CHOLELITHIASIS & CHELECYSTITIS Ms/00021/018

NORMAL ANATOMY

GROSS HISTOLOGY
❖ Pear shaped ,9cm in length ,capacity= 50mg ❖ Mucosal layer – column epithelium which is folded
❖ Parts : fundus, body and neck (opens into cystic duct) ❖ Smooth muscle layer
❖ Function : store and concentrate bile ❖ Peri muscular layer – fibrous layer and fat cell
❖ Contraction and relaxation under influence of CCK ❖ serosa
(from neuroendocrine cells of duod. and jejunum)
BILIARY TREE
BILE COMPOSITION
❖ Water
❖ Bile salts
❖ Bilirubin
❖ Inorganic salts
❖ Cholesterol
❖ Fatty acids
❖ lecithin

CONGENITAL ANOMALIES
Uncommon
❖ Agenesis
❖ Duplication
❖ Heterotopic tissue
❖ Congenital cystic lesions of bile ducts
• congenital intrahepatic biliary dilatation
(Caroli’s disease)
• choledochal cysts
• congenital hepatic fibrosis
 CHOLELITHIASIS
Stone formation in gall bladder
Gall stone composition in general- cholesterol, bile pigment and calcium salts

COMMON RISK FACTORS - Given acronym fat female fertile forty

❑ Age – increased occurrence with advancing age especially after 40
❑ Sex – F>>M, higher prevalence in multiparous women
❑ Obesity- increased synthesis of cholesterol from fat stores and consequently increased secretion

OTHER RISK FACTORS

❑ Diet- deficiency of dietary fiber, alcoholism
❑ Genetics-mutations in CYP7A1 results in deficiency cholesterol 7 hydroxylase leading to hypercholesterolemia
❑ Geography – higher prevalence in western world
❑ Gastrointestinal disease – those that compromise enterohepatic circulation of bile e.g. crohn’s disease, ileal by-pass
❑ Hemolytic anemias- increased unconjugated bilirubin in bile > pigment stones
Types of gall stones
 Pigment stones can be brown or black
Pigment stones can be brown or black
➢ black
➢ Brown
• sterile gall bladder
• formed in infected intrahepatic or extrahepatic ducts ,
• calcium salts e.g. calcium bilirubinate, mucin glycoproteins
• calcium soaps
and Chol.
• radiolucent
• radiopaque
 CHOLELITHOGENESIS
1) PATHOGENESIS OF CHOLESTRAL & MIXED GALL STONES
i) supersaturation of bile with cholesterol
due to factors that either increase chol. Levels or those that reduce bile acid/lecithin concentration
reduced bile acid pool e.g. compromised enterohepatic circulation
increased activity of HMG-CoA reductase activity > increased cholesterol synthesis
ii) cholesterol, as a compound, crystalizes out of solution and precipitates
iii) nucleation of cholesterol monohydrate crystals
iv) gall bladder hypomotility . Due to decreased CCK receptors in gall bladder > stasis of biliary sludge> lithogenesis

2) PATHOGENESIS OF PIGMENT GALL STONES

❖ chronic hemolysis > increased level of unconjugated bilirubin in bile> precipitation and stone formation
❖ alcoholic cirrhosis . Reduced conjugation of bilirubin
❖
CLINICAL FEATURES
• Excruciating pain which localizes to right upper quadrant or
• Epigastric region

COMPLICATIONS
• Cholecystitis
• Choledocholithiasis – gallstones in common bile duct
• Perforations and biliary fistula
• Gallstone ileus- gallstone I the intestine causing obstruction
• Empyema
 CHOLECYSTITIS
Inflammation of gall bladder .
Can be acute ,chronic or acute superimposed chronic cholecystitis
ACUTE CALCULUS CHOLECYSTITIS
Precipitated by obstruction of gall bladder neck or cystic duct (a complication of gallstones)
Pathogenesis
▪ Obstruction to bile flow
▪ Phospholipases hydrolyzes lecithin to lysolecithin which destroys glycoprotein mucous layer
▪ Epithelium is then exposes to direct detergent action of bile salts
▪ Prostaglandins are released as membrane phospholipids get broken down >pain
▪ Distention of bladder may compromise blood flow to mucosa >ischemia > infarction
▪ Secondary bacterial infection . E. Coli , Streptococcus faecalis

ACUTE ACALCULOUS CHOLECYSTITIS

Inflammation without the bar-ground of gallstones or obstruction
Common in seriously ill patients
Predisposing insults
▪ Major nonbiliary surgery
▪ Severe trauma, burns
▪ Sepsis/ bacteria contamination- enteric flora, e. coli, clostridia, salmonella
▪ Dehydration
▪ Edema of gallbladder valve
▪ shock
ACUTE CHOLECYSTITIS- MORPHOLOGY

GROSS
➢ Enlarged ,tense
➢ Bright red or blotched
➢ fibrinous or fibrinopurulent exudate on serosa
➢ Mucosal ulcer
➢ Lumen
• stone
• Cloudy bile that may contain fibrin ,blood or
pus(empyema)
➢ Severe case, gall bladder becomes Necrotic
(gangrenous necrosis) - green black
• gas-poducers e.g. e coli, clostridium.
HISTOLOGY
Usual pattern of inflammation e.g.
➢ Edema
➢ Leukocytic infiltration
CLINICAL PRESENTATION
severe pain in the upper abdomen, often radiates to the
right shoulder
guarding and hyperesthesia
The gallbladder is tender and may be palpable.
Fever
Leukocytosis with neutrophilia
Slight jaundice
DIAGNOSIS
detection of gallstones by ultrasonography,
typically accompanied by evidence of a
thickened gallbladder wall.
COMPLICATIONS
perforation
biliary fistula
recurrent attacks
adhesions
TREATMENT
cholecystectomy
 CHRONIC CHOLECYSTITIS

Almost always associated with gallstone

Risk factors- similar to cholelithiasis
PATHOGENESIS
1) May be sequel of bouts of acute cholecystitis
2) supersaturation of bile >chronic inflammation and stone formation

MORPHOLOGY

GROSS
➢ Generally contracted , may be normal or enlarged
➢ Thickened walls
➢ Mucosal folds- intact or thickened or flattened
➢ Lumen – stones

HISTOLOGY
➢ Hypertrophy and hyperplasia of smooth muscle cells
➢ Rokitansky Aschoff sinuses
➢ Inflammatory infiltrate – lymphocytes ,macrophage
➢ Variable degree of fibrosis
➢ Dystrophic calcification > porcelain gall bladder
Acute cholecystitis histopathology
Clinical presentation – chronic Cholecystitis
➢ Abdominal distension/ epigastric pain especially after fatty meal
➢ Dull ache in right hypochondrium or epigastric region
➢ Tenderness
➢ Nausea
➢ Flatulence
DIAGNOSIS
biopsy
Treatment
➢ Cholecystectomy

Acute on chronic cholecystitis

morphological changes of acute cholecystitis superimposed on chronic cholecystitis

 X-RAY IMAGING

Porcelain gallbladder emphysematous gallbladder Gall stones

Reference
1. Kubas, abbas, aster (2013). Robbins basic pathology, 9th
Edition
2. Mohan H (2010). Textbook of pathology , 6th edition
3.Heuman D(2019). Gallstones . Published by Medscape :
https://emedicine.Medscape.com/article/175667-overview