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to the ileocecal valve, sweeping away food particles and
other intestinal contents. The MMC has been aptly called
the “housekeeper potential.” Other mechanisms include
gastric acid, the secretion of immunoglobulins, and the
normal postprandial peristalsis. The concentration of bacteria in the small intestine is estimated at 10
5
/ml, with a
greater concentration in the ileum and a lower concentration in the jejunum. The ileocecal valve helps prevent
reflux of colonic bacteria into the ileum, but the ileocecal
valve is not always competent.
Bacterial overgrowth syndromes can be caused by
structural or motor abnormalities that favor luminal stagnation. Structural abnormalities include a blind loop, a
poorly emptying segment of bowel, strictures, fistulas,
and diverticula. Motor abnormalities may be caused by
primary failure of the MMC or by conditions such as
scleroderma and pseudo-obstruction. Consequences of
bacterial overgrowth include:
1. Deconjugation of bile salts, leading to impaired
micelle formation and causing fat malabsorption and
steatorrhea.
2. Malabsorption of fat-soluble vitamins (A, D, E, K)
because of 1.
3. Malabsorption of vitamin B
12
, leading to megaloblas-
tic anemia.
4. Malabsorption of other nutrients (carbohydrates and
proteins).
5. Hypocalcemia due to chelating action of unabsorbed
fatty acids.
CROHN’S DISEASE
Crohn’s disease (CD) is a granulomatous, transmural
inflammation of unknown origin that can affect any part
of the GI tract. Although the first case may have been documented by Morgani in 1761, and subsequent reports
occurred in the 19th and early 20th century, it is the classic
clinical and pathological description by Crohn, Ginzburg,
and Oppenheimer from Mount Sinai Hospital in New
York that best captured the concept of the disease.
3
Although the small and large intestine and rectum are the
most frequent targets, CD can affect the mouth (6% to
9%), the esophagus (<1%), and the stomach and duodenum (1% to 5%). It occurs with equal frequency in both
sexes. In Wales, the incidence of CD increased from 0.18
per 100,000 people per year in the 1930s to 8.3 per 100,000
people per year in 1980.
4
The essentials of Crohn’s disease
are summarized in Table 8.7.
Etiology and Pathogenesis
An interplay of genetic and environmental factors are
believed to cause Crohn’s disease. No convincing evidence
has been provided for an infectious cause.
Environmental Factors
INFECTIOUS AGENTS Two mycobacteria (Mycobac-
terium paratuberculosis and M. tuberculosis) have been
considered possible etiologic agents because they cause
granulomatous inflammation of the gut. Attempts to identify M. tuberculosis DNA in affected intestinal tissue by
polymerase chain reaction have had varying results. Some
investigators have identified such DNA, and CD has been
treated with variable success using antimycobacterial
drugs.
5
Persistent measles virus and Yersinia enterocolitica
have also been implicated. No specific viral cause has been
identified.
D
IET A dietary cause(s) has been suspected because of
the finding of several antibodies against food antigens (e.g.,
milk, baker’s yeast) in patients with Crohn’s disease. Of
course, this finding may simply represent increased permeability to antigens in the diseased bowel.
S
MOKING Smoking is an independent risk factor
for clinical, surgical, and endoscopic recurrence of CD.
Smoking does not have such an adverse effect on ulcerative
colitis. CD is twice as common in smokers than in
nonsmokers.
Genetic Factors
The risk of developing CD is 30 times higher in siblings of
patients with the disease than in normal subjects whose
siblings do not have CD.
6
CD is also associated with
other genetically determined diseases such as ankylosing
spondylitis and tyrosine-positive albinism. A weak correlation with some human leukocyte antigens (HLA) and an
inverse correlation with others have been made. Increased
P athophysiology ................................................................................................................................. 259
TABLE 8.7. Essentials: Crohn’s Disease
Pathology
䊏
Chronic transmural granulomatous inflammation
䊏
Involvement
➢ Small bowel alone: 35%
➢ Colon alone: 20%
➢ Both small bowel and colon: 45%
Etiology
䊏
Unknown
䊏
Mycobacterium paratuberculosis manifest in 66% of tissue
cultures
Symptoms
䊏
Diarrhea: 90%
䊏
Abdominal pain: 80%
䊏
Anemia: 33%
䊏
Anorectal disease: 35%–50%
䊏
Arthritis, arthralgia: 20%
Complications
䊏
Bowel osbstruction: 33%
䊏
Enteroenteric fistula: 25%
䊏
Enterocutaneous fistula: 20%
䊏
Enterovesical, enterovaginal fistula: 5%–10%
levels of haptoglobin type Hp1-I were found in Japanese
patients with CD compared with normal subjects.
