PANCREATITS

Dr Hira Faisal
Senior Lecturer
Dept of Pathology, BUMDC
 PANCREATITIS

• Pancreatitis is inflammation in the pancreas

associated with injury to the exocrine parenchyma.
• ranges in severity from a mild, self-limited disease to
a life-threatening acute inflammatory process
• In acute pancreatitis the gland can return to normal
if the underlying cause of the pancreatitis is
removed.
• Chronic pancreatitis is defined by the irreversible loss
of exocrine pancreatic parenchyma.
 ACUTE PANCREATITIS

• REVERSIBLE PANCREATIC PARENCHYMAL

INJURY ASSOCIATED WITH INFLAMMATION.
• ETIOLOGY:
– Impacted gallstones in CBD obstructing flow of
pancreatic juices through Ampulla of
Vater( gallstone pancreatitis)
– Alcohol excess intake
 ETIOLOGY
GALLSTONE PANCREATITS Obstruction of CBD and AOV by
gallstones
ALCOHOLIC PANCREATITIS Excessive Alcohol intake
NON GALL STONE Cancer, divisum, biliary sludge or parasites
RELATED OBSTRUCTION
MEDICATION INDUCED thiazides, antiepileptics
PANCREATITIS
PANCREATITIS DUE TO Mumps, CX virus
INFECTION
METABOLIC DISORDERS Hypertriglyceridemia, hypercalcemia,
hyperthyroidism
VASCULAR PROBLEMS Shock, ischaemia, atheroembolism
TRAUMA blunt abdominal injury
GERMLINE MUTATIONS PRSS1, SPINK 1
IDIOPATHIC PANCREATITIS CFTR Mutations
 PATHOGENESIS
• Autodigestion by activated pancreatic
enzymes
• Unleashing of proenzymes
• Tissue injury and inflammation
• Trypsin prekallikrein activation of kinin
system activation of factor VIII
activation of complement
 PATHWAYS
• PANCREATIC DUCT OBSTRUCTION
– Causes accumulation of enzymes
– Lipase secreted in active form…..this causes local fat
digestion of omental area
– Leucocytes, myofibroblasts and injured tissues release
cytokines promoting inflammation and oedema
– Compromised blood flow leads to primary acinar cell
injury (ischemic injury)
– Defective intracellular transport-lysosomal hydrolase
and proenzymes packed together creating havoc
• ALCOHOL CONSUMPTION
– Causes increased contraction of Sphincter of oddi
– Increases pancreatic exocrine function
– Increased oxidative stress on acinar cells causes
membrane damage
– With chronicity, deposition of protein plugs and
small duct obstruction
 MORPHOLOGY
• The basic alterations are:
(1) microvascular leakage causing edema,
(2) necrosis of fat by lipolytic enzymes,
(3) acute inflammation,
(4) proteolytic destruction of pancreatic parenchyma,
and
(5) destruction of blood vessels and subsequent
interstitial hemorrhage.
ACUTE NECROTIZING PANCREATITIS:
• GROSS:
– Red black hemorrhagic areas with yellow white chalky fat
necrosis
– Peritoneum has serous, turbid brown fluid with fat
globules
• HISTOPATHOLOGY:
– Extreme parenchymal necrosis and diffuse hemorrhage
Acute pancreatitis. The microscopic field shows a region of fat necrosis on the
right and focal pancreatic parenchymal necrosis (center
 Acute pancreatitis. The pancreas has been sectioned longitudinally to reveal dark
areas of hemorrhage in the head of the pancreas and a focal area of pale fat necrosis
in the peripancreatic fat (upper left).
 CLINICAL FEATURES
1. Abd pain- cardinal
2. Acute abdomen- guarding, pain and absent
bowel sounds
3. DIC, ARDS, Renal Failure
4. Shock and Endotoxemia
 LAB DIAGNOSIS
• 1st 24 hrs: raised Amylase
• 72-96 hrs: increasing lipase levels
• Hypocalcemia-poor prognostic factor
• CT Scan
• MRI
 MANAGEMENT
• Supportive
• Maintain BP and Analgesia
• Resting pancreas(restricted oral intake)
• Sequalae: abscess or pseudocyst
 CHRONIC PANCREATITIS
• defined as inflammation of the pancreas with irreversible
destruction of exocrine parenchyma, fibrosis, and, in the late
stages, the destruction of endocrine parenchyma.
• By far the most common cause of chronic pancreatitis is long-
term alcohol abuse, and these patients are usually middle-
aged males.
 ETIOLOGY

ALCOHOLIC PANCREATITIS Long term alcohol abuse

Duct Obstruction:
pseudocysts, calculi,
neoplasms and divisum

TROPICAL PANCREATITIS

HEREDITARY PANCREATITIS PRRS1 and SPINK1 gene

CHRONIC PANCREATITIS CFTR MUTATIONs
AUTOIMMUNE PANCREATITIS Ig4 secreting plasma cells
Polymorphisms in
carboxypeptidases A1(CPA1)
and Lipase (EL)
 PATHOGENESIS.

• Ductal obstruction by concretions(calcium carbonate

precipitates)
• Toxic metabolites due to alcohol consumption
• Oxidative stress leads to IL 8 release ,promotes the
fusion of lysosomes and zymogen granules, acinar cell
necrosis, inflammation, and fibrosis.
• Inappropriate activation of pancreatic enzymes
• Chemokines esp transforming growth factor β (TGF-β)
and platelet-derived growth factor(PDGF) induce the
activation and proliferation of periacinar
myofibroblasts (pancreatic stellate cells), resulting in
the deposition of collagen and ultimately fibrosis
 MORPHOLOGY:
• parenchymal fibrosis,
• reduced number and size of acini with relative sparing of the islets
of Langerhans, and
• variable dilation of the pancreatic ducts
• accompanied by a chronic inflammatory infiltrate around lobules
and ducts. The interlobular and intralobular ducts are frequently
dilated and contain protein plugs in their lumens.
• Acinar loss-constant feature.
• The remaining islets of Langerhans become embedded in the
sclerotic tissue and may fuse and appear enlarged. Eventually, they
too disappear.
It is important to recognize lymphoplasmacytic sclerosing
pancreatitis, since it can clinically mimic pancreatic cancer and also
because it responds to steroid therapy.
• Grossly, the gland is hard, sometimes with
extremely dilated ducts and visible calcified
concretions.
• Lymphoplasmacytic sclerosing pancreatitis –
swirling fibrosis (autoimmune pancreatitis)
characterized by a duct-centric mixed
inflammatory cell infiltrate, venulitis, and
increased numbers of IgG4-producing plasma
cells
A, Extensive fibrosis and atrophy has left only residual islets (left) and ducts
(right), with a sprinkling of chronic inflammatory cells and acinar tissue. B,
A higher power view demonstrating dilated ducts with inspissated
eosinophilic ductal concretions in a person with alcoholic pancreatits
 CLINICAL FEATURES:
1. Repeated bouts of jaundice, vague
indigestion
2. Persistent or recurrent abdominal and back
pain
3. Weight loss
4. Hypoalbuneimic edema from malabsorption
5. Diabetes Mellitus
6. CT- may show pancreatic calcification
 COMPLICATIONS
• Severe chronic pain
• Pancreatic PSEUDOCYSTS
• Chronic Malabsorption
• Diabetes Mellitus
• Pancreatic Cancer esp with PRSS1 mutations
THANK YOU