5 Path Practical Liver

Liver, gall bladder and pancreas pathology practical

Content Normal liver Fatty liver Liver cirrhosis. Bile duct cholestases (stone) Hepatic adenoma. Hepatocellular carcinoma. Liver hemangioma. Liver cyst. Liver abscess. Gall bladder stones. Gall bladder carcinoma. Pancreas carcinoma.


This is an in-situ photograph of the chest and abdominal contents. As can be seen, the liver is the largest parenchymal organ, lying just below the diaphragm. The right lobe (at the left in the photograph) is larger than the left lobe. The falciform ligament is the rough dividing line between the two lobes.

This is the external surface of a normal liver. The color is brown and the surface is smooth. A normal liver is about 1200 to 1600 grams.

Liver is divided histologically into lobules. The center of the lobule is the central vein. At the periphery of the lobule are portal triads. Functionally, the liver can be divided into three zones, based upon oxygen supply. Zone 1 encircles the portal tracts where the oxygenated blood from hepatic arteries enters. Zone 3 is located around central veins, where oxygenation is poor. Zone 2 is located in between.


This liver is slightly enlarged and has a pale yellow appearance, seen both on the capsule and cut surface. This uniform change is consistent with fatty change.

This is the histologic appearance of hepatic fatty change. The lipid accumulates in the hepatocytes as vacuoles. These vacuoles have a clear appearance with H&E staining. The most common cause of fatty change in developed nations is alcoholism. In developing nations, kwashiorkor in children is another cause. Diabetes mellitus, obesity, and severe gastrointestinal malabsorption are additional causes.

Here are seen the lipid vacuoles within hepatocytes. The lipid accumulates when lipoprotein transport is disrupted and/or when fatty acids accumulate. Alcohol, the most common cause, is a hepatotoxin that interferes with mitochondrial and microsomal function in hepatocytes, leading to an accumulation of lipid.


Grossly, there are areas of necrosis and collapse of liver lobules seen here as ill-defined areas that are pale yellow. Such necrosis occurs with hepatitis.

Viral hepatitis leads to liver cell destruction. A mononuclear inflammatory cell infiltrate extends from portal areas and disrupts the limiting plate of hepatocytes which are undergoing necrosis, the so-called "piecemeal" necrosis of chronic active hepatitis. In this case, the hepatitis B surface antigen (HbsAg) and hepatitis B core antibody (HbcAb) were positive.

Individual hepatocytes are affected by viral hepatitis. Viral hepatitis A rarely leads to signficant necrosis, but hepatitis B can result in a fulminant hepatitis with extensive necrosis. A large pink cell undergoing "ballooning degeneration" is seen below the right arrow. At a later stage, a dying hepatocyte is seen shrinking down to form an eosinophilic "councilman body" below the arrow on the left.


This is a case of viral hepatitis C, which in half of cases leads to chronic liver disease. The extent of chronic hepatitis can be graded by the degree of activity (necrosis and inflammation) and staged by the degree of fibrosis. In this case, necrosis and inflammation are prominent, and there is some steatosis as well. Regardless of the grade or stage, the etiology of the hepatitis must be sought, for the treatment may depend upon knowing the cause, and chronic liver diseases of different etiologies may appear microscopically and grossly similar.

This is a case of viral hepatitis C which is at a high stage with extensive fibrosis and progression to macronodular cirrhosis, as evidenced by the large regenerative nodule at the center right. At present, the sole laboratory test for identification of this form of viral hepatitis is the hepatitis C antibody test. Hepatitis C accounts for most (but not all) cases formerly called "non-A, non-B hepatitis".

This trichrome stain demonstrates the collapse of the liver parenchyma with viral hepatitis. The blue-staining areas are the connective tissue of many portal tracts that have collapsed together.


Ongoing liver damage with liver cell necrosis followed by fibrosis and hepatocyte regeneration results in cirrhosis. This produces a nodular, firm liver. The nodules seen here are larger than 3 mm and, hence, this is an example of "macronodular" cirrhosis.

Here is another example of macronodular cirrhosis. Viral hepatitis (B or C) is the most common cause for macronodular cirrhosis. Wilson's disease and alpha-1-antitrypsin deficiency also can produce a macronodular cirrhosis.

