GI tract Flashcards
Normal non-keratinizing esophageal squamous mucosa is seen here at the left, and there is underlying submucosa containing mucus glands, with a duct surrounded by lymphoid tissue. At the right is the muscularis with smooth muscle as well as outer skeletal muscle.
Acute esophagitis is manifested here by increased neutrophils in the submucosa as well as neutrophils infiltrating into the squamous mucosa at the right. The acute inflammation can be caused by infections, ingestion of irritative chemicals, drugs such as NSAIDS, chemotherapy, and radiation.
The lower esophagus here shows sharply demarcated ulcerations that have a brown-red base, contrasted with the normal pale white esophageal mucosa at the far left. Such “punched out” ulcers are suggestive of herpes simplex infection.
A herpetic ulcer is seen microscopically to have a sharp margin. The ulcer base at the left shows loss of overlying squamous epithelium with only necrotic debris remaining. In the upper GI endoscopic view below, there are rounded, erythematous ulcerations of the lower esophagus. Biopsies of these lesions reveals intranuclear inclusions in squamous epithelial cells indicative of herpes simplex virus esophagitis. This patient was immune compromised from chemotherapy.
At high magnification, the squamous mucosa at the margin of the herpetic ulcer shows pale pink “ground glass” inclusions within squamous epithelial cells. Some of the inclusions are clustered together– multinucleation is another common viral cytopathic effect.
A common cause for inflammation is a so-called “Barrett esophagus” with epithelial metaplasia to gastric-type mucosa above the gastroesophageal junction. The metaplasia results from chronic gastroesophageal reflux disease (GERD). Note the columnar epithelium to the left and the squamous epithelium at the right. This is “typical” Barrett mucosa, because there is intestinal metaplasia as well (note the goblet cells in the columnar mucosa).
These two endoscopic views demonstrate Barrett esophagus areas of mucosal erythema of the lower esophagus, with islands of normal pale esophageal squamous mucosa. If the area of Barrett mucosa extends less than 2 cm above the normal squamocolumnar junction, then the condition is called “short segment” Barrett esophagus, as shown below.
A history of smoking and/or alcoholism is often present in patients with esophageal squamous carcinoma, while a history of Barrett esophagus precedes development of esophageal adenocarcinoma in many cases. Here, an ill-defined mass at the gastroesophageal junction produces mucosal ulceration and irregularity, which led to the clinical symptoms of pain and difficulty swallowing.
At the upper left is a remnant of squamous esophageal mucosa that has been undermined by an infiltrating squamous cell carcinoma of the mid-esophagus. Solid nests of neoplastic cells are infiltrating down through the submucosa at the right. Esophageal cancers often spread to surrounding structures, making surgical removal difficult.
At high power, these infiltrating nests of neoplastic cells have abundant pink cytoplasm and distinct cell borders typical for squamous cell carcinoma. Esophageal carcinomas are not usually detected early and, therefore, have a very poor prognosis
This is the normal appearance of the gastric fundal mucosa, with short pits lined by pale columnar mucus cells leading into long glands which contain bright pink parietal cells that secrete hydrochloric acid.
This is a more typical acute gastritis with a diffusely hyperemic gastric mucosa. There are many causes for acute gastritis: alcoholism, drugs, infections, etc.
Here are some larger areas of gastric hemorrhage that could best be termed “erosions” because the superficial mucosa is eroded away. Such erosions are typical for the pathologic process termed gastropathy, which describes gastric mucosal injury without significant inflammation. The findings here fit with acute erosive gastropathy, but there are other patterns. Etiologies for the various gastropathies can include: alcohol, drugs such as NSAIDS, stress, uremia, bile reflux, portal hypertension, radiation, and chemotherapy.
On microscopic examination at high power, this gastric mucosa shows infiltration by neutrophils. This is acute gastritis.
Microscopically, the ulcer here is sharply demarcated, with normal gastric mucosa on the left falling away into a deep ulcer whose base contains infamed, necrotic debris. An arterial branch at the ulcer base is eroded and bleeding.
