lec 5-9 Gastrointestinal System pdf - د. ندوى

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Gastrointestinal System

The gastrointestinal (GI) tract is a hollow tube extending from the oral
cavity to the anus that consists of anatomically distinct segments,
including the esophagus, stomach, small intestine, colon, rectum, and
anus

Oral Cavity

The mouth is subject to the same types of lesions as other

sites in the body, but these often show distinct features

peculiar to the mouth. In addition, there are a number of

specific lesions related to the teeth and their supporting tissues.

LEUCOPLAKIA

Leucoplakia and erythroplakia are potentially malignant lesions.
Leucoplakia is a white patch which cannot be attributed to any specific
disease

erythroplakia is the analogous term for the less frequent red patches.

 Smoking and frictional irritation are common aetiological factors,

but many cases are of unknown aetiology.

 Microscopically.

hyperkeratosis of the linning epithelium, and a variable inflammatory
infiltrate is present. A small proportion show dysplasia.

The more severe the dysplasia microscopically, the greater risk of
malignancy.

• High-risk sites for malignant change are floor of mouth, ventral and
lateral of the tongue.

SALIVARY GLANDS

• There are three major salivary glands

parotid, submandibular, and sublingual

• as well as numerous minor salivary glands distributed throughout

the mucosa of the oral cavity.

All these glands are subject to inflammation or to the development of
neoplasms.

Inflammation (Sialadenitis)

Causes :

 Trumatic

 Viral (Mumps)

 Bacterial

 Autoimmune (Sjögren syndrome)

 Tumors of Salivary glands

Epithelial salivary gland neoplasms are a complex

group, mostly benign.

• 80% of salivary gland tumors involve the parotid

gland.

• Pleomorphic adenomas account for over 70% of

tumors.

• There is a higher relative incidence of carcinomas in minor salivary
glands.

PLEOMORPHIC ADENOMA

 60% of tumors in the parotid, are less common in the

submandibular glands, and rarely in minor

 benign tumors that consist of a mixture of ductal (epithelial) and

myoepithelial cells, and therefore they show both epithelial and
mesenchymal differentiation.

 epithelial elements dispersed throughout the matrix along with

varying degrees of myxoid, hyaline, chondroid (cartilaginous), and
even osseous tissue

WARTHIN TUMOR (papillary cystadenoma lymphomatosum)

 almost exclusively in the parotid

 more commonly in males than in females, usually in the fifth to

seventh decades of life.

 On microscopic examination cystic spaces are lined by a double

layer of neoplastic epithelial cells resting on a dense lymphoid
stroma

Adenoid cystic carcinoma

 uncommon tumor, which in approximately 50% of cases is found

in the minor salivary glands , the major salivary glands affected are
parotid & submandibular

 Microscopically: solid growth of small hyperchromatic neoplastic

cells surrounding small (microcystic) spaces filled with mucinous
secretions giving rise to cribriform appearance

THE OESOPHAGUS

25 cm in length, the oesophagus is a muscular

tube with a well-defined origin

Its function is a simple one, namely the conduction of food from the
pharynx to the stomach.

The mucosal lining is of stratified squamous  epithelium, while the
underlying  submucosa includes numbers of mucinous glands The muscle
coat is an inner circular and outer longitudinal coats.

MOTOR DISORDERS

 Achalasia

 Hiatal Hernia (sliding [95%], paraesophageal)‏

 “ZENKER” diverticulum

 Esophagophrenic diverticulum

 Mallory-Weiss tear

Achalasia

 Achalasia is a Greek term meaning „failure to relax‟ is

characterized by poor relaxation of the functional lower
oesophageal sphincter.

Causes: most of the cases is unknown ,but could be due to systemic
sclerosis and South American trypanosomiasis (Chagas‟ disease)

 may present at any stage in life, usually with dysphagia and

regurgitation of undigested food material. Aspiration pneumonia is
a significant problem

Microscopically, the disease is characterized by a reduction in the
numbers of neurones in the muscular (myenteric) plexus of the lower
oesophagus, dilatation of proximal esophagus ,Inflammation &ulceration
of mucosa .