Here is another example of macronodular cirrhosis. The fibrosis and the loss of the normal architecture of liver lobules leads to obstruction of portal venous blood flow. This results in portal hypertension, one of the most serious consequences of cirrhosis. Portal hypertension leads to ascites, splenomegaly, and to esophageal varices.


This is an example of a micronodular cirrhosis. The regenerative nodules are quite small, averaging less than 3 mm in size. The most common cause for this is chronic alcoholism. The process of cirrhosis develops over many years.

Here is another example of micronodular cirrhosis. Note that the liver also has a yellowish hue, indicating that fatty change (also caused by alcoholism) is present.

A close-up view of a micronodular cirrhosis in a liver with fatty change demonstrates the small, yellow nodules. Micronodular cirrhosis may also be seen with Wilson's disease, primary biliary cirrhosis, and hemochromatosis.


Microscopically with cirrhosis, the regenerative nodules of hepatocytes are surrounded by fibrous connective tissue that bridges between portal tracts. Within this collagenous tissue are scattered lymphocytes as well as a proliferation of bile ducts.

Micronodular cirrhosis is seen along with moderate fatty change. Note the regenerative nodule surrounded by fibrous connective tissue extending between portal regions.

At high magnification can be seen globular red hyaline material. This is Mallory's hyaline, also known as "alcoholic" hyaline because it is most often seen in conjunction with chronic alcoholism. The globules are aggregates of intermediate filaments in the cytoplasm resulting from hepatocyte injury.


Here is an example of intrahepatic obstruction with a small stone in an intrahepatic bile duct. This could produce a localized cholestasis, but the serum bilirubin would not be increased, because there is plenty of non-obstructed liver to clear the bilirubin from the blood. However, the serum alkaline phosphatase is increased with biliary tract obstruction at any level.

At the upper right is a well-circumscribed neoplasm that is arising in liver. This is an hepatic adenoma.


The cut surface of the liver reveals the hepatic adenoma. Note how well circumscribed it is. The remaining liver is a pale yellow brown because of fatty change from chronic alcoholism.

The cut surface of the hepatic adenoma demonstrates greenish bile staining, indicating that it is of hepatocyte origin (no other neoplasm could accumulate bile pigment). Such neoplasms are rare. One setting for their occurrence is young women taking oral contraceptives.

Normal liver tissue with a portal tract is seen on the left. The hepatic adenoma is on the right and is composed of cells that closely resemble normal hepatocytes, but the neoplastic liver tissue is disorganized hepatocyte cords and does not contain a normal lobular architecture.


Here is an hepatocellular carcinoma. Such liver cancers arise in the setting of cirrhosis.Worldwide, viral hepatitis is the most common cause, but in the U.S., chronic alcoholism is the most common cause. The neoplasm is large and bulky and has a greenish cast because it contains bile. To the right of the main mass are smaller satellite nodules.

The satellite nodules of this hepatocellular carcinoma represent either intrahepatic spread of the tumor or multicentric origin of the tumor.

Here is another hepatocellular carcinoma with a greenish yellow hue. One clue to the presence of such a neoplasm is an elevated serum alpha-fetoprotein. Such masses may also focally obstruct the biliary tract and lead to an elevated alkaline phosphatase.


The malignant cells of this hepatocellular carcinoma (seen mostly on the right) are well differentiated and interdigitate with normal, larger hepatocytes (seen mostly at the left).

Note that this hepatocellular carcinoma is composed of liver cords that are much wider than the normal liver plate that is two cells thick. There is no discernable normal lobular architecture, though vascular structures are present.

At the right is an area of necrosis and hemorrhage in this hepatocellular carcinoma. Liver cell carcinomas are very prone to necrosis and hemorrhage. In fact, hemorrhage from such an hepatocellular carcinoma at the liver capsule may lead to hemoperitoneum.


Note the numerous mass lesions that are of variable size. Some of the larger ones demonstrate central necrosis. The masses are metastases to the liver. The obstruction from such masses generally elevates alkaline phosphatase, but not all bile ducts are obstructed, so hyperbilirubinemia is typically not present. Also, the transaminases are usually not greatly elevated.

