Acute Pancreatitis Flashcards
(26 cards)
protection from pancreatitis
- lysosomal and digestive enzymes are packaged separately
- trypsin inhibitor is packaged into each vesicle
- ## alpha-1 anti-trypsin protects against autodigestion in the bloodstream
cascade of pancreatitis
- trypsin is activated by cathepsin B from lysozymes or other trypsin
- trypsin then activates other pro-enzymes into active form
- active enzyme then affect other targets in the body
- AMYLASE AND LIPASE ARE THE ONLY ENZYMES WITHOUT A PRO-ENZYME
activation of chymotrypsin and kallikrein by trypsin
- leaky vessels
activation of elastase by trypsin
- weakens artery walls and leads to aneurysms and hemorrhage
activation of thrombin by trypsin
- DIC
activation of complement by trypsin
- WBC chemotaxis
release of lipase
- fat necrosis
activation of phospholipase A2 by trypsin
- ARDS
macroamylassemia
- hereditary condition in which macromolecules of amylase exist
- creatinine nearly zero
creatine levels in acute pancreatitis
- elevated
- nearly zero in macroamylassemia
etiologies of high amylase
- if its salivary amylase - diabetic ketoacidosis
- if its pancreatic amylase - pancreatitis
factors predictive of gallstone pancreatitis
- the more the risk factors the more likely gallstones are the cause and not alcohol
- age > 50
- female
- amylase > 400
- AST > 100
- ALP > 300
etiologies of high lipase
- lipase is only elevated in pancreatitis
Ranson’s criteria, at admission
- age > 55
- WBC > 16,000
- glucose > 200
- LDH > 350
- AST > 250
Ranson’s criteria, during initial 48 hours
- Hct decrease of > 10
- BUN increase of > 5
- Ca < 8
- PaO2 < 60
- Base deficit > 4
- fluid sequestration > 6
Ranson’s criteria
- if over the levels, the more likely to develop severe pancreatitis
- if 3-5 criteria met, about 20% mortality
- 6-8, 60% mortality
- 9-11, 80% mortality
rapid IV bolus contrast CT scan
- used to indicate viable vs necrotic pancreas and delineates pancreas from extrapancreatic fluid
- if whole pancreas takes up dye there is no necrosis
- if necrotic it will look black on CT
necrosis with infection
- bad prognosis
- about 30% mortality
3 sequelae of pancreatitis
- pseudocyst
- phelgmon
- necrosis
Grey-Turner sign
- bruising on flank from bleeding and rupture of splenic artery
- if bruising is by umbilicus its called Cullen’s sign and is a sign of retroperitoneal hemorrhage
treatment of acute pancreatis
- hemodynamic and renal monitoring
- FLUID, FLUID, FLUID
- NPO
- antibiotics with pancreas penetration
- O2 as needed for ARDS
- ERCP for biliary pancreatitis IF STABLE, especially in severe cases WITHIN 24 HOURS of presentation to relieve obstruction by stone
calcium and albumin levels
- normally decrease together
- if calcium drops by itself by binding to free fatty acids it can lead to cardiac problems and neuromuscular irritability
indications for intervention of pseudocysts
- larger than 5 cm, lasts > 4-6 weeks, severe pain, rapid expansion, complications
ERCP
- scope passed into 2nd part of duodenum where papilla is located, catheter is passed via scope into pancreatic or bile ducts and dye injected
- X-rays then obtained to see if filling defects of either duct
- spincterotomy can be performed with stone removal or stent placement
- drainage of pseudocyst can be accomplished through stomach or duodenum