Esophagitis:

 Inflammation of esophageal mucosa

Causes:

o Reflux oesophagitis : refluxed gastroduodenal contents

o Infectious agents (Candida, herpes simplex

virus) rarely in immunocompromised patient.

The oesophagus may be involved in Crohn‟s disease and in
systemic sclerosis.

o Oesophageal obstruction (tumour, achalasia)

leads to a secondary proximal oesophagitis.

Barrett Esophagus:

 characterized by intestinal metaplasia within the esophageal

squamous mucosa

 10% of individuals with symptomatic Gastroesophageal reflux

diseases

 most common in white males and it typically presents between 40

and 60 years of age.

 The signifigance of it: an increased risk of esophageal

adenocarcinoma.

ESOPHAGEAL VARICES

 development of a congested subepithelial and submucosal venous

plexus within the distal esophagus. These vessels, termed varices,

 develop in 90% of cirrhotic patients, most commonly in association

with alcoholic liver disease. Hepatic schistosomiasis is the second
most common cause of varices.

 they may rupture, causing massive hematemesis half of the patients

die from the first bleeding episode either as a direct consequence of
hemorrhage or following hepatic coma triggered by hypovolemic
shock.

Squamous Cell Carcinoma

Arise from Sq.epithelium as exophytic, ulcerative

masses that partly or almost totally occlude the lumen.

Adenocarcinomas

generally arise in Barrett‟s oesophagus, this is a disease of Western
society

Lec:

If you think of the acid production in the stomach to be ONLY in the
mid-BODY, and the proximal and distal ends as chiefly mucous to
protect the esophagus and duodenum from the harsh acid, then you will
understand the histology.

Acute Gastritis

is a transient mucosal inflammatory process

Pathogenesis:

Acute or chronic gastritis can occur following disruption of any of these
protective mechanisms

 Mucin secreted by surface foveolar cells forms a thin layer of

mucus (defect occur as in elderly,

 bicarbonate ion secretion ( NSAI drugs reduce producti on),

chemotherapy

 rich vascular supply

Clinically:

Mild cases the pt. presented with nausea, vomiting in severe cases causes
bleeding

Microscopically :

Mild condition show neutrophils infiltrated the surface epithelium &
glands in lamina propria with lymphocytes and plasma chronic
inflammatory cells

In severe cases there are erosion of surface epithelium , ulceration ,
bleeding and hemorrhage.

ACUTE GASTRIC ULCERATION

Pathogenesis.

 Stress ulcers are most common in individuals with shock, sepsis, or

severe trauma

 Ulcers occurring in the proximal duodenum and associated with

severe burns or trauma are called Curling ulcers.

 Gastric, duodenal, and esophageal ulcers arising in persons with

intracranial disease are termed Cushing ulcers and carry a high
incidence of perforation.

Acute gastritis: hyperemic erythmatous edematous gastric mucosa with
foci of superficial erosions. There are many causes for acute gastritis:
alcoholism, drugs, infections, etc

Chronic Gastritis

Causes :

 The most common cause of chronic gastritis is infection with the

bacillus Helicobacter pylori.

 Others : psychological stress, caffeine, alcohol, and tobacco .

 Autoimmune gastritis ( cause atrophic gastritis, 10%of chronic

gastritis in the absence of H.pylori)

 Less common causes : radiation injury, chronic bile reflux,

mechanical injury, and involvement by systemic disease such as
Crohn disease, amyloidosis, or graft-versus-host disease.

HELICOBACTER PYLORI GASTRITIS

o spiral-shaped or curved bacilli

o Presented in almost all patients with duodenal ulcers and the

majority of individuals with gastric ulcers or chronic gastritis.

o H. pylori has important roles in gastric and duodenal diseases.(

peptic ulcer disease, increased risk of gastric cancer)

H-pylori This small curved to spiral rod-shaped bacterium is found in the
surface epithelium of most patients with active gastritis. The rods are seen
here with a methylene blue stain.

Pathogenesis.

H.Pylori causes Antral gastritis with high acid secretion , progress to
involve the fundic and body mucosa , in advanced untreated conditions
lead to pangatritis associated with multifocal mucosal atrophy, reduced
acid secretion, intestinal metaplasia, and increased risk of gastric
adenocarcinoma.

