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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_734_Библиотеки_им_академика_М_И_Перельмана.pdf
4
J. Heard et al.
The foregut will form gastrointestinal tissue from the oropharynx to the duodenum proximal to the major papilla in addition to the special digestive organs: the
liver, gallbladder, and pancreas. The celiac artery is the primary vessel supplying the
structures of the embryologic foregut. The midgut develops into the distal duodenum through the proximal transverse colon. The primary arterial supply of the midgut is derived from the superior mesenteric artery (SMA). Finally, the hindgut forms
the distal transverse colon through the anus with its primary blood supply provided
via the inferior mesenteric artery.
During the fth embryonic week, proliferation of the primitive gut tube continues at a prolic rate resulting in occlusion of the lumen of the tube and the pancreatic buds rst appear. These buds develop as direct outgrowths of the duodenal
endoderm and as such, they too are covered on their ventral surface by splanchnic
mesoderm. The dorsal pancreatic bud is relatively larger than the ventral pancreatic
bud which is associated with the developing common bile duct, gallbladder,
and liver.
By the end of the seventh embryonic week, the stomach completes a 90-degree
clockwise rotation dragging with it the duodenum, the ventral pancreatic bud, and
common bile duct. This rotation has several results, namely it creates the characteristic “C” of the duodenum, brings the pancreas and all but the most proximal duodenum into the retroperitoneum, and it puts the ventral pancreatic bud into contact
with the posterior aspect of the dorsal pancreatic bud. The pancreatic buds, partially
sandwiching the common bile duct, will then fuse by the end of week eight. The
superior pancreatic head, neck, body, and tail originate from the dorsal pancreatic
bud while the inferior pancreatic head and uncinate process are formed by the ventral bud. The main pancreatic duct (duct of Wirsung) is formed by fusion of the
distal two thirds of the dorsal pancreatic duct with the entire ventral duct. The accessory pancreatic duct (duct of Santorini) is formed by the persistence of the proximal
one third of the dorsal pancreatic duct, but the duct may completely regress in up to
40% of cases.
Prior to the arrival of week 10, the lumen of the gut is once again fully patent due
to apoptosis of some endodermal cells. By the completion of week 10, acinar and
primitive islet cells can be found within the pancreas of the embryo. Both exocrine
and endocrine pancreatic cells form from endodermal buds. There is then an amplication of endocrine cells, particularly beta cells. By week 13, alpha, beta, and delta
cells are present in the islets [2–4].
1 Anatomy andPhysiology
5
Normal Anatomy
Duodenal Anatomy
The duodenum is the rst 20 to 25cm of small bowel and connects the stomach to
the jejunum. It is found in the upper abdomen, generally between lumbar vertebra
one and three. Unlike the remainder of the small bowel, the duodenum does not
have a mesentery. Its course forms a characteristic “C” shape which is divided into
four parts: superior (D1), descending (D2), inferior (D3), and ascending (D4). D1
travels superiorly from the pylorus of the stomach. Approximately the rst half of
D1 is located intraperitoneally prior to transitioning to a retroperitoneal location.
The hepatoduodenal ligament attaches D1 to the inferior aspect of the liver. D2
courses inferiorly, as the name implies, and curves around the head of the pancreas.
It contains the major and minor duodenal papillae by which the liver and pancreas
drain. D3 crosses from right to left, passing over the great vessels and behind the
superior mesenteric vessels. Once the duodenum crosses over the aorta, it begins an
anterosuperior ascension and is called D4. The most distal segment of D4 transitions into the intraperitoneal space and its terminal point is marked by a peritoneal
fold, known as the ligament of Treitz (suspensory muscle of the duodenum). The
ligament of Treitz creates a sharp anteroinferior turn known as the duodenojejunal
exure and signies the start of the jejunum [2, 3, 5, 6].
Pancreatic Anatomy
Also located primarily in the retroperitoneum, the pancreas is positioned posterior
to the stomach and mesentery of the transverse colon. It also is divided into four
major sections: head, neck, body, and tail. The head is the most right-sided major
division of the pancreas and can be found nestled within the C-loop of the duodenum, which overlies the inferior vena cava (IVC). The uncinate process, a subdivision of the head, extends inferiorly and medially to hook behind the superior
mesenteric vein (SMV). The uncinate process generally terminates prior to the
superior mesenteric artery (SMA). The neck is a short segment that connects the
head and body of the pancreas and is located directly anterior to the SMV. The gastroduodenal artery (GDA) is located on the anterior surface of the pancreas and can
be used to identify the border between the head and neck of the pancreas. The body
then extends across the midline, crossing over the aorta and SMA. The tail lies anterior to the left kidney and can be intimately related to the splenic hilum and left
colonic exure. The splenic vein courses along the posterior surface of the body and
tail, while the splenic artery runs along their superior surface [6–8].
