Chronic pancreatitis

1. Maj Vipul Kumar
Dr Manjunath

2.  Pancreas derived from Greek word ‘pan’(all) and
‘kreas’(flesh).
 Weight-80 g ,15-20 cm long.
 Lies transversely along the posterior wall of
stomach.
 Between 2nd part of duodenum and spleen.
 Divided into Head, neck, body and tail.

4. Nestled in the C shaped duodenum.
Lies posterior to transverse mesocolon.
Posterior to head lies vena cava, right renal
artery and both renal veins.

5.  Iies anterior to portal veins.
 Inferior border smv joins with splenic vein.

6. Continues from the neck and lies to the left of
the superior mesentric vessels.
Passes over the L2 vertebra and
Aorta.
Posterior surface is devoid of
Peritoneum and is in contact
With aorta, left suprarenal gland
and renal vessels.

7.  Lies anterior to left kidney.
 Closely related to splenic hilum and colic
flexure.

10.  Head drains into anterior and posterior
pancreaticoduodenal veins.
 The posterior superior pancreaticoduodenal
veins enters SMV laterally at he superior
border of the neck of the pancreas.
 The anterior superior pancreaticoduodenal
veins enters the right just before its
confluence with the SMV at the inferior border
of the pancreas.

13.  Exocrine pancreas begins development during 4th
week gestation.
 Pleuripotent pancreatic epithelial stem cells give
rise to exocrine and endocrine cells lines as well
as the intricate pancreatic ductal network.
 Dorsal and ventral buds appear from the
primitive duodenal endoderm.
 Dorsal bud typically appears first and ultimately
develops into the superior head, neck ,body and
tail of the mature pancreas.

14.  Ventral bud will become the inferior part of
the head and uncinate process of the gland.
 Between 4th and 8th ,the ventral bud rotates
posteriorly in a clockwise fashion to fuse with
dorsal bud.
 At approximately 8 weeks of gestation ,dorsal
and ventral buds are fused.

15.  Pancreatic Divisum.
 Annular Pancreas.
 Ectopic Pancreas.

16.  Failure of the dorsal and ventral ducts to fuse
during embryogenesis.
 Ventral pancreatic duct and common bile
duct that enter the duodenum through a
major papilla.
 Dorsal pancreatic duct enters through a
minor papilla that is slightly proximal.

17.  Aberrant migration of the ventral pancreas
bud.
 Leading to circumferential or near
circumferential pancreas tissue surrounding
the second portion of the duodenum.

18.  Arise anywhere along the primitive foregut
most common in the stomach, duodenum
and Meckel’s diverticulum.

19.  Pancreas is a complex gland with both
endocrine and exocrine functions.
 Acinar cells (85% of the glands) and islet
cells(2%)cells embedded in a complex
extracellular matrix, comprising 10% of the
gland.
 Remaining 3-4% composed of epithelial duct
and blood vessels.

20.  Main exocrine function is to provide enzymes
for alimentary digestion.
 Acinar cells synthesize many enzymes
(proteases),such as trypsin, chymotrypsin,
carboxypeptidases, and elastases that digest
food proteins.

22.  Cephalic phase-pancreas stimulated by vagus
nerve in response to the sight, smell or taste
of food.(20-25% of the daily secretion).
 Gastric phase-10% of the secretion.
 Intestinal phase-(60-65%) mediated by
secritin and CCK.

23.  Persistent progressive irreversible damage of
the pancreas due to chronic inflammation.
 Atrophy of the pancreatic parenchyma.
 3-10/100,000.

24.  T-Toxic
 I-Idiopathic
 G-Genetic
 A-Autoimmune
 R-Recurrent attacks.
 O-Obstructive.

25.  Metabolic-oxidative stress theory.
 Ductal obstruction hypothesis.
 SAPE Hypothesis.

26.  Normal acinar cell function and zymogen
release is disrupted by stress.

27.  Mechanical role for ductal plug and stone.
 Disruption of the integrity of acinar cells.

28.  Local cytokines activate the circulating
macrophages.
 Stellate cells also get activated.
 During subsequent healing phase, anti
inflammatory mediators(like TGF-B).
 Drive the stellate cells and tissue
macrophages to synthesis and deposit the
fibrogenic matrix protein.

29.  Alcohol Abuse.
 Smoking.
 Gene Mutations.

30.  Most important risk factors.
 3-7% heavy drinkers develop chronic
pancreatitis.
 Exerts noxious effects.
 Increases total protein concentration.

31.  Promotes synthesis and secretion of
lithostathine by acinar cells and increases
glycoprotein 2 secretion in pancreatic juice.
 These factors lead to protein precitation and
subsequent formation of protein plugs and
eventually stone inside the pancreatic duct.
 As a result of obstruction, acinar cells are no
longer able to secrete pancreatic enzymes
and are predisposition to autodigestion.

32.  Increases the risk of alcohol induced chronic
pancreatitis.
 Active smokers develop pancreatitis at a
younger age.

33.  Mutations in PRSS1,SPINK1 and CFTR genes.
 PRSS1 gene located on chromosome 7
regulates trypsinogen production.
 SPINK1 peptide secreted by acinar cells that
regulates premature activation of
trypsinogen.
 CFTR gene affecting normal secretion of
bicarbonate.

34.  Autoimmune pancreatitis.
 Tropical pancreatitis
 Idiopathic pancreatitis.

35.  Two different histological variants.
 Type 1 is the most common, characterised by
dense, periductal lymphoplasmacytic
infiltrates.
 Type 2 pancreas is infiltrated by neutrophils,
lymphocytes and plasma cells that destroy
and obliterates the epithelium in the
pancreatic duct.

36.  Common in tropical areas, particularly India.
 Associated with cassava ingestion and SPINK1
mutations.

37.  10-20% of the patients with chronic
pancreatitis.

38.  Pain.
 Weight loss and Malnutrition.
 Jaundice .
 Nausea and vomiting.
 Steatorrhea.

39.  Occurs late.
 Diabetes is the more common in alcohol
associated pancreatitis.
 Destruction of all cell types within the islets
of langerhans.

40.  Pseudocyst of pancreas.
 Pancreatic Ascitis.
 CBD stricture due to edema or inflammation.
 Portal thrombosis.
 Peptic ulcer.
 Carcinoma pancreas.
 Pancreatic fistula.

41.  Carcinoma head of pancreas.
 Retroperitoneal tumour.