MBS 208

Introduction to Basic and Clinical Anatomy

GI System:
Midgut and Hindgut
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Today:
Recap of Foregut and Mesenteries
Midgut & Hindgut:
Small intestine Blood Supply, Venous Drainage and Innervation
Brief Introduction to GI Embryology
The Colon Blood Supply, Venous Drainage and Innervation
Porto-Caval Anastamoses
Concept of Referred Pain

GI System

Divided into:
Foregut
Midgut
Hindgut
Based on blood
supply
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Blood Supply to GI
System
Celiac trunk
(foregut)

Superior
mesenteric Artery
(midgut)

Inferior mesenteric
Artery (hindgut)

Dorsal mesentery

Ventral mesentery

The GI Tract
Foregut

Lower Esophagus

Celiac Trunk

Stomach
Spleen
Liver
Gall Bladder

1st, 2nd parts of duodenum, part of pancreas

Midgut

3rd, 4th parts of duodenum, part of pancreas

jejeunum, ileum

Superior Mesenteric
Artery

cecum
appendix

ascending colon, proximal 2/3 of transverse colon

Hindgut

distal 1/3 of transverse colon

descending colon, sigmoid colon
rectum

Inferior mesenteric
Artery

l. Gastric a.

Proper hepatic a.

Gastroduodenal .

r. gastric a.

Biliary System

Hepatic
duct
Cystic duct
Common bile
duct
7

Common bile
duct

pancreas

papilla
Main pancreatic duct
8

Ampulla (of Vater)

Porta Hepatis Portal Triad

Portal vein
Cystic artery

Hepatic duct
Common
hepatic artery

Splenic artery

10

Lesser omentum connecting liver to the

stomach and upper duodenum, composed of
the hepatoduodenal ligament inferiorly and
the hepatogastric ligament superiorly; the
hepatoduodenal ligament contains the portal
triad and forms the roof of the epiploic forament
of Winslow (connecting the greater and lesser
sacs)

Falciform ligament with

ligamentum teres

Gastro-hepatic
ligament
Lesser
sac

Hepato-duodenal
ligament
Lesser omentum
Foramen of
Winslow

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Greater omentum

STOMACH MESENTERIES
Coronary ligament

Visceral
peritoneum

Falciform ligament

Umbilical vein

Ligamentum teres hepatis

(remnant of umbilical vein)

12

Ligamentum teres = obliterated

umbilical vein passing in lower free
edge of falciform ligament

Falciform
ligament
Ligamentum
teres
Umbilical vein

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Midgut
Distal part of 2nd portion of duodenum
Part of pancreas
Small intestine jejeunum, ilium
Cecum
Appendix
Ascending Colon
Proximal 2/3 of transverse colon
All of these structures are supplied by the
Superior mesenteric Artery
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Digestion in the Small Intestine

As chyme enters the duodenum:
Carbohydrates and proteins are only partially
digested
No fat digestion has taken place
Digestion continues in the small intestine:
Chyme is released slowly into the duodenum
Because it is hypertonic and has low pH, mixing is
required for proper digestion
Required substances needed are supplied by the liver
Virtually all nutrient absorption takes place in the
small intestine
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THE DUODENUM

foregut
midgut

16

G -shaped

Arteries of Duodenum and Head of Pancreas

Celiac trunk
Splenic artery

Posterior superior
pancreatico-duodenal
artery
Anterior superior
pancreatico-duodenal
artery

SMA

Pancreas is
considered part of
both foregut and
midgut

Posterior branch of
inferior pancreaticoduodenal artery
Anterior branch of
inferior pancreaticoduodenal artery
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Right crus of
diaphragm

Ligament of Treitz

Celiac
trunk

Duodenojejeunal junction

SMA

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Greater
omentum

Transverse
colon

Small
intestine
(jejeunum
and ileum)

Ascending
colon

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Small bowel has valvulae

conniventes (plicae
circulares), mucosal folds
that extend across the
entire diameter of the
bowel

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Superior
mesenteric a.
jejeunum

Mesentery of small
intestine

cecum

Ileo-jejeunal
branches of SMA

ilieum

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Superior Mesenteric Artery Syndrome

Compression of the 3rd part of Duodenum by SMA
Causes dilation of 1st, 2nd parts
Causes bilious vomiting, (curdled milk mixed with bile), nausea
SMA may also compress left renal vein
May be relieved by having patient lean forward when eating

stomach

duodenum

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Another cause of obstruction

in the foregut Congenital
Pyloric Stenosis

Cardiac
region

fundus

pylorus

body

antrum
Symptoms of congenital pyloric
stenosis
Non-bilious Vomiting (projectile)
Abdominal pain
Dehydration
Failure to gain weight
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Congenital Hypertrophic Pyloric Stenosis

