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Most gallbladder diseases are associated with the formation of gallstones (cholelithiasis). Gallstones are usually formed in the gallbladder and rarely in the common bile duct.
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Cholesterol-Based Gallstones
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Pure, mixed, and combined cholesterol-based gallstones are common and are formed when the concentration of cholesterol is increased or when bile salts are decreased. (Bile salts keep cholesterol in solution.) Women are more apt to be affected. Middle age, obesity, and multiparity (“fat, fertile females in their forties and fifties”) increase the risk to as high as 20%. Oral contraceptives increase biliary cholesterol excretion and predispose to gallstones. Three fourths of Native American women develop gallstones. The incidence is also high in South American and Mexican women.
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In patients with terminal ileal disease such as Crohn's disease or those who have undergone ileal resection and ileal bypass surgery, failure of bile salt reabsorption in the terminal ileum is associated with decreased bile salt levels in bile and formation of gallstones.
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Patients with diabetes mellitus also have an increased incidence of cholesterol gallstones, probably related to increased cholesterol levels in bile.
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Pigment (Bilirubin) Stones
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These are uncommon and occur (1) in patients suffering from chronic hemolytic anemias such as sickle cell disease and thalassemia, in whom bilirubin excretion is greatly increased; and (2) in patients with parasitic infestations, most commonly Clonorchis sinensis, in whom the parasite ova form a nidus for pigment stones (see Oriental Cholangiohepatitis, Chapter 42: The Liver: I. Structure & Function; Infections).
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Clinicopathologic Syndromes
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Asymptomatic Gallstones
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Thirty percent or more of patients with gallstones have no symptoms, and gallstones are frequently found incidentally at radiologic examination. Only about 25% of gallstones contain sufficient calcium to be visible on plain x-rays, but ultrasonography and computerized tomography are highly effective at detecting gallstones. The presence of asymptomatic gallstones is not an indication for surgical removal.
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Acute cholecystitis rarely occurs in the absence of gallstones. In 80% of cases, a stone is found obstructing the cystic duct, leading to stasis of bile in the gallbladder. The residual bile becomes highly concentrated and causes a chemical acute inflammation. The damaged gallbladder is then susceptible to infection by bacteria; Escherichia coli and other gram-negative bacilli are cultured from the bile in 80% of cases.
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Pathologically, the gallbladder shows congestion, thickening of the wall by edema, mucosal ulceration, and fibrinous exudation. Large numbers of neutrophils are present. The gallbladder may become filled with pus (empyema of the gallbladder). In severe cases, necrosis of the wall occurs, with greenish-black discoloration (gangrenous cholecystitis). Perforation may lead to local abscess formation or to generalized peritonitis.
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Clinically, acute cholecystitis produces acute onset of fever and right upper quadrant pain. An enlarged, tender gallbladder is palpable in 40% of cases; mild jaundice may be seen in about 20%. Treatment is with antibiotics and surgical drainage or cholecystectomy.
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Chronic Cholecystitis
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Chronic cholecystitis almost never occurs without gallstones. Pathologically, the gallbladder is contracted and its wall thickened by fibrosis (Figure 44-4), with infiltration by lymphocytes, plasma cells, and macrophages. Calcification may occur in the wall; when extensive, the gallbladder is outlined on abdominal x-ray (porcelain gallbladder). The mucosa of the gallbladder may be near normal or thinned by pressure of a stone, or it may show yellow flecks due to accumulation of cholesterol-filled foamy macrophages in the mucosa (cholesterolosis).
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Symptoms are usually vague; abdominal pain, often related to the ingestion of fatty foods, is the most common feature. Biliary colic—severe intermittent right upper quadrant pain—may occur when the cystic duct is obstructed.
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Movement of Gallstones
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Migration of gall-stones from the gallbladder may cause obstruction or fistula formation.
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Cystic duct obstruction is characterized by distention of the gallbladder with watery bile (hydrops) or mucus (mucocele). Acute cholecystitis also complicates duct obstruction.
Common bile duct obstruction may be intermittent, with attacks of biliary colic, jaundice, and high fever due to cholangitis (Charcot's triad of symptoms). Less commonly, obstruction is complete, leading to deep jaundice. In patients with obstructive jaundice resulting from stones, the presence of chronic cholecystitis prevents dilation of the gallbladder (Courvoisier's law; see Figure 44-2). Impaction of a gallstone in the ampulla of Vater may obstruct the pancreatic duct, leading to acute pancreatitis.
Fistulous tracts develop rarely between the gallbladder and intestine due to the chronic inflammation. A large gallstone may then pass directly through such a cholecystoenteric fistula into the intestine, causing intestinal obstruction (gallstone ileus).