Morphological Features of H.pylori asssociated chronic gastritis:

 H.Pylori is concentrated within the superficial mucus overlying

epithelial cells in the surface and neck regions.

 H. pylori are typically found in the antrum ,

neutrophilic cells infiltration within the lamina propria

 In addition, the superficial lamina propria includes large numbers

of plasma cells, often in clusters or sheets, and increased numbers
of lymphocytes and macrophages.

PEPTIC ULCER DISEASE

85% -100% are duodenal ulcers

65% gastric ulcer

Epidemiology.

 The imbalances of mucosal defenses and damaging forces that

cause chronic gastritis are also responsible for PUD

 the main causes for hyperacidity: H.pylori, parietal cell

hyperplasia, hypergastrinemia, ….

 Co-factors NSAIDrugs direct injury to the mucosa

 Smoking , alcohol consumption affect the blood supply of mucosa

Morphology:

 Duodenal ulcers involve the anterior duodenal wall.

 Gastric peptic ulcers are predominantly located along the lesser

curvature near the interface of the body and antrum.

 80% solitary ,round to oval, sharply punched-out defect, hang out

the surrounding mucosa

 The base show fibrinoid material, Beneath this, active granulation

tissue infiltrated with mononuclear leukocytes and a fibrous or
collagenous scar

• Complications of Peptic Ulcers:

• Bleeding

– Occurs in 15% to 20% of patients

– Most frequent complication

– May be life-threatening

– Accounts for 25% of ulcer deaths

– May be the first indication of an ulcer

• Perforation

– Occurs in about 5% of patients

– Accounts for two thirds of ulcer deaths

– Rarely, is the first indication of an ulcer

• Obstruction from edema or scarring

– Occurs in about 2% of patients

– Most often due to pyloric channel ulcers

– May also occur with duodenal ulcers

– Causes incapacitating, crampy abdominal pain

– Rarely, may lead to total obstruction with intractable

vomiting

– Malignant transformation of peptic ulcers is very rare

Would this slide be seen in a REAL classroom to those sitting in the back
row?

GASTRIC TUMORS

• BENIGN:

– “POLYPS*” (HYPERPLASTIC vs. ADENOMATOUS)

– LEIOMYOMAS

– LIPOMAS

• MALIGNANT

– (ADENO)-Carcinoma

– LYMPHOMA

Others

– Gastro-Intestinal “Stromal” Tumor (GIST)

– CARCINOID (NEUROENDOCRINE)

In general. A “polyp*” can be thought of as ANYTHING which projects
as a bump or nodule from a mucosal surface.

HYPERPLASTIC POLYPS are considered to be NON-neoplastic, and
therefore NEVER turn into cancers. ADENOMATOUS polyps are true
benign neoplasms and MAY turn into carcinomas, particularly if the
exhibit DYSPLASIA on biopsy.

This SAME general principle, is even MORE true of the colon!

But in general, you know the drill: 1) Benign, 2) Malignant, and 1)
epithelial, 2) stromal, and 3) lymphoid

RISK FACTORS

o H. Pylori

o Type of food : Nitrites, smoked meats, pickled, salted, chili

peppers,

o Low Socioeconomic

o tobacco

Chronic gastritis, Barrett‟s, adenomas

o Family history

Morhophology: Adenocrcinoma

Intestinal Type :

Grossly : Exophytic , Nodular, ulcerative Excavaeted.

Microscopically: glandular component of malignant cells.

Diffuse type:

Infitrative to gastric wall , malignant cells had intracellular mucin push
the nucleus to the periphery (Linitis Plastica)

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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

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

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.

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

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.

 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

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,

Lec:8

Inflammatory Bowel Disease

is a chronic condition resulting from inappropriate mucosal immune
activation

 IBD includes Crohn disease and ulcerative colitis

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.

 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

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.

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.

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

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Diverticulosis :

 Acquired pseudo-diverticular outpouchings of the colonic

mucosa and submucosa.

 Rare in persons under age 30, but the prevalence approaches

50% in Western adult populations over age 60.