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J. Heard et al.
Ductal Anatomy
The extrahepatic biliary ducts ultimately ow into the common bile duct, which
travels in the hepatoduodenal ligament. The common bile duct passes posterior to
D1, courses within a deep pancreatic groove on the posterior surface of the pancreatic head until eventually becoming intrapancreatic prior to its termination in the
duodenum. The normal internal diameter of the common bile duct is less than 6mm.
The main pancreatic duct is responsible for drainage of the entire length of the
pancreas. It eventually joins the distal common bile duct to drain via the major duodenal papilla. The diameter of the main duct increases gradually as it travels from
the tail to the pancreatic head with normal diameters of 1–2mm in the tail, 2–3mm
in the body, and 3–4mm in the head. The accessory duct drains the anterosuperior
aspect of the pancreatic head. Approximately 60% of people have a bid pancreatic
duct conguration with the main and accessory pancreatic ducts both present
although the main duct maintains the dominant role of drainage. The accessory
pancreatic duct typically drains via the minor duodenal papilla, which is located
within D2 proximal to the major duodenal papilla.
The ampulla of Vater (hepatopancreatic ampulla) contains the dilated fusion of
the distal portion of the common bile and main pancreatic ducts. It is located within
the wall of D2, in the most common conguration, producing a short common channel. The sphincter of Oddi (hepatopancreatic sphincter), a smooth muscle complex,
is located within the ampulla of Vater and controls the ow of bile and pancreatic
enzymes into the duodenum and prevents reux into the common bile and main
pancreatic ducts [2, 7, 9, 10].
Vasculature
The duodenum and head of the pancreas obtain their blood supply by a highly
redundant arterial collateralization from branches of both the celiac trunk and
SMA. The celiac trunk gives rise to the common hepatic artery. The common
hepatic artery branches to form the gastroduodenal artery, which then gives off the
anterior and posterior superior pancreaticoduodenal arteries. These supply D1 to the
major duodenal papilla in D2. Meanwhile, the inferior pancreaticoduodenal artery,
a branch of the SMA, bifurcates into the anterior and posterior inferior pancreaticoduodenal arteries. The paired inferior pancreaticoduodenal arteries provide for D2,
distal to the major papilla, through D4. Together, the four pancreaticoduodenal
arteries supply the head and uncinate process of the pancreas. The pancreatic neck,
body, and tail all receive their arterial supply from branches of the splenic artery via
the celiac trunk. The splenic artery produces several small branches along its length
to supply the superior aspect. The inferior aspect of the neck, body, and tail are supplied by the dorsal (superior) and inferior (transverse) pancreatic arteries.
1 Anatomy andPhysiology
Venous drainage of the area generally mirrors that of the arterial system. All of
the pancreaticoduodenal veins ultimately drain into the SMV. While the anterior
and posterior inferior veins directly conuence with the SMV at the inferior border
of the uncinate process, the posterior superior pancreaticoduodenal vein joins the
SMV at the superior border of the pancreatic neck. The anterior superior ows into
the right gastroepiploic vein prior to entering the SMV at the inferior border of the
pancreas. Venous outow of the pancreatic body and tail is via the branches of the
splenic vein [2, 6].
7
Lymphatics
The body and tail of the pancreas directly drain to the pancreaticosplenic lymph
nodes (stations 18, 10, 11), which subsequently go to the celiac lymph nodes (station 9). The head and neck of the pancreas primarily drain to the supra- and infrapyloric lymph nodes (stations 5 and 6), anterior to the common hepatic artery
(station 8a), around the cystic and common bile ducts (stations 12b1, 12b2, 12c),
anterior and posterior to the head of the pancreas (stations 13a, 13b, 17a, 17b), and
along the proximal SMA [14]. The duodenal lymphatics are located anterior and
posterior to the head of the pancreas and around the SMA [11, 12].