The mucosa at the upper right merges into the ulcer at the left which is eroding through the mucosa. Ulcers will penetrate over time if they do not heal. Penetration leads to pain. If the ulcer penetrates through the muscularis and through adventitia, then the ulcer is said to “perforate” and leads to an acute abdomen. An abdominal radiograph may demonstrate free air with a perforation.
Chronic gastritis and peptic ulcer disease are often accompanied by infection with Helicobacter pylori. This small curved to spiral rod-shaped bacterium is found in the surface epithelial mucus of most patients with active gastritis. The rod-shaped bacteria are seen here with a methylene blue stain.
Another association with gastritis is pernicious anemia. Chronic atrophic gastritis is associated with autoantibodies that block or bind intrinsic factor. Another type of autoantibody demonstrated here is anti-parietal cell antibody. The bright green immunofluorescence is seen in the paritetal cells of the gastric mucosa.
The stomach is opened here to reveal a gastric adenocarcinoma In the U.S., most gastric cancers are discovered at a late stage when the neoplasm has invaded and/or metastasized. In Japan, where the incidence of gastric cancer is high, endoscopic screening is conducted, and more cancers are detected at an early stage. ALL gastric ulcers and ALL gastric masses must be biopsied, because it is not possible to tell from gross appearance alone which are benign and which are malignant. In contrast, virtually all duodenal peptic ulcers are benign.
This is an example of linitis plastica, a diffuse infiltrative gastric adenocarcinoma which gives the stomach a shrunken “leather bottle” appearance with extensive mucosal erosion and a markedly thickened gastric wall. This type of carcinoma has a very poor prognosis. The endoscopic view of this lesion is shown below, with extensive mucosal erosion.
A moderately differentiated gastric adenocarcinoma is infiltrating up and into the submucosa below the squamous mucosa of the esophagus. The neoplastic glands are variably sized.
At higher magnification, the infiltrating neoplastic glands of gastric adenocarcinoma show mitoses, increased nuclear/cytoplasmic ratios, and hyperchromatism. There is a desmoplastic stromal reaction to the infiltrating glands.
At high power, this gastric adenocarcinoma is so poorly differentiated that glands are not visible. Instead, rows of infiltrating neoplastic cells with marked pleomorphism are seen. Many of the neoplastic cells have clear vacuoles of mucin pushing the cell nucleus to one side, giving them a ‘signet ring’ appearance.
This is a signet ring cell pattern of adenocarcinoma in which the cells are filled with mucin vacuoles that push the nucleus to one side, as shown at the arrow.
This is an immunohistochemical stain with antibody to cytokeratin, which is positive in the poorly differentiated neoplastic cells seen here infiltrating through the gastric wall. Cytokeratin staining is typical for neoplasms of epithelial origin (carcinomas).
This is the normal appearance of small intestinal mucosa with long villi that have occasional goblet cells. The villi provide a large area for digestion and absorption.
Normal small intestinal mucosa is seen at the left. The mucosa involved by celiac disease (sprue) at the right has blunting and flattening of villi. Celiac disease most often becomes apparent either in infancy, or in young to middle age adults. It is diagnosed in about 1 in 3000 persons in the U.S., but the prevalence is probably much greater. It is more common in Caucasians and uncommon in Blacks and Asians. In some European populations, it may be as prevalent as 1%. About 95% of patients have the HLA-DQ2 allele, which suggests a genetic basis.
At high magnification, the non-Hodgkin lymphoma cells have prominent clumped chromatin and nucleoli with occasional mitotic figures. Most gastrointestinal lymphomas are B-cell in origin.
This small adenomatous polyp (tubular adenoma) on a small stalk is seen microscopically to have more crowded, disorganized glands than the normal underlying colonic mucosa. Goblet cells are less numerous and the cells lining the glands of the polyp have hyperchromatic nuclei. However, it is still well-differentiated and circumscribed, without invasion of the stalk, and is benign. Two colonoscopic views of a small polyp that proved to be a tubular adenoma is seen below.
