Pancreatitis

• Fxns: make and secrete insulin and glucagon (islet of langerhaans) and make and secrete digestive enzymes (acinar cells)
• Stimuli: CCK from duodenum stimulates production of digestive proenzymes like chymotrypsinogen, trypsinogen, amylase, lipase, prophospholipase A2, carboxyesterase lipase which are secreted into the duodenum.
• In duodenum trypsinogen is activated by enterokinase to trypsin.
• Trypsin then activates the pro-enzymes into active enzymes in the duodenum.
• Secretin from the duodenum goes to pancreas and stimulates bicarb and water to move into duodenum which creates a protective pH in the duodenum so the digestive enzymes aren't denatured.

• Gallstones
• ethanol
• hypertriglyceridemia (rarely)
• alcohol
• Drugs: furosemide and thiazides, sulfonamides, valproate

• alcohol (70%)
• idiopathic (20%)

• amylase and lipase (don't tell severity)
• if only amylase is elevated, then it's probably a different problem, not pancreatitis

criteria used in pancreatitis. if you have 3 or less survival is about 100%. if you have more than 6, mortality is close to 100%.

• At admission
• age > 55
• WBC > 16,000
• blood glucose > 11 mmol/L (> 200 mg/dL)
• AST > 250
• LDH > 350
• At 48 hours
• serum calcium < 2.0 mmol/L (<8.0 mg/dL)
• PO2 < 60 mmHg (hypoxemia)
• BUN increased by 5 or more after IV fluids
• Base deficit > 4
• Sequestration of fluids > 6L

• Stop offending drug (if drug induced)
• #1 priority is fluid resuscitation
• #2 priority is pain control (hydromorphone may be preferred)
• Parenteral nutrition or enteral feedings distal to the jejunum (b/c the jejunum is after the duodenum and we don't want any more enzyme production)
• H2RAs and PPIs don't work

• octreotide - reduces secretions
• antibiotic prophylaxis with ceftazidime, metronidazole, amikacin, imipenem-cilastatin

• Acute
• interstitial - interstitial edema and inflamm cells
• necrotizing - pancreatic enzymes auto-digest the pancreatic tissue
• pseudocysts - pockets of auto-digestion walled off by fibrosis

• Chronic
• inflammation -> plugging of ducts -> calcification -> fibrosis -> loss of enzymes especially lipase
• Presentation - early: wt loss, abd pain after eating; later: malabsorption and diarrhea, diabetes, lipase and amylase usually normal

Pain management (in an addicted person - b/c 70% of the cause is alcohol) - enteric coated pancreatic enzymes with a PPI (questionable efficacy for pain - work well for malabsorption - keep pH around 5), NSAIDs, tricyclics