7
Potentially pathogenetic immune defects that have been identified in individuals with CD [e.g., complement C3-F,
increased cytotoxicity against intestinal cell antigen, and
epithelial Ca
++
channels (ECaC)] have been found in unaffected relatives.Using complex familial segregation studies,
Mousen et al. have suggested that “CD is an oligogenetically
inherited disease with one recessive major gene locus and
one modifier gene with a penetrance of 27%.”
8
The most exciting recent contribution of molecular
genetics to our understanding of the etiology of CD has
been the identification of the NOD2 gene. Genome-wide
linkage analysis studies by Hugot and colleagues have
identified NOD2 mutations that are present only in
patients with CD, suggesting a causal relationship.
9
NOD2
is an intracellular protein with homology to disease resistance (R) genes present in plants.
Immune System
Patients with CD seem to be unable to shut off activation
of the gut inflammatory immune responses to luminal
bacteria and dietary antigens. Immune dysregulation in
CD-affected intestine is suggested by the anatomic distribution of MHC class II antigens in the intestine, which is
strikingly similar to the distribution of inflammation of
CD. Also, CD epithelial cells inappropriately induce proliferation of T-helper cells, in contrast to normal epithelial cells, which stimulate proliferation of T-suppressor
cells. Unopposed T-helper cell proliferation may then
nonspecifically induce the cascade of immune activation
effects typical of CD.
Psychological Factors
Prospective studies have failed to show that stressful life
events precipitate exacerbation of CD. Despite this, successful treatment of patients with CD cannot be provided
without attention to psychosocial factors.
Pathology
Anatomic Distribution
CD affects the small intestine alone in 30% to 40% of
patients, both small and large bowel in 40% to 55%, and
colon only in 15% to 25%. Thus, the small intestine is
affected in more than 75% of patients with CD, and the
terminal ileum in more than 90% of these. When only the
colon is involved, disease tends to primarily involve the
distal colon. Perirectal and perianal lesions occur in 33%
of patients. In recent years, the incidence of Crohn’s
disease in the colon has increased. Also, isolated colon
lesions are more common in the elderly.
Gross and Microscopic Picture
The involved bowel and its mesentery are thickened, and
all layers of the bowel wall are affected (Figure 8.18).
Mesenteric fat will be seen creeping onto the serosal
surface of the bowel, accompanied by diffuse, nonspecific
transmural inflammation (Figure 8.19). Involvement is
segmental, with normal intervening portions of bowel.
Noncaseating granulomas are present in 50% of cases and
may be found in the bowel wall, the mesentery, lymph
nodes, or on the peritoneal surface. The inflammatory cells
are made up of macrophages, lymphocytes, and plasma
cells. As disease progresses, deep transverse and longitudi-
10
FIGURE 8.18. Crohn’s disease. The resection specimen of Crohn’s ileitis shows a section of bowel with
marked cobblestoning of the mucosa and thickening. (Courtesy of Theodore Schrock, MD.)
260 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.19. (A) The colon resection specimen shows Crohn’s disease with thickening and stricture
formation. Notice also the transmural character of the process and the fat that creeps to the anterior
surface of the colon. (B) Occasionally, a well-formed, noncaseating granuloma may be encountered.
(Courtesy of Linda D. Ferrell, MD.)
nal mucosal ulcerations develop, with nodular swelling of
Complications of Crohn’s Disease
the intervening mucosa, giving the characteristic cobblestone appearance. With time, the bowel wall becomes
thickened, fibrotic, and stenotic. Burrowing ulcers might
form fistulas into adjacent bowel or bladder. Free intestinal perforation is exceedingly rare.
P athophysiology ................................................................................................................................. 261
Three complications are commonly seen in Crohn’s
disease: obstruction, fistula formation, and extraintestinal
manifestations. Hemorrhage and malignancy are less common complications.