Nerves
The vagus nerves provide parasympathetic innervation to the duodenum and pancreas. The left and right vagus nerves divide to form the anterior and posterior vagal
trunks, respectively, which travel near the surface of the distal esophagus. The vagal
trunks then pass through the celiac plexus before branching to innervate the submucosal layer of the duodenum and the pancreatic acinar and islet cells. Thoracic-level
greater and lesser splanchnic nerves provide sympathetic innervation to both the
duodenum and pancreas after passing through the sympathetic chain to the celiac
and superior mesenteric plexuses [12, 13].
Clinically Relevant Anatomic Variations
Duodenum Inversum
In duodenum inversum, also known as inverted duodenum, the proximal duodenum
travels posterosuperiorly so that the D3 curves over D2 ultimately terminating at a
normally located ligament of Treitz. While the etiology is incompletely known, it is
8
Fig. 1.1 Abdominal
radiograph demonstrating
opacication of the
stomach and duodenum. It
is noted that the third part
of the duodenum passes in
a cranial direction over the
second portion
J. Heard et al.
thought to result from a persistent pancreatic dorsal mesentery resulting in incomplete embryologic rotation. The reported prevalence is less than 1%, with the majority of these patients incidentally identied on imaging. Among the few who develop
symptoms, nausea, vomiting, bloating, and epigastric pain are often seen. Notably,
duodenum inversum is often reported in patients also found to have pancreas divisum [14] (Fig.1.1).
Pancreas Divisum
Pancreas divisum is the most common pancreatic anatomic variant, occurring in up
to 14% of the population. There are three primary variants, all of which result in a
relative outow obstruction through the minor papilla and may result in recurrent
acute pancreatitis: type 1 (classical), type 2, and type 3 (incomplete). In type 1, there
is a complete failure of fusion of the dorsal and ventral pancreatic buds resulting in
the superior head, neck, body, and tail draining via the accessory duct and the minor
papilla while the inferior head and uncinate process drain through the main pancreatic duct and the major duodenal papilla (Fig.1.2). With type 2 pancreas divisum,
there is an absence of the main pancreatic duct and pancreatic drainage is thus
dependent upon the accessory duct alone. Type 3 is similar to type 1, except there is
a diminutive communicating ductal branch between the main and accessory ducts
[8, 10].
1 Anatomy andPhysiology
Fig. 1.2 An MRCP of
classical pancreas divisum
is shown. CBD common
bile duct, D duodenum,
DD dorsal duct, VD
ventral duct
Annular Pancreas
The prevalence rate of annular pancreas is thought to be 0.01% and results from a
failure of the ventral bud to properly rotate with the second portion of the duodenum
during embryologic development. This results in complete, or partial, encasement
of the duodenum by pancreatic tissue. There are two types: extramural and intramural. The most common type, extramural, occurs when the ventral pancreatic duct
traverses posteriorly around the duodenum to join the main pancreatic duct in the
usual fashion. When symptomatic, this often presents as a duodenal obstruction and
has been associated with Down syndrome. The second type, intramural, results in
many small ducts that drain directly into the duodenum from the ventral pancreatic
bud and may cause duodenal ulcerations [7, 10].
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Ectopic Pancreas
Ectopic pancreas occurs when normal pancreatic tissue exists without anatomic or
vascular communication with the main pancreatic gland. Typically, these are identied in the submucosa of the gastric antrum (30%), duodenum (50%), or the remainder of the small bowel (20%). The embryologic origin for these islands of pancreatic
tissue is thought to be residual primitive pancreatic cells that were not incorporated
into the pancreatic buds. Ectopic pancreas is most often an incidental nding, but
patients may develop abdominal pain, dyspepsia, or gastrointestinal bleeding.
Although rare, there are reports of malignancy that develops within the ectopic pancreatic tissue which may be signicant in patients with known pancreatic eld
defects [7, 8, 10].
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J. Heard et al.
Pancreatic Agenesis andHypoplasia
Total pancreatic agenesis is considered incompatible with life, but partial agenesis,
also known as hypoplasia, does occasionally occur as a result of a failure of the
ventral or dorsal pancreatic buds to develop. Total dorsal pancreatic agenesis (“short
pancreas”) is extremely rare and has been associated with visceral heterotaxy. More
commonly, partial dorsal agenesis occurs resulting in a variable degree of tail, body,
neck, or anterior head absence. In partial dorsal agenesis, the accessory pancreatic
duct and minor papilla are present, which differentiates it from total dorsal agenesis.
