This ppt. Is about surgical anatomy and physiology of pancreas. Anatomical anamolies of the pancreas and variation of the ducts has been touched also. Basic phsiology and pancreatic functions have been explanied with diagrams. This ppt is only for postgraduates.

1. ANATOMY AND
PHYSIOLOGY OF
PANCREAS
Dr. Sajad Nazir

2. ANATOMY
 The pancreas is a J
shaped
retroperitoneal organ
that lies in an
oblique position,
sloping upward from
the C-loop of the
duodenum to the
splenic hilum.
 In an adult, the
pancreas weighs 75
to 100 g and is about
15 to 20 cm long.

3. EMBROLOGY OF
PANCREAS
 The pancreas is formed by the fusion of a ventral and dorsal bud .
 The ventral anlage becomes the inferior portion of the pancreatic
head and the uncinate process, while the dorsal anlage becomes
the body and tail of the pancreas.
 The duct from the smaller ventral bud, which arises from the hepatic
diverticulum, connects directly to the common bile duct.
 The duct from the larger dorsal bud, which arises from the
duodenum, drains directly into the duodenum.
 The duct of the ventral anlage becomes the duct of Wirsung, and the
duct
from the dorsal anlage becomes the duct of Santorini.
 With gut rotation, the ventral anlage rotates to the right and around
the posterior side of the duodenum to fuse with the dorsal bud.
 The ducts from each anlage usually fuse together in the pancreatic
head such that most of the pancreas drains through the duct of
Wirsung, or main pancreatic duct, into the common channel formed
from the bile duct and pancreatic duct

5.  The main pancreatic duct is
usually only 2 to 3 mm in
diameter and runs midway
between the superior and
inferior borders of the
pancreas, usually closer to the
posterior than to the anterior
surface.
 Pressure inside the
pancreatic duct is about twice
that in the common bile duct,
which is thought to prevent
reflux of bile into the
pancreatic duct.
 The main pancreatic duct
joins with the common bile
duct and empties at the
ampulla of Vater or major
papilla, which is located on the
medial aspect of the second
portion of the duodenum.

6. PANCREATIC DUCT
VARIATIONS
• The length of the common channel is variable.
• In about one third of patients, the bile duct and
pancreatic duct remain distinct to the end of the
papilla, the two ducts merge at the end of the
papilla in another one third, and in the remaining
one third, a true common channel is present for a
distance of several millimeters.
• The muscle fibers around the ampulla form the
sphincter of Oddi, which controls the flow of
pancreatic and biliary secretions into the
duodenum.
• Contraction and relaxation of the sphincter is
regulated by complex neural and hormonal
factors.

8. PANCREAS DIVISUM
 Commonly, the duct from the dorsal
anlage, the duct of Santorini,
persists as the lesser pancreatic
duct, and sometimes drains directly
into the duodenum through the
lesser papilla just proximal to the
major papilla.
 In approximately 30% of patients,
the duct of Santorini ends as a blind
accessory duct and does not empty
into the duodenum. In 10% of
patients, the ducts of Wirsung and
Santorini fail to fuse.
 This results in the majority of the
pancreas draining through the duct
of Santorini and the lesser papilla,
while the inferior portion of the
pancreatic head and uncinate
process drains through the duct of
Wirsung and major papilla.
 This normal anatomic variant, which
occurs in one out of 10 patients, is
referred to as pancreas divisum.

9. TYPES
• Type I, or classic pancreatic divisum, is a
complete failure of the dorsal and ventral
buds to fuse.
• Type II pancreatic divisum is characterized by
the absence of the ventral duct, so the minor
papilla drains the entire pancreas and the
major papilla drains some of the common bile
duct.
• Type III presents with a small remnant
communication between the dorsal duct and
ventral duct

11.  In a minority of these patients, the
minor
papilla can be inadequate to handle the
flow of pancreatic juices from the
majority of the gland.
This relative outflow obstruction can
result in pancreatitis and is sometimes
treated by sphincteroplasty of the minor
papilla.

12. PARTS OF PANCREAS

13.  The location of pathology within the
pancreas in relation to four regions: the
head, neck, body, and tail.
 HEAD
 The head of the pancreas is nestled in
the C-loop of the duodenum and is
posterior to the transverse mesocolon.
 3 borders ; superior, inferior and right
lateral.
 2 surfaces; anterior and posterior.
 Uncinate process
 Just posterior to the head of the
pancreas lie the vena cava, the right
renal , and both renal veins.

