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õ
Continuing pancreatic
inflammation à
Irreversible
damage à
Pain ± permanent loss of function.
N.B.
Acute pancreatitis (e.g. from gallstones) doesn’t lead to
chronic pancreatitis.
Etiology
q
Alcohol
(> 85%) à
chronic calcifying pancreatitis.
q
Tropical
(nutritional).
q
Recurrent
attacks of acute pancreatitis.
q
Hereditary
(rare).
q
Idiopathic.
Pathogenesis:
N.B.
Obstruction
à
Cyst formation.
Ultimately,
exocrine tissue is damaged largely.
Clinical
features:
§
Abdominal
pain: same features as in the
acute disease
§
Anorexia à
Severe weight loss.
§
Pancreatic exocrine
insufficiency à
↓↓↓ Lipase secretion à
Maldigestion à
Lack of absorption of fats
à
Steatorrhea.
§
Pancreatic endocrine
insufficiency à
DM.
Investigations:
o
ERCP:
the gold standard, to outline duct system.
o
Endoscopic
US: very specific for
diagnosis.
o
CT
scan.
o
Lundh
test:
ü
For patients presenting
steatorrhea.
ü
Estimates exocrine
function: meal is given to patient (instead of secretin/ CCK).
ü
Rarely used if
pancreatic imaging is diagnostic.
Combination
of all tests is often required.
Treatment:
ü
Stop
drinking alcohol.
ü
Control
pain with narcotics (problem
with addiction!)
ü
Surgery.
ü
Treat
steatorrhea: low-fat diet +
pancreatic supplements + cimitidine.
ü
Treat
DM.
Complications:
Duct
obstruction by protein plugs:
à
Calcification in protein plugs in ducts à
Calculi.
à
Cyst à
Rupture into surrounding tissue à
Granulation tissue reaction à
Pseudocyst
à
Rupture into peritoneal cavity
à
Hemorrhagic
ascites.
N.B.
Pseudocyst:
ü
Commonest complication.
ü
Occurs in the lesser sac, intra- / peripancreatic.
ü
Has ↑ amylase
content.
ü
Lined by granulation tissue (no capsule, cf. true
cyst = lined by epithelium).
written
by:
Khalid Bin Yaroof. FMHS, UAE University.
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