 Occurs due to increased intraluminal pressure in the sigmoid ,

due to constipation (low fiber diet)

Pathogenesis:

 Increased intraluminal pressure is probably due to exaggerated

peristaltic contractions.

 may be enhanced by diets low in fiber, which reduce stool bulk,

particularly in the sigmoid colon.

 nerves, arterial vasa recta, and their connective tissue sheaths

penetrate the inner circular muscle coat, focal discontinuities in
the muscle wall are created.

Morphology:

colonic diverticula are small, flask-like outpouchings, usually 0.5 to 1
cm in diameter

regular distribution alongside the taeniae coli

Microscopically :

 Colonic diverticula have a thin wall composed of a flattened or

atrophic mucosa, compressed submucosa, and attenuated or,
most often, totally absent muscularis propria

 Obstruction of diverticulae leads to inflammatory changes,

producing diverticulitis and peri-diverticulitis

Complication

 Ulceration

 Bacterial infection & abscess formation

 Perforation & peritonitis

 Fistula formation (with bladder , vagina)

Intestinal Polyps :

 Non-neoplastic polyp

• Inflammatory polyp : form as a result of chronic cycles of

injury and healing. ( seen in large bowel in Inflammatory
disases as crohn’s disease or ulcerative colitis)

• Hamartomatous polyp tumor-like growths composed of mature

tissues that are normally present at the site in which they
develop e.g/ autosomal dominant inherited condition of Peutz–
Jeghers syndrome,

 Neoplastic polyp:

 more common in the large than small bowel , about one-third of

individuals at 60-70 years of age.

the most common and clinically important neoplastic polyps are colonic
adenomas, benign polyps that are precursors to the majority of colorectal
adenocarcinomas.

 Adenomas are intraepithelial neoplasms that range from small,

often pedunculated polyps to large sessile lesions

 Most adenomas are clinically silent, with the exception of large

polyps that produce occult bleeding and anemia and rare
villous adenomas that cause hypoproteinemic hypokalemia by
secreting large amounts of protein and potassium

Morphology

• Adenomas can be classified as tubular, tubulovillous, or villous

based on their architecture

• Tubular adenomas tend to be small, pedunculated polyps composed

of small rounded, or tubular, glands

• villous adenomas, which are often larger and sessile, are covered

by slender villi

• Tubulovillous adenomas have a mixture of tubular and villous

• Histologically, the cytologic hallmark of epithelial dysplasia is

nuclear hyperchromasia, elongation, and stratification.

The tubular adenoma:

FAMILIAL ADENOMATOUS POLYPOSIS

Familial adenomatous polyposis (FAP) is an autosomal dominant
disorder in which patients develop numerous colorectal adenomas as
teenagers. It is caused by mutations of the adenomatous polyposis coli,
or APC, gene.

 At least 100 polyps are necessary for a diagnosis of classic FAP

 Colorectal adenocarcinoma develops in 100% of untreated FAP

patients, often before age 30.

As a result, prophylactic colectomy is the standard therapy for
individuals carrying APC mutations.

Adenocarcinoma

Adenocarcinoma of the colon is the most common malignancy of the
GI tract and is a major cause of morbidity and mortality worldwide

Low fiber diet , high intake of refind carbohydrate &Fat.

Low antioxidant Vit A,C,E

(all had a role in developing adenocarcinoma of large bowel).

Morphology :

 About one-half are found in the rectum, a further

one-third in the sigmoid, and the rest are spread equally

across the remainder of the colon

 Tumors of proximal colon appear as exophytic or ulcerative mass

rarely cause obstruction

In distal part presented as annular lesion cause narrowing of lumen
and obstruction .

 Tumors composed of glandular structures lined by malignant cells

at different differentiation

 Some times signet ring ca. as in gastric Ca.

Colorectal carcinoma. A, Circumferential, ulcerated rectal cancer.
Note the anal mucosa at the bottom of the image. B, Cancer of the
sigmoid colon that has invaded through the muscularis propria and
is present within subserosal adipose tissue (left). Areas of chalky
necrosis are present within the colon wall (arrow).