Obstruction
Hemorrhage
CD may cause partial and reversible bowel obstruction or
fibrostenotic and fixed irreversible obstruction. In acute
Crohn’s ileitis, distal small bowel obstruction may be a
presenting problem. In longstanding cases, multiple areas
of fibrotic stenosis may coexist at different levels of the
small intestine.
Fistula Formation
The most common fistulas are into adjacent bowel: ileoileal, ileocecal, or ileosigmoid. Less frequently, cologastric
or coloduodenal fistulas may form (Figure 8.20). While
enteroenteric and even enterocolic fistulas may remain
asymptomatic, cologastric or coloduodenal fistulas produce feculent vomiting and diarrhea. Other common
types include enterovesical fistulas, which produce recurrent attacks of polymicrobial urinary tract infection and
enterovaginal fistulas, which may result in enteric contents
discharging from the vagina. Occasionally, enterocutaneous fistulas develop.
Intra-abdominal Abscess
Intraperitoneal abscesses develop frequently. The abscess
may sometimes be retroperitoneal, anterior to the psoas
muscle, where it may entrap the ureters and cause
hydroureter. Intra-abdominal abscesses usually produce
fever, sweating, pain, and leukocytosis.
Massive hemorrhage is rare, occurring in less than 1% of
patients. However, it may be life-threatening, sometimes
requiring emergency operation.
Growth Retardation
Crohn’s disease retards growth in 15% to 30% of affected
children. The combination of chronic inflammation, subclinical sepsis, and malabsorption are contributing factors.
Occasionally, failure to thrive is an indication for surgery.
Carcinoma
Carcinoma is not a common complication of CD as it is
of ulcerative colitis. Nevertheless, prevalence figures of 0%
to 6% for small intestinal cancer and 1% to 4% for colonic
cancer have been reported.
11
Extraintestinal Manifestations
CD has a variety of extraintestinal manifestations that may
accompany or even precede the intestinal disease. These
include:
1. Dermatological. Associated skin diseases include
erythema nodosum, pyoderma gangrenosum, and
metastatic Crohn’s disease. The latter is an ulcerating skin
FIGURE 8.20. A barium upper GI study and small bowel follow-through examination demonstrate a
duodenal (D)-ileal (I) fistula (arrows) in a patient with Crohn’s disease. The duodenal segment is distorted because of the disease, and the fistula is clearly visible because it is surrounded by fat, which
effectively prevents the small bowel from obscuring it on x-ray (so-called creeping fat). (Courtesy of
Henry I. Goldman, MD.)
262 ................................................................................................................ Small and L arge Intestine
lesion, which on biopsy demonstrates granulomatous
inflammation.
2. Oral. Oral manifestations include aphthous stomatitis, which on biopsy shows chronic granulomatous
inflammation.
3. Ocular. Episcleritis or anterior uveitis may be related
to CD.
4. Musculoskeletal. These manifestations include
clubbing, ankylosing spondylitis, pelvic osteomyelitis,
osteomalacia, and aseptic necrosis. Patients with ankylosing spondylitis exhibit HLA B27 phenotype. Osteomalacia
is caused by vitamin D and calcium deficiency due to malabsorption. Aseptic necrosis is less a complication of CD
than of steroid therapy.
5. Renal. Kidney stones, typically oxalate stones, are
due to enteric hyperoxaluria.
6. Hepatobiliary. Gallstones may occur due to defective
enterohepatic circulation of bile salts, which occurs in
Crohn’s ileitis. Primary sclerosing cholangitis and its complication cholangiocarcinoma occur less commonly in CD
than in ulcerative colitis.
7. Amyloidosis. Amyloidosis may occur in longstanding CD.
CHRONIC ULCERATIVE COLITIS
Chronic ulcerative colitis (CUC) is a chronic inflammatory disease of unknown origin that affects the mucosa of
the rectum and colon. It was first recognized in 1859 by
Samuel Wilks of Guy’s Hospital, London,
12
but it was
Hawkins in 1909 who gave an excellent description of the
disease and its natural history.
13
Subsequently, Sir Arthur
Hurst described the sigmoidoscopic appearance and
clearly differentiated it from bacillary dysentery.
14
Epidemiology
Western Europe, North America, and Australia have a
high incidence of the disease, varying from 4.3 to
11.3 cases per 100,000.
15
Unlike CD, the incidence of
CUC has remained stable. Incidence rates in Eastern
Europe, Asia, and South America are tenfold lower.
