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Gastrointestinal pathology

Irianiwati
Department of Pathology
GMU, Yogyakarta

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ORAL PATHOLOGY
I. Diseases of the Mouth & Jaw
A. Congenital Disorders
B. Inflammatory disorders
C. Tumors and tumor-like conditions

II. Diseases of the Salivary Glands


A. Sialadenitis
B. Acute parotitis
C. Mucocele
D. Tumors of the salivary gland

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Inflammatory disorders

Oral candidiasis:
- local lesion, white, membranous, caused by Candida albican
- occurs most commonly in debilitated infants and children,
immunocompromized patient, and diabetics
- White plaques consisting of enmeshed fungal hypae
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Vesicles

Ground glass cells


Multinucleated cells

Herpes labialis:
- most common lesion caused by HSV (HSV-1)
- tends to recur, with activation by febrile illness, trauma,
sunshine, menstruation
- vesiculation, ulceration of the oral mucosa
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Ulceration

Granulation process

Apthous stomatitis:
- Single/ multiple small ulcers in the oral mucosa
- painful, heal spontaneously after several days
-Tend to recurrent
-Microscopic: ulcer, granulation
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Lymphocytes

Tubercle epitheloid

Caseous necrosis

Langhans type giant cell

Tuberculosa

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hyperkeratosis

acanthosis

Leucoplakia:
- white patches of keratosis :
- premalignant lesion
- hyperkeratosis, hyperplasia of the squamous epithelium
- dysplastic changes

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Nests of epithelial tumor

Hydropic degenaration

Adamantinoma: tumor of odontogenic epithelial origin


Slow growing, locally invasive,
Ro: multilocular radiolucent lesion/ soap bubble

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Dermoid cyst (mature teratoma):
ecodermal
Mesodermal
endodermal

Epidermoid cyst
Keratin mass

Epidermal layer

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lumen

Granulation tissue

Ranula: mucocele in the floor of the mouth


Pseudo cyst

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Diseases of the esophagus:
Tracheo-esophageal fistula
Heterotopic of gastric tissue
Esophageal diverticula
Achalasia
Esophageal varices
Hernia esophagus
Inflammatory disease
Barrets esophagus
Neoplasma of the esophagus

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Pleomorphic adenoma

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Tumor of salivary glands
Cylindroma/ adenoid cystic carcinoma

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Tracheoesophageal fistula

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III. Diseases of the Esophagus
A.1. Tracheoesophageal fistula
Congenital disorder, is suggested in a newborn by copious salivation associated with
choking, coughing, and cyanosis on attempts at food intake

The most common variant (90%), the lower portion of the esophagus communicates
With the trachea near the tracheal bifurcation, the upper esophagus ends in a blind
pouch
Associated abnormality: maternal polyhydramnion

The second most common variant, fistulous connection


between the upper esophagus and the trachea; the lower
esophageal segment is not connected to the upper esophagus

The third variant, fistulous connection between


the tachea and a completely patent esophagus
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III. Diseases of the Esophagus
A.2. Heterotopic tissue

patches of fundic-type gastric mucosa are


occasionally found above the distal sphincter
separated from the columnar lining of the distal
esophagus
congenitally misplaced gastric tissue (heterotopic)
can lead to ulceration and stricturing due to
local acid/pepsin secretion

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III. Diseases of the Esophagus
C. Achalasia

-Contractility of the lower esophagus is lost and


there is failure of relaxation at the sphincter
(cardiospasm)

-Mechanism: fibrosis and atrophy of smooth muscle


(reduced number number of ganglion cells in the
myenteric plexus: Chagas disease & other
unknown etiology).

-Clinically: slowing / retention of the food


dilatation dysphagia

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III. Diseases of the Esophagus
D. Esophageal varices
-Localized dilatation of veins

-Portal hypertension

- cirrhosis hepatis

- Haematemesis

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Dilated veins in the mucosa and muscularis propria of the esophagus

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III. Diseases of the Esophagus
F. Inflammatory and related disorders
of the esophagus

1. Gastroesophageal reflux
2. Barrets esophagus
3. Candida esophagitis
4. Viral esophagitis
5. Esophageal stricture

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III. Diseases of the Esophagus
F. 1. Gastroesophageal reflux
Reflux of gastric acid contents into the esophagus esophagitis,
stricture, ulceration, or columnar metaplasia (Barrets esophagus)
Usually characterized by burning pain (often manifests by substernal
pain or heartburn) relieved by antacids

Associated:
- most commonly with hiatal hernia and incompetent lower
esophageal sphincter
- with excessive use of alcohol & tobacco, and with increased gastric
volume

