2018\3\11 ‫امراض‬ ‫ندوى‬.

‫د‬
lec:7+8 ‫\موصل‬3\‫م‬ ) 7 ( ‫عدد االوراق‬
SMALL INTESTINE AND COLON
• The small intestine and colon account for the majority of GI
tract length and are the sites of a broad array of diseases
SI = 6 meters (100% intraP, except for duodenum), LI = 1.5 meters
(50% retroP)
Mucosa, submucosa, muscularis, serosa

Intestinal Obstruction
small intestine is most often involved because of its relatively narrow
lumen.
 Hernias,
 Intestinal adhesions,
 Intussusception
 Volvulus account for 80% of mechanical obstructions

1
HERNIAS
Any weakness or defect in the wall of the peritoneal cavity may
permit protrusion of a serosa-lined pouch of peritoneum (hernial sac)
The inguinal and femoral canals or umbilicus, or at sites of surgical
scars
Pressure at the neck of the pouch may impair venous drainage of the
entrapped viscus , in severe cases both arterial & venous blood
supply lead to strangulation &infarction

ADHESIONS
Surgical procedures, infection, or other causes of peritoneal
inflammation, such as endometriosis, may result in development of
adhesion,
These fibrous bridges can create closed loops through which other
viscera may slide and become entrapped

VOLVULUS
Complete twisting of a loop of bowel about its mesenteric base of
attachment
occurs most often in large redundant loops of sigmoid colon, followed
in frequency by the cecum, small bowel, stomach, or, rarely,
transverse colon.

INTUSSUSCEPTION
when a segment of the intestine, constricted by a wave of peristalsis,
telescopes into the immediately distal segment
In infant & young children when a segment of the intestine,
constricted by a wave of peristalsis, telescopes into the immediately
distal segment
In older children and adults an intraluminal mass or tumor generally
serves as the point of traction that causes intussusception

2
Malabsorption:
defective absorption of fats, fat- and water-soluble vitamins, proteins,
carbohydrates, electrolytes and minerals, and water.
Clinically :
Chronic malabsorption can be accompanied by weight loss, anorexia,
abdominal distention, borborygmi, and muscle wasting. A hallmark
of malabsorption is steatorrhea
• Diseases that cause Malabsorbtion:
 Celiac Disase
 Cystic Fibrosis
 Chronic pancreatitis
 Primary bile acid malabsorption
 Carcinoid syndrome
 Autoimmune enteropathy
 Disaccharidase deficiency
 Whipple disease
 Inflammatory bowel disease

Mechanisms of Malabsorbtion
Malabsorption results from disturbance in at least one of the four
phases of nutrient absorption:

(1) intraluminal digestion( proteins, carbohydrates, and fats)

(2) terminal digestion, which involves the hydrolysis of carbohydrates
and peptides by disaccharidases and peptidases, respectively, in the brush
border of the small intestinal mucosa
(3) transepithelial transport, in which nutrients, fluid, and electrolytes are
transported across and processed within the small intestinal epithelium
(4) lymphatic transport of absorbed lipids.

3
CELIAC DISEASE
 celiac sprue or gluten-sensitive enteropathy
 It is an immune-mediated enteropathy triggered by the
ingestion of gluten-containing cereals, such as wheat, rye, or
barley
 genetically predisposed individuals
• Pathogenesis.
 Gluten is the major storage protein of wheat and similar grains, and
the alcohol-soluble fraction of gluten
 is digested by luminal and brush-border enzymes into amino acids
and peptides
 Some gliadin peptides induce epithelial cells to express IL-15,
which in turn triggers activation and proliferation of CD8+
intraepithelial lymphocytes
 induced to express NKG2D, a natural killer cell marker

4
Morphology.
 Biopsy specimens from the second portion of the duodenum or
proximal jejunum
 increased numbers of intraepithelial CD8+ T lymphocytes
(intraepithelial lymphocytosis), crypt hyperplasia, and villous
atrophy
 Other features of fully developed celiac disease include increased
numbers of plasma cells, mast cells, and eosinophils,

Clinical Features:
 Pediatric celiac disease, which affects males and females equally,
may present with malabsorption, disease typically begins between
ages of 6 and 24 months,
 In adults, celiac disease presents most commonly between the ages
of 30 and 60.
 Symptomatic adult celiac disease is often associated with anemia,
chronic diarrhea, bloating, or chronic fatigue.

