آزمايشگاه رز - Ackerman Atlas(chaptr19)

Liver Non-neoplastic

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Figure 19.1 Lipofuscin appears as a finely granular brown pigment within hepatocytes, most prominent in zone 3

Figure 19.2 "Surgical hepatitis" features a neutrophilic infiltrate associated with necrosis of single hepatocytes or small groups of hepatocytes

Figure 19.3 Acute hepatitis B infection characterized by ballooning of hepatocytes, lobular disarray, and mononuclear (mainly lymphocytic) inflammatory infiltration

Figure 19.4 Acute viral hepatitis with scattered apoptotic hepatocytes (arrow) and cholestasis

Figure 19.5 Severe Necrotizing Acute Viral Hepatitis B. There is mild to moderate mononuclear cell infiltration in portal tracts, as well as bridging portal-central confluent lytic necrosis with parenchymal loss

Figure 19.6 Fibrosing Cholestatic Hepatitis C. A, Fibrous expansion of portal areas with marked ductular reaction. There is mild hepatocyte ballooning and hepatocellular cholestasis. B, Cytokeratin 7 immunostain highlights the ductular reaction

Figure 19.7 Bridging confluent lytic necrosis in severe chronic viral hepatitis B, connecting an inflamed portal tract with a centrilobular area (lower left). The upper right part corresponds to an area of extensive lytic necrosis and postnecrotic collapse of the reticulin framework

Figure 19.8 Severe Chronic Viral Hepatitis B. Several small islands of surviving hepatocytes, appearing swollen and pale, and sometimes arranged in tubular fashion ("hepatitic-type liver cell rosettes"), are present within an area of postnecrotic collapse and early fibrosis

Figure 19.9 Marked interface hepatitis ("piecemeal necrosis") in chronic viral hepatitis B. Note the inflamed portal tract (upper right) with an irregular interface between the portal periphery and adjacent parenchyma

Figure 19.10 A, Ground-glass hepatocytes, characterized by eosinophilic, homogeneous and paler cytoplasm than surrounding normal hepatocytes. B, Note the artifactual cleft between the ground-glass cytoplasm and the hepatocellular cell membrane

Figure 19.11 Chronic Viral Hepatitis B, Viral Replicative Phase. Hepatitis B core antigen is localized in hepatocellular nuclei and, in several hepatocytes, also in the cytoplasm and cell membrane. (Immunoperoxidase stain for HBcAg.)

Figure 19.12 Chronic Viral Hepatitis B, Viral Replicative Phase. Hepatitis B surface antigen is localized in variable quantities in the cytoplasm and in the cell membrane of several hepatocytes. Note there is only a mild lymphocytic infiltrate in the portal tract and lobule. (Immu- noperoxidase stain for HBsAg.)

Figure 19.13 Chronic Viral Hepatitis B, Viral Nonreplicative (Integra- tion) Phase. Hepatitis B surface antigen is localized in considerable quantity in the cytoplasm of a contiguous group ("clone") of hepatocytes. Note the relatively mild lymphocytic infiltrate in the portal tract and lobule. The more intensely staining cells appear as "ground-glass hepatocytes" on H&E staining. (Immunoperoxidase stain for HBsAg.)

Figure 19.14 Chronic Viral Hepatitis C. Low-power view of two portal tracts connected by bridging fibrosis, with dense mononuclear cell infil- tration and a prominent lymphoid aggregate. The portal-parenchymal interface is irregular due to interface hepatitis. Minimal steatosis is also present

Figure 19.15 Chronic Viral Hepatitis C. Detail of a portal tract showing a lymphoid follicle containing an irregular and damaged bile duct near its center. Note the biliary epithelial irregularity and intramural lymphocytic infiltrate

Figure 19.16 Chronic viral hepatitis C showing moderate to marked steatosis in addition to portal inflammation and mild interface hepatitis

Figure 19.17 A, A poorly formed basophilic, granular CMV inclusion is present within an endothelial cell (arrow) in the sinusoids. There is sur- rounding patchy inflammation and scattered apoptotic hepatocytes. B, Several "owl's-eye" inclusions are seen within biliary epithelial cells (arrow)

Figure 19.18 EBV hepatitis showing dense lymphocytic portal infiltrates, and a sinusoidal lymphocytosis in a "string of beads" configuration

Figure 19.19 Mycobacterium Avium-Intracellulare Complex in the Liver. A, A foamy macrophage infiltrate with virtually no other atten- dant inflammation. B, Ziehl-Neelsen stain highlights organisms within macrophages

Figure 19.20 Foamy cytoplasmic vacuoles, ballooning, and numerous Mallory-Denk bodies characterize amiodarone toxicity