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Reflux esophagitis: edema epithelial
leucocytes pmn and eosinoplilia
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III. Diseases of the Esophagus
F.2. BARRETS ESOPHAGUS

Columnar metaplasia (often of intestinal type with prominent goblet cells) of


esophageal squamous epithelium.
Complication of long-standing gastroesophageal reflux, to be a well-known
precursor of esophageal adenocarcinoma
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Barrets esophagus

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Adenocarcinoma in barrets esophagus
Invasive to the cardia

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III. Diseases of the Esophagus
F. 3. Candida esophagitis
Etiology: Candida (Monilia) albicans
Manifest clinically by white adherent mucosal patches and
painful, difficult swallowing
Often assciated with:
- antibiotic therapy
- diabetes mellitus
- malignancy
- immunodeficiency

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III. Diseases of the Esophagus
F. 4.a. Viral esophagitis

Herpetic esophagitis
Characterized by painful and difficult swallowing
Tends to occur in immunosuppressed patient, caused
by HSV-1 infection

Cytomegalovirus (CMV) infection


Less common

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III. Diseases of the Esophagus
F. 4.b. Other esophagitis

Less common form of esophagitis


Caused by: uremia, radiation therapy, graft-versus-host
(GVH) disease

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III. Diseases of the Esophagus
F. 5. Esophageal stricture

Most often results from prolonged esophageal


gastric acid reflux
May also be caused by suicidal or accidental
ingestion of corrosive agent (acid or alkaline)

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III. Diseases of the Esophagus
G. Carcinoma of the esophagus
Aggressive tumor manifest clinically by dysphagia, weight loss,
and anorexia, and occasionally by pain or hematemesis

In the USA the incidence of SC and adenocarcinoma are equal

May be manifest pathologically by protrusion into the


esophageal lumen

Spread by local extension to adjacent structure: trachea,


bronchi, aorta, or diffuse infiltration into esohageal wall

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Squamous cell carcinoma of the esophagus

Flat type of SCC ply[oid type of SCC


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III. Diseases of the Esophagus
G.1. Squamous Cell Carcinoma

Arises most frequently in the upper and middle thirds


of the esophagus

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III. Diseases of the Esophagus
G2. Adenocarcinoma

Arises most frequently in the lower third, and mostly from


aberrant gastric mucosa or Barrets esophagus

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Pathology of the

LOWER ALIMENTARY TRACT


I. Diseases of the Stomach
II. Diseases of the Small Intestine
III. Diseases of the Colon
IV. Diseases of the Appendix
STOMACH

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I. Diseases of the Stomach
A. Congenital Pyloric Stenosis
B. Gastritis
C. Peptic Ulcer of the Stomach
D. Malignant Tumor of the Stomach

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I. Diseases of the Stomach

A. Congenital Pyloric Stenosis


Is caused by hypertrophy of circular muscular layer of the pylorus
often results as papable mass

obstruction of gastric outlet episodes of projectile vomiting


(beginning in the first 2 weeks of life)

Much more common in boys


Is corrected by surgical incision of the hypertrophied muscle

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I. Diseases of the Stomach
B. Gastritis: 1. Acute (erosive) gastritis
a. Causes
- Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Cigarette smoking
- heavy alcohol intake
- Burn injury (severe) Curling ulcer
- ingestion of strong acid or alkaline
b. Characteristic
- focal damage of mucosa with acute inflammation, necrosis,
and hemorrhage
- may be manifest as gastric ulcer often multiple

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Acute gastritis

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I. Diseases of the Stomach
B. Gastritis: 2. Chronic gastritis
- Helicobacter pylori associated gastritis
- gram neg. organism, in the surface
epithelium beneath the mucous barrier
- cells desquamation and lead to polymorph
and chronic inflammatory cells
- predominantly affects the anthrum
- most common form of gastritis
- often has increased gastric acid
- young adulthood and early middle age
- associated with gastric cancer

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HISTOLOGIC PICTURE OF CHRONIC
GASTRITIS

Early stage: inflammation affects the superficial parts of


the mucosal layers superficial chronic gastritis
Next stage: the inflammation affects all mucosal and
submucosal layers with germinal center
1. Inflammatory cells: mononuclear cells; active netrophil (+)
2. Metaplasia: intestinal metaplasia pre-malignant
condition
3. Glandular atrophy: glandular tissue is reduced in
amount and undergoes to intestinal metaplasia
4. H. pylori
5. Dysplasia: carcinoma

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ATROPHIC
GASTRITIS

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H.pylori

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H. PYLORY AND CHRONIC GASTRITIS

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OTHER GASTRITIS

Eosinophyillic gastritis: food allergy ?


