Gallstones are formed from constituents of the bile (viz. cholesterol, bile pigments and calcium salts) along with other organic components. Accordingly, the gallstones commonly contain cholesterol, bile pigment and calcium salts in varying proportions. They are usually formed in the gall bladder, but sometimes may develop within extrahepatic biliary passages, and rarely in the larger intrahepatic bile duct.

The incidence of gallstones varies markedly in different geographic areas, age, sex, diet and various other risk factors.

The mechanism of cholesterol gallstone formation or lithogenesis is determined by 3 major factors, namely supersaturation of bile with cholesterol, cholesterol nucleation, and the hyperfunction of gallbladder.

Types of gallstones. As stated before, gallstones contain cholesterol, bile pigment and calcium carbonate, either in pure form or in various combinations. Accordingly, gallstones are of 3 major types — pure gallstones, mixed gallstones and combined gallstones. Mixed gallstones are the most common while pure and combined gallstones comprise 10% each. In general, gallstones are formed most frequently in the gallbladder but may occur in extrahepatic as well as intrahepatic biliary passages.

Numerous complications develop in cholelithiasis. They are cholecystitis, choledocholithiasis, mucocele or hydrops of the gallbladder, biliary fistula, gallstone ileus, gallbladder cancer.


Cholecyscitis or inflammation of the gallbladder may be acute, chronic, or acute superimposed on chronic. Though chronic cholecyscitis is more common.

Acute Cholecystitis

In many ways, acute cholecystitis is similar to acute appendicitis. The condition usually begins with obstruction, followed by infection later.

Based on the initiating mechanisms, acute cholecystitis occurs in two types of situations — acute calculous and acute acalculous cholecystitis.

In majority of cases, acute cholecystitis is caused by obstruction in the neck of the gallbladder or in the cystic duct by a gallstone. The commonest location of impaction of a gallstone is in Hartman's pouch. After that secondary bacterial infection, for instance E. coli and Streptococcus faecalis, supervenes.

Acute acalculous cholecystitis. The remaining 10% cases of acute cholecystitis do not contain gallstones. In such cases, a variety of causes have been assigned such as previous non-biliary surgery, multiple injuries, burns, severe sepsis, diabetes mellitus, etc.

Morphology. Except for the presence or absence of calculi, the two forms of acute cholecystitis are morphologically similar. Macroscopically, the gallbladder is distended and tense. The serosal surface is coated with fibrinous exudate with congestion and hemorrhages. The mucosa is red. The lumen is filled with pus mixed with green bile. In calculous cholecystitis, a stone is generally impacted in the neck or in the cystic duct. When obstruction of the cystic duct is complete, the lumen is filled with purulent exudate and the condition is known as empyema of the gall bladder. Microscopically, wall of the gall bladder shows marked inflammatory edema, congestion and neutrophilic exudate. There may be frank abscesses in the wall and gangrenous necrosis with rupture into the peritoneal cavity (gangrenous cholecystitis).

Chronic Cholecystitis

Chronic cholecystitis is the commonest type of clinical gall bladder disease. The association of chronic cholecystitis with mixed and combined goll-stones is virtually always present.

Morphology. Macroscopically, the gall bladder is generally contracted but may be normal or enlarged. The wall of the gall bladder is thickened which on cut section is grey-white due to dense fibrosis or may be even calcified. The mucosal folds may be intact, thickened, or flattened and atrophied. The lumen commonly contains multiple mixed stones or a combined stone. Microscopically, the following signs may be observed: thickened and congested mucosa but occasionally mucosa may be totally destroyed; penetration of the mucosa deep into the wall of the gall bladder up to muscular layer to form Rokitansky-Aschoff sinuses; variable degree of chronic inflammatory reaction, consisting of lymphocytes, plasma cells and macrophages, present in the lamina propria and subserosal layer; variable degree of fibrosis in the subserosal and subepithelial layers.


