This document provides an overview of chronic pancreatitis, including its pathophysiology, etiology, clinical features, diagnosis, and management. It discusses how chronic pancreatitis represents a continuous inflammatory and fibrosing process of the pancreas resulting in permanent dysfunction. The main causes are alcohol use and genetic factors. Patients present with abdominal pain in 95% of cases and can develop weight loss, steatorrhea, and diabetes. Diagnosis involves tests of pancreatic function and imaging tests looking for features like calcification. Treatment focuses on pain control, managing maldigestion with pancreatic enzyme replacement, and addressing complications like pseudocysts and stenosis.

1. Guide : Dr V A KOTHIWALE
Co Guide : Dr Raju Badiger
Presenter : Dr Prudhvi Krishna

2. References▪ Sleisenger and
Fordtran’s - 9th edition.
▪ Harrison Principles of
internal medicine –
18th edition.

3. Chronic pancreatitis represents a continuous,
prolonged, inflammatory and fibrosing process of
the pancreas with irreversible morphologic changes
resulting in permanent endocrine and exocrine
pancreatic dysfunction.
-Harrisons 18th Ed.
Acute pancreatitis and chronic pancreatitis are assumed to be
different disease processes, and most cases of acute
pancreatitis do not result in chronic disease.

4. PREVALANCE
10-15/1,00,000 in western
countries.
114-200/1,00,000 in southern
India.
Typical age 35-55

5. Chronic pancreatitis
Pathophysiology
Etiology
Clinical features
Diagnosis
Management
Complications

6. PATHOPHYSIOLOGY
Incompletely understood
Why 10% heavy alcoholics develop
chronic pancreatitis and the rest not, or
limited to asymptomatic pancreatic fibrosis
Alcohol is the most studied

7. Ductal obstruction hypothesis
Chronic
alcohol use
acinar and
ductal cell
protein rich
pancreatic
juice, low in
volume and
HCO3
formation
of protein
precipitates
– plug
calcificatio
n of ppt –
ductal
stone
formation
ductule
obstruction
parenchym
al damage
Pancreatic ductal stone are seen in
alcoholic, tropical, hereditary, idiopathic
Sleisenger and Fordtran’s - 9th edition.

8. Toxic metabolic hypothesis
(alcohol) Direct injurious effect on acinar and ductal cells
Increased membrane lipid peroxidation (oxidative stress),
free radical production
Increase acinar cell sensitivity to pathogenic stimuli
Stimulate CholeCystoKinin(CCK) production (duodenal I
cells) – activation of proinflammatory transcription factor

9. Necrosis fibrosis hypothesis
Repeated episodes of acute pancreatitis with cellular
necrosis or apoptosis, healing replaces necrotic tissue
with fibrosis
Evidence from natural history studies - more severe and
frequent attacks

10. • Cystic fibrosis is assosiated with
abnormalities of HCO3 secretion, ductal
dilatation, ppt formation, pancreatic atrophy
• Seen in 50% of idiopathic CP, not common
in alcoholic CP
CFTR –
cystic fibrosis
trans-membrane
conductance
regulator
• Seen in pediatric Idiopathic CP, hereditary
Pancreatitis, Tropical Pancreatitis; but not
in chronic alcoholic pancreatitis
SPINK1 - serine
protease inhibitor
Kazal type 1
Genetic forms
• Once trypsinogen is activated to trypsin,
becomes resistant to inactivation and
activate other proenzymes leading to
episodes of acute pancreatitis– like
necrosis fibrosis theory
PRSS1 – cationic
trypsinogen gene

11. Etiologic factors associated With CP: TIGAR-O

12. TROPICAL PANCREATITIS
Africa, India, Brazil
A disease of early childhood and youth
> 90% before age of 40yrs
Prevalence in endemic areas: 1 in 500-800
Abdominal pain, malnutrition, exocrine and endocrine insufficiency
Pancreatic caliculi – 90%
50% SPINK1 gene mutation.