Here are multiple tubular adenomas (adenomatous polyps) of the cecum. A small portion of terminal ileum appears at the right. This is a patient with hereditary non-polyposis colon carcinoma (HNPCC) syndrome. Compared to adenomatous polyposis coli (APC), in HNPCC there are fewer polyps and an older age for development of carcinoma. The defect in HNPCC is the inheritance, in an autosomal dominant fashion, of a faulty DNA mismatch repair gene, and most HNPCC tumors demonstrate microsatellite instability (variations in dinucleotide repeat sequences).
A microscopic comparison of normal colonic mucosa on the left and that of an adenomatous polyp (tubular adenoma) on the right is seen here. The neoplastic glands are more irregular with darker (hyperchromatic) and more crowded nuclei. This neoplasm is benign and well-differentiated, as it still closely resembles the normal colonic structure.
The distal encircling mass of firm adenocarcinoma in this colon opened along its length is typical for adenocarcinomas arising in the descending colon. A change in stool or bowel habits can be created by the mass effect. By colonoscopy, a fungating, ulcerating mass is seen in the views below.
This adenocarcinoma is arising in a villous adenoma. The surface of the neoplasm is polypoid and reddish pink. Hemorrhage from the surface of the tumor creates a guaiac positive stool. This neoplasm was located in the sigmoid colon, just out of reach of digital examination, but easily visualized with sigmoidoscopy.
The edge of the carcinoma arising in the villous adenoma is seen here. The neoplastic glands are long and frond-like, similar to those seen in a villous adenoma. The growth is primarily exophytic (outward into the lumen) and invasion is not seen at this point. Grading and staging of the tumor is done by the surgical pathologist who will examine multiple histologic sections of the tumor.
Microscopically, a moderately differentiated adenocarcinoma of colon is seen here. There is still a glandular configuration, but the glands are irregular and very crowded. Many of them have lumens containing bluish mucin.
Here is an adenocarcinoma in which the glands are much larger and filled with necrotic debris.
At high magnification, the neoplastic glands of adenocarcinoma have crowded nuclei with hyperchromatism and pleomorphism. No normal goblet cells are seen.
This is another example of Crohn disease involving the small intestine. Here, the mucosal surface demonstrates an irregular nodular appearance with hyperemia and focal ulceration. The distribution of bowel involvement with Crohn disease is irregular with more normal intervening “skip” areas.
The etiology for Crohn disease is unknown, though infectious and immunologic mechanisms have been proposed. The NOD2/CARD15 gene produces a bacterial lipopolysaccharide receptor in mucosal Paneth cells, and mutations in this gene affect activation of nuclear factor kappa B that is part of an innate immune response. CD patients generally have a pANCA negative / ASCA positive serologic pattern. There is a bimodal incidence for CD and an increased incidence in women and persons of Caucasian race.
Microscopically, Crohn disease is characterized by transmural inflammation. Here, inflammatory cells (the bluish infiltrates) extend from mucosa through submucosa and muscularis and appear as nodular infiltrates on the serosal surface adjacent to fat. Note the granulomatous inflammation.
On microscopic examination at high magnification the granulomatous nature of the inflammation of Crohn disease is demonstrated here with epithelioid cells, giant cells, and many lymphocytes. Special stains for organisms are negative.
The clinical manifestations of CD are variable and can include diarrhea, fever, and pain, as well as extraintestinal manifestations of arthritis, uveitis, erythema nodosum, and ankylosing spondylitis.
One complication of transmural inflammation with Crohn disease is fistula formation. Seen here is a fissure extending through mucosa into the submucosa toward the muscular wall, which eventually will form a fistulous tract. Fistulae can form between loops of bowel, bladder, and even skin. With colonic involvement, perirectal fistulae are common.