Figure 19.21 Hypervitaminosis A. Increased numbers of enlarged hepatic stellate cells (arrows) with clear cytoplasm and delicate cytoplasmic processes

Figure 19.22 Canalicular cholestasis with bile plugs (arrows) and minimal associated inflammation in this cholestatic drug reaction secondary to antibiotics

Figure 19.23 A, Centrilobular necrosis with minimal attendant inflammation in acetaminophen toxicity. Reactive binucleated hepatocytes are also present. B, Acute drug-induced liver injury featuring lobular inflammation, prominent Kupffer cells forming small clusters, and apoptotic hepatocytes (arrow). Fibrosis is absent by definition

Figure 19.24 A, Fat and abundant Mallory-Denk bodies in amiodarone toxicity. B, Steatosis, reactive hepatocellular changes, and stellate cell hyperplasia secondary to HAART therapy

Figure 19.25 A, Lymphocytic cholangitis and interlobular bile duct damage associated with Bactrim use. B, Neutrophilic cholangitis and interlobular bile duct damage (arrow) secondary to the anti-hypertensive lisinopril. This would be difficult to distinguish from large bile duct obstruction. C, Vanishing bile duct syndrome leading to biliary cirrhosis and liver transplant secondary to antibiotic administration

Figure 19.26 A, Noncaseating epithelioid granuloma in a portal tract, secondary to allopurinol. B, Loosely formed granuloma with numerous associated eosinophils from an adverse reaction to echinacea tea

Figure 19.27 TPN-associated injury in an infant featuring ductular and canalicular cholestasis, marked ductular reaction, portal inflammation, and reactive hepatocellular changes

Figure 19.28 Macrovesicular steatosis featuring large droplets of fat

Figure 19.29 Accumulation of Tiny Lipid Droplets in Microvesicular Steatosis

Figure 19.30 Lipogranuloma featuring adipocytes mixed with lymphocytes and macrophages. (Courtesy Dr. Joe Misdraji.)

Figure 19.31 A, Alcoholic liver disease featuring marked hepatocyte ballooning, a neutrophilic infiltrate, and Mallory-Denk bodies. Steatosis is minimal in this case. B, Steatosis with well-developed ballooning and "satellitosis" of neutrophils around apoptotic hepatocytes (arrow). C, Higher power view of Mallory-Denk bodies (arrows)

Figure 19.32 Mixed Macrovesicular and Microvesicular Steatosis

Figure 19.33 A, Pericellular or "chicken-wire" fibrosis ensheaths individual hepatocytes and small groups of hepatocytes, many of which show ballooning (Trichrome stain). B, Severe pericellular fibrosis in a case of sclerosing hyaline necrosis

Figure 19.34 A markedly enlarged, pale yellow liver with micronodular cirrhosis from the autopsy of a patient with alcoholic liver disease. (Courtesy Dr. George F. Gray, Jr.)

Figure 19.35 Non-alcoholic Fatty Liver Disease. A, Centrilobular area with predominantly macrovesicular steatosis and foci of inflammation. B, Higher power view shows numerous glycogenated nuclei, a common finding. (A, Courtesy International Liver Pathology Study Group [Gnomes].)

Figure 19.36 Non-Alcoholic Steatohepatitis. Centrilobular parenchyma with steatosis, hepatocellular ballooning, Mallory-Denk bodies, and inflammation. (Courtesy International Liver Pathology Study Group [Gnomes].)

Figure 19.37 Glycogenic hepatopathy featuring enlarged, markedly pale, swollen hepatocytes due to glycogen accumulation

Figure 19.38 Marked bilirubinostasis in hepatocytes and bile canaliculi, leading to bile plugs in the latter (arrows)

Figure 19.39 Erythropoietic Protoporphyria. A, Dark brownish-black deposits of protoporphyrin in hepatocytes, canaliculi, Kupffer cells, and ductules. B, The deposits are birefringent under polarized light, and show a Maltese cross configuration of red birefringence in the larger deposits

Figure 19.40 Cholate stasis in periphery of parenchymal nodule in cirrhotic liver of patient with end-stage primary sclerosing cholangitis. The hepatocytes near the fibrous septum (lower part) show hydropic swelling, clumping of the cytoplasm, and Mallory bodies

Figure 19.41 A, Cholate stasis in chronic cholestatic liver disease. The picture shows orcein-positive granules in periportal hepatocytes, represent- ing lysosomal localization of copper binding protein (metallothionein). B, Lysosomal copper-metallothionein complexes appear as red-stained granules in the copper-specific rhodanine stain

