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UNIVERSITY OF THE GAMBIA
SCHOOL OF MEDICINE & ALLIED HEALTH
            SCIENCES
       ACADEMIC YEAR 2007-2008


     MEDICAL PROGRAMME
  4th YEAR SECOND SEMESTER
          MEDICINE I

        COURSE 2007 - 2008
Dr Ygber Luis Gonzalez de la Cruz

      Consultant phycisian
              R.V.T.H


         Visiting Lecturer
Pancreatitis
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
Etiologic factors
Acute Pancreatitis




Interstitial         Necrotizing
Pancreatitis         Pancreatitis
PATHOLOGY
    Interstitial
1.   The gland is edematous, but its gross
     architecture is preserved
2.   Parenchymal inflammatory cells are present
3.   Reduced enzyme secretion
4.   Partial cell necrosis may allow the acinus to
     regenerate rapidly after injury.
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.
PATHOPHYSIOLOGY

    Three major pathological processes within the
     acinar cell
1.   Inactive digestive zymogens are converted into
     active enzymes
2.   Pancreatic exocrine secretion is inhibited
3.   The pancreas generates pro-inflammatory
     mediators
Activation of Pancreatic Zymogens
     May be the first step in a process that leads to
      pancreatic auto-digestion
     Potential consequences are
1.    damaging local effects
2.    Attack on other tissues
3.    Promotion or activation of additional
      pathways leading to tissue injury
Inhibition of Secretion
   Retention of active enzymes within the acinar
    cell instead of their secretion into the pancreatic
    duct
DIAGNOSIS
   Presence of severe abdominal pain
   Biochemical evidence of pancreatic injury
Symptoms
    Pain
1.   Occurs in 95% of patients
2.   Often located in the epigastric and umbilical
     region
3.   Deep, visceral pain is among the most severe
     described
4.   Nausea and vomiting are present in 85%
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
Grey Turner’s sign in acute pancreatitis
Markers of Pancreatic Injury
    A number of factors influence the level of
     serum markers of Pancreatitis
1.   Serum levels of pancreatic enzymes are the
     sum of tissue production, release into the
     blood, and clearance
2.   In patients with renal failure, the serum
     amylase may increase
   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
Markers of Pancreatic Injury
   Amylase
   Lipase
   Urinary enzymes (urinary trypsinogen 2)
   Trypsinogen activation peptide
Inflammatory Markers
   Inflammatory cells release neutrophil-specific
    elastase
    Interleukin-6 (IL-6)
   C-reactive protein
Markers of Biliary Tract Involvement
   alanine aminotransferase (ALT)
   Ratio of lipase to amylaseratio of lipase to
    amylase in alcoholic
   Serum bilirubin level over 3
Imaging
    Abdominal Radiographs to exclude non-
     pancreatic diseases
    Radiographic findings
1.   Pleural effusions
2.   Intestinal gas patterns may demonstrate an
     ileus pattern
3.   Isolated dilated loop of small bowel overlying
     the pancreas
4.   Colon cutoff sign
5.   Loss of the psoas margins
6.   Pancreatic calcification or calcified gallstones
    Sonography
1.   appears hyp-oechoic
    Computed Tomography
1.   Pancreatic enlargement
2.   Inhomogeneity of the pancreatic parenchyma
3.   Fluid infiltrating the peri-pancreatic fat
    Endoscopic Cholangiopancreatography
LOCAL COMPLICATIONS
   Acute Fluid Collections
   Necrosis and Infected Necrosis
   Pseudocysts
   Pancreatic Abscesses
   Ascites and Fistulae
   Vascular and Splenic Complications
   Gastrointestinal Obstruction
   Gastrointestinal Obstruction
Pancreatitis
Pancreatitis
Pancreatitis

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Pancreatitis

  • 1. UNIVERSITY OF THE GAMBIA SCHOOL OF MEDICINE & ALLIED HEALTH SCIENCES ACADEMIC YEAR 2007-2008 MEDICAL PROGRAMME 4th YEAR SECOND SEMESTER MEDICINE I COURSE 2007 - 2008
  • 2. Dr Ygber Luis Gonzalez de la Cruz Consultant phycisian R.V.T.H Visiting Lecturer
  • 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
  • 6. Acute Pancreatitis Interstitial Necrotizing Pancreatitis Pancreatitis
  • 7. PATHOLOGY  Interstitial 1. The gland is edematous, but its gross architecture is preserved 2. Parenchymal inflammatory cells are present 3. Reduced enzyme secretion 4. Partial cell necrosis may allow the acinus to regenerate rapidly after injury.
  • 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. PATHOPHYSIOLOGY  Three major pathological processes within the acinar cell 1. Inactive digestive zymogens are converted into active enzymes 2. Pancreatic exocrine secretion is inhibited 3. The pancreas generates pro-inflammatory mediators
  • 10. Activation of Pancreatic Zymogens  May be the first step in a process that leads to pancreatic auto-digestion  Potential consequences are 1. damaging local effects 2. Attack on other tissues 3. Promotion or activation of additional pathways leading to tissue injury
  • 11. Inhibition of Secretion  Retention of active enzymes within the acinar cell instead of their secretion into the pancreatic duct
  • 12. DIAGNOSIS  Presence of severe abdominal pain  Biochemical evidence of pancreatic injury
  • 13. Symptoms  Pain 1. Occurs in 95% of patients 2. Often located in the epigastric and umbilical region 3. Deep, visceral pain is among the most severe described 4. Nausea and vomiting are present in 85%
  • 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. Grey Turner’s sign in acute pancreatitis
  • 16. Markers of Pancreatic Injury  A number of factors influence the level of serum markers of Pancreatitis 1. Serum levels of pancreatic enzymes are the sum of tissue production, release into the blood, and clearance 2. In patients with renal failure, the serum amylase may increase
  • 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.
  • 19. Markers of Pancreatic Injury  Amylase  Lipase  Urinary enzymes (urinary trypsinogen 2)  Trypsinogen activation peptide
  • 20. Inflammatory Markers  Inflammatory cells release neutrophil-specific elastase  Interleukin-6 (IL-6)  C-reactive protein
  • 21. Markers of Biliary Tract Involvement  alanine aminotransferase (ALT)  Ratio of lipase to amylaseratio of lipase to amylase in alcoholic  Serum bilirubin level over 3
  • 22. Imaging  Abdominal Radiographs to exclude non- pancreatic diseases  Radiographic findings 1. Pleural effusions 2. Intestinal gas patterns may demonstrate an ileus pattern 3. Isolated dilated loop of small bowel overlying the pancreas
  • 23. 4. Colon cutoff sign 5. Loss of the psoas margins 6. Pancreatic calcification or calcified gallstones
  • 24. Sonography 1. appears hyp-oechoic  Computed Tomography 1. Pancreatic enlargement 2. Inhomogeneity of the pancreatic parenchyma 3. Fluid infiltrating the peri-pancreatic fat  Endoscopic Cholangiopancreatography
  • 25.
  • 26. LOCAL COMPLICATIONS  Acute Fluid Collections  Necrosis and Infected Necrosis  Pseudocysts  Pancreatic Abscesses  Ascites and Fistulae  Vascular and Splenic Complications  Gastrointestinal Obstruction  Gastrointestinal Obstruction

Editor's Notes

  1. 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
  2. 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
  3. Once injury has been initiated, it is perpetuated and amplified by other processes, including the inflammatory cascade and vascular damage
  4. This characteristic discoloration in both flanks results from the tracking of blood from the pancreatic area of the retroperitoneum
  5. have prognostic value
  6. Differentiation between biliary and nonbiliary forms of pancreatitis has important implications for treatment