Patients with dorsal agenesis are at elevated risk for diabetes as the islet cells are
primarily located in the pancreatic tail [7, 8, 10].
Ansa Pancreatica
The rarest pancreatic duct anomaly, ansa pancreatica, is associated with the development of recurrent acute pancreatitis. In this anomaly, there is an obliteration of
the accessory duct prior to joining the main pancreatic duct. This missing segment
is replaced with a dilated branch of the main duct which takes an “S-shaped” or
looping path to the remnant accessory duct allowing for drainage through the minor
papilla [7, 15].
Pancreaticobiliary Maljunction
Pancreaticobiliary maljunction (anomalous pancreaticobiliary junction) occurs
when the common bile duct and main pancreatic duct fuse prior to entering the
duodenal wall which results in a long common channel (>15mm) outside of the
purview of the sphincter of Oddi. The estimated prevalence is near 3% worldwide
although signicantly higher rates are observed in Asia. In recent years, studies
have associated pancreaticobiliary maljunction with development of biliary tract
malignancies and pancreatitis, which are believed to result from bidirectional reux
of pancreatic juices and bile. While pancreaticobiliary maljunction is associated
with a choledochal cyst (types A and C) in 70% of cases, it also occurs without dilation (type B) or as a product of annular pancreas, pancreas divisum, or other atypical
duct congurations (type D) [16–18].
1 Anatomy andPhysiology
11
Duplication Anomalies
Duplication cysts are characterized by an epithelial mucosal lining, a smooth muscle layer, and an attachment, whether communicating or non-communicating, to the
native alimentary tract. They may occur anywhere along the gastrointestinal tract
and are named for their native-organ attachment from which they obtain their blood
supply. Notably, up to 35% of duplication cysts contain ectopic tissue with gastric
and pancreatic being common. Overall, the incidence of duplication cysts is 1in
4500 births with duodenal duplication cysts accounting for 5% of those identied.
Pancreatic duplication cysts are exceedingly uncommon with less than 75 reported
cases in the literature.
Generally, duodenal duplication cysts are identied in early childhood as a result
of abdominal pain, gastrointestinal bleeding, or intestinal obstruction although
severe pancreatitis and cyst rupture do occur. Duodenal duplication cysts are typically located in the second or third portion of the duodenum and may communicate
with the native duodenum, the pancreatic duct, or the common bile duct. Very little
is known about pancreatic duplication cysts, but they are thought to have a connection with the native pancreatic duct [19–21].
Physiology
Duodenal Physiology
Mechanical Function
The migrating motor complex (MMC) is a recurring gastrointestinal pattern that
occurs every 90min in the fasted state. The MMC is thought to originate in the
gastric antrum or duodenum and propagate a peristaltic contraction distally in order
to propel residual material toward the colon. The MMC occurs in four phases with
the third affecting the strongest contractions. Motilin, an active gastrointestinal peptide, is known to play a large role during phase III MMC contractions [22].
During the fed state, the duodenal motion serves two purposes: to mix the chyme
deposited from the stomach and to increase the chyme’s contact with the brush border of the intestines (segmentation contractions) and to propel the chyme forward
through the intestinal tract (peristalsis) [23]. Peristalsis is increased by cholecystokinin, gastrin, serotonin, and insulin and decreased by glucagon and secretin [24].
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J. Heard et al.
Digestive andAbsorptive Functions
The duodenum is a signicant location for digestion of fats, carbohydrates, and
proteins within the gastrointestinal tract and is primarily responsible for the absorption of starches, amino acids, vitamins, minerals, and water.
Oral and pancreatic amylase debranch almost all dietary starches (lactulose,
sucrose, maltose) to maltose, saccharides, and dextrins prior to their passage into
the jejunum. The more simplied starches then come into contact with the brush
border of the intestines which completes the process of converting them primarily
to glucose. SGLT1 transporters, present on the brush border in the upper one third
of the small bowel, allow active transport of glucose and galactose from the digestive tract. GLUT5 allows for the facilitated diffusion of fructose across the brush
border of the small intestines.
Denatured proteins, present in chyme, are further broken down by secreted pancreatic enzymes that are activated by the duodenal brush border in a cascade-like
manner. Trypsin, activated from the secreted enzyme trypsinogen, then activates
other proteolytic enzymes such as chymotrypsin, elastase, and carboxypeptidase.