Figure 19.42 Keratin 7 immunostain highlights an increase in the number of ductular structures at the portal tract periphery; expression of keratin 7 in periportal hepatocytes is an indicator of early cholate stasis. A few scattered, small keratin 7 positive cells at some distance from the portal tract are presumed hepatic progenitor cells

Figure 19.43 Cholestatic Liver Cell Rosettes. A, Liver biopsy of patient with primary sclerosing cholangitis. The involved hepatocytes form small tubules or rosettes. B, Immunostaining for keratin 7. Normal hepatocytes do not express keratin 7, whereas cells in cholestatic rosettes express this intermediate filament to variable extent

Figure 19.44 Ductular Reaction in Chronic Cholestasis. Liver biopsy from a patient with primary sclerosing cholangitis. The picture shows a mildly inflamed portal tract with ductular reaction at the periphery

Figure 19.45 Ductular bilirubinostasis featuring markedly dilated ductules filled with bile concrements

Figure 19.46 A portal tract in primary biliary cirrhosis contains a nodular mixed inflammatory infiltrate consisting of lymphocytes, plasma cells, numerous eosinophils, and histiocytes. There is a damaged bile duct in the center of the portal tract

Figure 19.47 Florid Duct Lesion in Primary Biliary Cirrhosis. A loose portal granuloma with admixed lymphocytes and plasma cells is centered on a damaged duct that is infiltrated by lymphocytes and shows marked epithelial disarray

Figure 19.48 Biliary-type cirrhosis in primary biliary cirrhosis, featuring irregular cirrhotic nodules, lymphocytic interface hepatitis, and ductopenia

Figure 19.49 A, Primary sclerosing cholangitis showing a damaged bile duct with surrounding edema, concentric fibrosis, and lymphoplasmacytic inflammation. B, Detail of portal tract with moderately dense inflammatory infiltrate (mainly lymphocytes, some eosinophils) and concentric, lamellated, periductal fibrosis ("onion skin" fibrosis) around the interlobular bile duct

Figure 19.50 Primary sclerosing cholangitis featuring nonspecific ductular reaction, changes of chronic cholestasis, and a markedly atrophic duct (arrow). Inflammation is minimal

Figure 19.51 Primary Sclerosing Cholangitis. Overview of portal tract and periportal parenchyma. This portal tract shows only mild inflammation; two interlobular bile ducts show clear-cut thickening of their basement membrane on PAS/diastase, a helpful diagnostic feature

Figure 19.52 IgG4-associated sclerosing cholangitis featuring marked periductal lymphoplasmacytic inflammation and surrounding storiform fibrosis in a large intrahepatic bile duct

Figure 19.53 Extrahepatic large bile duct obstruction featuring portal edema, a mixed portal inflammatory infiltrate, and ductular reaction with admixed neutrophils

Figure 19.54 Autoimmune Hepatitis. A, Needle biopsy showing lobular disarray, feathery cytoplasmic degeneration, and a hepatocyte rosette (arrow). B, Broad zones of bridging necrosis with parenchymal collapse. Note the prominent plasma cells. C, Portal tract with lymphoplasmacytic inflammation and interface activity. Bile ducts show reactive changes and are focally infiltrated by inflammatory cells

Figure 19.55 Detail from micronodular cirrhosis, reticulin stain

Figure 19.56 Detail from macronodular cirrhosis, reticulin stain. Note larger nodules, thin, fibrous septa, and irregular orientation of liver cell plates

Figure 19.57 "Incomplete septal-type" cirrhosis can be considered a macronodular variety of cirrhosis with large multilobular nodules, thin, incomplete septa, and little inflammatory activity (Sirius red stain)

Figure 19.58 Biliary Atresia. Early disease featuring cholestasis and neonatal giant cell transformation

Figure 19.59 Biliary Atresia. Expanded portal tract with marked ductular reaction and ductular cholestasis

Figure 19.60 Detail of a bile duct from a neonate with biliary atresia, showing an irregular outline and epithelial damage including vacuolization of some cholangiocytes, apoptosis in others, and some inflammatory cells inside the basement membrane

Figure 19.61 Biliary atresia, "early severe" type with advanced fibrosis. The picture shows part of a large, fibrous portal area, with recognizable hepatic artery branches, barely visible or no portal vein branches, and bile duct structures in ductal plate configuration ("ductal plate malforma- tion"). The lining cholangiocytes show involutional changes such as flattening, shrinkage, and nuclear pyknosis

Figure 19.62 Cystic Fibrosis. An expanded portal tract has associated ductular reaction and inspissated pink-brown concretions (arrows)

Figure 19.63 Alpha1-Antitrypsin Deficiency. A, Cirrhosis with numerous globules present on H&E stain. B, High-power view of globules of various sizes in periportal hepatocytes