15
The
incidence appears to be high in Ashkenazi Jews and low in
black Americans. CUC is a disease of the young, occurring
most commonly between ages 20 and 40 years. A secondary peak of incidence in the elderly has also been
described.
Etiology and Pathogenesis
The etiology has remained elusive. Several theories have
been proposed including infection, dietary allergy, autoimmunity, immune reaction to bacteria, and psychosomatic causes. In addition, a genetic predisposition has
been identified.
Genetics
About 10% to 20% of patients have one or more affected
family members. A study in twins has shown that, of 20
dizygote twins, all 20 were affected, while only one of 16
monozygotic twins had the disease.
16
Nevertheless, the
genetic influences are greater in CD than in CUC.
Infection
No specific infecting microorganism has been consistently
isolated, so CUC is unlikely to be due to infection. E. coli
isolated from CUC patients express higher amounts of
adhesion molecules, suggesting they may adhere better to
and damage the colonic mucosa.
Dietary Allergy
Sensitivity to milk has long been suspected as a trigger.
Controlled clinical trials suggest that 20% of patients
might benefit from a milk-free diet, and increased antibodies to milk proteins have been shown in these
patients.
17
Despite these observations, there is little evi-
dence that food allergy is the primary cause.
Autoimmune Response
Antibodies against polymorphonuclear neutrophils
(PMNs) or perinuclear antineutrophil cytoplasmic antibodies (pANCAs) have been shown to be more prevalent
in CUC, especially in the aggressive form. But the true relevance of these autoantibodies is unknown.
Immune Response
Both humoral and cell-mediated responses are probably
involved in the pathogenesis of inflammation. In the
inflamed tissue, cells that produce IgG are disproportionately increased, but this finding may be an epiphenomenon. In active disease, T cells and macrophages are
activated and release an array of cytokines including IL1b, TNF, and IL-6. Class II antigens are induced in the
epithelial cell surface, making it capable of behaving as an
antigen-presenting cell. In addition to cytokines, other
substances released from activated mucosal cells include
leukotrienes, thromboxane, platelet-activating factor, and
reactive oxygen metabolites. This process contributes to
the cause of diarrhea.
Role of Tachykinins
Neurogenic inflammation, mediated by substance P (SP)
and the neurokinin-1 receptor (NK
1
R), may be important
in CUC. Both SP levels and SP-containing neurons are
markedly increased in the colon in CUC.
Psychosomatic Causes
No convincing evidence exists to show that CUC is a psychosomatic disease. Many of the psychologic findings in
patients with CUC are likely to be secondary to the chronic
and anxiety-producing symptoms of the disease.
P athophysiology ................................................................................................................................. 263
Pathology
Distribution of Disease
In 20% of patients, the disease involves the whole colon;
in 30% to 40% the disease involves the rectum and
sigmoid only, and in 40% to 50% disease is limited to the
rectum. Disease is often more severe in the rectum.
Macroscopic Features
On sigmoidoscopy, the rectal mucosa is hyperemic, edematous, and granular, and it bleeds when touched with an
instrument. More advanced disease is characterized by
ulcers that look like they might penetrate into the lamina
propria. In longstanding cases, pseudopolyps are present
in the colon. At laparotomy, the involved bowel is not
thickened as in CD and, since the disease is mucosal, bowel
may appear nearly normal on the serosal surface. In
advanced cases, however, the colon wall is thin and gray in
appearance. The bowel is often foreshortened and haustral
folds may be lost. Small abscesses may be present within
the mesentery and the colon may dilate and perforate
(Figure 8.21).
Microscopic Features
Inflammation is largely confined to the mucosa. The
lamina propria is edematous and infiltrated with neutrophils, lymphocytes, plasma cells, and macrophages.
Crypt abscesses may be present (Figure 8.22).
Complications of Ulcerative Colitis
Gastrointestinal Complications
HEMORRHAGE Hemorrhage occurs in 5% of cases.
Emergency colectomy should be performed if 6 to 8U of
blood for transfusion are required per 24h.
P
ERFORATION Perforation may occur with or without
toxic megacolon.Perforation is associated with a high mortality rate.
