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2011-04-07 21:49:31
Therapeutics Exam6

Therapeutics Exam6 Pancreatitis Dr. Jameson
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  1. 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.
  2. Causes of Acute pancreatitis
    • Gallstones
    • ethanol
    • hypertriglyceridemia (rarely)
    • alcohol
    • Drugs: furosemide and thiazides, sulfonamides, valproate
  3. Causes of chronic pancreatitis
    • alcohol (70%)
    • idiopathic (20%)
  4. 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
  5. 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
  6. 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
  7. Treatment of severe acute pancreatitis
    • octreotide - reduces secretions
    • antibiotic prophylaxis with ceftazidime, metronidazole, amikacin, imipenem-cilastatin
  8. Differences between acute and chronic pancreatitis
    • 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
  9. 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