Acute necrotizing pancreatitis, hemorrhagic pancreatitis. Chronic pancreatitis. Etiology & pathogenesis. Microscopic & gross pathomorphology
Pancreatitis is inflammation of the pancreas, it can be acute or chronic.
The most common causes are gallstones and alcohol use, as well as trauma, infectious agents and tumours.
Acute pancreatitis
- The exocrine part of the pancreas secretes digestive enzymes into the duodenum that break down carbohydrates, lipids and proteins. As these are found in the pancreas itself, the pancreas secretes inactive forms, which are then activated by proteases in the duodenum.
- If these enzymes activate too early, they can cause acute pancreatitis. One such example is the enzyme Trypsinogen.
- Etiology:
- Alcohol induced
- Alcohol increases trypsinogen secretion but decreases fluid and bicarbonate in the pancreatic ducts. This thickens the pancreatic juices, and makes them very viscous.
- The viscous pancreatic fluid can form a plug in the pancreatic duct, causing backing up of the juices.
- This can cause the inactive Trypsinogen to fuse with lysosomes, converting it to Trypsin and activating it.
- Trypsin, now active then begins autodigestion of the pancreas
- Gallstones
- Gallstones can get lodged in the sphincter of Oddi (where both the common bile duct and pancreatic duct come together to excrete into the duodenum). This blockage once again causes clogging of the pancreatic duct and therefore a build up of pancreatic juices.
- From here the pathogenesis is the same as the alcohol induced form.
- Other causes are Idiopathic, trauma (puncture), steroids, mumps, autoimmune disease, scorpion sting, hypercalcemia, endoscopic retrograde cholangiopancreatography and drugs (I GET SMASHED). Additionally, Cystic Fibrosis can cause acute pancreatitis, due to the fact it makes pancreatic secretions thicker.
- Eventually, acute pancreatitis can lead to pancreatic tissue destruction, triggering an inflammatory response, and liquefactive hemorrhagic necrosis.
- Clinical signs
- Nausea
- Vomiting
- Pain
- Hypocalcemia
- Bruising around belly button and flank
- Complications include pancreatic pseudocyst which itself can become an abscess, rupture and others. Additionally, bleeding, disseminated intravascular coagulation and acute respiratory distress syndrome can all occur.
Remember: periumbilical bruising is Cullen’s sign and flank bruising is Grey Turner’s sign – both mark retroperitoneal bleeding in severe necrotizing pancreatitis. The hypocalcaemia comes from fat necrosis: fatty acids released by lipase bind calcium into chalky white soaps (saponification).
The Pathomorphological changes in acute pancreatitis are:
- Microvascular leakage causing edema
- Necrosis of fat by lipases
- Acute inflammatory reaction
- Proteolytic destruction of pancreatic parenchyma
- Destruction of blood vessels leading to interstitial hemorrhage