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Acute pancreatitis
(AP) is an inflammatory process of the pancreas that
involves peripancreatic tissues and remote organs
Chronic pancreatitis
(CP) is an inflammatory disorder that causes anatomic
changes, including infiltration of chronic inflammatory
cells and fibrosis of the pancreas.
The endocrine and exocrine portions of the pancreas
gland are depicted in Figure 1B.
The chief endocrine unit is called the Islets of
Langerhan where alfa,beta, and ? cells are present and
produce insulin, glucagon, and somatostatin,
respectively.
Acinar cells make up the exocrine portion of the gland
and are where digestive enzymes are produced.
The acinar cells are connected to the pancreatic duct
by ductules lined by columnar epithelium that secrete a
bicarbonate-rich fluid.
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The digestive enzymes are stored in an inactive
precursor form inside zymogen granules within the
acinar cells to prevent autodigestion of the pancreas.
When neurohumoral factors stimulate the pancreas to
secrete digestive enzymes, the zymogen granules fuse
with the apical surface of the acinar cell and are
secreted into the ductular system of the pancreas.
Under normal circumstances, enterokinase, a brush
border enzyme of the duodenal mucosa, partially
digests the pancreatic enzyme trypsinogen and
releases trypsin, which is responsible for activating
most of the other pancreatic enzymes within the lumen
of the small bowel.
Pathophysiology
The key event in the initiation of acute pancreatitis is
acinar cell injury and the subsequent activation of
trypsinogen to trypsin that leads to autodigestion of the
gland.
Acinar Cell Injury
A number of factors have been implicated in causing
injury to the pancreatic acinar cells.
- Alcohol,trauma, viruses, ischemia, and toxins
cause primary acinar cell injury.
Autodigestion
The proteolytic enzymes secreted by the acinar cells
can digest the pancreas itself, but under normal
circumstances, the pancreas is protected from
autodigestion by several mechanisms, which are listed
in Table 2.
The first line of defense is the production of the
digestive enzymes in an inactive precursor form and
storage in zymogen granules.
Pancreatic stellate cells (PaSCs or PSCs) are myofibroblast-like cells that can switch between
the quiescent and activated phenotypes, like hepatic stellate cells.[2] PaSCs reside
in exocrine areas of the pancreas. When activated (by cytokines from macrophage), PaSCs
migrate to the injured location, and participate in tissue repair activities,
secreting ECMcomponents. PaSCs may play a role in the pathogenesis
of pancreatitis and pancreatic cancer.[1]
fever,
nausea,
vomiting, and
adynamic ileus.
fever in the initial stage of acute pancreatitis is not an expression of a bacterial inflammatory
process or even of underlying necrotizing pancreatitis but rather of a systemic process
and thus does not represent an automatic indication for antibiotic treatment
Clinical Findings
Typically, the patient is agitated, tachycardic, and often looks ill.
The abdomen is very sensitive to touch and palpation usually reveals an abdomen with
moderate guarding which, however, is distinguishable from the board-like rigidity of
classic peritonitis.
The tenderness (pain or discomfort) is usually most marked in the upper abdomen, but it may
also be
diffuse.
Complication
Depending on the severity of the inflammation and the inflammatory response in both the
pancreas and the peripancreatic region, a spectrum of complications can arise in the
pancreas itself and in the adjacent structures.
The most serious complication is necrosis of the pancreatic parenchyma as well as extensive
fat necrosis in the peripancreatic retroperitoneum which may extend down to the pelvis and
rostrally up to the mediastinum.
Chronic Pancreatitis