithin, which is toxic to the mucosa.biliary lecithin to lysolecithin, which is toxic to the mucosa.  Distention and increased intraluminal pressure may alsoDistention and increased intraluminal pressure may also compromise blood flow to the mucosa.compromise blood flow to the mucosa.  These events occur in the absence of bacterial infection; only laterThese events occur in the absence of bacterial infection; only later may bacterial contamination develop.may bacterial contamination develop.
  • 12. MorphologyMorphology  GB is enlarged ,tensed, redGB is enlarged ,tensed, red  Shows evidence of acute inflammation- congestion, edema, and Fibrinous orShows evidence of acute inflammation- congestion, edema, and Fibrinous or suppurative exudate on serosasuppurative exudate on serosa On being openedOn being opened  Obstructive stone in neck or cystic ductObstructive stone in neck or cystic duct  The lumen is filled with cloudy fluid, may contain several stoneThe lumen is filled with cloudy fluid, may contain several stone  Empyema of GB – when it contains frank pusEmpyema of GB – when it contains frank pus Wall of GBWall of GB  ThickenedThickened  Gangrenous cholecystitis – may be necrosis of mucosa with small to largeGangrenous cholecystitis – may be necrosis of mucosa with small to large ulcersulcers  It may perforate or ruptureIt may perforate or rupture
  • 13. HistologyicallyHistologyically  The microscopic features are classical for acute inflammation andThe microscopic features are classical for acute inflammation and include hyperemia, polymorphonuclear leukocyte infiltration, edemainclude hyperemia, polymorphonuclear leukocyte infiltration, edema and in severe cases, necrosis of the wall of the gall bladder.and in severe cases, necrosis of the wall of the gall bladder.
  • 14. SequelaeSequelae  SubsideSubside  Chronic CholecystitisChronic Cholecystitis  Sub acute cholecystitisSub acute cholecystitis  Porcelain (calcified) GBPorcelain (calcified) GB  Carcinoma of GBCarcinoma of GB
  • 15. ComplicationsComplications  Gangrene of the gallbladderGangrene of the gallbladder  Perforation and peritonitisPerforation and peritonitis  Fistula formation and gallstone ileusFistula formation and gallstone ileus  Ascending cholangitisAscending cholangitis  Liver abscess, sub hepatic or subdiaphragmatic abscessLiver abscess, sub hepatic or subdiaphragmatic abscess  SepticaemiaSepticaemia
  • 16. Mucocele of GBMucocele of GB  Distention of GB filled by clear, watery, mucinous secretionDistention of GB filled by clear, watery, mucinous secretion PathogenesisPathogenesis  Total obstruction of cystic ductTotal obstruction of cystic duct  Trapped bile is absorbedTrapped bile is absorbed  GB becomes filled with clear, mucinous secretions from mucosal cellsGB becomes filled with clear, mucinous secretions from mucosal cells AppearanceAppearance  Enlarged, tense & translucentEnlarged, tense & translucent  Wall becomes thinWall becomes thin
  • 17. Chronic cholecystitisChronic cholecystitis It is the continuous chronic inflammation of the gallbladder usuallyIt is the continuous chronic inflammation of the gallbladder usually caused by gallstonescaused by gallstones Aetiology – Probable actorsAetiology – Probable actors  Sequelae to acute cholecystitisSequelae to acute cholecystitis  Always associated with gall stonesAlways associated with gall stones  Supersaturation of bile – (Chemical injury)Supersaturation of bile – (Chemical injury)  Infection – enteric bacteriaInfection – enteric bacteria
  • 18. MacroscopicMacroscopic  GB – contracted, normal or enlargedGB – contracted, normal or enlarged  Wall is hypertrophic or atrophicWall is hypertrophic or atrophic  Flattening of mucosal folds, thinning & atrophy of mucosaFlattening of mucosal folds, thinning & atrophy of mucosa
  • 19. Micro:Micro:  Chronic inflammation and Rokitansky-Aschoff sinuses (OutpouchingsChronic inflammation and Rokitansky-Aschoff sinuses (Outpouchings of the mucosa through the wall)of the mucosa through the wall) Late complication:Late complication:  Calcification of the gallbladder ("porcelain gallbladder")Calcification of the gallbladder ("porcelain gallbladder")  Carcinoma of gall bladder.Carcinoma of gall bladder.
  • 20. Carcinoma of GallbladderCarcinoma of Gallbladder  Malignant epithelial tumor of the gallbladder, commonly of theMalignant epithelial tumor of the gallbladder, commonly of the adenocarcinoma type.adenocarcinoma type.  Squamous cell carcinoma or adenosquamous carcinoma may ariseSquamous cell carcinoma or adenosquamous carcinoma may arise from squamous metaplasisafrom squamous metaplasisa EtiologyEtiology  Cancer of the gallbladder is strongly associated with stone disease.Cancer of the gallbladder is strongly associated with stone disease.  Even in patients with gallstones, the risk of carcinoma is low.Even in patients with gallstones, the risk of carcinoma is low. PathogenesisPathogenesis  Unknown,Unknown,
  • 21. Gross PathologyGross Pathology Mass that may be:Mass that may be:  diffuse (70%)diffuse (70%)  polypoid (30%)polypoid (30%) growing in diffuse fashion in the wall of the gallbladder, associated with extensive involvement of the liver. Adenocarcinoma of the gallbladder having a predominantly papillary configuration.