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Liver 3
 

Liver 3

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    Liver 3 Liver 3 Presentation Transcript

    • Title : LiverObjectives : to1. Describe α1- Anti trypsin deficiency disorder.2. Explain intrahepatic biliary tract diseases.3. Identify benign tumors of liver.4. Study malignant tumors of liver.5. Out line metastatic tumors to liver.
    • α1-ANTITRYPSIN DEFICIENCY : Autosomal-recessive disorder. Low serum levels of protease inhibitor(α1-antitrypsin). Leads to pulmonary emphysema and liver diseases. Gene which located on chromosome 14is very polymorphic (75 forms identified). Most common genotype is PiMM ( 90% of individuals). Most common mutation (homozygotes PiZZ) withcirculating α1-antitrypsin level only 10% of normal.
    • Morphology:round-to-oval cytoplasmic inclusionsin hepatocytes which are acidophilic inH &E stains, and strongly PAS-positive.Clinical Features:• Neonatal hepatitis with cholestatic jaundice .• In adolescence: hepatitis or cirrhosis.• Disease may remain silent until cirrhosis appearsin middle to later life.• Hepatocellular carcinoma in 2% to 3% of PiZZ adults,usually in setting of cirrhosis.
    • Intrahepatic Biliary Tract DiseaseSecondary Biliary Cirrhosis :Etiology: Extrahepatic bile duct obstruction by:-• biliary atresia.• Gallstones.• Stricture.• carcinoma of pancreatic head.Sex predilection: None.Symptoms and signs:Pruritus, jaundice, malaise, dark urine, light stools ,and hepatosplenomegaly.
    • Lab. findings:• Conjugated hyperbilirubinemia.• increased serum level of : alkaline phosphatase,bile acids, and cholesterol.Morpholgy:• Prominent bile stasis in bile ducts.• bile ductular proliferation with surrounding neutrophils.• portal tract edema.Secondary biliary cirrhosis ischaracterized by regenerationnodules, surrounded byfibrous septa. biliary ducts( proliferated or distended ).
    • Primary Biliary Cirrhosis:Etiology: autoimmune, 90% of patients havecirculating antimitochrondrial antibodies .Sex predilection: Female to male: 6:1Symptoms and signs: Same assecondary biliary cirrhosis ; insidious onset.Lab. findings: Same as secondary biliary cirrhosis,plus elevated serum IgM autoantibodies( M2 form of antimitochondrial antibody-AMA).Morphology:• Dense lymphocytic infiltrate in portal tracts.• granulomatous destruction of bile ducts.
    • PRIMARY BILIARY CIRRHOSIS: This imageshows dense lymphoid infiltrate in a portaltract . This stage is also known as “floridduct lesion”Liver, primary biliary cirrhosis:non-necrotizing granuloma
    • Primary Sclerosing Cholangitis:Etiology: Unknown, possibly autoimmune;50–70% have inflammatory bowel disease.Sex predilection: Female to male: 1:2Symptoms and signs: Same assecondary biliary cirrhosis; insidious onset.Lab. findings: Same as secondary biliary cirrhosis,plus elevated serum IgM.Morphology : concentric Periductal portaltract fibrosis(onion-skin fibrosis) segmental stenosis ofextrahepatic and intrahepaticbile ducts.
    • BENIGN NEOPLASMS :Cavernous hemangiomas : Blood vessel tumors. Red -blue soft nodules, less than 2 cm. Often occur directly beneath the capsule. Not be mistaken for metastatic tumors. Blind percutaneous biopsies not be performed on them.
    • Liver cell adenomas: Benign neoplasms developing from hepatocytes. Occur in young women who used oral contraceptivesand regress on discontinuance of their use. When present as intrahepatic mass, may be mistakenfor hepatocellular carcinoma. Subcapsular adenomas have tendency to rupture. Rarely, may harbor hepatocellular carcinoma.
    • Morphology:Grossly:• Yellow-tan bile-stained nodules, often presentbeneath capsule.• Usually well demarcated, encapsulationmight not be present.Microscopically :• Sheets and cords of cells that may resemble normalhepatocytes or have some variation in cell and nuclear size.• Abundant glycogen generate a clear cytoplasm.• Portal tracts are absent.
