Pancreas

The pancreas is a soft, finely lobulated, elongated exo-endocrine

gland. The exocrine part secretes the pancreatic juice and the
endocrine part secretes the hormones, viz.,insulin, etc. The
pancreas (in Greek pan: all, kreas: flesh). Pancreas named
because of its fleshy appearance. The pancreatic juice helps in
the digestion of lipids, carbohydrates, and proteins, whereas
the pancreatic hormones maintain glucose homeostasis.
The pancreas lies more or less horizontally on the
posterior abdominal wall. In the epigastric and
left hypochondriac regions. It crosses the
posterior abdominal wall obliquely from concavity
of the duodenum to the hilum of spleen opposite
the level of T12– L3 vertebrae. The greater part of
the gland is retroperitoneal behind the serous
floor of the lesser sac.
The pancreas is “J”-shaped or retort shaped being
set obliquely. The bowl of retort represents its
head and the stem of retort represents its neck,
body, and tail. Its measurements are: Length:
12–15 cm. Width: 3–4 cm. Thickness: 1.5–2
cm. Weight: 80–90 g.
 ducts of the pancreas
The exocrine pancreas is drained by two ducts, 1.The main pancreatic duct
(duct of wirsung) 2. the accessory pancreatic duct( duct of santorini);

The main pancreatic duct (duct of wirsung) lies near the posterior surface
of the pancreas and is recognised easily by its white colour. With in the
head of the pancreas the pancreatic duct is related to the bile duct which
lies on its right side. The two ducts enter the wall of the second part of
the duodenum , and join to form the hepatopancreatic ampulla of vater . 
The accessory pancreatic duct( duct of santorini)
begins in the lower Part of the head , crosses
the front of the main duct with which it
communicates an opens into the duodenum
at the minor duodenal papilla.
 Arterial Supply of Pancreas
pancreatic branches of
the splenic artery;
-the superior
pancreaticoduiodena
l artery;
-the inferior
pancreaticoduodenal
artery;
 Venous Drainage of Pancreas
Vein drain into splenic, superior mesenteric and
portal veins 
 Lymphatic drainage
Rich periacinar network that drain into 5 nodal
groups – Superior nodes – Anterior nodes –
Inferior nodes – Posterior PD nodes – Splenic
nodes
 THE EXOCRINE PANCREAS
This consists of a large number of lobules made
up of small acini, the walls of which consist of
secretory cells. • Each lobule is drained by a tiny
duct and these unite eventually to form the
pancreatic duct, which extends the whole length
of the gland and opens into the duodenum. •
The function of the exocrine pancreas is to
produce pancreatic juice containing enzymes
that digest carbohydrates , proteins and fats.
 The endocrine pancreas
Distributed throughout the gland are groups of
specialised cells called the pancreatic islets
(islets of langerhans). • The islets have no
ducts so the hormones diffuse directly into the
blood. • The endocrine pancreas secretes the
hormones insulin and glucagon, which are
principally concerned with control of blood
glucose levels.
 Imaging investigations
• Ultrasonography
Ultrasonography is the initial investigation of choice in
patients with jaundice to determine whether or not the
bile duct is dilated, the coexistence of gallstones or gross
disease within the liver, such as metastases. It may also
define the presence or absence of a mass in the pancreas.
However, obesity and overlying bowel gas often make
interpretation of the pancreas itself unsatisfactory;
Computed tomography;
Magnetic resonance imaging;
Endoscopic retrograde cholangiopancreatography;
Endoscopic ultrasound;
 PANCREATITIS
Pancreatitis is inflammation of the gland parenchyma of the
pancreas. It is divided into acute, which presents as an
emergency, and chronic, which is a prolonged and frequently
lifelong disorder resulting from the development of fibrosis
within the pancreas. It is probable that acute pancreatitis is
but a phase of chronic pancreatitis.
Acute pancreatitis is defined as an acute condition
presenting with abdominal pain and is usually associated
with raised pancreatic enzyme levels in the blood or urine
as a result of pancreatic inflammation. Acute pancreatitis
may recur. The underlying mechanism of injury in
pancreatitis is thought to be premature activation of
pancreatic enzymes within the pancreas, leading to a
process of autodigestion. Anything that injures the acinar
cell and impairs the secretion of zymogen granules, or
damages the duct epithelium and thus delays enzymatic
secretion, can trigger acute pancreatitis. Once cellular injury
has been initiated, the inflammatory process can lead to
pancreatic oedema, haemorrhage and, eventually, necrosis.
Acute pancreatitis may be categorised as mild or severe.
Mild acute pancreatitis is characterised by interstitial
oedema of the gland and minimal organ dysfunction. Eighty
per cent of patients will have a mild attack of pancreatitis,