Use of biologic agents such as adalimumab and infliximab, which are monoclonal antibodies targeting tumor necrosis factor (TNF), has improved therapy for Crohn disease. A biologic agent plus the immunosuppressant azathioprine can be effective in diminishing the inflammation and tissue destruction, with reduction in complications.
Here is another example of extensive ulcerative colitis (UC). The ileocecal valve is seen at the lower left. Just above this valve in the cecum is the beginning of the mucosal inflammation with erythema and granularity. As the disease progresses, the mucosal erosions coalesce to linear ulcers that undermine remaining mucosa. Colonoscopic views of less severe UC are seen below, with friable, erythematous mucosa with reduced haustral folds.
At higher magnification, the pseudopolyps can be seen clearly as raised red islands of inflamed mucosa. Between the pseudopolyps is only remaining muscularis.
Pseudopolyps are seen here in a case of severe ulcerative colitis. The remaining mucosa has been ulcerated away and is hyperemic. A colonoscopic view of active ulcerative colitis, but not so eroded as to produce pseudopolyps, is seen below
Microscopically, the inflammation of ulcerative colitis is confined primarily to the mucosa. Here, the mucosa is eroded by an inflammatory process with ulceration that undermines surrounding mucosa. The resulting ulceration often has a flask shape (Erlenmeyer flask…triggering flashbacks to organic chemistry).
Zinc is a key micronutrient for both microbial pathogens and human host cells, particularly immune cells. Zinc can be concentrated by phagocytic cells, particularly neutrophils containing a cytoplasmic protein call calprotectin. These phagocytes can then signal T lymphocytes for an adaptive immune response, and they can concentrate free zinc toxic to microbes. Measurement of calprotectin can provide a means for assessing the magnitude of an inflammatory reaction, such as stool calprotectin measurement to gauge inflammatory bowel disease.
On microscopic examination at higher magnification, the intense inflammation of the mucosa is seen. The colonic mucosal epithelium demonstrates loss of goblet cells. The shape of the crypts is distorted. An exudate is present over the surface. Both acute and chronic inflammatory cells are present.
The colonic mucosa of active ulcerative colitis shows “crypt abscesses” in which a neutrophilic exudate is found in glandular lumens of crypts of Lieberkuhn. The submucosa shows intense inflammation. The glands demonstrate loss of goblet cells and hyperchromatic nuclei with inflammatory atypia.
Over time, there is a risk for adenocarcinoma with ulcerative colitis. Here, more normal glands with abundant goblet cells are seen at the left, but the glands at the right are more irregular in shape and demonstrate dysplasia with darker crowded nuclei. Dsyplasia is the first indication that there is a move towards neoplasia.
Clinical findings can include diarrhea, but the amount of diarrheal stool is not great, and is often accompanied by tenesmus. Patients with prolonged UC are at increased risk for developing colon cancer. Colonic biopsy can be used to detect dysplasia, a neoplastic change in the mucosa which implies an increased probability of malignancy. Patients with UC are also at risk for development of liver diseases including sclerosing cholangitis and bile duct carcinoma.
The cut surface of a normal liver has a brown color. Near the hilum here, note the portal vein carrying blood to the liver, which branches at center left, with accompanying hepatic artery and bile ducts. At the lower right is a branch of hepatic vein draining blood from the liver to the inferior vena cava.
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 metamorphosis (fatty change).
This is a larger liver with more pronounced steatosis (fatty change). Such fatty change is most often “nutritional” in etiology when diet is poor in protein and/or when fatty acid metabolism is deranged and/or when liver cell function is impaired. Non-alcoholic fatty liver (NAFL) is frequent due to metabolic syndrome, obesity, and diabetes mellitus (all of which are related).
Chronic alcohol abuse may lead to hepatic steatosis. The carbohydrate deficient transferrin (CDT) test measures isoforms of iron transport protein transferrin. Consumption of ethanol more than 50 to 80 g/day for 2-3 weeks may increase serum CDT. The CDT may be higher in chronic heavy drinkers than light social drinkers.