15. ANTERIOR SURFACE

16. POSTERIOR SURFACE

17. UNCINATE PROCESS

18. NECK
 The neck of the
pancreas lies directly
anterior to the portal
vein.
 At the inferior border
of the neck of the
pancreas, the
superior mesenteric
vein joins the splenic
vein and then
continues toward the
porta hepatis as the
portal vein.

19.  The inferior
mesenteric vein
often joins the
splenic vein near its
junction with the
portal vein.
 Sometimes, the
inferior mesenteric
vein joins the
superior mesenteric
vein or merges with
the superior
mesenteric portal
venous junction to
form a trifurcation .

21.  The neck of the pancreas is anterior to
the vertebral body of L1 and L2, and
blunt anteroposterior trauma can
compress the neck of the pancreas
against the spine, causing
parenchymal and, sometimes, ductal
injury.
 The neck divides the pancreas into
approximately two equal halves.

22. BODY
 3 borders: anterior, superior
and inferior.
 The splenic artery runs
parallel and just superior to
the vein along the posterior
superior edge of the body and
tail of the pancreas. The
splenic artery often is
tortuous.
 The anterior surface of the
body of the pancreas is
covered by peritoneum.
 Once the gastrocolic omentum
is divided, the body and tail of
the pancreas can be seen
along the floor of the lesser
sac, just posterior to the
stomach.

23.  The body of the
pancreas is
anterior to the
aorta at the origin
of the superior
mesenteric artery.

24. TAIL
 The small portion of
the pancreas anterior
to the left kidney is
referred to as the tail
and is nestled in the
hilum of the spleen
near the splenic
flexure of the left
colon.
 Awareness of these
anatomic relationships
is important to avoid
injury to the pancreatic
tail during left
colectomy or
splenectomy.

25. PANCREAS INSITU

26. BLOOD SUPPLY
 The blood supply to the pancreas comes from multiple branches
from the celiac and superior mesenteric arteries . The common
hepatic artery gives rise to the gastroduodenal artery before
continuing toward the porta hepatis as the proper hepatic artery.
 The gastroduodenal artery then travels inferiorly anterior to the neck
of the pancreas and posterior to the duodenal bulb.
 At the inferior border of the duodenum, the gastroduodenal artery
then gives rise to the right gastroepiploic artery then continues on as
the anterior superior pancreaticoduodenal artery, which branches
into the anterior and posterior superior pancreaticoduodenal arteries.
 As the superior mesenteric artery passes behind the neck of the
pancreas, it gives off the inferior pancreaticoduodenal artery at the
inferior margin of the neck of the pancreas. This vessel quickly
divides into the anterior and posterior inferior pancreaticoduodenal
arteries.
 The superior and inferior pancreaticoduodenal arteries join together
within the parenchyma of the anterior and posterior sides of the
head of the pancreas along the medial aspect of the C-loop of the
duodenum to form arcades that give off numerous branches to the
duodenum and head of the pancreas. Therefore, it is impossible to
resect the head of the

28.  pancreas without devascularizing the duodenum,
unless a rim of pancreas containing the
pancreaticoduodenal arcade is preserved.
 Variations in the arterial anatomy occur in one out of
five patients. The right hepatic artery, common hepatic
artery, or gastroduodenal arteries can arise from the
superior mesenteric artery.
 In 15% to 20% of patients, the right hepatic artery will
arise from the superior mesenteric artery and travel
upwards toward the liver along the posterior aspect of
the head of the pancreas (referred to as a replaced right
hepatic artery). It is important to look for this variation
on preoperative computed tomographic (CT) scans and
in the operating room so the replaced hepatic artery is
recognized and injury is avoided.