Together these enzymes complete the digestion of proteins to amino acids allowing
for up to 90% of protein absorption by the end of the jejunum.
The duodenum is responsible for the uptake of several vitamins and minerals.
Duodenal active transport of calcium is enhanced by the relatively acidic environment, vitamin D, and parathyroid hormone. Similarly, iron, in its ferrous form or as
heme, is actively transported primarily in the duodenum by the transporter DMT1.
Ferric iron is reduced to the ferrous form by brush border enzyme cytochrome b.
DMT1 also transports zinc and copper within the duodenum. Finally, vitamin B12
(cobalamin), absorbed in the terminal ileum, requires pancreatic proteases in the
duodenum to cleave intrinsic factor from B12 to allow for future absorption [25].
Endocrine Function
The second portion of the duodenum is the entry point for both stomach contents
and pancreatic uid into the small bowel. The duodenum plays an important role in
hormone secretion in several negative feedback loops. G cells, primarily located in
the gastric antrum, can be found in the duodenum. G cells are stimulated to release
gastrin in response to vagal stimulation and gastrin-releasing peptide (bombesin)
due to protein ingestion, gastric distention, and an elevated gastric pH.Gastrin stimulates gastric parietal cells to acidify the stomach, stimulates gastrointestinal mucosal growth, and increases gastric motility [26].
Cholecystokinin (CCK) is produced by I-cells in the duodenum, but also the
jejunum, in response to the release of fats and digested proteins deposited from the
stomach. CCK’s primary functions are known to aid in digestion. It stimulates the
gallbladder to contract, relaxes the sphincter of Oddi, inhibits further stomach contraction, and plays a role in inducing satiety. Additionally, CCK stimulates
1 Anatomy andPhysiology
13
pancreatic release of bicarbonate rich uid although to a much lesser extent than
that of secretin [27].
Passage of gastric chyme into the duodenum and jejunum also stimulates the S
cells to produce secretin. Specically, a pH less than 4.5, fatty acids, and bile salts
have been shown to stimulate secretin production. Secretin limits further gastrin
release in the stomach and induces the pancreas to produce a high-volume bicarbonate uid to neutralize the acidic chyme and digestive enzymes to aid fat digestion.
Somatostatin (SST) is produced by D cells in the pancreas as well as in the gastric antrum, duodenum, and central nervous system. Within the gut, SST is secreted
in the presence of acid, fat, proteins, glucose, and cholecystokinin and acts as an
inhibitor of pancreatic, biliary, gastric, and colonic secretion. Additionally, it inhibits the release of vasoactive intestinal peptide (VIP) [28].
Gastric inhibitory peptide (GIP) is produced primarily by the K cells of the duodenum and proximal jejunum, yet can be found throughout the small intestine. GIP
is secreted in response to intraluminal glucose, high concentrations of amino acids,
or long-chain fatty acids. The gastrointestinal related effects of GIP include stimulation of pancreatic islet cells to increase insulin levels and inhibition of G cell gastrin
secretion [27, 29].
M cells, found in the duodenum, produce motilin which aids in propulsion of
food through the gastrointestinal tract, increases gallbladder contractility, increases
the lower esophageal sphincter tone, increases gastric pepsin release, and is thought
to play a role in increasing hunger. Several factors increase motilin release including
prolonged fasting and the presence of fat or acid in the duodenum [30, 31].
VIP, like SST, has a multitude of roles throughout the body. In the gastrointestinal tract, it is produced by the myenteric and submucosal plexus nerves in the intestinal walls and by the islet cells of the pancreas in response to vagal stimulation.
Generally, VIP results in smooth muscle relaxation of the lower esophageal sphincter, stomach, gallbladder, small bowel, and blood vessels. Additionally, it causes
secretion of water and electrolytes from the small bowel and bicarbonate rich uid
from the pancreas. Finally, in the stomach it reduces gastrin-related acid production [32].
Pancreatic Physiology
Exocrine Physiology
The exocrine structures of the pancreas make up about 80–90% of the pancreatic
mass, and the endocrine structures contribute to about 2% of the pancreas. The rest
of the pancreas is made up of the extracellular matrix, blood vessels, and ductal
structures. The function of the exocrine pancreas is to aid in the digestion of carbohydrates, fats, and proteins.
There are two main components of the exocrine pancreas: the acinar cells and the
ductal system. The pancreas secretes about 1L of pancreatic uid daily, containing