Steatosis is reversible over weeks to months. Reduce alcohol consumption. Adopt a diet and exercise program to lose weight (a 10% weight reduction helps to prevent progression of steatosis to steatohepatitis and to cirrhosis).
Here are large lipid vacuoles within hepatocytes in a case of macrovesicular steatosis (fatty change). The lipid accumulates when lipoprotein transport is disrupted and/or when fatty acids accumulate. Alcohol (ethanol), for example, is a hepatotoxin that interferes with mitochondrial and microsomal function in hepatocytes, leading to an accumulation of lipid.
The definitive diagnosis of non-alcoholic liver disease (NAFLD) steatosis is liver biopsy, but this is uncommonly done because a good history and physical examination will provide clues in most cases. An overweight person (even a child) with a mild to moderately elevated serum alanine transferase (ALT) is suggestive, in the absence of drug usage or causes for hepatitis. Right upper quadrant pain may be present from liver enlargement. Imaging studies include ultrasound examination, with diffusely increased echogenicity, or CT scan showing diffusely decreased attenuation, are supportive evidence for NAFLD.
This is the histologic appearance of hepatic macrovesicular steatosis (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 termed non-alcoholic fatty liver (NAFL) disease (diabetes mellitus, obesity, metabolic syndrome). Poor socioeconomic status contributes to kwashiorkor in children. Diseases causing severe gastrointestinal malabsorption are additional causes.
Polymorphisms in the patatin-like phospholipase domain containing 3 (PNPLA3) gene encoding for a triacylglycerol lipase involved in lipid regulation may explain greater propensity to develop steatosis in some populations.
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.
Portal hypertension results from the abnormal blood flow pattern in liver created by cirrhosis. The increased pressure is transmitted to collateral venous channels. Sometimes these venous collaterals are dilated. Seen here is “caput medusae” which consists of dilated veins seen on the abdomen of a patient with cirrhosis of the liver.
A much more serious problem produced by portal hypertension results when submucosal veins in the esophagus become dilated. These are known as esophageal varices. Varices are seen here in the lower esophagus as linear blue dilated veins. There is hemorrhage.around one of them. Such varices are easily eroded, leading to massive gastrointestinal hemorrhage.
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.
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.
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 (macrovesicular steatosis). Note the regenerative nodule surrounded by fibrous connective tissue extending between portal regions.
At high magnification can be seen globular red hyaline material within hepatocytes. 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.
Mallory’s hyaline is seen here, but there are also neutrophils, necrosis of hepatocytes, collagen deposition, and fatty change. These findings are typical for acute alcoholic hepatitis. Such inflammation can occur in a person with a history of alcoholism who goes on a drinking “binge” and consumes large quantities of alcohol over a short time.
The hepatocytes and Kupffer cells here are full of granular brown deposits of hemosiderin from accumulation of excess iron in the liver. The term “hemosiderosis” is used to denote a relatively benign accumulation of iron. The term “hemochromatosis” is used when organ dysfunction occurs. The iron accumulation may lead to a micronodular cirrhosis (so called “pigment” cirrhosis).
A Prussian blue iron stain demonstrates the blue granules of hemosiderin in hepatocytes and Kupffer cells. Hemochromatosis can be primary (the cause is probably an autosomal recessive genetic disease) or secondary (excess iron intake or absorption, liver disease, or numerous transfusions). Hemochromatosis leads to bronze pigmentation of skin, diabetes mellitus (from pancreatic involvement), and cardiac arrhythmias (from myocardial involvement).
The pale golden brown finely granular pigment seen here in nearly all hepatocytes is lipchrome (lipofuscin). One such deposit within a hepatocyte is marked by the arrow. This is a “wear and tear” pigment from the accumulation of autophagolysosomes over time. This pigment is of no real pathologic importance.