29. BODY AND TAIL
 The body and tail of the pancreas are supplied by
multiple branches of the splenic artery.
 The splenic artery arises from the celiac trunk and
travels along the posterior-superior border of the body
and tail of the pancreas toward the spleen.
 The inferior pancreatic artery usually arises from the
superior mesenteric artery and runs to the left along the
inferior border of the body and tail of the pancreas,
parallel to the splenic artery.
 Three vessels run perpendicular to the long axis of the
pancreatic body and tail and connect the splenic artery
and inferior pancreatic artery.
 They are, from medial to lateral, the dorsal, great, and
caudal pancreatic arteries. These arteries form arcades
within the body and tail of the pancreas, and account for
the rich blood supply of the organ.

31. VENOUS DRAINAGE
 The venous drainage of the pancreas follows a pattern similar to that
of the arterial supply. The veins are usually superficial to the arteries
within the parenchyma of the pancreas.
 There is an anterior and posterior venous arcade within the head of
the pancreas.
 The superior veins drain directly into the portal vein just above the
neck of the pancreas.
 The posterior inferior arcade drains directly into the inferior
mesenteric vein at the inferior border of the neck of the pancreas.
These venous tributaries must be divided during a Whipple
procedure.
 The anterior inferior pancreaticoduodenal vein joins the right
gastroepiploic vein and the middle colic vein to form a common
venous trunk, which enters into the superior mesenteric vein.
 Traction on the transverse colon during colectomy can tear these
fragile veins, which then retract into the parenchyma of the
pancreas, making control tedious. There also are numerous small
venous branches coming from the pancreatic parenchyma directly
into the lateral and posterior aspect of the portal vein. Venous return
from the body and tail of the pancreas drains into the splenic vein.

33. LYMPHATICS
 The lymphatic drainage from the pancreas is diffuse and
Widespread.
 The profuse network of lymphatic vessels and lymph nodes
draining the pancreas provides egress to tumor cells arising
from the pancreas. This diffuse lymphatic drainage
contributes to the fact that pancreatic cancer often presents
with positive lymph nodes and a high incidence of local
recurrence after resection.
 Lymph nodes can be palpated along the distal bile duct and
posterior aspect of the head of the pancreas in the
pancreaticoduodenal groove, where the mesenteric vein
passes under the neck of the pancreas, along the inferior
border of the body, at the celiac axis and along the hepatic
artery ascending into the porta hepatis, and along the splenic
artery and vein.
 The pancreatic lymphatics also communicate with lymph
nodes in the transverse mesocolon and mesentery of the
proximal jejunum.
 Tumors in the body and tail of the pancreas often metastasize
to these nodes and lymph nodes along the splenic vein and in

35. Neuroanatomy
 The pancreas is innervated by the sympathetic and parasympathetic
nervous systems.
 The acinar cells responsible for exocrine secretion, the islet cells
responsible for endocrine secretion, and the islet vasculature are
innervated by both system.
 The parasympathetic system stimulates endocrine and exocrine
secretion and the sympathetic system inhibits secretion.
 The pancreas is also innervated by neurons that secrete amines and
peptides, such as somatostatin, vasoactive intestinal peptide (VIP),
calcitonin gene-related peptide (CGRP), and galanin.
 The exact role of these neurons in pancreatic physiology is
uncertain, but they do appear to affect both exocrine and endocrine
function.
 The pancreas also has a rich supply of afferent sensory fibers, which
are responsible for the intense pain associated with advanced
pancreatic cancer, as well as acute and chronic pancreatitis.
 These somatic fibers travel superiorly to the celiac ganglia .
 Interruption of these somatic fibers can stop transmission of pain
sensation.

36. HISTOLOGY
 The exocrine pancreas accounts for about 85% of the
pancreatic mass; 10% of the gland is accounted for by
extracellular matrix, and 4% by blood vessels and the major
ducts, whereas only 2% of the gland is comprised of
endocrine tissue.
 The endocrine and exocrine pancreas are sometimes thought
of as functionally separate, but these different components of
the organ are coordinated to allow an elegant regulatory
feedback system for digestive enzyme and hormone
secretion.
 This complex system regulates the type of digestion, its rate,
and the processing and distribution of absorbed nutrients.
 This coordination is facilitated by the physical approximation
of the islets and the exocrine pancreas, the presence of
specific islet hormone receptors on the plasma membranes of
pancreatic acinar cells, and the existence of an islet-acinar
portal blood system

37. Exocrine Pancreas
 The pancreas secretes
approximately 500 to 800 mL per
day of colorless, odorless, alkaline,
isosmotic pancreatic juice.
 Pancreatic juice is a combination of
acinar cell and duct cell secretions.
 The acinar cells secrete amylase,
proteases, and lipases, enzymes
responsible for the digestion of all
three food types: carbohydrate,
protein, and fat.
 The acinar cells are pyramid
shaped, with their apices facing the
lumen of the acinus.
 Near the apex of each cell are
numerous enzyme-containing
zymogen granules that fuse with the
apical cell membrane .