the mortality from which is around 1 per cent. Severe acute
pancreatitis is characterised by pancreatic necrosis, a severe
systemic inflammatory response and often multi-organ
failure. In those who have a severe attack of pancreatitis,
the mortality varies from 20 to 50 per cent. About one-third
of deaths occur in the early phase of the attack, from
multiple organ failure, while deaths occurring after the first
week of onset are due to septic complications.
Chronic pancreatitis is defined as a continuing
inflammatory disease of the pancreas characterised by
irreversible morphological change typically causing
pain and/or permanent loss of function. Many patients
with chronic pancreatitis have painful exacerbations,
but the condition may be completely painless.
 Aetiology
The two major causes of acute pancreatitis are biliary calculi, which
occur in 50–70 per cent of patients, and alcohol abuse, which
accounts for 25 per cent of cases. Gallstone pancreatitis is thought to
be triggered by the passage of gallstones down the common bile
duct. If the biliary and pancreatic ducts join to share a common
channel before ending at the ampulla, then obstruction of this
passage may lead to reflux of bile or activated pancreatic enzymes
into the pancreatic duct. Patients who have small gallstones and a
wide cystic duct may be at a higher risk of passing stones. The
proposed mechanisms for alcoholic pancreatitis include the effects of
diet, malnutrition, direct toxicity of alcohol, concomitant tobacco
smoking, hypersecretion, duct obstruction or reflux, and
hyperlipidaemia. The remaining cases may be due to rare causes or
be idiopathic
 Clinical presentation
Pain is the cardinal symptom. It characteristically develops quickly, reaching
maximum intensity within minutes rather than hours and persists for hours
or even days. The pain is frequently severe, constant and refractory to the
usual doses of analgesics. Pain is usually experienced first in the epigastrium
but may be localised to either upper quadrant or felt diffusely throughout
the abdomen. There is radiation to the back in about 50 per cent of patients,
and some patients may gain relief by sitting or leaning forwards. The
suddenness of onset may simulate a perforated peptic ulcer, while biliary
colic or acute cholecystitis can be mimicked if the pain is maximal in the right
upper quadrant. Radiation to the chest can simulate myocardial infarction,
pneumonia or pleuritic pain. In fact, acute pancreatitis can mimic most
causes of the acute abdomen and should seldom be discounted in differential
diagnosis.
Nausea, repeated vomiting and retching are usually marked
accompaniments.
 Investigations
Typically, the diagnosis is made on the basis of the
clinical presentation and an elevated serum
amylase level. A serum amylase level three to four
times above normal is indicative of the disease. A
normal serum amylase level does not exclude
acute pancreatitis, particularly if the patient has
presented a few days later.
 Management
If after initial assessment a patient is considered to have a mild attack
of pancreatitis, a conservative approach is indicated with intravenous
fluid administration and frequent, but non-invasive, observation. A
brief period of fasting may be sensible in a patient who is nauseated
and in pain, but there is little physiological justification for keeping
patients on a prolonged ‘nil by mouth’ regimen. Antibiotics are not
indicated. Apart from analgesics and anti-emetics, no drugs or
interventions are warranted, and CT scanning is unnecessary unless
there is evidence of deterioration. However, if a stable patient meets
the prognostic criteria for a severe attack of pancreatitis, then a more
aggressive approach is required, with the patient being admitted to a
highdependency or an intensive care unit and monitored invasively
Patients with a severe attack should be admitted to an
intensive care or high-dependency unit. Adequate
analgesia should be administered. Aggressive fluid
resuscitation is important, guided by frequent
measurement of vital signs, urine output and central
venous pressure. Supplemental oxygen should be
administered and serial arterial blood gas analysis
performed. The haematocrit, clotting profile, blood
glucose and serum levels of calcium and magnesium
should be closely monitored
If gallstones are the cause of an attack of predicted or proven
severe pancreatitis, or if the patient has jaundice, cholangitis or
a dilated common bile duct, urgent ERCP should be carried out
within 72 hours of the onset of symptoms. There is evidence
that sphincterotomy and clearance of the bile duct can reduce
the incidence of infective complications in these patients. In
patients with cholangitis, sphincterotomy should be carried out
or a biliary stent placed to drain the duct. ERCP is an invasive
procedure and carries a small risk of worsening the pancreatitis.