Acute Pancreatitis

Classification
Navid Khezri – 351
 Endocrine

Exocrine OpenStax, Anatomy & Physiology. OpenStax CNX.

Digestive Enzymes

Proenzyme Active Form

Lipase

Amylase

Trypsinogen Trypsin

Proelastase Elastase

Pandol SJ. The Exocrine Pancreas. San Rafael (CA): Morgan & Claypool Life Sciences; 2010. Digestive Enzymes.
Normal Histology

Lamps, LW. Pancreas. Images: Lobular pancreas, acinar parenchyma. ExpertPath.

 Acute Pancreatitis
- Reversible inflammatory
process of the pancreas
- Often mild, but severe
disease can have a
mortality
rate of up to 30%
- Common cause of
hospitalization

https://radiologyassistant.nl/abdomen/pancreas/acute-pancreatitis
Pathophysiology
- Caused by auto digestion
- Pancreatic cell damage occurs leading to activation of trypsinogen
- Other digestive enzymes are activated
- Macrophages and neutrophils are recruited resulting in inflammation
- Cell damage is potentiated and the tissue is destroyed

Trypsinogen
Pancreatic
Insult
cell damage
Tissue
Trypsin Recovery
destruction

Inflammation Other enzymes

activated
 Phases of the course of acute pancreatitis

Edematous (interstitial) pancreatitis

in frequency it occupies 80-85% in the structure of the disease. It is characterized by a mild
severity of the disease and a rare development of local complications or systemic
disorders.

Walled-off pancreatic necrosis (WOPN) is a late complication of acute pancreatitis, although it can occur in chronic pancreatitis or as a
result of pancreatic trauma. Differentiation of WOPN from pancreatic pseudocyst is essential because management differs. WOPN may
need aggressive treatment to avoid complications.
WOPN usually occurs four weeks after the episode of acute pancreatitis. Before this time, it is referred to as an acute necrotic collection
(ANC).
Terminology
The following are the latest terms according to the updated Atlanta classification to describe fluid collections associated with acute
pancreatitis
• fluid collections associated with interstitial edematous pancreatitis (i.e. minimal or no necrosis)
• acute peripancreatic fluid collections (APFC): in the first 4 weeks: non-encapsulated peripancreatic fluid collections
• pseudocysts: develop after 4 weeks; encapsulated peripancreatic or remote fluid collections
• fluid collections associated with necrotizing pancreatitis
• acute necrotic collections (ANCs): in the first 4 weeks; non-encapsulated heterogeneous non-liquefied material
• walled-off necrosis (WON or WOPN): develop after 4 weeks; encapsulated heterogeneous non-liquefied material
Acute mild pancreatitis
Pancreatic necrosis with this form of acute pancreatitis is not formed (edematous
pancreatitis) and organ failure does not develop

Acute pancreatitis of moderate degree

It is characterized by the presence of either one of the local manifestations of the disease:
acute peripancreatic fluid accumulation, acute necrotic accumulation, peripancreatic
infiltrate, delimited necrosis, or / and the development of general manifestations in the form
of transient organ failure (no more than 48 hours)

Acute severe pancreatitis

Characterized by the presence of either infected pancreatic necrosis (purulent-necrotic
parapancreatitis) or/and the development of persistent organ failure (more than 48 hours)
 Moderate and severe severity of the course
IA phase
usually the first week of illness
The formation of foci of necrosis in the parenchyma of the pancreas or the surrounding tissue of various sizes and the
development of endotoxicosis.
Endotoxicosis is manifested by mild or deep systemic disorders in the form of organ (multi-organ) failure.
There is an accumulation of enzymatic effusion (enzymatic peritonitis parapancreatitis), which is one of the sources of
endotoxicosis

IB phase
usually the second week of illness
It is characterized by the reaction of the body to the formed foci of necrosis (both in the pancreas and in the
parapancreatic tissue)

Clinically, the phenomena of resorptive fever prevail,

a peripancreatic infiltrate is formed.