38.  Pancreatic amylase is secreted in its active form and
completes the digestive process already begun by
salivary amylase.
 Amylase is the only pancreatic enzyme secreted in its
active form, and it hydrolyzes starch and glycogen to
glucose, maltose, maltotriose, and dextrins.
 These simple sugars are transported across the brush
border of the intestinal epithelial cells by active
transport mechanisms.
 Gastric hydrolysis of protein yields peptides that enter
the intestine and stimulate intestinal endocrine cells to
release cholecystokinin (CCK)-releasing peptide, CCK,
and secretin, which then stimulate the pancreas to
secrete enzymes and bicarbonate into the intestine.

39.  The proteolytic enzymes are secreted as proenzymes
that require activation.
 Trypsinogen is converted to its active form, trypsin, by
another enzyme, enterokinase, which is produced by
the duodenal mucosal cells. Trypsin, in turn, activates
the other proteolytic enzymes.
 Trypsinogen activation within the pancreas is prevented
by the presence of inhibitors that are also secreted by
the acinar cells.
 A failure to express a normal trypsinogen inhibitor,
pancreatic secretory trypsin inhibitor (PSTI), also known
as serine protease inhibitor Kazal type 1 (SPINK1), is a
cause of familial pancreatitis. Inhibition of trypsinogen
activation ensures that the enzymes within the
pancreas remain in an inactive precursor state and are
activated only within the duodenum.

40.  Chymotrypsinogen is activated to form
chymotrypsin.
 Elastase, carboxypeptidase A and B, and
phospholipase are also activated by
trypsin.
 Trypsin, chymotrypsin, and elastase
cleave bonds between amino acids
within a target peptide chain, and
carboxypeptidase A and B cleave amino
acids at the end of peptide chains.
 Individual amino acids and small
dipeptides are then actively transported
into the intestinal epithelial cells.

41.  Pancreatic lipase hydrolyzes triglycerides to 2-monoglyceride
and fatty acid.
 Pancreatic lipase is secreted in an active form. Colipase is
also secreted by the pancreas and binds to lipase, changing
its molecular configuration and increasing its activity.
 Phospholipase A2 is secreted by the pancreas as a
proenzyme that becomes activated by trypsin. Phospholipase
A2 hydrolyzes phospholipids and, as with all lipases, requires
bile salts for its action.
 Carboxylic ester hydrolase and cholesterol esterase
hydrolyze neutral lipid substrates like esters of cholesterol,
fat-soluble vitamins, and triglycerides.
 The hydrolyzed fat is then packaged into micelles for
transport into the intestinal epithelial cells, where the fatty
acids are reassembled and packaged inside chylomicrons for
transport through the lymphatic system into the bloodstream.

44. Endocrine Pancreas
 There are nearly 1 million
islets of Langerhans in the
normal adult pancreas.
They vary greatly in size
from 40 to 900 μm.
 Larger islets are located
closer to the major
arterioles and smaller islets
are embedded more deeply
in the parenchyma of the
pancreas. Most islets
contain 3000 to 4000 cells
of five major types:
 alpha cells that secrete
glucagon, β-cells that
secrete insulin, delta cells
that secrete somatostatin,
epsilon cells that secrete
ghrelin, and PP cells that
secrete PP.

45. INSULIN
 Insulin is the best-
studied pancreatic
hormone. The
discovery of insulin
in 1920 by Frederick
Banting, an
orthopedic surgeon,
and Charles Best, a
medical student, was
recognized with the
awarding of the
Nobel Prize in
Physiology or
Medicine.

