GASTROINTESTINAL TRACT

SMALL AND LARGE INTESTINES

DR. KACHINDA W.

Dec.2012
 Most of the length of the gastrointestinal
tract
 Affect nutrient and water transport
 Site where the immune system interfaces
with a diverse array of antigens present in
food and gut microbes.
 Most common site of gastrointestinal
neoplasia
 Hernias, intestinal adhesions, intussusception,
and volvulus
account for 80% of mechanical obstructions ,
while tumors and infarction account for most of
the remainder
 Hirschsprung
 Abdominal Hernia
 Weakness or defect in the wall of the
peritoneal cavity
 Serosa-lined pouch of peritoneum
called a
hernia sac.
 Pressure at the neck of the pouch may impair
venous drainage, leading to stasis and
edema.
 Permanent entrapment, or incarceration,
and over time, arterial and venous
compromise, or strangulation, can result in
infarction
 Gastrointestinal tract is supplied by the
celiac, superior mesenteric, and inferior
mesenteric arteries.
 As they approach the intestinal wall, the
superior and inferior mesenteric arteries fan
out to form the mesenteric arcades
 Small intestine and colon to tolerate
slowly progressive loss of the blood
supply from one artery
 Ischemic
Bowel Disease
 Hemorrhoids
 Ischemic damage to the bowel wall
 Mucosal infarction, extending no deeper
than the muscularis mucosa;
 Transmural infarction involving all three
layers of the wall
 Mucosal or mural infarctions often are
secondary to acute or chronic
hypoperfusion
 Transmural infarction is generally

caused by acute vascular obstruction.

 5% of the general population
 Dilated anal and perianal collateral vessels
that connect the portal and caval venous
systems to relieve elevated venous pressure
within the hemorrhoid plexus.
 Factors that predispose to hemorrhoids are
constipation and associated straining, which
increase intra-abdominal and venous
pressures, venous stasis of pregnancy, and
portal hypertension.
 External hemorrhoids Collateral vessels
within the inferior hemorrhoidal plexus are
located below the anorectal line
 Internal hemorrhoids dilation of the
superior hemorrhoidal plexus within the
distal rectum
 On histologic examination, hemorrhoids
consist of thin-walled, dilated submucosal
vessels that protrude beneath the anal or
rectal mucosa.
 Clinical Features
 Hemorrhoids often manifest with pain and
rectal bleeding, particularly bright red blood
seen on toilet tissue.
 Except in pregnant women, hemorrhoids are
rarely encountered in persons younger than
30 years
 Malabsorptive
 Infectious Enterocolitis
 Cystic Fibrosis
 Celiac Disease
 Environmental (Tropical) Enteropathy
 Lactase (Disaccharidase) Deficiency
 Abetalipoproteinemia
 Irritable Bowel Syndrome
 Microscopic Colitis
 Graft-Versus-Host Disease
 Defective absorption of fats, fat- and water-
soluble vitamins, proteins, carbohydrates,
electrolytes and minerals, and water.
 Chronic malabsorption causes weight loss,
anorexia, abdominal distention, borborygmi,
and muscle wasting.
 Hallmark of malabsorption is steatorrhea,
characterized by excessive fecal fat and
bulky, frothy, greasy, yellow or clay-colored
stools
 Diarrhea is defined as an increase in stool
mass, frequency, or fluidity, typically to
volumes greater than 200 mL per day
 Painful, bloody, small-volume diarrhea is
known as dysentery
 Secretory diarrhea is characterized by
isotonic stool and persists during fasting.
 Osmotic diarrhea, is due to osmotic forces
exerted by unabsorbed luminal solutes
 Malabsorptive diarrhea caused by
inadequate nutrient absorption is associated
with steatorrhea and is relieved by fasting
 Exudative diarrhea is due to inflammatory
disease and characterized by purulent,
bloody stools that continue during fasting
 Disturbance in at least one of the four phases
of nutrient absorption:
 Intraluminal digestion,
 Terminal digestion
 Transepithelial transport
 Lymphatic transport
 Diarrhea, abdominal pain, urgency,
perianal discomfort, incontinence, and
hemorrhage.
 INFECTIOUS COLITIS
1. Cholera
2. Campylobacter enterocolitis
3. Shigellosis
4. Escherichia coli
5. Salmonellosis
6. Pseudomembranous colitis
 Multivisceral chronic disease
 Malabsorption
diarrhoea,lymphadenopathy,arthritis of
undefined origin
 Foamy macrophage having argyrophilic
rods
 Gram positive actinomycetes..Tropheryma
whippelli
ACCUMULATE IN LAMINA PROPRIA AND
MESENTRIC LYMPHNODES CAUSING
LYMPHATIC OBSTRUCTION
 PAS POSITIVE DIASTASE RESISTANT GRANULES
IN LYSOSOMES
 Chronic relapsing abdominal pain,bloating
and changes in bowel habits
 Syndrome with multiple illnesses
 Rome criteria
 Pathogenesis unknown
 Psychosocial,diet,gut factors
 Constipation predominant,diarrhoea
predominant
 Bile acid malabsorption
 20 to 40years age/female
 3days per month for over 3 months
 acquired pseudodiverticular outpouchings of
the colonic mucosa and submucosa.
 rare in persons younger than 30 years of age,
but the prevalence approaches 50% in
Western adult populations beyond the age of
60
 under conditions of elevated intraluminal
pressure in the sigmoid colon
chronic condition resulting from
inappropriate mucosal immune activation.