Marked thickening of the
pylorus
Results in narrowing of the
pyloric canal and
obstruction to passage of
food
Stomach becomes
markedly distended and
infants expel food with
nonbilious projectile
vomiting
Progressive loss of fluid,
H-, Cl- leads to metabolic
alkalosis and dehydration
Can be treated surgically
with pylorotomy
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GI Embryology 101
(in 3-minutes)
All you need to know:
Once upon a time, the GI system was a simple
tube suspended in the abdominal cavity by a
double layer of peritoneum (a mesentery) which
connected the tube to the posterior wall (dorsal
mesentery) and the anterior wall (ventral
mesentery) of the abdomen

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MESENTERIES

A ventral mesentery is formed from the terminal part of esophagus down to the initial
portion of the duodenum; this is formed when the liver penetrates the mesenchyme of
septum transversum, causes it to bulge down and form the mesentery; the liver divides this
mesentery into two parts: the dorsal part connecting the liver to the terminal part of
esophagus down to the initial part of duodenum (called the lesser omentum) and a ventral
part connecting the liver to the ventral body wall (called the falciform ligament)

26

Cylindrical
human body
plan, day 28
(about cm)

Simplified
cross section
through
abdomen of
an adult
(essentially the
same as above)

27

Rotation of the Stomach The developing stomach rotates 90 degrees in a

clockwise direction around its longitudinal axis. The original left side becomes the
ventral surface, while the original right side becomes the dorsal surface. The greater
curvature comes to lie somewhat caudally and to the left; the lesser curvature will be
located cranially and to the right. The left vagal trunk will be pulled anteriorly, while the
right vagus is pushed posteriorly (Remember the mnemonic LARP for left anterior,
right posterior)
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STOMACH MESENTERIES

As a result of the rotation of the stomach, the greater omentum is pulled to the
left, forming a space behind the stomach (the lesser sac or omental bursa), and
also bulges down in front of the transverse colon; later its two layers fuse to form a
single sheet that also fuses with the transverse mesocolon

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STOMACH MESENTERIES

As a result of the rotation of the stomach, the greater omentum is pulled to the left,
forming a space behind the stomach (the lesser sac or omental bursa), and also
bulges down in front of the transverse colon; later its two layers fuse to form a
single sheet that also fuses with the transverse mesocolon
When the spleen primordium appears in the dorsal mesogastrium, the portion
behind it becomes the lienorenal ligament (or splenicorenal ligament) and the
anterior part forms the gastrolienal ligament

Lesser sac

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STOMACH MESENTERIES

As a result of the rotation of the stomach, the greater omentum is pulled to the
left, forming a space behind the stomach (the lesser sac or omental bursa),
and also bulges down in front of the transverse colon; later its two layers fuse to
form a single sheet that also fuses with the transverse mesocolon
(Lesser
sac)

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THE PANCREAS

The pancreas develops from two buds: a dorsal bud from the duodenum, and a ventral bud from the
origin of the liver bud; as the duodenum rotates to the right, the bile duct and the ventral pancreatic bud
also rotate until they lie posteriorly; the ventral bud thus lies below and behind the dorsal bud
The ventral bud forms the uncinate process and part of head of pancreas; the rest is formed by the
dorsal bud; the main pancreatic duct is formed from the entire ventral duct and the distal part of the
dorsal duct; the proximal part of the dorsal duct often forms an accessory pancreatic duct
Islets of Langerhans form from pancreatic parenchyma (derived from endoderm) in the 3rd month; insulin
secretion begins in the 5th month; connective tissue is derived from the splanchnic mesoderm
Pancreas becomes secondarily retroperitoneal as its mesentery fuses with the posterior abdominal wall

Dorsal
pancreatic
bud

ventral
pancreatic
bud

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Annular Pancreas
The ventral pancreas may consist of two lobes. If the lobes migrate around the
duodenum in opposite directions to fuse with the dorsal bud, an annular pancreas is
formed.