T
OXIC MEGACOLON The diagnosis of toxic megacolon
is made when the diameter of the transverse colon is 6 cm
or more. The incidence is 5%. Factors that precipitate the
development of toxic megacolon include the use of opiates
(particularly in conjunction with anticholinergics), hypokalemia, and barium enema or colonoscopy during the
course of severe acute colitis.
A
CUTE TOXIC COLITIS Severe toxic colitis can occur
without the development of megacolon. Patients with toxic
colitis are septic and have peritoneal symptoms. Signs and
symptoms of peritonitis may be partially masked by steroid
therapy. An important symptom is frequent bloody
diarrhea.
C
ARCINOMA OF THE COLON The incidence of colon
cancer is 7.2% and 16.5% with 20- and 30-year history
of disease, respectively.
18
Colon cancer is usually preceded with dysplasia. Performing colectomy if dysplasia
is present prevents the development of carcinoma. There is
the impression that colon cancer associated with CUC is
more virulent than that occurring in an otherwise normal
colon.
S
CLEROSING CHOLANGITIS AND CHOLANGIOCARCINOMA
Sclerosing cholangitis has a significant association with
ulcerative colitis. It can antedate the development of the
disease or develop in the course of the disease. There
appears to be, however, no relationship between the severity of ulcerative colitis and the develoment of sclerosing
cholangitis. Sclerosing cholangitis is a significant risk factor
for cholangiocarcinoma.
E
XTRAGASTROINTESTINAL COMPLICATIONS These in-
clude:
1. Ocular: episcleritis and anterior uveitis.
2. Oral: Aphthus ulcers in the buccal mucosa.
3. Dermatologic: Pyoderma gangrenosa and erythema
nodosum. Severe pyoderma gangrenosa is occasionally
an indication for colectomy.
4. Musculoskeletal: sacroileitis, ankylosing spondilitis.
The musculoskeletal complications of ulcerative colitis
are rarely an indication for colectomy.
DIVERTICULAR DISEASE OF
THE COLON
Diverticula, or outpouchings from the colon wall, may be
true or false. True diverticula, which involve all layers of
the colonic wall, are infrequent and occur singly or in multiples, mostly in the right colon. Pseudodiverticula, which
lack muscular coat, are more common and are responsible for most diverticular diseases of the colon.
Epidemiology
Around the world, an inverse relationship exists between
the prevalence of diverticular disease and colonic
volvulus.
19
Diverticular disease is an affliction of Western
civilization, most common in North America and
Western Europe, where the incidence of volvulus of the
colon is small. By contrast, volvulus is common in Eastern
Europe, Asia, and Africa, where diverticular disease is rare.
This epidemiologic contrast has been ascribed to dietary
habits. In North America and Western Europe, the diet is
low in fiber content. As a result, the stools are small, and
the colon has a narrow caliber and is not fecally loaded.
The opposite is true in areas where a high-fiber diet is
consumed.
264 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.21. (A) Total colectomy specimens in severe ulcerative colitis show foreshortening of the
bowel, loss of haustral markings, and (B) severe pseudopolyposis. (Courtesy of Theodore Schrock, MD,
and Linda D. Ferrell, MD.)
P athophysiology ................................................................................................................................. 265
A
B
FIGURE 8.22. Ulcerative colitis. (A) Microscopically, pseudopolyps are formed as islands of inflamed
mucosa by ulceration and denudation of surrounding mucosa. (B) Complications of ulcerative colitis
include crypt abscess formation, in this case with a large collection of inflammatory cells and superficial inflammation, and (C) cancer, demonstrating high-grade dysplasia with overt carcinoma formation.
(Courtesy of Linda D. Ferrell, MD.)
C
266 ................................................................................................................ Small and L arge Intestine
FIGURE 8.23. Diverticulitis. CT scan of the pelvis with contrast material in the sigmoid colon and small
bowel shows sigmoid thickening, stranding of the pericolonic fat, and an air collection in the thickened wall (black arrows). These features are typical of diverticulitis with small intramural abscess. A
few simple diverticula (white arrows) are also present. (Figure courtesy of Henry I. Goldman, MD.)
Distribution
Diverticulosis is a condition of the elderly. Its incidence is
less than 10% under the age of 40 years and more than
40% after the age of 80 years. The sigmoid colon is
involved in 95% of cases. Involvement decreases progressively as the disease moves proximally. In a small percentage of patients, the disease is distributed throughout the
colon (Figure 8.23). Diverticula limited to the right colon
are likely to be true diverticula and appear to be more frequent in Asian populations.