46.  Insulin was subsequently purified and found to be a 56-
amino acid peptide with two chains, an α and a β chain,
joined by two disulfide bridges and a connecting
peptide, or C-peptide.
 Proinsulin is made in the endoplasmic reticulum and
then is transported to the Golgi complex, where it is
packaged into granules and the C-peptide is cleaved
off.
 There are two phases of insulin secretion. In the first
phase, stored insulin is released. This phase lasts about
5 minutes after a glucose challenge.
 The second phase of insulin secretion is a longer,
sustained release due to ongoing production of new
insulin.
 β-cell synthesis of insulin is regulated by plasma
glucose levels, neural signals, and the paracrine
influence of other islet cells.

47.  Insulin secretion by the β-cell is also
influenced by plasma levels of amino
acids such as arginine, lysine, leucine,
and free fatty acids.
 Glucagon, GIP, GLP-1, and CCK
stimulate insulin release, while
somatostatin, amylin, and pancreastatin
inhibit insulin release.
 Cholinergic fibers and beta sympathetic
fibers stimulate insulin release, while
alpha sympathetic fibers inhibit insulin
secretion.

48.  Insulin’s glucoregulatory function is to
inhibit endogenous (hepatic) glucose
production and to facilitate glucose
transport into cells, thus lowering
plasma glucose levels. Insulin also
inhibits glycogenolysis, fatty acid
breakdown, and ketone formation, and
stimulates protein synthesis.

50. GLUCAGON
 Glucagon is a 29-amino-acid, single-chain peptide that
promotes hepatic glycogenolysis and gluconeogenesis and
counteracts the effects of insulin through its hyperglycemic
action.
 Glucose is the primary regulator of glucagon secretion, as it is
with insulin, but it has an inhibitory rather than stimulatory
effect.
 Glucagon release is stimulated by hypoglycemia, and by the
amino acids arginine and alanine. GLP-1 inhibits glucagon
secretion in vivo, and insulin and somatostatin inhibit
glucagon secretion in a paracrine fashion within the islet.
 The same neural impulses that regulate insulin secretion also
regulate glucagon secretion, so that the two hormones work
together in a balance of actions to maintain glucose levels.
 Cholinergic and beta sympathetic fibers stimulate glucagon
release, while alpha sympathetic fibers inhibit glucagon
release.

53. Islet Distribution
 The β-cells are generally located in the central portion
of each islet and make up about 70% of the total islet
cell mass. The other cell types are located
predominantly in the periphery.
 The delta cells are least plentiful, making up only 5%;
the α-cells make up 10%, and the PP cells make up
15%.
 In contrast to the acinar cells that secrete the full gamut
of exocrine enzymes, the islet cells seem to specialize
in the secretion of predominantly one hormone.
 However, individual islet cells can secrete multiple
hormones.
 There is diversity among the islets depending on their
location within the pancreas

54.  The α- and δ-cells are evenly distributed throughout the
pancreas, but islets in the head and uncinate process
(ventral anlage) have a higher percentage of PP cells
and fewer α-cells, whereas islets in the body and tail
(dorsal anlage) contain the majority of α-cells and few
PP cells.
 This is clinically significant because
pancreatoduodenectomy removes 95% of the PP cells
in the pancreas. This may partially explain the higher
incidence of glucose intolerance after the Whipple
procedure compared to a distal pancreatectomy with an
equivalent amount of tissue resected.
 In addition, chronic pancreatitis, which
disproportionately affects the pancreatic head, is
associated with PP deficiency and pancreatogenic
diabetes.
 The relative preponderance of α-cells in the body and
tail of the pancreas explains the typical location of
glucagonomas

55. Pancreatic function tests
 Exocrine function assessment.
 Endocrine assessment.

56. ASSESSMENT OF EXOCRINE
FUNCTION
 DIRECT AND INDIRECT TESTS.
 indirect tests monitor the intestinal
effects of secreted pancreatic digestive
enzymes.
 Direct tests monitor the actual secretion
of pancreatic exocrine products
(enzymes, fluid, and bicarbonate).
 The indirect tests are the least invasive
and most widely available of the tests,
but they also are the least sensitive, and
such tests are most likely to be normal in
patients with mild degrees of pancreatic
functional loss.