Symptoms and signs in infants:

feeding intolerance
bilious vomiting
abdominal distension
In adults: abdominal pain, nausea, vomiting,
upper GI bleeding (from stomach ulceration),
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acute or chronic pancreatitis

MIDGUT

Elongation of the midgut forms the primary intestinal loop which is connected at its apex to
the vitelline duct; the superior mesenteric artery forms the axis of the loop; the cephalic
limb of the loop later forms the rest of the duodenum, jejunum, and part of ileum; the
caudal limb forms the rest of the ileum, cecum and appendix, ascending colon, and
proximal two-thirds of transverse colon
The loop elongates rapidly, especially at the cephalic limb; because of enlargement of liver,
the abdominal cavity temporarily cannot accommodate the loop and it herniates into the
extraembryonic cavity in the 6th week (called physiological umbilical herniation)

Vitelline
duct
(connection
to yolk sac)
Vitelline
duct
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Development of Midgut Midgut development is characterized by rapid elongation of the

gut and mesentery. This process occurs at a time when the body cavity is still relatively
small, so the primary intestinal loop undergoes a process known as physiological
herniation into the umbilical cord, beginning at about 6 weeks of development.
The apex of the midgut loops remains in continuity with the yolk sac via the vitelline
duct.
During its growth spurt, the intestinal loop rotates around a central axis formed by the
artery of the midgut, the superior mesenteric artery. The rotation is counterclockwise,
and totals 270 degrees.
By the 10th week, the intestinal loops begin their return to the abdominal cavity.
Proximal jejunum is the first to re-enter, and comes to lie on the left side; later returning
parts come to lie more and more to the right. The prospective cecum is the last part of
the intestinal loop to return to the body cavity. At first, it lies directly below the liver, but
from there it normally descends to the right iliac fossa. Failure of this part of the gut tube
to descend may result in subhepatic appendix.
As the ascending and descending colon press against the posterior body wall, their
mesenteries fuse with the posterior layer of parietal peritoneum, causing these
structures to become secondarily retroperitoneal. Abnormalities in midgut rotation can
result in conditions such as left-sided colon and reversed rotation of the intestinal loop.
Twisting (volvulus) of the gut tube and compromised blood supply can occur.
Occasionally, part of the vitelline duct may persist, forming an ileal (Meckels
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diverticulum)

MIDGUT ROTATION

During the herniation, the

loop rotates 90o
counterclockwise (when
viewed ventrally);
later the loop returns to the
abdominal cavity; the cause
for this return may be
attributed to degeneration of
mesonephric kidneys,
reduced growth of the liver,
and expansion of abdominal
cavity; during the retraction,
the loop rotates another 180o
counterclockwise

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Abnormalities of Midgut Rotation

A. Nonrotation
B. Mixed rotation
and volvulus
C. Reversed
rotation
D. Subhepatic
cecum and
appendix
E. Internal Hernia
F. Midgut
volvulus

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Omphalocele failure
of umbilicus to close
completely

Ectopia Cordis
failure of abdominal
wall closure more
superiorly
38

Gastroschisis
abdominal wall does
not involve the
umbilicus

Meckels
Diverticulum

ileum

Meckels Diverticulum abnormality of vitelline duct

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40

Cecum and Appendix

Cecum is a small sac (blind pouch) at lower end of
ascending colon
Valve prevents a back up of fecal matter to ileum
Appendix
Lymph tissue neutralizes bacteria
Diverticulosis a small outward herniation of colon,
especially sigmoid
Diverticulitis infection with leaks into peritoneal cavity
may lead to peritonitis

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Cecum and Appendix

Iliocecal valve
appendix
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43

1/3 distance
from ASIS to
umbilicus

Variations in position of
appendix/cecum due to
malrotation of gut

45

Appendicitis
Obstruction of appendiceal
lumen leads to
inflammation and/or
rupture
Typically present with
fever, nausea/vomiting, and
periumbilical/right lower
quadrant pain
Presence of calcified
appendicolith (7-15%) and
abdominal pain = 90%
probability of acute
appendicitis
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Appendicitis
Normal

Inflamed

Inflamed appendix

Appendicolith seen on bone window 47

A ruptured appendix may lead to

Peritonitis: inflammation of the parietal and visceral peritoneum.
Peritonitis may be localized or generalized, and may result from
infection or from a non-infectious process.
The main manifestations of peritonitis are acute abdominal pain,
abdominal tenderness, and abdominal guarding, which are
exacerbated by moving the peritoneum, e.g. coughing (forced
cough may be used as a test), flexing one's hips,
Abdominal guarding is the tensing of the abdominal wall muscles
to guard inflamed organs within the abdomen from the pain of
pressure upon them. The tensing is detected when the abdomen
wall is pressed.

