Pathology of the Billiary tract

Dr Janaki Hewavisenthi Department of Pathology Faculty of Medicine Ragama.

Pathology of the Billiary tract

Anatomy & Physiology Congenital abnormalities Cholelithiasis Acute cholecystitis. Chronic cholecystitis. Miscellaneous Tumours of the billiary tree.

Physiology

Function - concentration and storage of bile. (liver secretes 0.5 - 1 litre of bile / d cf: the capacity of the Gall bladder is 50ml)
Cholesterol is not soluble in bile but maintained in solution by micelle formation with bile acids.

Histology

Compared with the GIT Single mucosal lining of tall columnar cells. A fibromuscular subserosal layer. A layer of subserosal fat. Peritoneal coverings except where embedded in the liver.

Congenital anomalies Developmental

Absence. Bilobed gall bladder. Duplication. Folded fundus - Phyrigian cap anomaly (Clinical significance of above )

Agenesis / atretic narrowing of the billiary system which leads to obstructive Jaundice.

Cholelithiasis - Gall stones.

INCIDENCE AND RISK FACTORS. Ethnic / Genetic factors. Age Sex Diet and Obesity Drugs Eg: Clofibrate Gastrointestinal disorders Crohns disease.

Pathogenesis

Stages involved in the formation of Gall stones 1. Supersaturation of bile 2. Nucleation or initiation of stone formation. 3. Growth by accretion.

Supersaturation of bile.

Deficient secretion of bile acid (salts) or lecithin is lithogenic. Supersaturation / increased secretion of cholesterol. Increased reabsorption of water.

Stage 1 - Supersaturation of bile

Cholesterol is maintained in solution by micell formation with bile salts.

Stage 2 - Nucleation / initiation of stone formation

Nucleating factors- (increased) Mucin - in bile supersaturated with cholesterol forms a sludge. Prostaglandins - promote mucin secretion.
Antinucleating factors - (Decreased) Apoproteins / Serum lippoproteins.

Morphology

3 types of stones Pure cholesterol stones. Mixed stones Pigment stones. Pure cholesterol stones Multiple rarely single. 1 - several cms in size. C/S glistening radiating crystalline pallisade. NOT RADIOLUCENT.

Morphology

Mixed stones varying proportion of calcium carbonates, phosphates and bilirubin. 1 - 3 cms in size. Rounded / faceted exterior. C/S lamellated and variable in colour Because of the varying proportions of calcium substances. Depending on the amount of calcium RADIOPAQUE.

Pigment stones.

More common in Orientals. Pathogenesis - Chronic haemolysis, ?? Opisthorchis sinesis Alcoholic cirrhosis Billiary infection Advancing age. Composed of pure Calcium bilirubinate. Rarely >1.5cm in size. Jet black in colour.

Clinical picture

50% patients with gall stones are asymptomatic. Symptoms - indigestion Intolerance of fat Nausea and vomiting. ?? Are these symptoms non specific. Most of the definitive symptoms are due the complications of Gall stones. (See next slide)

Clinical implications

Obstruction of the bile ducts. Biliary colic Cholecystitis and Ascending cholangitis. Obstructive jaundice. Formation of empyema or hydrops (Mucocoele) Gall stone ileus. Carcinoma.

CHOLECYSTITIS

ACUTE CHOLECYSTITIS ACALCULOUS surgery, Trauma Prolonged labour DM & PAN Infections Cholera Salmonella

CHRONIC CHOLECYSTITIS

CALCULOUS

Acalculous vs Calculous Acute cholecystitis

Less common. Predisposition See The common denominator being transient invasion of the blood stream by infective organisms and seeding in the GB / Ischaemic compromise. Signs and symptoms and morphology of the GB are the same in both conditions.

Clinical picture

RHC pain. Pain radiates to right shoulder and scapular and interscapular regions. Palpably enlarged exceedingly tender GB Murphy sign. Leukocytosis Fever and Jaundice - uncommon.

Macroscopy

- Gall bladder is enlarged. Red - violaceous - green black discolouration due to subserosal haemorrhage. Serosa - fibrin layered. Cloudy turbid bile in the lumen or purulent material . Wall is thickened. Mucosa - hyperaemic, patchily destroyed or denuded.

Acute Cholecystitis

Microscopy

All the features of acute inflammation. The inflammatory reaction is replaced by chronic inflammation. Calcification in the resolving phase may lead to Porcelain Gall bladder. In some cases (incidence unknown) Acute cholecystitis leads to Chronic cholecystitis.

Chronic cholecystitis

Virtually always associated with Calculi. ? Predisposing factor ? Same factors predisposing to calculous disease. May be the sequel to repeated attacks of acute cholecystitis. Sometimes develops without antecedent acute attacks.

Morphology

Macroscopy Normal, small or enlarged. (This depends on the balance between fibrosis and obstruction in the genesis of inflammation.) Serosa is dulled by subserosal fibrosis. Wall thickened. - Opaque gray white. Stones are present in almost all cases.

Chronic Cholecystitis

Morpholgy

Presence of calculi even in the absence of significant inflammation taken to indicate Chronic cholecystitis. MICROSCOPY Varying degrees of chronic inflammation. Fibrosis. Rokitansky Aschoff sinuses in the wall.

Miscellaneous conditions.

Porcelain Gall bladder.

Inflammatory polyps. Cholesterosis of the Gall bladder (Strawberry gall bladder) Hydrops or mucocoele of the Gall bladder.

Tumours of the Gall bladder

Benign - Adenomas and Papillomas. Branching pedunculated masses <1.0cm in diameter. (adenomas - sessile) Malignant - Adenocarcinoma (Carcinoma of the Gall bladder)

Papillary adenocarcinoma