Pathophysiology of pancreatitis

1. PANCREATITIS
BY
IBEKWE CHIGOZIE BLESSING
GROUP 310

2. Brief overview of the pancreas
• The pancreas is a large gland behind the stomach
and next to the small intestine. It does two main
things
 releases powerful digestive enzymes into the small
intestine to aid food digestion. (Exocrine function)
Releases the hormones insulin and glucagon into the
bloodstream. These hormones help to control how
the body uses food for energy. (Endocrine fuction)

4. Definition
• Inflammatory disorders of the pancreas. The
damage occurs when the digestive enzymes
are activated before they are released into the
small intestine and begin attacking the
pancreas

5. Types
• Acute pancreatitis
Sudden inflammation that lasts for a short time. It
may range from a mild discomfort to a severe life
threatening illness. Most people with acute
pancreatitis recover completely after getting the
proper treatment.
In sever cases, it can lead to bleeding into the
gland, serious tissue damage, infection and cyst
formation, and can harm vital organs such as the
heart, lungs and kidneys

6. Phases of acute pancreatitis
Early phase(within 1 week)
• Characterized by SIRS
+/organ failure
• Severity assessed by
functional/clinical Severity
Scoring System
(Ranson/Galsgow etc)
Late Phase (>1 week)
• Characterized by local
complication
• Severity assessed by
morphological scoring
system(Balthazar Scoring)

7. • Chronic pancreatitis
Long lasting inflammation which most often
happens after a episode of acute pancreatitis.

8. Etiology of Acute pancreatitis
 Metabolic
Alcoholism
Hyperlipoproteinemia
Hypercalcemia
Drugs (e.g azathioprine)
 Genetic
 Mutation in the
cationic trypsinogen
(PRSS1) and trypsin
inhibitor (SPINK1) genes
• Mechanical
Gallstones
Trauma
Iatrogenic injury
Perioperative injury
Endoscopic procedures
with dye injection.
 Vascular
Shock
Atheroembolism

9. Etiology of chronic pancreatitis
• Heavy alcohol consumption for a long time
• Certain hereditary conditions, such as cystic
fibrosis
• Gallstones
• Conditions such as high triglycerides and lupus

10. Clinical Manifestations
• ABDOMINAL PAIN-CARDINAL SYMPTOM
SITE: usually experienced first in the epigastrium
but may be localized to either upper quadrant or
felt diffusely throughout the abdomen or lower
chest
ONSET: characteristically develops quickly,
generally following substantial meal
SEVERITY: frequently severe, reaching max.
intensity within minutes
NATURE: “boring through”, “knifing” (illimitable
agony)

11. DURATION: hours-days
COURSE: constant (refractory to usual doses of
analgesics, not relieved by vomiting)
RADIATION: directly to back(50%), chest or flanks
AGGRAVATING FACTOR: food/alcohol intake,
walking, lying supine.
RELEIVING FACTOR: sitting or leaning/stooping
forward (MUHAMMEDAN PRAYER SIGN)

12. Pathophysiology
• Acute pancreatitis appears to be caused by
autodigestion of the pancreas by inappropriately
activated pancreatic enzymes.
• Trypsin, as we know, when it activated, it will
lead to activation of other pancreatic enzymes (
phospholipase and elastase) as well as more
trypsin. This will lead to autodigestion.
• Trypsin also activates the kinin system, that will
lead to activation of factor XII ( Hageman's factor
), and this will activate clotting & complement
system.

13. • Causes that lead to initial activation of
pancreatic enzymes are:
 Pancreatic duct obstruction.
 Primary acinar cell injury.
 Defective intracellular transport of proenzymes
within acinar cells.
 Alcohol

14. Pancreatic duct obstruction
• Due to the effect of lipase, since it is secreted
in active form, any obstruction will cause fat
necrosis and produce an inflammatory
response.

15. Primary acinar cell injury
• Acinar cells could be primarily been damaged
by:
 ischemia
 viral infections (e.g., mumps)
 Drugs
 Direct trauma to the pancreas.

16. Defective intracellular transport of
proenzymes within acinar cells
• Pancreatic proenzymes ( in zymogen granules
) and lysosomal hydrolases ( in lysosomes )
become packaged together. This results in
proenzyme activation, lysosomal rupture
(action of phospholipases), and local release
of activated enzymes.
• The role of this mechanism in human acute
pancreatitis is not clear.

17. Alcohol
• Several mechanisms involved in alcohol-induced
pancreatitis :
 increases pancreatic exocrine secretion and
contraction of the sphincter of Oddi (the muscle
regulating the flow of pancreatic juice through papilla
of Vater).
 induction of oxidative stress in acinar cells, which
leads to membrane damage.
 chronic alcohol ingestion results in the secretion of
protein-rich pancreatic fluid, which leads to the
deposition of inspissated protein plugs and
obstruction of small pancreatic ducts.

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