Histologic appearance of colorectal carcinoma. A, Well-differentiated
adenocarcinoma. Note the elongated, hyperchromatic nuclei.
Necrotic debris, present in the gland lumen, is typical. B, Poorly
differentiated adenocarcinoma forms a few glands but is largely
composed of infiltrating nests of tumor cells. C, Mucinous
adenocarcinoma with signet-ring cells and extracellular mucin pools.

 The two most important prognostic factors are depth of invasion

and the presence or absence of lymph node metastases.

 Invasion into the muscularis propria confers significantly

reduced survival that is decreased further by the presence of
lymph node metastases

• Many systems for staging of colorectal ca. one of them Dukes

Staging System

ANAL CANAL CARCINOMAS

MORE LIKELY TO BE SQUAMOUS, or “basaloid”

WORSE IN PROGNOSIS

HPV RELATED

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Hemorrhoids:

affect about 5% of the general population and develop secondary to
persistently elevated venous pressure within the hemorrhoidal plexus

The most frequent predisposing influences are straining at stool
because of constipation and the venous stasis of pregnancy.

Morphology.

Collateral vessels within the inferior hemorrhoidal plexus are located
below the anorectal line and are termed external hemorrhoids

while those that result from dilation of the superior hemorrhoidal plexus
within the distal rectum are referred to as internal hemorrhoids

Histologically,

thin-walled, dilated, submucosal vessels that protrude beneath the anal or
rectal mucosa.

In their exposed position, they are subject to trauma and tend to
become inflamed, thrombosed, and, in the course of time,
recanalized. Superficial ulceration may occur.

THE APPENDIX

 is a normal true diverticulum of the cecum that is prone to

acute and chronic inflammation

 Acute Appendicitis

o initiated by progressive increases in intraluminal pressure that

compromise venous outflow. In 50% to 80% of cases, acute
appendicitis is associated with overt luminal obstruction caused
by stool (fecolith, oxyuriasis vermicularis (worm), tumor…)

o Microscopically: transmural infiltration of neutrophils with

ulceration of linning mucosa

ACUTE APPENDICITIS

What is the white junk coating the surface? Answer: FIBRIN

The presence of neutrophils invading the muscularis is the diagnostic
criteria needed to diagnosis or confirm, acute appendicitis!

Tumors of the Appendix

The most common tumor of the appendix is the carcinoid

discovered incidentally at the time of surgery or examination of a
resected appendix

At the tip of appendix , a solid bulbous swelling up to 2 to 3 cm in
diameter

• Other tumors of Appendix :

Mucocele, a dilated appendix filled with mucin, may simply represent
an obstructed appendix containing inspissated mucin or be a
consequence of mucinous cystadenoma or mucinous
cystadenocarcinoma.

THE PERITONIUM

Inflammatory Disease: could be bacterial infection or chemical irritants

 Leakage of bile or pancreatic enzymes

 Perforation or rupture of the biliary system

 Acute hemorrhagic pancreatitis

 Foreign material, including that introduced surgically (e.g., talc

and sutures)

 Endometriosis

 Perforation of abdominal viscera

PERITONEAL INFECTION

Bacterial peritonitis occurs when bacteria from the gastrointestinal lumen
are released into the abdominal cavity, typically following perforation

acute appendicitis, peptic ulcer, cholecystitis, diverticulitis, and
intestinal ischemia. Acute salpingitis, abdominal trauma, and
peritoneal dialysis are other potential sources of contaminating
bacteria.

Morphology.

• loss of glistening serosal and peritoneal surfaces

• serous or slightly turbid fluid begins to accumulate within 2 to 4

hours of infection.

• As the infection progresses, creamy suppurative material that may

be extremely viscous accumulates.

• The cellular inflammatory response is composed primarily of

dense collections of neutrophils and fibrinopurulent debris that
coat the viscera and abdominal wall.

Tumors

Most tumors of the peritoneum are malignant and can be divided
into primary and secondary forms

Primary tumors arising from peritoneal lining are mesotheliomas (are
almost always associated with significant asbestos exposure.)

Secondary tumors of the peritoneum are, in contrast, quite common.
In any form of advanced cancer, direct spread to the serosal surface
or metastatic seeding (peritoneal carcinomatosis) may occur.(ovarian
and pancreatic adenocarcinoma, Appendiceal mucinous carcinomas
are the most common malignant tumor)