Other Pathology

Ninety percent of patients (>60 years, F:M 1:1) present with jaundice and diagnosis is by cholangiography (retrograde endoscopic or percutaneous transhepatic) supplemented by FNA/brushings/washings cytology and/or biopsy.

Frozen section diagnosis of bile duct carcinoma can be difficult due to the presence of ductulo-glandular structures in normal bile duct sub-mucosa and the distortion that can occur in inflammatory strictures.

Dysplasia of adjacent bile duct mucosa can have a flat or micropapil-lary epithelial pattern and must be noted at the resection limits. Intra-ductal papillary neoplasia or biliary papillomatosis is also a precancerous lesion.

Chronic inflammatory bowel disease (ulcerative colitis), primary sclerosing cholangitis, gall stones and choledochal cysts all show an increased incidence. Radiologically it can be difficult to distinguish between primary sclerosing cholangitis and a stenotic carcinoma.

Epithelium

Subepithelial connective tissue

Fibromuscular layer

Perifibromuscular connective tissue

Epithelium

Subepithelial connective tissue

Fibromuscular layer

Perifibromuscular connective tissue

Adjacent structures pTI : confined to the bile duct wall (mucous membrane plus muscularis) pI2: beyond the bile duct wall Figure 9.2. Extrahepatic bile duct carcinoma.

liver,gall bladder, pancreas and/or unilateral portal vein or hepatic artery main portal vein or its bilateral tributaries, common hepatic artery, or colon, stomach, duodenum, abdominal wall n >

Immunophenotype

Markers (e.g. cytokeratins, CEA) may be helpful in identifying poorly differentiated single-cell infiltration on biopsy: other markers of bile duct carcinoma are cytokeratins 7 and 19, EMA and CA19-9. There is also overexpression of p53 in contradistinction to normal duct structures. Perineural invasion can point to a diagnosis of malignancy

Prognosis

Prognosis is worse for carcinoma of the upper third and hilum which is diffuse and/or multifocal. Distal lesions that are polypoid or nodular are potentially resectable with better prognosis. Despite being a sclerotic, diffuse tumour, hilar Klatskin lesions have a well-differentiated morphology and indolent time course. Prognosis of bile duct carcinoma is poor with most patients dead within 2-3 years. It relates to tumour location, stage, histological type and grade. Overall survival is 10% with 25% for lesions of the distal third and resectable lesions with negative margins. This can improve to 50-80% 5-year survival if the tumour is ampullary and of early stage (pT1: limited to the sphincter of Oddi). Treatment for proximal lesions (not as high as the hilar plate) is resection (±hepatic lobectomy) with hepatojejunostomy; a Whipple's procedure is indicated for distal lesions. Palliative treatment can involve biliary drainage, stenting or radiotherapy.

9. OTHER MALIGNANCY

Lymphoma/leukaemia

— secondary to systemic/nodal disease.

Sarcoma

— embryonal (botryoid) rhabdomyosarcoma in children with direct invasion of abdominal structures, metastases to bone and lungs and poor prognosis. Desmin/myo D1/myogenin positive small cells, subepithelial cellular cambium layer, deeper myxoid zone.

— leiomyosarcoma, angiosarcoma.

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