58. FAECAL FAT STAINING
 Conceptually, fecal fat analysis is the simplest of the indirect
pancreatic function tests.
 It is based on the fact that pancreatic lipase is the enzyme
responsible for most fat digestion, and diminished lipase
secretion results in fat malabsorption.
 Fecal fat analysis can be accomplished by staining stool
samples for fat with Sudan stain or by quantifying fecal fat
when the patient is on a controlled-fat diet (Chowdhury &
Forsmark, 2003; Lieb
 & Draganov, 2008).
 In the latter case, the patient is placed on a diet consisting of
100 g of fat per day for 5 days.
 Stool is collected on days 3 to 5, and fat content is measured.
Fecal fat output of greater than 7 g/day is considered to be
abnormal and diagnostic of steatorrhea.
 but fecal fat measurement is notoriously insensitive for the
diagnosis of chronic pancreatitis, and it is most commonly
abnormal only in patients with overtly symptomatic
steatorrhea.

59. The bentiromide and the
pancreolauryl tests
 The bentiromide and the pancreolauryl tests
are noninvasive, indirect pancreatic function
tests.
 The former involves ingestion of the
chymotrypsin substrate bentiromide, which is
hydrolyzed by chymotrypsin to yield
paraaminobenzoic acid, which is absorbed in
the small intestine, conjugated in the liver,
and excreted in the urine.
 The test is completed by collecting urine for 6
hours and quantifying urinary
paraaminobenzoic acid recovery, which is
considered to be abnormal if less than 50%
(Niederau & Grendell, 1985).

60. the pancreolauryl tests
 The pancreolauryl test involves
ingestion of fluorescein dilaurate,
which is hydrolyzed by pancreatic
esterases to yield lauric acid and free
fluorescein.
 The pancreolauryl test is completed by
collecting urine, in this case for 10
hours, and measuring fluorescein
excretion; in this test, excretion is
compared with the patient’s excretion
of orally ingested free fluorescein
several days later.

61. DIRECT TESTS
 Direct pancreatic function tests can be subdivided further into
noninvasive and invasive tests.
 The noninvasive tests involve measuring fecal or serum
levels of pancreas-derived digestive enzymes (serum
trypsinogen, fecal chymotrypsin, and fecal elastase).
 Recently, direct function tests combining MRCP with
secretagogue stimulation have been proposed (Schneider et
al, 2006; Czako, 2007).
 These MRCP functional tests aim to either quantify juice flow
into the duodenum or to provide contrast enhancement of the
pancreatic parenchyma after hormonal stimulation; to date,
however, the overall sensitivity and specificity of these
MRCP-based tests remain to be determined, and their overall
value as diagnostic tests for early chronic pancreatitis is
unproven.
 The invasive tests involve placing a collecting device into the
duodenum or pancreatic duct, stimulating pancreatic exocrine
secretion, and measuring the output or concentration of
exocrine pancreatic products.

62. TRYPSINOGEN
 Circulating levels of trypsinogen are
easily measured and frequently low in
patients with severe pancreatic
insufficiency (Jacobson et al, 1984).
 Although measurement of serum
trypsinogen may be helpful in
evaluating the severity of chronic
pancreatitis, the test has low
sensitivity for the diagnosis of mild
pancreatitis.

63. chymotrypsin and elastase
 Fecal levels of chymotrypsin and
elastase also can be measured and used
to assess exocrine pancreatic function
(Dominguez-Munoz et al, 1995; Dominici
& Franzini, 2002; Goldberg, 2000;
Katschinski et al, 1997; Loser et al,
1996; Luth et al, 2001).
 The levels of these enzymes are
reduced in patients with advanced
chronic pancreatitis.
 However, the sensitivity of fecal
chymotrypsin and elastase measurement
in diagnosing mild or moderate
pancreatic insufficiency is only 40% to

64. invasive, direct pancreatic
function
 The invasive, direct pancreatic
function tests are the most sensitive of
the tests used to identify patients with
mild to moderate chronic pancreatitis.
 In these tests, pancreatic secretions
are continuously aspirated from either
the duodenum or the pancreatic duct
after administration of a pancreatic

65.  stimulant; this stimulant varies among
the different tests.
 In some, secretin is administered to
stimulate pancreatic secretion, and
bicarbonate in duodenal juice is
measured.
 In others, a combination of secretin
and CCK or one of its analogs is used,
and bicarbonate and protein (or
pancreatic enzymes) in duodenal juice
are measured (Chowdhury &
Forsmark, 2003).