13. AutoImmune Pancreatitis
5% of CP, more in males, middle age
12 – 50% ass. With other autoimmune diseases
abdominal pain, weight loss, jaundice
Imaging studies show focal or diffuse (sausage
shaped) enlargement
Diagnosis – clinical, imaging, IgG4, autoantibodies
Treatment – glucocorticoids 1-2m and tappering in 3-
4m

14. Idiopathic Pancreatitis
Early onset
• 20yr mean age, male=female
• 96% pain
• Calcification, exocrine or endocine insufficiency
develop slowly over time – 25, 26 -27.5 yrs
• CFTR, SPINK1 genes
Late onset
• Pain is less frequent 54%-75%
• Age of onset 56yrs, m=f
• 90% calcification is seen

15. Diabetes mellitus
1% of DM from CP
In DM - pancreas is smaller,
• abnormal duct in 40-50% ,
• abnormal pancreatic function in 40-50%
Insulin is a trophic factor for exocrine function of the
pancreas
Insulin deficiency + microangiopathy of DM lead to
pancreatic damage
DM and CP cause effect relation is not clear

16. • Chronic pancreatitis is a relapsing condition that
presents with abdominal pain, occurring in 95% of
cases.
• Pain can be episodic, lasting hours to days, or it can
persist for months or even years. The pain is
characteristically steady in the epigastrium, and it
frequently radiates to the back.
• Weight loss, Steatorrhea.
Clincal features

17. Diagnosis
▪ No single test is adequate
▪ Tests for function
▪ Tests for structure
▪ Both are more accurate in advanced
disease .

18. Tests of function – hormone stimulation
• Direct Tests
• Secretin/ secretin CCK test
• Indirect Tests
• Fecal elastase
• Fecal chymotrypsin
• Serum trypsinogen (trypsin)
• Fecal fat
• Blood glucose
Tests of structure
• Plain film of the abdomen
• CT
• Ultrasonography
• MRI, particularly MRCP
• ERCP

20. Routine labarotory tests
Serum amylase and lipase
• May be elevated in acute exacerbations
• Also found increased in pseudocyst, ductal
stricture, internal pancreatic fistula,pancreatic
carcinoma,cholecystitis,ectopic pregnancy

21. Classics of Chronic pancreatitis
Pancreatic calcification
Steatorrhea
Diabetes mellitus
Found in less than a third of pts with CP
• abnormal secretin stimulations test when >60 %
affected
• Serum trypsinogen < 20ng/ml,
• Fecal elastase < 100mcg/mg stool - severe
exocrine insuf.

22. • Pancreatic calcifications are shown in 25-59% of patients.
• This feature is pathognomonic for chronic pancreatitis.
• Calcification is punctate or coarse, and it may have a focal, segmental, or
diffuse distribution.
chronic pancreatitis with
marked calcification of the
pancreatic parenchyma.
Plain films

23. The anatomic proximity of the pancreatic head and stomach antrum is
constant, and enlargement of the pancreatic head usually causes
effacement of the antrum. This finding has been termed the pad sign.
Upper gastrointestinal tract barium
study shows a reverse 3 in the
duodenum due to chronic pancreatitis.
Pancreatic carcinoma can have a
similar appearance
Upper GI tract barium series

24. Currently, CT is regarded as the
imaging modality of choice for the
initial evaluation of suggested
chronic pancreatitis.
The diagnostic features of:
• pancreatic enlargement,
• pancreatic calcifications,
• pancreatic ductal dilatation,
• thickening of the peripancreatic
fascia, and
• bile duct involvement
are depicted well on CT scans.
CT Findings

25. The sensitivity of plain film for detection of pancreatic calcifications
is about 80 %, which is higher than that of sonography but lower
than that of CT.
CT Findings

26. • Ultrasonography is the first
modality to be used in
patients presenting with
upper abdominal pain,
although the direct diagnosis
of chronic pancreatitis is not
always possible.
• In early disease, the pancreas
may be enlarged and
hypoechoic, with ductal
dilatation. Later, the pancreas
becomes heterogeneous,
with areas of increased
echogenicity and focal or
diffuse enlargement.
Chronic pancreatitis in phase of
exacerbation - an uneven outline of the
gland and heterogeneous structure
of pancreatic tissue.
ULTRASOUND

