06.GB Pathology

7/27/2019 06.GB Pathology

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Pathology of the Billiary

tract

Dr Janaki Hewavisenthi

Department of Pathology

Faculty of Medicine

Ragama.


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Pathology of the Billiary

tract

Anatomy & Physiology

Congenital abnormalities

Cholelithiasis Acute cholecystitis.

Chronic cholecystitis.

Miscellaneous Tumours of the billiary tree.


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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.


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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 embeddedin the liver.


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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.


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Cholelithiasis - Gall stones.

INCIDENCE AND RISK FACTORS.

- Ethnic / Genetic factors.

- Age- Sex

- Diet and Obesity

- Drugs Eg: Clofibrate

- Gastrointestinal disorders -Crohns disease.


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Pathogenesis

Stages involved in the formation of Gall

stones1. Supersaturation of bile

2. Nucleation or initiation of stone

formation.

3. Growth by accretion.


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Supersaturation of bile.

Deficient secretion of bile acid (salts) or

lecithin is lithogenic.

Supersaturation / increased secretion of

cholesterol.

Increased reabsorption of water.


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Stage 1 - Supersaturation of

bile

Cholesterol is maintained in solution by

micell formation with bile salts.


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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.


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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.


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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 ofcalcium substances. Depending on the

amount of calcium RADIOPAQUE.


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Pigment stones.

More common in Orientals.

Pathogenesis - Chronic haemolysis,?? Opisthorchis sinesisAlcoholic cirrhosisBilliary infectionAdvancing age.

Composed of pure Calcium bilirubinate.

Rarely >1.5cm in size.

Jet black in colour.


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Clinical picture

50% patients with gall stones are

asymptomatic.

Symptoms - indigestionIntolerance of fat

Nausea and vomiting.

?? Are these symptoms non specific.

Most of the definitive symptoms are duethe complications of Gall stones.

(See next slide)


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Clinical implications

Obstruction of the bile ducts.Biliary colicCholecystitis and Ascending

cholangitis.Obstructive jaundice.

Formation of empyema or hydrops(Mucocoele)

Gall stone ileus.

Carcinoma.


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CHOLECYSTITIS

ACUTE CHOLECYSTITIS CHRONIC CHOLECYSTITIS

ACALCULOUS

surgery, Trauma

Prolonged labour

DM & PAN

Infections -

Cholera

Salmonella

CALCULOUS

C


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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 ofthe GB are the same in both conditions.


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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.


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Macroscopy

- Gall bladder is enlarged.

Red - violaceous - green black

discolouration due to subserosalhaemorrhage.

Serosa - fibrin layered.

Cloudy turbid bile in the lumen or purulent

material .

Wall is thickened.

Mucosa - hyperaemic, patchily destroyed

or denuded.


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Acute Cholecystitis


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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.


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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 antecedentacute attacks.


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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.


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Chronic Cholecystitis


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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.


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Miscellaneous conditions.

Porcelain Gall bladder.

Inflammatory polyps.

Cholesterosis of the Gall bladder

(Strawberry gall bladder)

Hydrops or mucocoele of the Gall bladder.


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Tumours of the Gall bladder

Benign - Adenomas and Papillomas.

Branching pedunculated masses


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Papillary adenocarcinoma

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06.GB Pathology