What are the 2 main functions of the pancreas? What are the most important stimuli?
- 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.
Causes of Acute pancreatitis
- hypertriglyceridemia (rarely)
- Drugs: furosemide and thiazides, sulfonamides, valproate
Causes of chronic pancreatitis
- alcohol (70%)
- idiopathic (20%)
What are the standard lab tests for pancreatitis?
- amylase and lipase (don't tell severity)
- if only amylase is elevated, then it's probably a different problem, not pancreatitis
What are Ranson's criteria?
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
Treatment of acute pancreatitis
- 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
Treatment of severe acute pancreatitis
- octreotide - reduces secretions
- antibiotic prophylaxis with ceftazidime, metronidazole, amikacin, imipenem-cilastatin
Differences between acute and chronic pancreatitis
- Acuteinterstitial - 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
Treatment of chronic pancreatitis
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