tumors of liver

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CLASSIFICATION OF TUMORS OF THE LIVER: I. Primary Tumors of the liver A.Benign tumors of the liver 1.Hepatic Adenoma 2.Cavernous hemangiomas B. Malingnant Tumors of the liver 3.Hepatocellular carcinoma ( HCC ) 4.Hepatoblastoma 5.Cholangiocarcinoma a) Intra Hepatic CCA b) Extra Hepatic CCA

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Page 1: Tumors of Liver

CLASSIFICATION OF TUMORS OF THE LIVER:I. Primary Tumors of the liver

A. Benign tumors of the liver 1. Hepatic Adenoma2. Cavernous hemangiomas

B. Malingnant Tumors of the liver 3. Hepatocellular carcinoma ( HCC ) 4. Hepatoblastoma5. Cholangiocarcinoma

a) Intra Hepatic CCA b) Extra Hepatic CCA

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II . METASTATIC TUMORS Common metastatic tumors are notably arising from:

a. Breast b. Colon c. Lungs d. Leukemias e. Lymphomas f. Melanomas g. Pancreas

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HEPATOBLASTOMA

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Hepatoblastoma

• Most common primary hepatic tumour, 0.5% of all pediatric tumors

• 90% less than 5 years age• Male predominance: 2:1• Fatal if left untreated• 5% assoc congenital abnormality• High AFP levels• Trisomy 2,8,20

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MorphologyGROSS:• Tan-green, solitary mass, smooth/lobulated,

solid/cystic• Right lobe, 3-20 cm• Epithelial: soft, fleshy• Mesenchymal: Firm and calcified

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Microscopic1. The epithelial type : – Small polygonal fetal cells

or smaller embryonal cells forming acini, tubules and papillary structures for the development of liver

2. The mixed epithelial and mesenchymal type : • Foci of mesenchymal

differentiating type - primitive mesenchyme osteoid, cartilage and striated muscle

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HEPATOCELLULAR CARCINOMA

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• ~ 90% of all primary hepatic malignancies• Eighth most prevalent worldwide• Male to female ratio is 3:1 to 6:1• Age• Pathogenesis– Any condition associated with chronic hepatic

injury– Results in hepatocyte hyperplasia, increased

susceptibility to carcinogens and greater risk of chromosomal damage

– Two pathways: Chromosomal stability pathways (β Catenin & 8p losses) and chr instability pathway (HBV)

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• 76% of HCC in Asia, followed by Africa

• Countries with high rates of chronic HBV infection

• Vertical transmission of HBV from mother to child, 200 fold increase for development of HCC by adulthood

• Aflatoxins in diet- derived from fungus aspergillus flavus

• Other pre disposing factors- cirrhosis, liver cell dysplasia, tyrosynemia, schistosomiasis

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Clinical findings

• Pain, fullness, mass or related to cirrhosis

• Rarely metastatic at initial presentation

• Screening of patients with CLD– USG– Serum AFP levels (>10-20 ng/ml)– Higher in HBV and HCV related

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Small HCC

GROSS• < 2 cm, Nodule with distinct or indistinct capsule• Bulge from liver surface, greenish, yellow

MICROSCOPY• <1 cm, WD-HCC, thin trabeculae (3 cell thick),

little atypia • Nuclear density greater than twice normal, mild

but definite nuclear atypia

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Advanced HCC

Gross appearance

– In normal liver as homogenous mass, occasionally with satellite nodules (Massive or expanding type)

–Nodular type or multiple small nodules – Diffuse type

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MICROSCOPY:

• Appearance of tumor cells resembling hepatocytes typically arranged as trabeculae (at least focally) outlined by sinusoids

• 4 architectural patterns:– Trabecular, solid, acinar, scirrhous

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Grading of HCCEdmondson & SteinerWHO:• Well Diff (I/II): – Thin plates three or less cells thick, smaller than normal

hepatocytes, mild nuclear atypia, increased Nuclear density

• Mod Diff (II/III): – > three cell thick, large cells , abundant eosiniphilic

cytoplasm, prominent nucleoli

• Poorly Diff (III/IV): – Solid growth pattern, pleomorphism, spindled or small cell

areas

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• IHC- AFP, Cam 5.2(keratins 8,18,19),EMA

• The better differentiated the tumor , the more difficult the diagnosis on morphology

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