Pancreatitis is inflammation of the pancreas with acinic cell injury. It is classified into acute and chronic forms both of which are two distinct entities.

Acute Pancreatitis

Acute pancreatitis is an acute inflammation of the pancreas. The severe form of the disease associated with macroscopic hemorrhages and fat necrosis in and around the pancreas is termed acute hemorrhage pancreatitis or acute pancreatic necrosis. The condition occurs in adults between the age of 40 and 70 years and is commoner in females than in males.

The onset of acute pancreatitis is sudden, occurring after about of alcohol or a heavy meal. The patient presents with abdominal pain, vomiting and collapse and the condition must be differentiated from other diseases producing acute abdomen such as acute appendicitis, perforated peptic ulcer, acute cholecystitis.

Etiology. The two leading causes associated with acute pancreatitis are alcoholism and cholelithiasis, both of which are implicated in more than 80% of cases. Less common causes of acute pancreatitis include trauma, ischemia, shock, extension of inflammation from the adjacent tissues, blood-borne bacterial infection, viral infections, certain drugs, etc.

Morphology. The morphology of acute pancreatic necrosis stems directly from the action of activated pancreatic enzymes that are released into the pancreatic substance. The basic alterations are proteolytic destruction of pancreatic substance, necrosis of blood vessels with subsequent hemorrhage, necrosis of fat,

and an accompanying inflammatory reaction. The extent and predominance of each of these features depend on the duration and severity of the process, in the very early stages, only interstitial edema is present. Soon after, focal and confluent areas of frank necrosis of endocrine and exocrine tissue are found. Neutrophilic infiltration and interstitial hemorrhage eventually ensue. The most characteristic histologic lesions of acute pancreatic necrosis are the focal areas of fat necrosis that occur in the pancreatic and peripancreatic fat. Following enzymatic destruction, adipocytes are transformed into shadowy outlines of cell membranes filled with pink, granular, opaque precipitates. Amorphous basophilic calcium precipitates may be visible within the necrotic focus.

With severe pancreatic necrosis, a variegated pattern of blue-black hemorrhages and gray-white necrotic softening alternates with sprinkled foci of yellow-white, chalky fat necrosis.

Complications. A patient of acute pancreatitis who survives may develop a variety of systemic and local complications. Systemic complications are chemical and bacterial peritonitis, endotoxic shock, acute renal failure. Local complications are pancreatic abscess, pancreatic pseudocyst, duodenal obstruction.

Chronic Pancreatitis

Chronic pancreatitis is the progressive destruction of the pancreas due to repeated mild and subclinical

attacks of acute pancreatitis. Most patients present with recurrent attacks of severe abdominal pain at intervals of months to years. Weight loss and jaundice are often associated. Later manifestations include associated diabetes mellitus and steatorrhea.

Etiology. Most cases of chronic pancreatitis are caused by the same factors as for acute pancreatitis.

Morphology. Chronic pancreatitis is distinguished by irregularly distributed fibrosis, reduced number and size of acini with relative sparing of the islets of Langerhans, and variable obstruction of pancreatic ducts of all sizes. The lesions have a macroscopic lobular distribution and may involve portions or all of the pancreas. A chronic inflammatory infiltrate around lobules and ducts is usually present. The interlobular and intralobular ducts are dilated and contain protein plugs in their lumina. The ductal epithelium may be atrophied or hyperplastic or may show squamous metaplasia. Macroscopically, the gland is hard and exhibits foci of calcification and fully developed pancreatic calculi. These concretions vary from calculi invisible to the naked eye, to stones 1 cm to several centimeters in diameter, giving rise to the term «chronic calcifying pancreatitis'. With chronic ductal obstruction, the distribution of lesions is irregular, and the ductal epithelium generally is less severely damaged. Protein plugs and calcified stones are rare.

Complications. Last stage of chronic pancreatitis may be complicated by diabetes mellitus, pancreatic

insufficiency with steatorrhea and malabsorption and formation of pancreatic pseudocysts.

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