Page 662 - Textbook of Pathology, 6th Edition

646 PANCREATITIS leakage of pancreatic enzymes from the ductules into the
Pancreatitis is inflammation of the pancreas with acinic cell interstitial tissue.
injury. It is classified into acute and chronic forms both of Block in exocytosis of pancreatic enzymes occurring from
which are distinct entities. nutritional causes results in activation of these intracellular
enzymes by pancreatic lysosomal hydrolases.
Acute Pancreatitis
MORPHOLOGIC FEATURES. Grossly, in the early stage,
Acute pancreatitis is an acute inflammation of the pancreas
presenting clinically with ‘acute abdomen’. The severe form the pancreas is swollen and oedematous. Subsequently,
of the disease associated with macroscopic haemorrhages in a day or two, characteristic variegated appearance of
grey-white pancreatic necrosis, chalky-white fat necrosis
and fat necrosis in and around the pancreas is termed acute and blue-black haemorrhages are seen. In typical case, the
haemorrhagic pancreatitis or acute pancreatic necrosis. The
condition occurs in adults between the age of 40 and 70 years peritoneal cavity contains blood-stained ascitic fluid and
and is commoner in females than in males. white flecks of fat necrosis in the omentum, mesentery
The onset of acute pancreatitis is sudden, occurring after and peripancreatic tissue. The resolved lesions show areas
a bout of alcohol or a heavy meal. The patient presents with of fibrosis, calcification and ductal dilatation.
abdominal pain, vomiting and collapse and the condition Microscopically, the following features in varying grades
must be differentiated from other diseases producing acute are noticeable:
abdomen such as acute appendicitis, perforated peptic ulcer, 1. Necrosis of pancreatic lobules and ducts.
acute cholecystitis, and infarction of the intestine following 2. Necrosis of the arteries and arterioles with areas of
sudden occlusion of the mesenteric vessels. Characteri- haemorrhages.
stically, there is elevation of serum amylase level within the 3. Fat necrosis.
first 24 hours and elevated serum lipase level after 3 to 4 days, 4. Inflammatory reaction, chiefly by polymorphs, around
the latter being more specific for pancreatic disease. the areas of necrosis and haemorrhages.
Glucosuria occurs in 10% of cases.
COMPLICATIONS. A patient of acute pancreatitis who
ETIOLOGY. The two leading causes associated with acute survives may develop a variety of systemic and local
pancreatitis are alcoholism and cholelithiasis, both of which complications.
are implicated in more than 80% of cases. Less common
causes of acute pancreatitis include trauma, ischaemia, shock, Systemic complications:
SECTION III
extension of inflammation from the adjacent tissues, blood- 1. Chemical and bacterial peritonitis.
borne bacterial infection, viral infections, certain drugs (e.g. 2. Endotoxic shock.
thiazides, sulfonamides, oral contraceptives), hypothermia, 3. Acute renal failure.
hyperlipoproteinaemia and hypercalcaemia from hyperpara-
thyroidism. Rarely, familial pancreatitis is encountered. In a Local sequelae:
proportion of cases of acute pancreatitis, the etiology remains 1. Pancreatic abscess.
unknown (idiopathic pancreatitis). 2. Pancreatic pseudocyst.
3. Duodenal obstruction.
PATHOGENESIS. The destructive changes in the pancreas
are attributed to the liberation and activation of pancreatic Mortality in acute pancreatitis is high (20-30%). Patients
enzymes. Though more than 20 enzymes are secreted by succumb to hypotensive shock, infection, acute renal failure,
exocrine pancreas, 3 main groups of enzymes which bring and DIC.
Systemic Pathology
about destructive effects on the pancreas are as under:
1. Proteases such as trypsin and chymotrypsin play the most Chronic Pancreatitis
important role in causing proteolysis. Trypsin also activates Chronic pancreatitis or chronic relapsing pancreatitis is the
the kinin system by converting prekallikrein to kallikrein, progressive destruction of the pancreas due to repeated mild
and thereby the clotting and complement systems are and subclinical attacks of acute pancreatitis. Most patients
activated. This results in inflammation, thrombosis, tissue present with recurrent attacks of severe abdominal pain at
damage and haemorrhages found in acute haemorrhagic intervals of months to years. Weight loss and jaundice are
pancreatitis. often associated. Later manifestations include associated
2. Lipases and phospholipases degrade lipids and membrane diabetes mellitus and steatorrhoea. Abdominal radiographs
phospholipids. show calcification in the region of pancreas and presence of
3. Elastases cause destruction of the elastic tissue of the blood pancreatic calculi in the ducts.
vessels.
The activation and release of these enzymes is brought ETIOLOGY. Most cases of chronic pancreatitis are caused
about by one of the following mechanisms: by the same factors as for acute pancreatitis. Thus, most
Acinic cell damage caused by the etiologic factors such as commonly, chronic pancreatitis is related to chronic alcoholism
alcohol, viruses, drugs, ischaemia and trauma result in with protein-rich diet, and less often to biliary tract disease.
release of intracellular enzymes. Familial hereditary pancreatitis, though uncommon, is more
Duct obstruction caused by cholelithiasis, chronic frequently chronic than the acute form. Other rare causes of
alcoholism and other obstructing lesions is followed by chronic pancreatitis are hypercalcaemia, hyperlipidaemia