27. • In late stages of the disease, the pancreas becomes atrophic and
fibrotic, and it shrinks. These changes result in a small, echogenic
pancreas with a heterogeneous echotexture.
• Pseudocysts may occur, and focal hypoechoic inflammatory
masses may mimic pancreatic neoplasia.
• Calculi and calcification in the gland result in densely echogenic
foci, which may show shadow
ULTRASOUND

28. ERCP is the most sensitive and specific technique in the investigation of
chronic pancreatitis, although it is invasive and may cause an acute episode
of pancreatitis and ascending cholangitis.
Endoscopic retrograde cholangiopancreatography (ERCP)
ERCP of normal
pancreatic and
biliary ducts.
ERCP

29. Endoscopic retrograde cholangiopancreatography (ERCP)
Mild pancreatitis
may present with
minimal dilation of
the main
pancreatic duct
and some clubbing
of the side
branches of the
duct
ERCP

30. Chronic Pancreatitis
Endoscopic retrograde cholangiopancreatography (ERCP)
The patient with
moderately-
staged chronic
pancreatitis
shows moderate
dilation of the
main pancreatic
duct (1.5 times
the normal size)
This is
accompanied by
moderate
clubbing of the
side branches of
the main
pancreatic duct
ERCP

31. Chronic Pancreatitis
Endoscopic retrograde cholangiopancreatography (ERCP)
A characteristic "chain of
lakes" appearance of the
main pancreatic duct can
be noted on ERCP in
patients with severe
chronic pancreatitis.
The main pancreatic duct
is enlarged (greater than
1.5 times) with increased
tortuosity.
There is severe clubbing
and dilation of the side
branches.
Stone formation and
occlusion of the
pancreatic duct may
occur in this stage of the
disease
ERCP

32. Chronic Pancreatitis
MRI, particularly MRCP,
is a noninvasive
technique.
The combination of
pancreatic parenchyma
imaging sequences
with MR angiography
and secretin-enhanced
MRCP offers the
possibility of a
comprehensive
examination within a
single diagnostic
modality for evaluation
of the full range of
pancreatic diseases. (A) MRCP demonstrates a "double duct" stricture with proximal dilatation
of the common bile duct and pancreatic duct (arrow). A cystic lesion is seen
between the common bile duct and the duodenal wall. (B) Fat-suppressed
TSE T1-weighted image. Unenhanced (C) and delayed gadolinium-
enhanced (D) T1-weighted images, demonstrate diffuse enhancement of the
sheetlike mass, which corresponded to fibrotic tissue.
Groove pancreatitis
MRI

33. 34

34. Treatment
▪ Aim - Pain control and management of maldigestion
▪ Pain
▪ Avoid alcohol
▪ Low fat meals
▪ Antipain – narcotics tramadol,codeine(addiction)
▪ Surgical pain control
▪ Resection (local - - - - 95%) –causes pancreatic insufficiency
▪ Splanchinectomy, celiac ganglionectomy, nerve block
▪ Endoscopic treatment
▪ Sphinctorotomy, dilatation of strictures, caliculi removal, duct stenting
▪ Complications– acute pancreatitis, abscess, ductal damage, death
▪ Pancreatic enzymes- Non enteric coated
Pancrelipase  CREON,Ultresa.

35. Treatment of maldigestion
▪ Pancreatic enzyme replacement
▪ 2-3 enteric coated with meals
▪ adjuvants with conventional tablets – H2 blockers, PPI,
Na bicarbonate,
▪ Steatorrhea can be abolished if 10 % of normal
lipase amount can be delivered to the duodenum
at the right time.

36. Approach

37. Chronic Pancreatitis
Complications of chronic pancreatitis include:
• Pseudocyst formation
• Fistula formation
• Pseudoaneurysms of large arteries close to the
pancreas
• Stenosis of the common bile duct
• Splenic and/or portal venous obstruction
• Diabetes can develop in 70-90% of patients with
chronic calcific pancreatitis
Complications

38. Thank you