The pale golden brown finely granular pigment seen here in nearly all hepatocytes is lipchrome (lipofuscin). One such deposit within a hepatocyte is marked by the arrow. This is a “wear and tear” pigment from the accumulation of autophagolysosomes over time. This pigment is of no real pathologic importance.
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.
Shown here is a well-circumscribed neoplasm that is arising within the liver. This is an hepatic adenoma. The smooth border and circumscribed nature of this mass suggest that it is benign. Howver, adenomas are much less common than carcinomas in the liver.
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.
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 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 on the right) are well differentiated and interdigitate with normal hepatocytes arranged in regular cords (seen at the left).
Deaths from liver cancer are increasing due to increasing nonalcoholic fatty liver disease, cost of drugs to treat hepatitis C virus (HCV), the high stage of the cancer at detection, and the lack of effective chemotherapy.
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.
The carcinoma at the left has a glandular appearance that is most consistent with a cholangiocarcinoma. A liver cancer may have both hepatocellular as well as cholangiolar differentiation. Cholangiocarcinomas do not make bile, but the cells do make mucin, and they can be almost impossible to distinguish from metastatic adenocarcinoma on biopsy or fine needle aspirate.
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 apoptosis. A mononuclear inflammatory cell infiltrate extends from portal areas and disrupts the limiting plate of hepatocytes which are undergoing apoptosis, the so-called interface hepatitis of chronic active hepatitis. In this case, the hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (HBcAb) were positive, but anti-HBs (seen with recovery) was negative. Presence of hepatitis B e antigen (HBeAg) is associated with an increased risk for hepatocellular carcinoma regardless of serum level of alanine aminotransferase (ALT).
The severity of infection relates to the immune system’s ability to clear the virus. If clearance is delayed, a chronic persistent hepatitis can occur. A poor response can lead to chronic active hepatitis with ongoing hepatocellular damages and liver remodeling, with consequences of cirrhosis and potentially hepatocellular carcinoma.
Hepatitis B viral DNA can be measured by PCR. HBV DNA >2000 copies/mL along with an elevated alanine aminotransferase (ALT) suggests further workup and possible therapy is needed. Viral copies/mL above 10,000 suggest ongoing hepatitis with greater risk for carcinoma.
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. The screening laboratory test for 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”. In addition to this serologic test PCR and genotyping can be performed.
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.
There is extensive hepatocyte necrosis seen here in a case of acetaminophen overdose. The hepatocytes at the right are dead, and those at the left are dying. This pattern can be seen with a variety of hepatotoxins. Acute liver failure leads to hepatic encephalopathy
This is a case of primary biliary cholangitis, a rare autoimmune disease (mostly of middle-aged women) that is characterized by destruction of bile ductules within the triads of the liver. Seen here at medium power are intense mononuclear inflammatory infiltrates in portal tracts with loss of bile ductules. The inflammatory infiltrate can have granulomatous features as well.
This immunofluorescence pattern is positive for anti-mitochondrial antibody (AMA) which has an association with primary biliary cholangitis. The tissue substrate for this test is renal parenchyma, and the tubule cells have lots of mitochondria, which stain bright green.
This 3 month old child died with extrahepatic biliary atresia, a disease in which there is inflammation with stricture of hepatic or common bile ducts. This leads to marked cholestasis with intrahepatic bile duct proliferation, fibrosis, and cirrhosis. This liver was rock hard. The dark green color comes from formalin acting on bile pigments in the liver from marked cholestasis, turning bilrubin to biliverdin.
Microscopically, extrahepatic biliary atresia leads to this appearance in the liver, with numerous brown-green bile plugs, bile duct proliferation (seen at lower center), and extensive fibrosis. If a large enough bile duct can be found to anastomose and provide bile drainage, then surgery can be curative.
This trichrome stain of the liver demonstrates extensive portal tract fibrosis with sclerosing cholangitis. The hepatocytes are normal.
Microscopically, this bile duct in a case of sclerosing cholangitis is surrounded by marked collagenous connective tissue deposition.