    • MALIGNANT TUMORS:Hepatoblastoma : Most common liver tumor of young childhood. Usually fatal within few years if not resected. Has two variants:o Epithelial type:composed of small polygonal fetal cells forming acini,tubules, or papillary structures resembling liver development.o Mixed epithelial and mesenchymal type:contains foci of mesenchymal differentiation thatmay consist of primitive mesenchyme, osteoid, cartilage,or striated muscle.
    • Hepatoblastoma revealing thepresence of embryonal epithelial cellsarranged in sheets.Mesenchymal component including osteoidmaterial in mixed type hepatoblastoma
    • Angiosarcoma : Resembles those occurring elsewhere. Its association with exposure to vinyl chloride,arsenic, or Thorotrast (formerly used in radiography). Latency period after exposure may be several decades. Highly aggressive neoplasms metastasize widelyand generally kill within a year.
    • Hepatocellular Carcinomas : Constitute 5.4% of all cancers in human. Blacks affected threefold higher than others . Male predominance . Three major etiologic associations :-1- viral infection (HBV, HCV).2- chronic alcoholism .3- food contaminants ( aflatoxins ).Others include : tyrosinemia and hereditaryhemochromatosis.
    • Morphology:Grossly:(1) unifocal (usually large) mass.(2) multifocal nodules of variable size.(3) diffusely infiltrative cancer.Microscopically: Range from well-differentiated to highly anaplasticundifferentiated lesions. In well-differentiated and moderately differentiated tumors,cells are disposed either in trabecular pattern(recapitulating liver cell plates) or in acinar pattern . In poorly differentiated forms, tumor cells arepleomorphic with numerous anaplastic giant cells.
    • H.C.C- acinar and trabecular patterns Poorly differentiated H.C.C
    • Fibrolamellar carcinoma: Variant of hepatocellular carcinoma. Occurs in young male and female (20 to 40 years )with equal incidence. No association with HBV or cirrhosis risk factors,and has better prognosis. Grossly: Presents as single large hard "scirrhous" tumorwith fibrous bands coursing through it.
    •  Microscopically: composed of well-differentiatedpolygonal cells growing in nests or cords and separatedby parallel lamellae of dense collagen bundles .
    • Clinical Features of H.C.C: Upper abdominal pain. Malaise, fatigue, weight loss. abdominal mass or abdominal fullness. Jaundice, fever, and esophageal variceal bleeding.Lab. studies: Elevated levels of serum α-fetoprotein (in 50% to 75%of patients ). False -positive results: in yolk-sac tumors andnon-neoplastic conditions( cirrhosis, massive liver necrosis,chronic hepatitis, and normal pregnancy). Radiologic studies: US, hepatic angiography , CT scan,and MRI.
    • Prognosis: Hematogenous metastases: especially to lung,occur late in disease. Lymph node metastases: to perihilar, peripancreatic,and para-aortic nodes in less than half of cases. Death occurs from:(1) cachexia(2) GIT or esophageal variceal bleeding.(3) liver failure with hepatic coma.(4) rarely, rupture of tumor with fatal hemorrhage. Fibrolamellar variant has favorable outlook.
    • Metastatic Tumors: More common than primary neoplasia. Most common primaries: breast, lung, and colon. Metastasis may be present in absence of clinical orlab. evidence of hepatic functional insufficiency. However, with massive destruction of liver substanceor direct obstruction of major bile ducts, jaundiceand elevations of liver enzymes may appear.
    • Summary:1. α1- antitrypsin deficiency is a metabolic liver disease.2. Intrahepatic biliary tract diseases : primary andsecondary biliary cirrhosis, and primary sclerosingcholangitis.3. Benign tumors of liver: cavernous hemangioma, andliver cell adenomas.4. Malignant tumors : Hepatoblastoma, Angiosarcoma,and H.C.C.5. Metastatic tumors to liver are more common thanprimary neoplasia.
    • Questions:1. Mention morphological changes of hepatocellularcarcinoma?2. Write short assay on primary biliary cirrhosis?THANK YOU