Monoclonal antibody production by hybridoma technology
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
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
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
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
Notes de l'éditeur
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