Two major entities

1. Crohn disease and
2.. U lcerative colitis
CROHN’S ULCERATIVE COLITIS

Ileum ± colon Colon only

Skip lesions Diffuse

Transmural inflammation Limited to mucosa and

submucosa
Toxic megacolon + Toxic megacolon -

Ulcers Deep, knifelike Superficial, broad-based

Stricture Yes Stricture rare

 more common in females and
frequently present during
adolescence or in young adults.
 The cause(s) of IBD remains uncertain
 a combination of errant host interactions with
intestinal microbiota, intestinal epithelial
dysfunction, and aberrant mucosal immune
responses.
1. Genetics
2. Mucosal immune responses
3. Epithelial defects
4. Microbiota
 terminal ileum, ileocecal valve, and
cecum.
 Disease is limited to the small intestine
alone in about 40% of cases; the small
intestine and the colon both are involved in
30% of patients; and the remainder of
cases are characterized by colonic
involvement only.
 The presence of multiple, separate, sharply
delineated areas of disease, resulting in skip
lesions, is characteristic of Crohn disease
 Strictures are common
 The microscopic features of active Crohn
disease include abundant neutrophils that
infiltrate and damage crypt epithelium.
 Clusters of neutrophils within a crypt are
referred to as a crypt abscess and often are
associated with crypt destruction.
 Ulceration is common in Crohn disease, and
there may be an abrupt transition between
ulcerated and normal mucosa.
 Repeated cycles of crypt destruction and
regeneration lead to distortion of mucosal
architecture.
 In most patients, disease begins with
intermittent attacks of relatively mild
diarrhea, fever, and abdominal pain.
 Right lower quadrant pain, fever, and bloody
diarrhea that may mimic acute appendicitis
or bowel perforation.
 Periods of active disease typically are
interrupted by asymptomatic intervals that
last for weeks to many months
 Extraintestinal manifestations of Crohn
disease include uveitis, migratory
polyarthritis, sacroiliitis, ankylosing
spondylitis, erythema nodosum, and clubbing
of the fingertips, any of which may develop
before intestinal disease is recognized
 involved colonic mucosa may be slightly red and
granular-appearing or exhibit extensive broad-
based ulcers.
 The transition between diseased and
uninvolved colon can be abrupt.
 Ulcers are aligned along the long axis of the
colon but typically do not replicate the
serpentine ulcers of Crohn disease.
 Isolated islands of regenerating mucosa often
bulge into the lumen to create small elevations,
termed pseudopolyps.
 Chronic disease may lead to mucosal atrophy
and a flat, smooth mucosal surface lacking
normal folds.
 mural thickening is absent, the serosal
surface is normal, and strictures do not
occur.
 Inflammation and inflammatory mediators
can damage the muscularis propria and
disturb neuromuscular function leading
tocolonic dilation and toxic megacolon,
which carries a significant risk of
perforation.
 Histologic features of mucosal disease in
ulcerative colitis are similar to those in
colonic Crohn disease and include
inflammatory infiltrates, crypt abscesses,
crypt distortion, and epithelial metaplasia.
However, skip lesions are absent and
inflammation generally is limited to the
mucosa and superficial submucosa
 Ulcerative colitis is a relapsing disorder
characterized by attacks of bloody diarrhea
with expulsion of stringy, mucoid material and
lower abdominal pain and cramps that are
temporarily relieved by defecation.
 One of the most feared long-term
complications of ulcerative colitis and
colonic Crohn disease is the development of
neoplasia.
 This process begins as dysplasia, which, just
as in Barrett esophagus and chronic gastritis,
is a step along the road to full-blown
carcinoma.
 Risk increases sharply 8 to 10 years after
disease initiation.
 Patients with pancolitis are at greater risk
than those with only left-sided disease.
 common in the colon but may occur in the
esophagus, stomach, or small intestine
 Without stalks are referred to as sessile.
 stalks are termed pedunculated
 classified as nonneoplastic or neoplastic.
 inflammatory,
 hamartomatous, or
 hyperplastic.
 Neoplastic
 Adenomas
 Familial syndromes ---FAP(Familial
Adenomatous Polyposis) /HNPCC
 Adenocarcinoma
 the most common malignancy of the
gastrointestinal tract
 Colorectal cancer incidence peaks at 60 to 70
years of age, and less than 20% of cases
occur before age 50. Males are affected
slightly more often than females
 The combination of molecular events that
lead to colonic adenocarcinoma is
heterogeneous and includes genetic and
epigenetic abnormalities. At least two
distinct genetic pathways APC/β-catenin
pathway, have been described.
END