ACUTE PANCREATITIS
Etiology
"I GET SMASHED": I = Idiopathic, G = Gall stones(most common, biliary pancreatitis)
, E=Ethanol, T = Trauma, S = Steroids, M = Mumps, A = Autoimmune and
rheumatological disordes (e.g. Sjôgren syndrome), S = Scorpion
poison, H= Hypercalcemia, Hypertriglyceridemia, E = ERCP, D = Drugs.(steroids
azathioprine sulfonamides furosemide estrogen protease inhibitors NRTIs)
Pathophysiology(video osmosis)
Sequence of events leading to pancreatitis:
1. Intrapancreatic activation of pancreatic enzymes: secondary
to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or
direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
Alcohol can also be responsible for blocked ducts by increasing zymogen
secretion (elevating pancreatic juice’s viscosity) and decreasing of fluid secretion
in the interstitial tissu, that leads to membrane trafficking, fusing of zymogens
and autodigestion
2. Enzymatic autodigestion of pancreatic parenchyma
3. Attraction of inflammatory cells (neutrophils, macrophages) → release of
inflammatory cytokines → pancreatic inflammation (pancreatitis)
Sequelae of pancreatitis (depending on the severity of pancreatitis)
1. Capillary leakage: Release of inflammatory cytokines and vascular injury
by pancreatic enzymes → vasodilation and increased vascular permeability
→ shift of fluid from the intravascular space into the interstitial space (third
space loss) → hypotension, tachycardia → distributive shock
2. Pancreatic necrosis: Uncorrected hypotension and third space loss →
decreased organ perfusion → multiorgan dysfunction (mainly renal)
and pancreatic necrosis
3. Hypocalcemia: Lipase breaks down peripancreatic and mesenteric fat →
release of free fatty acids that bind calcium → hypocalcemia