Pathogenesis
Diverticulosis
The presence of diverticula without inflammation is known
as diverticulosis. Two etiologic factors have been proposed:
NCREASED INTRALUMINAL PRESSURE High intralumi-
I
nal pressures due to colonic hypermotility occur in individuals whose diet has a low fiber content. The result is that
the colonic musculature becomes thickened and shortened—a condition known as mychosis. The colon, particularly the sigmoid, has a small caliber, and contractions of
its wall generate high luminal pressures. (This is in keeping
with LaPlace’s law, which states that the pressure within a
tubular structure is inversely proportional to its radius.)
The increased intraluminal pressure is believed to push out,
through areas of weakness in the colon wall such as the sites
of arterial entry, portions of mucosa surrounded by
submucosa (Figure 8.24). Evidence for increased intraluminal pressure has been provided with manometric
studies and demonstrations of occlusive contractions on
cineradiography.
EAKNESS OF COLONIC MUSCULATURE It is postulated
W
that the high frequency of diverticulosis in the elderly is
due to a weakness of the colonic musculature that develops with aging. Colonic diverticulosis is also associated
with connective tissue diseases such as Ehlers–Danlos and
Marfan’s syndromes. When connective tissue weakness is
present, pancolonic diverticulosis tends to develop.
Diverticulitis
When diverticula become inflamed, the precipitating
event is thought to be microperforation of individual
diverticuli due to increased intraluminal pressure. This
causes infection and inflammation in the peridiverticular
and pericolonic tissue. Obstruction of diverticular orifices
with fecalith may also precipitate inflammation without
initial perforation. At times, macroperforation of a
diverticulum may occur with more acute septic complications. Patients who perforate a diverticulum because of
steroids tend to develop free perforation and generalized
peritonitis.
Uncomplicated diverticulitis is, in essence, peridiverticulitis, usually due to microperforations of diverticula.
Macroperforation of diverticula may give rise to a pericolic
abscess if the process is walled off or to general peritonitis if it is not (Figure 8.25). Also, a pericolic abscess can
perforate secondarily to give rise to generalized peritonitis. Pericolic abscess or severe diverticulitis can lead to
sigmoid obstruction.
P athophysiology ................................................................................................................................. 267
A
B
FIGURE 8.24. (A) Gross appearance of diverticulosis coli. (B) Microscopically, diverticula are manifest as
outpouchings of the mucosa through the muscle wall and have no muscular coverings themselves (i.e.,
pseudodiverticula). (Courtesy of Linda D. Ferrell, MD.)
COMPLICATIONS Diverticulitis may be uncomplicated,
although complications often occur (see Table 8.8).
Colovesical fistula may manifest with recurrent polymicrobial urinary tract infections, pneumaturia, and fecaluria.
Ureteric obstruction or coloureteric fistula may be found
in rare cases. Bleeding is a feature of diverticulosis and is
less common in the presence of diverticulitis. Both rightsided and left-sided diverticula can bleed. At times, exsanguinating lower gastrointestinal hemorrhage can occur.
Bleeding is usually from ruptured vas rectum arterioles at
the dome of the diverticulum.
losis of the small intestine may occur as an isolated condition or as part of a multiorgan syndrome.
UODENAL DIVERTICULA All duodenal diverticula
D
occur on the inner (medial) aspect of the duodenum.
Periampullary Diverticula Periampullary diverticula
are common but most are asymptomatic. Nearly 70% are
found near the insertion of the ampulla of Vater. On occasion, the ampulla enters the apex of the diverticulum. Periampullar diverticula become symptomatic if they develop
diverticulitis or cause mechanical obstruction of the
common bile duct or pancreatic duct. These diverticuli
may lead to perforation. They may also make catheteriza-
Diverticula of the Small Intestine
Small intestinal diverticula may be solitary or multiple.
Solitary diverticula occur more commonly in the duodenum and in the ileum (Meckel’s diverticulum). Diverticu-
tion of the papilla more difficult during ERCP.
Diverticula of the Third and Fourth Portion of the Duodenum These diverticula are much less frequent than
those found in the periampullary region. They are clinically
268 ................................................................................................................ Small and L arge Intestine
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