Liver, Gallbladder, and Pancreas

Liver, Gallbladder, and Pancreas

The liver maintains the physiologic and metabolic balance of the body. Therefore, disease of the liver may have numerous effects throughout the body: it may cause disturbances in carbohydrate, lipid, amino acid, and vitamin metabolism and interfere with protein synthesis, blood clotting, and detoxification of endogenous and exogenous substances (Table 5-1).

Inflammatory Diseases of the Liver

Viral hepatitis is an acute inflammation of the liver, usually caused by the hepatitis viruses (HAV-HGV), rarely by such other viruses as enteroviruses and herpesviruses (CMV, EBV, HHV-6, or HSV). Symptoms do not develop until the onset of immune reactions against the virus or virus-infected cells, 2 to 26 weeks after infection (incubation period). Bacteria, fungi, and parasites also may cause hepatitis.

Noninfectious causes of liver inflammation include toxic and immunologic disorders of the liver (see Table 5-2). These are discussed together because certain forms of toxic hepatitis may mimic autoimmune disorders or may be mediated through hypersensitivity reactions. A large variety of substances can cause liver damage, and they are associated with an equally large variety of lesions. A selection is shown in Table 5-3.



Features AIH PBC PSC
Serology (autoantibodies) Antinuclear (ANA)
Anti–smooth muscle (ASMA)
Anti–liver/kidney membrane (LKM)
Antiliver (LSP)
Anti–native DNA
Antimitochondrial (AMA)
Anti–bile proteins
Antineutrophils (ANCA)
Anti–bile duct epithelia
Genetics Nonspecific Female predominance Male predominance
Increased expression: HLA-DR3, HLA-DRW52a, HLA-B8 (DR2,4, DRb12)
Associated diseases Rheumatoid arthritis
Pernicious anemia
Peripheral neuropathy
Hemolytic anemia
Raynaud syndrome
Thyroid dysfunction
Seronegative arthritis
Ulcerative colitis
Riedel thyroiditis
Retroperitoneal fibrosis
Orbital pseudotumor (may be complicated by cholangiocarcinoma)


Overlap syndromes combine features of cholestatic and chronic hepatitic forms of diseases, e.g., AIH + PBC, PBC + PSC, or PBC + sarcoidosis.

*AIH indicates autoimmune hepatitis; PBC, primary biliary cirrhosis; PSC, primary sclerosing cholangitis.

There are 3 major groups of autoimmune disorders affecting the liver: primary hepatic autoimmune diseases (Table 5-3), liver diseases with secondary autoimmune component, and systemic autoimmune diseases involving the liver.

Primary Tumors of the Liver

The most frequent tumors in the liver are metastases, often from the gastrointestinal (GI) tract, the lungs, or the mammary glands. Primary tumors originating in the liver consist of benign hepatic hamartomas and adenomas, bile duct angiomas, and cavernous hemangiomas. Two benign lesions must be distinguished from well-differentiated hepatocellular carcinoma (HCC): hepatocellular adenoma and focal nodular hyperplasia (FNH) of the liver. Adenomas (single or multiple) are well-circumscribed, yellowish masses of liver tissue with a fibrous capsule and histologically lobular architecture devoid of central vein, portal triads, and bile ductules. They occur preferentially in women of reproductive age and seem to be related to the use of oral contraceptives. FNHs, which occur equally in the two sexes, are solitary masses of hypertrophic hepatocellular nodules divided by fibrous septae, with prominent central scarring, large central nutritive vessels, bile ductules and cholestasis, and a pseudocapsule. The most frequent malignant tumors of the liver are HCC and cholangiocarcinoma (CAC). Less frequent are hepatoblastoma (in small children) and hemangiosarcoma.

Neoplasms of the Pancreas

Benign tumors of the exocrine pancreas are rare and consist essentially of ductal serous or mucinous cystadenomas. They must be distinguished clinically from inflammatory pseudocysts rather than from carcinoma. Carcinoma of the pancreas is the fourth most common tumor in the Western world, is even more frequent in the Pacific region, and is increasing in incidence. Approximately 23,000 new cases are diagnosed every year in the United States; only approximately 1% of these patients survive 5 years. No clear cause of human pancreatic cancer has been identified. Chronic pancreatitis is a recognized risk factor for carcinoma of the pancreas. Dietary factors, such as high fat and meat intake, may be contributory.



Name (Molecule) Family Transmission Incubation, weeks Disease Carrier Chronic Cancer
HAV (ssRNA) Picorna Enteral 2–6 Hepatitis, fulminant hepatitis 0 0 0
HBV (dsDNA) Hepadna Parenteral 4–26 Hepatitis, fulminant hepatitis, cirrhosis −1% −10% Yes
HCV (ssRNA) Flavivirus Parenteral 2–26 Hepatitis, cirrhosis, extrahepatic disorders −1% −50% Yes
HDV (ssRNA) Subviral satellite (HBV helper) Parenteral 4–7 (super- infection) Hepatitis, fulminant hepatitis −10% −5% 0
HEV (ssRNA) Calicivirus Enteral 2–8 Hepatitis ? 0 0
HGV (ssRNA) Flavivirus Parenteral ? Hepatitis, extrahepatic disorders in drug addicts −2% 0 ?


*ds indicates double-stranded; ss, single-stranded.



Gross Appearance Pathogenesis
Diffuse, finely nodular (classic Laennec type: with atrophy) Post–hepatitis virus cirrhosis
Same with or without fatty infiltration Post–alcoholic cirrhosis
Diffuse, medium-sized nodular, dark purple (classic Hanot type with hypertrophy) Chronic congestive (practically only seen in constrictive pericarditis)
Same with severe jaundice (green liver) Primary biliary cirrhosis or chronic sclerosing cholangitis
Same with “dirty” gray-brown appearance (and similarly pigmented pancreas) Hemochromatosis, Wilson disease
Diffuse, irregularly nodular, preferentially small- to medium-sized nodular Autoimmune hepatitis and cirrhosis
Irregular, medium- to large-sized nodular, with jaundice (green liver) Secondary biliary cirrhosis (i.e., extrahepatic bile duct obstruction)
Same with regular color or with fatty infiltration “Postnecrotic” cirrhosis of variable etiology (e.g., post-HSV + alcoholic or other toxic influences)

*HSV indicates herpes simplex virus.

Figure 5-1 Acute Viral Hepatitis
Acute viral hepatitis, an inflammatory disease of the hepatic parenchyma, is caused most frequently by the hepatitis viruses (HVs) and less frequently by other viruses (Table 5-4). In the Western world, HBV and HBC are most prevalent. Disease symptoms develop between 2 and 26 weeks after the onset of immune reactions against virus/virus-infected cells. The pathogenesis of liver injury in viral hepatitis is not completely clear, although a cytotoxic T-lymphocyte reaction against hepatocytes presenting viral antigens seems to be the key reaction. Histology shows many lymphocytes invading the liver parenchyma from portal triads, which causes adjacent hepatocellular necroses (piecemeal necroses). Infected hepatocytes change to a ground-glass appearance. In more severe disease, infected hepatocytes show ballooning degeneration. In addition, there are single or multiple hepatocellular coagulation necroses of virus-infected hepatocytes (Councilman bodies) or lytic necroses (dropout necroses).

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Jun 28, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Liver, Gallbladder, and Pancreas

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