LIVER

DR MAX G.M. HOVE

HISTOPATHOLOGY & CLINICAL PATHOLOGY
ANOMALIES OF THE BILIARY TRACT

VON MEYENBURG COMPLEXES (BILE DUCT

HARMATOMAS)
POLYCYSTIC LIVER DISEASE - BILIARY EPITHELIUM
LINED CYSTIC LESIONS ASSOCIATED WITH
POLYCYSTIC KIDNEY DISEASE
CONGENITAL HEPATIC FIBROSIS - INCOMPLETE
INVOLUTION OF EMBRYONIC DUCTAL STRUCTURES
CAROLIS DISEASE - DILATED LARGER INTRAHEPATIC
DUCTS
LIVER

MORPHOLOGIC PATTERNS OF HEPATIC INJURY-

RESPONSES
NECROSIS OR APOPTOSIS
DENEGERATION - SWELLING AND EDEMA
INFLAMMATION - HEPATITIS
REGENERATION - HEPATOCYTE NODULES
FIBROSIS - LEADS TO CIRRHOSIS
COMMON CAUSES OF CIRRHOSIS

ALCOHOLIC LIVER DISEASE

VIRAL HEPATITIS
BILIARY DISEASE
PRIMARY HEMACHROMATOSIS
WILSON DISEASE
ALPHA-1- ANTITRYPSIN
CRYPTOGENIC CIRRHOSIS
EXTRAHEPATIC BILIARY TRACT DISEASE

SECONDARY BILIARY DISEASE

COMMON CAUSES:
- CHOLELITHIASIS
- BILIARY ATRESIA
- MALIGNANCY - BILIARY TRACT
- HEAD OF PANCREAS
- STRICTURES
CIRRHOSIS - PATHOGENESIS

INTERSTITIAL COLLAGEN (TYPE I & III) IS NORMALLY

IN PORTAL TRACTS, AROUND CENTRAL VEINS AND
OCCASIONALLY IN SPACE OF DISSE.
IN CIRRHOSIS TYPE I & III COLLAGEN IS DEPOSITED
IN ALL PORTIONS OF LOBULE
ITO CELLS ARE MAJOR SOURCE OF EXCESS COLLGEN
ITO CELLS ARE NORMALLY VITAMIN A FAT-STORAGE
CELLS
CIRRHOSIS - PATHOGENESIS

ITO CELLS MAY BECOME ACTIVATED AND

TRANSFORM INTO MYOFIBROBLASTS - LIKE CELLS
COLLAGEN SYNTHESIS IS STIMULATED BY:
INFLAMMATORY CONDITIONS WITH CYTOKINES
CYTOKINE RELEASE BY KUPFFER CELLS
DISRUPTION OF NORMAL EXTRACELLULAR MATRIX
DIRECT TOXIC STIMULATION OF COLLAGEN
SYNTHESIS
PRIMARY BILIARY CIRRHOSIS (PBC)

A CHRONIC PROGRESSIVE CHOLESTATIC LIVER

DISEASE CHARACTERISED BY DESTRUCTION OF
INTRAHEPATIC BILE DUCTS, PORTAL
INFLAMMATION, SCARRING AND CIRRHOSIS.
A DISEASE OF MIDDLE AGED WOMEN
SERUM ANTIMITOCHONDRIAL ANTIBODIES
POSITIVE IN 90%
PRIMARY BILIARY CIRRHOSIS (PBC)

MORPHOLOGY
PORTAL TRACT LESION - DESTRUCTION AND
GRANULOMATOUS INFLAMMATION OF
INTERLOBULAR AND SEPTAL BILE DUCTS
PROGRESSIVE LESION - GLOBAL INVOLVEMENT OF
HEPATIC PORTAL TRACTS
END STAGE-INDISTINGUISHABLE FROM OTHER
CAUSES
PRIMARY SCLEROSING CHOLANGITIS (PSC)

CHRONIC PROGRESSIVE CHOLESTATIC LIVER

DISEASE, CHARACTERISED BY INFLAMMATION,
OBLITERATIVE FIBROSIS AND SEGMENTAL
DILATATION OF INTRAHEPATIC AND EXTRAHEPATIC
BILE DUCT
ASSOCIATED WITH ULCERATIVE COLITIS
MOST COMMON IN MIDDLE AGED MEN
ANTIMITOCHONDRIAL ANTIBODIES ARE ABSENT
PRIMARY SCLEROSING CHOLANGITIS (PSC)

SEGMENTAL INFLAMMATION
CONCENTRIC FIBROSIS AROUND BILE DUCTS
PROGRESSIVE ATROPHY AND OBLITERATION OF
BILE DUCTS
RESULTS IN CIRRHOSIS
TUMOURS AND TUMOROUS
CONDITIONS

NODULAR HYPERPLASIA
BENIGN HEPATOCELLULAR NODULES
A RESULT OF FOCAL OBLITERATION OF HEPATIC
VASCULATURE WITH COMPENSATORY LOBULAR
HYPERTROPHY
FOCAL NODULAR HYPERPLASIS (FNH)- WITHSCAR
NODULAR REGENERATIVE HYPERPLASIA
HEPATIC ADENOMA

BENIGN HEPATOCYTES NEOPLASM UP TO 30CM IN

FEMALES
ASSOCIATED WITH ORAL CONTRACEPTIVES
MAY RUPTURE AND CAUSE HEMOPERITONEUM
PORTAL TRACTS WITH BILE DUCTS ARE ABSENT
MALIGNANT TUMORS

MAJORITY ARE METASTATIC

PRIMARY
- HEPATOCELLULAR CARCINOMA
- HEPATOBLASTOMA
- ANGISARCOMA (VINYL
CHLORIDE, ARSENIC,
THOROTRAST)
HEPATOCELLULAR CARCINOMA (HCC)

ASSOCIATED HBV AND HCV

OTHER CAUSES:
- CIRRHOSIS
- CARCINOGENS: AFLATOXIN,
THOROTRAST
FIBROLAMELLAR VARIANT OF HCC

NO IDENTIFIED RISK FACTORS

OCCURS IN CHILDREN, ADOLESCENCE, YOUNG
ADULT
MORE RESECTABLE
60% - 5 YEAR SURVIVAL
PROMINENT FIBROUS BANDS
TRABECULAE OF LARGE, EOSINOPHILIC,
POLYGONAL HEPATOCYTES
CHOLAGIOCARCINOMA

ARISES FROM ELEMENTS OF INTRAHEPATIC BILIARY

TRACT
ASSOCIATED WITH THOROTRAST, CLONORCHIS
SINESIS AND CAROLIS DISEASE
TYPICALLY PALE - NOT BILE PRODUCING
EXTENSIVE DESMOPLASTIC REACTION AND MUCIN
PRODUCTION