Log in / Register Soon
Official Education Partner of the Delhi Medicos Premier League — free question bank for every player and college
SN4 SHORT NOTE 5M ★ High-yield

Classify gallstones. Describe their pathogenesis, complications and the pathology of cholecystitis.

Pathology · 2nd Professional — Para-Clinical

Gallstones — Types and Composition

Cholelithiasis is the formation of calculi within the biliary tract, most often the gallbladder.

TypeCompositionAppearanceAssociations
Cholesterol stones (about 80% in the West)Over 50% cholesterol monohydratePale yellow, ovoid, often solitary and large; radiolucentThe "four Fs" — Fat, Female, Forty, Fertile; also oestrogen and oral contraceptives, rapid weight loss, ileal disease, diabetes, family history
Pigment stones — blackCalcium bilirubinate; sterile bileSmall, black, multiple; often radio-opaqueChronic haemolysis — thalassaemia, sickle cell disease, hereditary spherocytosis, malaria; cirrhosis
Pigment stones — brownCalcium bilirubinate with bacterial depositsSoft, greasy, laminatedBiliary infection and infestation — E. Coli, Ascaris, Clonorchis; commoner in Asia
MixedCholesterol, pigment and calciumMultiple, faceted, laminated — the commonest overall in IndiaCombination of the above
  • Only 10 to 20% of gallstones are radio-opaque, so a plain radiograph is a poor test; ultrasound is the investigation of choice with over 95% sensitivity

Pathogenesis

  • 1. Supersaturation of bile with cholesterol — too much cholesterol or too little bile salt and lecithin to keep it in micelles → 2.
  • Nucleation — crystals form, promoted by mucin and by gallbladder hypomotility and stasis → 3.
  • Growth — crystals aggregate into stones → For pigment stones: increased unconjugated bilirubin from haemolysis, or bacterial beta-glucuronidase deconjugating bilirubin in infected bile

CLINICAL PEARL

Three factors are needed and stasis is the one most often forgotten. Supersaturated bile alone does not form stones — many people have lithogenic bile and no stones. It is hypomotility that allows crystals time to nucleate and aggregate, which is why pregnancy, rapid weight loss, prolonged fasting and total parenteral nutrition all predispose.

Complications of Gallstones

SiteComplication
GallbladderBiliary colic, acute and chronic cholecystitis, empyema, mucocoele, perforation, gangrene; carcinoma of the gallbladder
Bile ductsCholedocholithiasis with obstructive jaundice; ascending cholangitis; secondary biliary cirrhosis; mirizzi syndrome
PancreasAcute pancreatitis — gallstones are the commonest cause worldwide
IntestineGallstone ileus — a large stone erodes through a cholecystoduodenal fistula and obstructs at the ileocaecal valve; air in the biliary tree on a plain film

Cholecystitis

  • Acute cholecystitis — 90% are calculous, from a stone impacted in the neck or cystic duct; chemical irritation by concentrated bile with secondary bacterial infection. The gallbladder is enlarged, tense, red and covered by fibrinous exudate; MURPHY sign is positive
  • Acalculous cholecystitis (10%) — in critically ill, ventilated, burned or post-operative patients; carries a higher risk of gangrene and perforation and is easily missed
  • Chronic cholecystitis — a shrunken, thick-walled, fibrotic gallbladder with a chronic inflammatory infiltrate and rokitansky–aschoff sinuses (mucosal herniations through the muscle wall)
  • Porcelain gallbladder — a calcified wall from chronic inflammation; associated with a substantially increased risk of carcinoma, and an indication for cholecystectomy

Applied Aspects

  • Most gallstones are asymptomatic and are found incidentally; only about 20% ever cause symptoms, so silent stones are generally not operated on
  • Laparoscopic cholecystectomy is the treatment of choice for symptomatic stones
  • ERCP removes stones from the common bile duct and relieves obstruction and cholangitis
  • Carcinoma OF the gallbladder is strongly associated with gallstones, present in 80 to 90% of cases, and is notably common in north India, particularly along the Gangetic belt; it presents late and carries a poor prognosis
  • Charcot triad (fever with rigors, jaundice, right upper quadrant pain) indicates ascending cholangitis, a surgical emergency; the addition of shock and confusion makes Reynolds pentad
  • Consider haemolysis in a child or young adult with pigment stones, and investigate for thalassaemia, spherocytosis or sickle cell disease

All questions in Gastrointestinal & Hepatobiliary Pathology

  1. Q1Define peptic ulcer. Describe its aetiology, pathogenesis, morphology and complications. Differentiate benign from malignant gastric ulcer. ★
  2. Q2Describe the aetiology, classification, morphology and spread of gastric carcinoma. ★
  3. Q3Describe the viruses causing hepatitis. Explain the morphology of acute and chronic hepatitis and the interpretation of hepatitis B serology. ★
  4. Q4Define cirrhosis. Describe its causes, pathogenesis and morphological types. Add a note on portal hypertension. ★
  5. Q5Describe inflammatory bowel disease. Differentiate Crohn disease from ulcerative colitis. ★
  6. SN1Describe Barrett oesophagus and carcinoma of the oesophagus. ★
  7. SN2Classify colorectal polyps. Describe the adenoma-carcinoma sequence and the morphology of colorectal carcinoma. ★
  8. SN3Define jaundice. Classify it and describe how the types are distinguished. ★
  9. SN4Classify gallstones. Describe their pathogenesis, complications and the pathology of cholecystitis. ★
  10. SN5Differentiate amoebic from pyogenic liver abscess. ★
  11. SN6Classify malabsorption syndromes. Differentiate coeliac disease from tropical sprue. ★
  12. SN7Describe hepatocellular carcinoma with its aetiology, morphology and diagnosis.

Every Pathology chapter →

Scroll to Top