صور باثولوجى - Patholgy Slides : Liver, Biliary Tract and Pancreas

Patholgy Slides :  Liver, Biliary Tract and Pancreas

 

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Liver

Liver diseases with toxic (alcoholic or chemical) or viral etiology (hepatitis B, C or D virus) very often are the cause of cirrhosis. Independent of its' etiology, cirrhosis is considered to be a premalignant lesion for primary liver cancer (hepatocellular carcinoma). Nonetheless, about 95% of all liver cancers are secondary determinations (liver metastasis of other tumors).

Cholecystitis is the most frequent disease of the gallbladder.

Non-tumor pathology of the pancreas refers to acute hemorrhagic pancreatitis and chronic pancreatitis. Although it is the fifth as incidence among other cancers, carcinoma of the pancreas has an extremely severe prognosis

Fatty change (liver) - Steatosis

Fatty change or Steatosis represents the intracytoplasmic accumulation of triglyceride (neutral fats) of parenchimal organs, such as: liver, myocardium and kidney.

Mechanisms : increase of free fatty acids (starvation, diabetes and chronic ethylism/alcoholism), reduction of free fatty acids oxidation (hypoxia, toxins, chronic ethylism/alcoholism), increase of esterification of free fatty acids into triglycerides (due to increased free fatty acids or reduction of their oxidation, chronic ethylism/alcoholism) and reduced export of tryglicerides due to deficiency of lipid binding apoprotein (starvation/malnutrition, toxins). Initially, fatty change does not impair the cells function, being reversible.

At the beginning, the hepatocytes present small fat vacuoles in the vicinity of the endoplasmic reticulum (liposomes) - microvesicular fatty change (photo). In the late stages, the size of the vacuoles increases pushing the nucleus to the periphery of the cell - macrovesicular fatty change. These vesicles are well delineated and optically "empty" because fat solves during tissue processing (paraffin embedding). Large vacuoles may coalesce, producing fatty cysts - which are irreversible lesions. (HE, ob. x20)

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Viral chronic moderate hepatitis

Chronic hepatitis is characterized by hepatic necroinflammation (chronic inflammatory infiltrate and necrosis of hepatocytes), fibrosis and biochemical disorders lasting for more than 6 months. According to necroinflammatory activity, chronic hepatitis may be mild, moderate or severe. The stage of fibrosis depends on its' localization and degree of extension (absent, limited to portal tract without fibrous septa, complete or incomplete porto-portal fibrous septa and cirrhosis).
The main cause chronic hepatitis is viral infection : hepatitis B virus, hepatitis C virus, and others. Untreated, chronic viral hepatitis evolves into cirrhosis and hepatocellular carcinoma.

In moderate chronic hepatitis, the liver architecture is preserved, but portal tracts are enlarged (losing the normal triangular shape), with abundant chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages). Limiting plate of hepatocytes (which separates the portal tract from lobule) is interrupted (foci of hepatocyte necrosis surrounded by lymphocytes - piecemeal necrosis or interface hepatitis). This is followed by extension of inflammation into the periportal parenchyma. At this level, hepatocytes present hydropic change and/or fatty change. (H&E, ob. x20)

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Secondary biliary cirrhosis

Secondary biliary cirrhosis is produced by obstruction of extrahepatic biliary ducts and is characterized by regeneration nodules, surrounded by fibrous septa. In these nodules, regenerating hepatocytes are disorderly disposed. Biliary tract, central vein and the radiar pattern of hepatocytes are absent. Fibrous septa are important and may present inflammatory infiltrate (lymphocytes, macrophages) and biliary ducts (damaged, proliferated or distended - bile stasis). These dilated ducts contain inspissated bile which appear as bile casts or bile thrombi (brown-green, amorphous). Bile retention may be found also in the parenchyma, as the so called "bile lakes". (H&E, ob. x10)

Secondary biliary cirrhosis (detail)

Regeneration nodule in secondary biliary cirrhosis. (H&E, ob. x40)

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Poorly differentiated hepatocellular carcinoma

Hepatocellular carcinoma, poorly differentiated (photo - upper right), developed on liver cirrhosis. This malignant epithelial tumor consists in tumor cells, discohesive, pleomorphic, anaplastic, giant. The tumor has a scant stroma and central necrosis because of the poor vascularization. In well differentiated forms, tumor cells resemble hepatocytes, form cords and nests, and may contain bile pigment in cytoplasm. (H&E, ob. x20)

Poorly differentiated hepatocellular carcinoma. (H&E, ob. x20)

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Biliary Tract

Cholesterolosis (strawberry gallbladder)

Cholesterolosis is an intracellular accumulation of lipids (cholesterol). When cholesterol is in excess in the bile, it passes into the lamina propria where is phagocitated by macrophages. These macrophages become larger and polygonal, with foamy cytoplasm and small, hyperchromatic, central nucleus (xantic cells). Aggregation of xantic cells may enlarge the mucosal folds, producing a polypoid appearance of the mucosal surface. At gross examination, these yellow micropolyps (1-2 mm) contrasts with the red aspect of the surrounding mucosa, hence the term "strawberry gallbladder".

Sometimes, cholesterolosis is associated with inflammation of the gallbladder (cholecystitis) or with gallstones (cholelithiasis).

Cholesterolosis of the gallbladder. (HE, ob x4)

Cholesterolosis of the gallbladder (detail of an enlarged mucosal fold). (HE, ob x10)

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Pancreas

Acute pancreatitis (Acute hemorrhagic pancreatic necrosis)

The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzyme necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium (photo) and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. (H&E, ob.x10)

Acute pancreatitis (Acute hemorrhagic pancreatic necrosis) (detail)

The acute pancreatitis (acute hemorrhagic pancreatic necrosis). Area of fat tissue necrosis due to lipase activation in the pancreatic interlobular space. The adjacent vessel presents thrombosis and hemorrhage. (H&E, ob.x40)

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