Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

L33 ac pancreatiti st f

684 views

Published on

  • Be the first to comment

L33 ac pancreatiti st f

  1. 1. Lecture 33All FleshFinger of the liver
  2. 2. ACUTE PANCREATITIS• Acute pancreatitis is reversiblepancreatic parenchymal injury associatedwith inflammation.• Mild formSevere formAcute Interstitial PancreatitisAcute NecrotizingTwo Types:Edematous
  3. 3. Epidemiology• Acute pancreatitis is relatively common, withan annual incidence rate in Westerncountries of 10 to 20 cases per100,000 people.
  4. 4. Epidemiology• Biliary tract disease and•alcoholismaccount for approximately80% of cases inWestern countries.
  5. 5. EpidemiologyGallstonesare present in 35%to 60% of cases of acute pancreatitis,and about 5% of patients with gallstonesdevelop pancreatitis.
  6. 6. Epidemiology• The male-to-female ratio is 1 : 3 in thegroup with biliary tract disease and6 : 1 in those with alcoholism.
  7. 7. Etiologic factors
  8. 8. Tityus TrinitatisFound in Central/ South America andthe Caribbean»»
  9. 9. Pathogenesis• Pancreatic enzymes are synthesized in an inactiveproenzyme form. If trypsin is inappropriatelyactivated it can in turn activate other proenzymessuch as prophospholipase and proelastase.• Prophospholipase degrade fat cells andProelastase damage the elastic fibers of bloodvessels.Autodigestion
  10. 10. Pathogenesis cont.• Trypsin also converts prekallikrein to itsactivated form, thus bringing into play the kininsystem and, by activation of• Hageman factor (factor XII),• the clotting and• complement systems as well.• In this way inflammation and small-vesselthromboses are amplified.
  11. 11. Pathogenesis cont• The inappropriate activation oftrypsinogenis an important triggering event in acutepancreatitis.
  12. 12. Pathogenesis (Alcohol)1. Obstruction of small pancreatic ducts2.Contraction of Sphincter Oddi3. Direct toxic effects on acinar cells
  13. 13. Three proposed pathways in thepathogenesis of Acute Pancreatitis3 possible events in the pathogenesis ofacute pancreatitis:1.Duct obstruction2.Acinar Cell injury3.Defective intracellular transport
  14. 14. Morphology• Macroscopically, the pancreatic substanceshows areas of• red-black hemorrhage• interspersed with• foci ofyellow-white, chalky fatnecrosis.
  15. 15. Morphology cont.- Mild formMilder form, acute interstitialpancreatitis,1.Mild inflammation,2.Interstitial edema, and3.Focal areas of fat necrosisAcute Interstitial Pancreatitis
  16. 16. Morphology cont.• A hallmark of acute pancreatitis is amanifestation of the inflammatory response,namely the recruitment ofneutrophils to the pancreas.
  17. 17. Morphology cont. Severe Form• In the more severe form, acute necrotizingpancreatitis, the acinar and ductal tissues as wellas the islets of Langerhans are necrotic. Vascularinjury can lead to hemorrhage into theparenchyma of the pancreas.Acute Necrotizing Pancreatitis
  18. 18. Inflammatory SpreadDue to the pancreas lacking a capsule, the inflammation and necrosis can extend to
  19. 19. SignS &SymptomS• Severe epigastric abdominal pain - abrupt onset (mayradiate to back)• Nausea & Vomiting• Weakness• Tachycardia• +/- Fever; +/- Hypotension or shock– Grey Turner sign - flank discoloration due toretroperitoneal bleed in pt. with pancreatic necrosis (rare)– Cullen’s sign - periumbilical discoloration (rare)
  20. 20. • Grey Turner sign • Cullen’s sign
  21. 21. Clinical features• Full-blown acute pancreatitis is a medicalemergency. These patients usually have thesudden calamitous onset of an“acuteabdomen.”
  22. 22. DiagnoSiSLaboratory findings include marked elevation of1. serum amylase levels during the first 24hours,2. followed by a rising serum lipase level.3.Glycosuria occurs in 10% of cases.
  23. 23. 4. Hypocalcemia may result fromprecipitation of calcium soaps in necrotic fat;if persistent, it is a poor prognostic sign.5. Hyperglycemia6. Increased Hematocrit7. Leukocytosis8. Hyperbilirubinemia9. Inc. LDH10. Hypertriglyceridemia
  24. 24. Diagnosis• ↑ amylase…Nonspecific !!!– Amylase levels > 3x normal very suggestive of pancreatitis• May be normal in chronic pancreatitis!!!– Enzyme level ≠ severity– False (-): acute on chronic (EtOH); HyperTG– False (+): renal failure, other abdominal or salivary glandprocess, acidemia• ↑ lipase– More sensitive & specific than amylase
  25. 25. Imaging• Direct visualization of the enlarged inflamedpancreas by radiography is useful in thediagnosis of pancreatitis.
  26. 26. Prognosis• 85-90% mild, self-limited–Usually resolves in 3-7 days• 10-15% severe requiring ICUadmission–Mortality may approach 50% in severecases
  27. 27. Complications• Acute respiratory distress syndrome• Acute renal failure• A sterile pancreatic abscess• A pancreatic pseudocyst.
  28. 28. Treatment/ Management• The key to the management of acutepancreatitis is “resting” the pancreas bytotal restriction of oral intake and• by supportive therapy with intravenousfluids and analgesia.
  29. 29. Treatment

×