Morphology

Ranges from trivial inflammation and oedema to

severe extensive necrosis and hemorrhage.
In More severe form, acute necrotizing
pancreatitis
the acinar and ductal tissues as well as the
islets of Langerhans are necrotic.
Vascular injury can lead to hemorrhage into the
parenchyma of the pancreas.

Macroscopy Oedema and hyperaemia in early stages

2nd day- Variegated appearance
black haemorrhagic areas ,grey white necrotic
areas and chalky white areas of fat necrosis
Foci of fat necrosis may also be found in extrapancreatic collections of fat, such as the
omentum and the mesentery of the bowel,
and even outside the abdominal cavity, such
as in the subcutaneous fat.

Microscopy
(1) microvascular leakage causing oedema,
(2) fat necrosis
(3) acute inflammation
(4) proteolytic destruction of pancreatic
parenchyma
(5) destruction of blood vessels leading to
hemorrhage.
The extent of each of these alterations
depends on the duration and severity of
the process.

Normal pancrease

In the majority of cases the peritoneal cavity

contains blood stained ascitic fluid

Clinical features
Abdominal pain -Constant and intense and is often referred
to the upper back and occasionally can be associated with
referred pain to the left shoulder. Anorexia, nausea, and
vomiting
Full-blown acute pancreatitis is a medical emergency.
sudden onset of an acute abdomen.
Many of the systemic features of severe acute pancreatitis
can be attributed to release of toxic enzymes, cytokines,
and other mediators into the circulation and explosive
activation of the systemic inflammatory response,
resulting in leukocytosis, hemolysis, disseminated
intravascular coagulation, fluid sequestration, acute
respiratory distress syndrome, and diffuse fat necrosis.
Peripheral vascular collapse and shock with acute renal
tubular necrosis may occur.

Laboratory findings
marked elevation of serum amylase levels
during the first 24 hours,
followed within 72 to 96 hours by a rising
serum lipase level.
Glycosuria occurs in 10% of cases.
Hypocalcemia may result from precipitation
of calcium soaps in necrotic fat if persistent,
it is a poor prognostic sign.
Direct visualization of the enlarged
inflamed pancreas by radiography is useful
in the diagnosis of pancreatitis.

.
Prognosis
80% recover fully
15-20 %develop multiple organ failure
and pancratic necrosis
Mortality rate 20%

Systemic complications.
Acute respiratory distress syndrome
Acute renal failure
Endotoxic shock
Chemical and bacterial peritonitis
Local Sequelae
Sterile pancreatic abscess
Pancreatic pseudocyst
In 40% to 60% of patients with acute necrotizing
pancreatitis the necrotic debris becomes
infected, usually by gram-negative organisms
from the alimentary tract(bacterial
transposition)

Chronic Pancreatitis
Chronic pancreatitis is defined as chronic
inflammation of the pancreas with
irreversible destruction of exocrine
parenchyma, fibrosis, and, in the late stages,
the destruction of endocrine parenchyma.
Presents with recurrent attacks of severe
abdominal pain,weight loss ,DM and
steatorrhoea
Abdominal X ray calcification in the
pancreatic region
.

 Microscopically, there is acinar loss

with marked fibrosis

 Lymphoplasmacytic sclerosing
pancreatitis (autoimmune pancreatitis)
is a distinct form of chronic pancreatitis
characterized by a duct-centric mixed
inflammatory cell infiltrate, and
increased numbers of IgG4-producing
plasma cells. It is important to recognize
since it can clinically mimic pancreatic
cancer and also because it responds to
steroid therapy.

 most common cause of chronic pancreatitis

is long-term alcohol abuse
Less common causes are ;
Long-standing obstruction of the pancreatic
duct by pseudocysts, calculi, trauma,
neoplasms, or pancreas divisum. There is
often dilation of the pancreatic duct.
Tropical pancreatitis, which is a poorly
characterized heterogeneous disease seen in
Africa and Asia.Some cases have a genetic
basis.
Hereditary pancreatitis CFTR gene
mutations.

PSEUDOCYSTS
Pseudocysts are localized collections
of necrotic-hemorrhagic material rich
in pancreatic enzymes.Such cysts
lack an epithelial lining and account
for approximately 75% of cysts in the
pancreas.
Pseudocysts usually arise after an
episode of acute pancreatitis
Traumatic injury to the pancreas can
also give rise to pseudocysts.

Neoplasms
A broad spectrum of exocrine
neoplasms can arise in the pancreas.
cystic or solid
benign or malignant
CYSTIC NEOPLASMS
Serous cystadenomas
mucinous cystic neoplasms
Solid pseudopapillary tumours

Pancreatic carcinomas
Grossly, pancreatic carcinoma
presents as a hard infiltrative mass
that obstructs the pancreatic duct
frequently causing chronic
pancreatitis in the distal gland.
Carcinomas of the head tend to
obstruct the common bile duct
Tumors in the body and tail tend to
present late and be very large.

Factors associated with high incidence

Smoking

Diet with rich in calories and animal fatHigh incidence

Chronic pancreatitis
Obesity
Chemicals beta naphthaline ,nitrosamines
Long standing DM high incidence
H Pylori infection
Genetic factors-10% have FH

 Microscopically, over 90% of cases are

well-differentiated adenocarcinomas,
associated with marked fibrosis.
Perineural invasion is common
Carcinomas of the pancreas remain silent
until they invade into adjacent structures.
Pain is usually the first symptom, but by the
time pain appears these cancers are usually
beyond cure
Obstructive jaundice is associated with most
cases of carcinoma of the head of the
pancreas

 Weight loss, anorexia, and

generalized malaise and weakness
tend to be signs of advanced disease.
Migratory thrombophlebitis, known
as the Trousseau sign, occurs in
about 10% of patients and is
attributable to the elaboration of
platelet-aggregating factors and
procoagulants
Tumour markers -CA 19.9 ,CEA

Pancreatic neuroendocrine
tumors
Benign ormalignant
Pancreatic NETs are much less
common than pancreatic exocrine
tumors and have a better prognosis.
functionalornonfunctional

 Gastrinoma-most gastrinomas are

malignant
Insulinoma- usually benign (not
cancer).
glucagonoma