5
  Common extra-intestinal complaints include arthritis or joint pain,
seizure disorders, aphthous stomatitis, iron deficiency anemia,
pubertal delay, and short stature.
 itchy, blistering skin lesion, dermatitis herpetiformis
 The most common celiac disease–associated cancer is enteropathy-
associated T-cell lymphoma, to lesser extent adenocarcinoma of
small intestine

PSEUDOMEMBRANOUS COLITIS
known as antibiotic-associated colitis or antibiotic-associated
diarrhea
caused by Clostridium difficile
apply to diarrhea developing during or after a course of antibiotic
therapy

Pathogenesis:
 It is likely that disruption of the normal colonic flora by antibiotics
allows C. difficile overgrowth
 Immunosuppression is also a predisposing factor for C. difficile
colitis.
 Toxins released by C. difficile lead to disruption of the epithelial
cytoskeleton, tight junction barrier loss, cytokine release, and
apoptosis

Morphology.
• Fully developed C. difficile–associated colitis is accompanied by
formation of pseudomembranes
• layer of inflammatory cells and debris at sites of colonic mucosal
injury
• The surface epithelium is denuded, and the superficial lamina
propria contains a dense infiltrate of neutrophils and occasional
fibrin thrombi within capillaries

6
WHIPPLE DISEASE
 is a rare, multivisceral chronic disease
 Clinical symptoms occur because organism-laden macrophages
accumulate within the small intestinal lamina propria and
mesenteric lymph nodes, causing lymphatic obstruction.

Morphology.
• The morphologic hallmark of Whipple disease is a dense
accumulation of distended, foamy macrophages in the small
intestinal lamina propria
• The villous expansion caused by the dense macrophage infiltrate
imparts a shaggy gross appearance to the mucosal surface.
Lymphatic dilatation and mucosal lipid deposition account for the
common endoscopic detection of white to yellow mucosal plaques
• bacteria-laden macrophages can accumulate within mesenteric
lymph nodes, synovial membranes of affected joints, cardiac
valves, the brain,

7
Lec:8
Inflammatory Bowel Disease
is a chronic condition resulting from inappropriate mucosal immune
activation
 IBD includes Crohn disease and ulcerative colitis

8
Pathogenesis:
 IBD is an idiopathic disorder
 Genetics. Genetic factors contribute to IBD
 Mucosal immune responses. Although the mechanisms by
which mucosal immunity contributes to ulcerative colitis and
Crohn disease
 Epithelial defects

CROHN DISEASE
Morphology.
 Crohn disease may occur in any area of the GI tract, but the most
common sites involved at presentation are the terminal ileum,
ileocecal valve, and cecum.

9
 is limited to the small intestine alone in about 40% of cases; the
small intestine and colon are both involved in 30% of patients; and
the remainder have only colonic involvement.
 The presence of multiple, separate, sharply delineated areas of
disease, resulting in skip lesions,

 cobblestone appearance in which diseased tissue is depressed

below the level of normal mucosa
 Fissures frequently develop between mucosal folds and may extend
deeply to become fistula tracts or sites of perforation
 The intestinal wall is thickened and rubbery as a consequence of
transmural edema, inflammation, submucosal fibrosis, and
hypertrophy of the muscularis propria, all of which contribute to
stricture formation

• The microscopic features of active Crohn disease

1. Crypt abscesses : Clusters of neutrophils within a crypt .
2. Distortion of mucosal architecture : the normally straight and
parallel crypts take on bizarre branching shapes and unusual
orientations to one another
3. Epithelial metaplasia gastric antral-appearing glands , panth
cell metaplasia
4. Ulceration of the linning mucosa
5. Noncaseating granulomas a hallmark of Crohn disease, are
found in approximately 35% of cases, The absence of
granulomas does not preclude a diagnosis of Crohn disease

10
Microscopic pathology of Crohn disease. A, Haphazard crypt
organization results from repeated injury and regeneration. B,
Noncaseating granuloma. C, Transmural Crohn disease with
submucosal and serosal granulomas (arrows).

ULCERATIVE COLITIS
intestinal disease in ulcerative colitis is limited to the colon and
rectum
Common extra-intestinal manifestations of ulcerative colitis overlap
with those of Crohn disease and include
migratory polyarthritis, sacroiliitis, ankylosing spondylitis, uveitis,
skin lesions, pericholangitis, and primary sclerosing cholangitis

Morphology:
Grossly :
ulcerative colitis always involves the rectum and extends proximally
in a continuous fashion to involve part or all of the colon.
Most of the cases pancolitis , Limited distal disease may be referred
to descriptively as ulcerative proctitis or ulcerative proctosigmoiditis.

11
Grossly:
 involved colonic mucosa may be slightly red and granular or
have extensive, broad-based ulcers
 Isolated islands of regenerating mucosa often bulge into the
lumen to create pseudopolyps
 mural thickening is not present, the serosal surface is normal,
and strictures do not occur

• Histologic features :
the inflammatory process is diffuse and generally limited to the
mucosa and superficial submucosa
Granulomas are not present in ulcerative colitis.

Gross pathology of ulcerative colitis. A, Total colectomy with

pancolitis showing active disease, with red, granular mucosa in the
cecum (left) and smooth, atrophic mucosa distally (right). B, Sharp
demarcation between active ulcerative colitis (right) and normal
(left). C, Inflammatory polyps. D, Mucosal bridges.

12
Microscopic pathology of ulcerative colitis. A, Crypt abscess. B,
Pseudopyloric metaplasia (bottom). C, Disease is limited to the
mucosa

Colitis-Associated Neoplasia
Risk increases sharply 8 to 10 years after disease initiation
Patients with pancolitis are at greater risk than those with only left-
sided disease
Greater frequency and severity of active inflammation (characterized
by the presence of neutrophils) may increase risk

13