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Large Intestine
Most material has been digested by the time it reaches
Large Intestine
12-24 hours in large bowel
Little breakdown
Performs some absorption, especially water
Components
Ascending colon
Transverse colon
Descending colon
Sigmoid to rectum and anus
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Greater
omentum

Transverse
colon

Transverse
mesocolon

Small
intestine
(jejeunum
and ileum)

Ascending
colon
Right paracolic
gutter

Left paracolic
gutter

50

Greater
omentum

Transverse
colon

Transverse
mesocolon

Small
intestine
(jejeunum
and ileum)

Ascending
colon
Right paracolic
gutter

Left paracolic
gutter

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Large Intestine
Has three unique features:
Teniae coli three bands of longitudinal smooth
muscle in its muscularis
Haustra pocketlike sacs caused by the tone of the
teniae coli
Epiploic appendages fat-filled pouches of visceral
peritoneum
52

Right colic
(hepatic) flexure

left colic (splenic)

flexure

53

Small vs. Large

Intestine

Horton KM et al, Radiographics. 2000

Colon has sacculations called

haustra as teniae coli are
shorter than the colonic wall

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Colon is relatively peripheral

but can be very mobile

Barium X-ray
of large
intestine

55

L1 level

Transverse colon

Descending
colon

Small
intestine

56

L3 level

Transverse
colon
Small
intestine

Ascending
colon

nd
2 part of
duodenum

IVC

aorta

57

Descending
colon

Functions of the Large Intestine

Other than digestion of enteric bacteria, no
further digestion takes place
Vitamins, water, and electrolytes are
reclaimed
Its major function is propulsion of fecal
material toward the anus
Though essential for comfort, the colon is
not essential for life
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59

Transverse colon

Ascending
colon

Descending
colon

Sigmoid
colon
60

Foregut

Hindgut
Haustra

Middle colic a.
Marginal artery (of
Drummond)

Teniae coli

r. Colic a.
Iliocolic a.

l. colic a.

Superior rectal a.

62

Diverticulum

outpouchings of the colonic mucosa and

submucosa through weaknesses of muscle
layers in the colon wall

63

Due to low-fiber diets, constipation,

which increases intra-luminal pressure

Diverticulosis

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Herniation of mucosa and submucosa
through muscular layers

Colonic
intussusception
A section of the bowel tunnels into
an adjoining section, like a
collapsible telescope

Causes include:
benign or malignant growths

adhesions (scarlike tissue)

surgical scars in the small bowel
or colon

motility disorders (problems with

the movement of food through the
digestive tract)

long-term diarrhea

65

May interrupt normal blood

flow and necrosis of colon

Crohns Disease
Crohns disease (CD) is a chronic relapsing inflammatory condition
usually with flare-ups alternating with periods of remission, and an
increasing disease severity and incidence of complications as
time goes on.
It can affect any part of the gastrointestinal tract from the mouth to the anus.
For typical sites & proportion of patients affected see below:

Extensive Small
Bowel 5%

Terminal Ileum
only 20%

Ileocaecal 45%

Colon only 25%

66

Other: anorectal,
gastroduodenual, oral only
5%

Crohns Disease

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Clinical Features
The clinical presentation can be very variable depending upon the site and
predominant pathology of that site.
Major symptoms include:

Diarrhea (can be bloody with colonic involvement, or steatorrhea (fat in stool) in

small bowel disease)
Abdominal pain
Weight loss
Constitutional symptoms such as malaise, anorexia, nausea, vomiting and a low
grade fever.

To make things more complicated 15% of patients have no gastrointestinal

symptoms at all!

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Carcinoma
of the Cecum
2nd leading cause of
cancer death in western
world

69

Colon cancer is the most common

cancer of the GI Tract

CT colonography

Virtual

Mass protruding into lumen usually

arising from mucosa
Neoplastic, hyperplastic, or
inflammatory in etiology

70

Real

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Relationship of Rectum to Other Viscera

prostate

73

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To portal vein

Middle and
inferior rectal
veins to IVC

80

l. Gastric v.

Portal vein

SMV
Splenic v.

IMV

81

Paraumbilical v.s

Esophageal veins
l. Gastric v.

Portal vein

SMV
Splenic v.

IMV

Sup., middle, rectal v.s

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Inf. Rectal v.s

Caput medusae distended and engorged superficial veins which are

seen radiating from the umbilicus across the abdomen to join systemic
veins. They carry more blood than usual because the paraumbilical veins
cannot flow into the portal venous system due to cirrhosis of the liver

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84

Esophageal Varices

85

Most cases of hemorrhoids are

not due to portal hypertension
hard stool or constipation causes
increased pressure in rectum
which compresses rectal veins
need to eat more fiber and drink
more fluids!

Dilation of rectal veins due to anastamotic

connections between superior (portal system) and
middle and inferior (caval system) veins
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