Pancreatitis

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  • The first systematic analysis of pancreatitis was published by Reginald Fitz in 1889, Fitz’s report established the framework for studies and treatments of pancreatitis that have spanned more than a hundred years
  • Interstitial pancreatitis may lead to local and systemic complications but is rarely fatal; necrotizing pancreatitis may be fatal in up to 30% of cases. Interstitial
  • Once injury has been initiated, it is perpetuated and amplified by other processes, including the inflammatory cascade and vascular damage
  • This characteristic discoloration in both flanks results from the tracking of blood from the pancreatic area of the retroperitoneum
  • have prognostic value
  • Differentiation between biliary and nonbiliary forms of pancreatitis has important implications for treatment
  • Pancreatitis

    1. 1. UNIVERSITY OF THE GAMBIASCHOOL OF MEDICINE & ALLIED HEALTH SCIENCES ACADEMIC YEAR 2007-2008 MEDICAL PROGRAMME 4th YEAR SECOND SEMESTER MEDICINE I COURSE 2007 - 2008
    2. 2. Dr Ygber Luis Gonzalez de la Cruz Consultant phycisian R.V.T.H Visiting Lecturer
    3. 3. Pancreatitis
    4. 4. Acute Pancreatitis Is a clinical syndrome defined by a discrete episode of abdominal pain and elevations in serum enzyme levels Inflammation of the pancreas with varying amounts of injury to adjacent and distant organs more than 80% of the cases are related to biliary stones or alcohol use The criteria for diagnosing Pancreatitis areabdominal pain, fever, and jaundice, along with physical findings
    5. 5. Etiologic factors
    6. 6. Acute PancreatitisInterstitial NecrotizingPancreatitis Pancreatitis
    7. 7. PATHOLOGY Interstitial1. The gland is edematous, but its gross architecture is preserved2. Parenchymal inflammatory cells are present3. Reduced enzyme secretion4. Partial cell necrosis may allow the acinus to regenerate rapidly after injury.
    8. 8. Necrotizing Pancreatitis Marked tissue necrosis and hemorrhage Surrounding areas of fat necrosis Large hematomas often are located in the retroperitoneal space Vascular inflammation and thrombosis are common.
    9. 9. PATHOPHYSIOLOGY Three major pathological processes within the acinar cell1. Inactive digestive zymogens are converted into active enzymes2. Pancreatic exocrine secretion is inhibited3. The pancreas generates pro-inflammatory mediators
    10. 10. Activation of Pancreatic Zymogens May be the first step in a process that leads to pancreatic auto-digestion Potential consequences are1. damaging local effects2. Attack on other tissues3. Promotion or activation of additional pathways leading to tissue injury
    11. 11. Inhibition of Secretion Retention of active enzymes within the acinar cell instead of their secretion into the pancreatic duct
    12. 12. DIAGNOSIS Presence of severe abdominal pain Biochemical evidence of pancreatic injury
    13. 13. Symptoms Pain1. Occurs in 95% of patients2. Often located in the epigastric and umbilical region3. Deep, visceral pain is among the most severe described4. Nausea and vomiting are present in 85%
    14. 14. Signs Low-grade fevers are reported in 60% of patients Tachycardia and hypotension are found in up to 40% of patients Abdominal tenderness and guarding Bowel sounds are decreased or absent Pleural effusions Mild jaundice Dark discoloration in the back, flank, or the para- umbilical region
    15. 15. Grey Turner’s sign in acute pancreatitis
    16. 16. Markers of Pancreatic Injury A number of factors influence the level of serum markers of Pancreatitis1. Serum levels of pancreatic enzymes are the sum of tissue production, release into the blood, and clearance2. In patients with renal failure, the serum amylase may increase
    17. 17.  Measured enzyme activities may be influenced by a number of “serum factors” as hyperlipidemia Enzymes may be produced from non-pancreatic tissues Standard enzyme assays, such as amylase and lipase, provide no information on the severity of the pancreatitis
    18. 18. Markers of Pancreatic Injury Amylase Lipase Urinary enzymes (urinary trypsinogen 2) Trypsinogen activation peptide
    19. 19. Inflammatory Markers Inflammatory cells release neutrophil-specific elastase Interleukin-6 (IL-6) C-reactive protein
    20. 20. Markers of Biliary Tract Involvement alanine aminotransferase (ALT) Ratio of lipase to amylaseratio of lipase to amylase in alcoholic Serum bilirubin level over 3
    21. 21. Imaging Abdominal Radiographs to exclude non- pancreatic diseases Radiographic findings1. Pleural effusions2. Intestinal gas patterns may demonstrate an ileus pattern3. Isolated dilated loop of small bowel overlying the pancreas
    22. 22. 4. Colon cutoff sign5. Loss of the psoas margins6. Pancreatic calcification or calcified gallstones
    23. 23.  Sonography1. appears hyp-oechoic Computed Tomography1. Pancreatic enlargement2. Inhomogeneity of the pancreatic parenchyma3. Fluid infiltrating the peri-pancreatic fat Endoscopic Cholangiopancreatography
    24. 24. LOCAL COMPLICATIONS Acute Fluid Collections Necrosis and Infected Necrosis Pseudocysts Pancreatic Abscesses Ascites and Fistulae Vascular and Splenic Complications Gastrointestinal Obstruction Gastrointestinal Obstruction

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