Patho CA – Acute Pancreatitis KCMS

Acute Pancreatitis
 Inflammation and hemorrhage of the pancreas
 Due to autodigestion of pancreatic parenchyma by
pancreatic enzymes
 Premature activation of trypsin leads to activation of
other enzymes
 Normally produced as proenzymes; activated in duodenum
 Liquefactive necrosis of pancreas with extensive
hemorrhage
 Adipose tissue surrounding pancreas (peripancreatic fat)
will also be digested
 FA are released and undergo saponification  FAT
NECROSIS
 Most commonly due to alcohol and gallstones
 Alcohol
 Contraction at sphincter of Oddi decreasing drainage
of pancreatic enzymes
 Gallstones
 Blocks at ampulla and also blocks drainage
 Other causes
 Trauma (automobile accidents in children)
 Hypercalcemia, hyperlipidemia
 Calcium is an activator of enzymes
 Drugs
 Scorpion stings
 Mumps
 Has propensity to infect pancreas
 Rupture of posterior duodenal ulcer

Clinical Features
 Epigastric abdominal pain that radiates to the back
 Nausea and vomiting
 Periumbilical and flank hemorrhage
 Elevation of serum lipase and amylase
 Lipase is more specific for pancreatic damage
 Hypocalcemia
 Saponification uses up calcium
 Indicates severe necrosis

Complications
 Shock
 Pancreatic pseudocyst
 Pancreatic abscess
 Abdominal pain, high fever and persistently high
amylase
 DIC and ARDS
 Pancreatic enzymes can potentially enter into the
blood
 Can activate factors and chew on capillary interface
 ARDS