Figure 19.64 Niemann-Pick cells are pale, enlarged histiocytes with amphophilic foamy cytoplasm (arrows), which are clearly seen amidst the hepatocytes. Vacuolated pale inclusions are present within the cytoplasm

Figure 19.65 Glycogen storage disease type 1 featuring the characteristic "mosaic" pattern, featuring swollen hepatocytes with prominent cell membranes that compress sinusoids. Glycogenated nuclei are also easily visible

Figure 19.66 A, Biopsy from a patient with Wilson disease shows features of steatohepatitis. B, Patchy copper staining is a clue to the diagnosis (rhodanine stain)

Figure 19.67 Siderosis in Hepatocytes and Macrophages in Genetic Hemochromatosis. There is a decreasing portal-central gradient that can be appreciated even in advanced disease. (Perls iron stain.)

Figure 19.68 Neonatal hemosiderosis is characterized by iron deposition in hepatocytes and Kupffer cells, giant cell transformation, and increased fibrosis. Extramedullary hematopoiesis is also prominent in this case from a neonatal autopsy

Figure 19.69 Congenital Hepatic Fibrosis. Low-power view of needle biopsy specimen. Portal tracts are enlarged and joined by portal-portal fibrous connections. Bile ducts appear in their immature, embryonic shape (ductal plate malformation). Note the mature aspects of fibrous tissue and virtual absence of inflammation

Figure 19.70 Von Meyenburg complex featuring dilated bile ductules containing inspissated bile, embedded in dense fibrous stroma. The L lesion is located directly under the capsule

Figure 19.71 Intraoperative Photograph of Adult-Type Fibropolycystic Liver Disease. The liver is markedly enlarged and distorted by numerous cysts. (Courtesy Dr. George F. Gray, Jr.)

Figure 19.72 Adult-type polycystic liver/kidney disease featuring multiple cysts lined by a thin biliary epithelial lining, with a thick fibrous wall. Cysts are often associated with von Meyenburg complexes or congenital hepatic fibrosis

Figure 19.73 Acute hepatic venous outflow obstruction featuring sinusoidal dilatation in zone 3, with atrophy of the cell plates and extravasation of red blood cells

Figure 19.74 So-called cardiac cirrhosis, in which central vein to central vein fibrous bridges form nodules that encircle portal tracts. This patient had chronic congestive heart failure

Figure 19.75 Massive hepatic vein thrombosis in Budd-Chiari syndrome; note the marked congestion of the liver parenchyma ("nutmeg liver"). (Courtesy Dr. George F. Gray, Jr.)

Figure 19.76 Acute Fatty Liver of Pregnancy. Ballooned hepatocytes with microvesicular steatosis are present, with a small zone of spared parenchyma around the portal tract

Figure 19.77 Sarcoidosis. A, Multiple confluent, noncaseating, epithelioid granulomas with associated fibrosis. B, Cholestatic sarcoidosis mimicking primary biliary cirrhosis. Note bile duct damage (arrow)

Figure 19.78 Q Fever. Detail of lobular parenchyma with some steatosis and two fibrin ring granulomas. The granuloma is composed of a central fat vacuole, a layer of histiocytes and lymphocytes, a fibrin ring, and additional accumulation of inflammatory cells

Figure 19.79 Echinococcosis of the liver featuring multiple cysts in a resection specimen

Figure 19.80 Liver Abscess With Necrotic Center and Associated Fibrosis. (Courtesy Dr. George F. Gray, Jr.)

Figure 19.81 Amebic Abscesses Occupying Most of the Right Lobe of the Liver. Three distinct lesions are seen. (Courtesy Dr. RA Cooke, Brisbane, Australia; from Cooke RA, Stewart B. Colour Atlas of Anatomical Pathology. Edinburgh: Churchill Livingstone; 2004.)

Figure 19.82 Amyloidosis. A, Gross specimen showing sinusoidal amyloid deposition. B, Lobular parenchyma with massive amyloid deposi- tion in the space of Disse and corresponding marked atrophy of liver cell plates. (A, Courtesy Dr. George F. Gray, Jr.)

Figure 19.83 Light Chain Deposition Disease. Detail of lobular parenchyma with kappa chain deposition in the space of Disse. (Immu- nostain for kappa light chain.)

Figure 19.84 Acute cellular rejection of liver allograft, characterized by a dense mixed portal infiltrate (including eosinophils), endotheliitis, and lymphocytic cholangitis

Figure 19.85 Chronic "Ductopenic" Rejection of Liver Allograft. Portal tract without a bile duct and with very sparse lymphocytic infiltration