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MIT HST 121 - The Normal Liver

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The Normal Liver • Acinar/lobular architecture • Portal tracts • Hepatic plates & sinusoids • Central veins Harvard-MIT Division of Health Sciences and Technology HST.121: Gastroenterology, Fall 2005 Instructors: Dr. Jonathan GlickmanNormal liver architecture Figure removed due to copyright reasons.Histologic Types of Liver Injury • Necrosis • Hepatocyte degeneration/regeneration • Hepatitis (acute and chronic) • Steatosis (fatty change)/steatohepatitis • Cholestasis (bile accumulation) • Fibrosis and cirrhosisChronic Hepatitis Key Histologic Features • Portal tract mononuclear inflammation • Periportal activity – Extension beyond limiting plate (“piecemeal necrosis”) • Lobular Activity – Lobular mononuclear inflammation – Lobular hepatocyte necrosis • Fibrosis, CirrhosisAcute vs. Chronic Viral Hepatitis Acute Chronic Causes Inflamm-distrib Inflamm-cells Necrosis Sequelae HAV,HBV,HCV HBV,HCV Lobular Portal+lobular Lymphocytes Lymphocytes Macrophages Plasma cells + - +++ -/+ Resolution Chronic carrier Chronic hepatitis Cirrhosis Post-hepatitic scarringChronic Hepatitis- Etiologies •Viral – Hepatitis B,C • Autoimmune – Autoimmune hepatitis – Primary biliary cirrhosis • Drug reaction • Others (Wilson’s disease, lymphoma)Autoimmune hepatitis • Clinical: F>M, young-midage, abrupt or insidious onset, relapsing course; liver only or a/w systemic auoimmune phenomena • Labs: ↑transaminases; +ANA (type I), +α− LKM (type II), +α-SLA (type III) • Histology: – chronic hepatitis with marked piecemeal necrosis, lobular involvement – numerous plasma cellsPrimary Biliary Cirrhosis • Clinical: middle age, F>>M; insidious onset – a/w other autoimmune syndromes • Labs: inc. AP, +AMA • Histologic stages: –I. Florid duct lesion: BD damage, granulomas –II. Ductular proliferation, periportal hepatitis – III. Scarring and fibrosis –IV. CirrhosisChronic Hepatitis -Differential Diagnosis HCV AIH PBC Portal Inflamm. Piecemeal Necrosis Lobular Inflamm Plasma Cells BD Damage/Loss BD Proliferation Granulomas ++ + ++ ++ +++ + +/-+ +/-+ -/+ + -- -++ +++ ++ +++ +++ ++Cholestasis Definition: Accumulation of bile in hepatic tissue Etiologies: • Bile duct obstruction • Drug reaction •Sepsis • Acute viral hepatitis • Graft-versus-host disease • Other (cholestatic syndromes): – Cholestasis of pregnancy, benign recurrent cholestasisCholestasis-pathology Acute-Subacute • Bile accumulation – canalicular, centrilobular – (late) bile lakes • Hepatocyte “feathery” degeneration • Portal tract inflammation (PMNs) • Bile duct proliferation Chronic •FibrosisPrimary Sclerosing Cholangitis • Clinical: adults, M≈F, a/w ulcerative colitis jaundice, pruritus, RUQ pain · Radiology: Strictures (“beading”) of bile ducts · Histology: · Periductular concentric fibrosis · Bile duct inflammation, proliferation, and loss · Parenchyma: cholestasis · Progression: fibrosis, cirrhosisDrug-induced Liver Disease Microsteatosis Macrosteatosis Cholestasis Necrosis Hepatitis Granulomas Fibrosis/cirrhosis Venous occlusion Tetracycline, salicylates EtOH, methotrexate Cyclosporine, OCS Acetominophen Isoniazid, phenytoin Allopurinol, sulfonamides EtOH, methotrexate, amiodarone Cytotoxic chemotherapySteatosis- Etiologies • Microvesicular – Reyes Syndrome – Drug reactions (e.g. tetracycline) – Fatty liver of pregnancy •Macrovesicular – Alcohol – Drug reaction (e.g. steroids) – Others (obesity, diabetes, malnutrition)Cirrhosis-etiologies • Alcohol (60-70%) • Chronic viral hepatitis (10-20%) • Biliary (5-10%) – Primary biliary cirrhosis – Secondary (i.e.chronic biliary obstruction) • Metabolic (5%) – Hemochromatosis, Wilson’s disease −α1-antitrypsin deficiency • Cryptogenic (10-15%)Cirrhosis- assessment of cause • Pattern of nodules and fibrosis • Bile ducts • Blood vessels • Steatohepatitis? • Pattern of hepatitis • Abnormal depositsWilson’s disease • Autosomal recessive disorder of copper overload • Incidence 1:30,000 • Age of onset: 3-40 years • Molecular defect: – ATP7B gene, 13q12 – membrane ATPase with copper-binding domains – missense mutations in ATP-binding domainWilson’s disease- hepatic pathology • Early (precirrhotic): – chronic hepatitis, steatosis – balooning, Mallory bodies , apoptotic bodies – glycogenated nuclei – Cu stain may be negative • Fulminant hepatic failure • Late (cirrhotic)Hepatocellular Neoplasms and Masses With cirrhosis Without cirrhosis • Macroregenerative Nodule • Borderline (dysplastic) Nodule • Hepatocellular Carcinoma • Hepatic adenoma • Focal nodular hyperplasia • Fibrolamellar HCC • HCC • Nodular regenerative hyperplasiaHepatic malignancies • Overall, metastases most common Primary Hepatic malignancies • Hepatocellular CA 65-70% • Intrahepatic cholangioCA 20% • HCC-cholangioCA 2% • Sarcomas, lymphoma, other 2-3%HCCa vs regenerative nodule Feature HCC Regen nodule Plates>2 cells thick ++ -Small cell change ++ -/+ Portal tracts - + Infiltrative edge +/- -Fibrolamellar HCC • young adults, M=F •Low association with cirrhosis (<10%), HBV, HCV •Gross: Firm circumscribed mass, central fibrous septa •Micro: Nests, cords of eosinophilic tumor cells Lamellar bands of colagen surrounding tumor cells • Prognosis: slow growing, resected 5 year suvival 40-50% •Ddx: FNH, HCC, metastatic


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MIT HST 121 - The Normal Liver

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