Here are liver metastases from an adenocarcinoma primary in the colon, one of the most common primary sites for metastatic adenocarcinoma in liver.

Microscopically, metastatic infiltrating ductal carcinoma from breast is seen on the right, with normal liver parenchyma on the left.


This is a benign hemangioma of the liver just beneath the capsule. Perhaps one person in 50 has such a neoplasm, which is typically just an incidental finding, since most are 1 cm or less. They can sometimes be multiple.

Here are two simple cysts of the liver. The one at the right is seen to be fluid filled on the cut surface, and there is another just to the left of this that appears through the capsule. Benign cysts and hemangiomas can occasionally occur in liver. They are of no consequence except that they can appear with radiographic imaging procedures and must be distinguished from other lesions. Putting a biopsy needle through an hemangioma can be disconcerting.

Abscesses in liver may also occur with hematogenous spread from other areas of the body with septicemia. Here are seen many microabscesses in the liver in a patient with Candida septicemia.


A normal gallbladder is shown here with a velvety dark green mucosa and a thin wall. One minor variation is the small yellowish bulbous projection at the right known as a "Phrygian cap".

Two composite gallstones are seen here with a yellow to black appearance. Gallstones consist of a mixture of cholesterol, bilirubin, and calcium. Pure stones are uncommon, though jet black bilirubin stones suggest chronic hemolysis. These stones are squared off (faceted) because they sat together. Hint: if you find one faceted stone, there is probably at least one more somewhere else.

Multiple yellow-tan faceted gallstones are seen in the opened gallbladder pictured here. It is possible for a stone to exit the gallbladder via the cystic duct. It may then produce obstruction of cystic duct, or it may get into the common bile duct and obstruct that. It may obstruct at the ampulla of Vater and produce a pancreatitis. Biliary tract obstruction leads to jaundice with increased total and direct bilirubin in serum.


Yellow tan faceted gallstones are present. The gallbladder shows evidence of chronic cholecystitis because the mucosa is tan and the wall and surface are pale, suggesting collagenization as a result of scarring with chronic inflammation.

The neutrophils are seen infiltrating the mucosa and submucosa of the gallbladder in this patient with acute cholecystitis.


A gallbladder has been opended, and to the left of the pale porcelain gallstones (averaging 1 cm in size) is a fungating mass that extends into the gallbladder lumen and into the gallbladder wall. This is a primary adenocarcinoma of gallbladder. Gallstones accompany such carcinomas in up to 90% of cases.

At low power, the dysplastic epithelium can be seen at the left, and neoplastic glandular structures are invading into the muscular wall. Adenocarcinoma of the gallbladder is more common in the elderly and more frequently seen in women.

At high magnifcation, this adenocarcinoma of the gallbladder is composed of columnar cells forming glandular and papillary structures. The prognosis with adenocarcinoma of the gallbladder is usually poor, because they have often invaded and metastasized by the time they are discovered.


Here is the normal gross appearance of the adult pancreas; a small portion of duodenum is at the left next to the head; the tail of the pancreas is at the right. The pancreas has a tan, lobular architecture. Adjacent adipose tissue and lymph nodes are closely apposed.

An adenocarcinoma of the head of the pancreas is shown here obstructing the pancreatic duct. This may well have produced a "painless jaundice" in the patient. Adenocarcinomas at this site have a very poor prognosis, even if a Whipple procedure is done, as shown here.

This adenocarcinoma of the pancreas is very extensive, sparing only the uncinate process at the lower left center. Chronic biliary tract obstruction produced icterus, marked by the green color of the liver after formalin fixation. Tumor invades into the hilum of liver, and small metastases to liver are also present.


At low power there is an adenocarcinoma of the pancreas at the left, with normal pancreas at the right.

The medium power microscopic appearance of an adenocarcinoma of the pancreas is seen. Just to the left of center can be seen perineural invasion by the neoplasm, which is composed of very irregular glands.

At high magnification, the microscopic appearance of an adenocarcinoma of the pancreas is seen. At the left can be seen normal pancreatic acini, but the neoplasm is composed of small irregular glands.

At high magnification, this adenocarcinoma of the pancreas has very poorly differentiated glands and extensive desmoplasia (production of collagenous stroma).

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5 Path Practical Liver