Granulomatous gastritis: tuberculosis,
syphilis, sarcoidosis, fungi, Crohn disease
Reflux gastritis: duodenal and bile reflux
Menetrier disease (giant hypertrophic
gastritis)

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Menetrier disease (HYPERTROPHIC GASTROPATHY)
Severe hyperplasia of mucosal layer
cells + glandular atrophy extreme
enlargement of gastric rugae
Hypertrophic gastropathy + hyper-
secretion: mucosal cells, parietal and
chief cells hyperplasia.

Sometimes with severe loss of plasma


proteins from the altered mucosa
Risk of peptic ulcer

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I. Diseases of the Stomach

C. Peptic Ulcer of the Stomach


Most often at or near lesser curvature, in the anthral & pre-pyloric
region
Is not a precursor lesion of Ca of the stomac
Middle-later age group
Male > female, 1.5 to 2:1
Often solitary
>50% <2cm; 10% >4cm
<0,3 cm erosion; >0,6 cm ulcer

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PEPTIC ULCER

Etiopathogenic mechanism:

- H. pylori : 90-100% duodenal ulcer, 70% gastric ulcer; bacterial


urease & protease break down glycoprotein in gastric mucus
interfering with epithelial protection
- NSAID
- alcohol, smoke, blood-group, HLA-B5
- Increased permeability of the gastric mucosa to hydrogen ion
back diffusion of H2 ion injury to gastric mucosa
- Bile-induced gastritis leading to gastric ulceration

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TRIGER FACTORS OF PEPTIC ULCER

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Cylindric epithelia

Necrotic debris

Granulation tissue with lymphocytic infiltration

Glands hyperplasia

Edema

PEPTIC ULCER

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PEPTIC ULCER

Complications:

1. Bleeding
2. Perforation
3. Obstruction: due to Edema or cicatrix

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I. Diseases of the stomach
D. Tumors of the stomach (benign)
POLYP
Polypoid mass
>90% non neoplasm (inflammatory/ hyperplasia)
Sessile / pedunculated
20-25% multiple
Mostly occur in chronic gastritis
No malignant potential
ADENOMA
neoplasm 5-10% of gastric polyp
Sessile / pedunculated
distal anthrum predominant
Six decade, Male: female = 2:1
Some cases origin from chronic gastritis with intestinal
metaplasia

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hyperplastic polyp

Hyperplastic polyp

Peutz- jeghers
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I. Diseases of the stomach

D. Tumors of the stomach (malignant)


Adenocarcinoma is about 90-95% of gastric malignancy
High incidence: japan, Chili, Costa Rica, China
Location: - 40-50% pylorus/anthrum; 25% cardia
- 40% minor curvature; 12% c. major
- Etiology:
- Diet
- Chronic atrophic gastritis
- H. pylori infection
- partial gastrectomy
- Gastric Adenoma
- Genetic : A blood group, family factor

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GASTRIC CANCER
Invasion
Early ( mucosa and sub- mucosa)
Advanced (invade the sub- mucosa)
Macroscopic growth
Exophytic
flat/ depressed
Excavation
Linitis plastica tumor cells diffusely infiltrate gastric wall
Histology
intestinal gland type
Diffuse: signet-ring cell

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The Growth of Gastric Cancer

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Other gastric tumors
MALIGNANT LYMPHOMA
40% malignant lymphoma of GIT
5% of gastric malignancy
B cell type predominant, MALT origin
CARCINOID TUMOR Carcinoid syndrome
Low grade malignancy
Metastasis to the liver
Multiple lesions
LEIOMYOMA
SECONDARY TUMORS (METASTASIS)
rare
Mostly from leukemia or general lymphoma
From breast / lung cancer diffuse linitis
plastica

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GASTRIC CARCINOMA

Prognosis:
Depend on the depth of tumor invasion
and metastasis process

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ULCUS CARCINOMATOSA

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Adenocarcinoma, NOS

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Diseases of the Intestine
A. CONGENITAL ABNORMALITIES

REDUPLICATION STENOSIS DIVERTICULUM ATRESIA


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Diseases of the Intestine
B. INTESTINAL OBSTRUCTION
Mechanic obstruction Neurogenic obstruction Vascular obstruction
-atresia -paralytic - adinamic
-stenosis
-trombosis
-spastic - dinamic
-stricture -embolism
-hernia
-volvulus
-invagination / intususeption

HERNIA

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Volvulus: rotation of the gut on its own mesenteric axis

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Invagination/ intususseption

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II. Diseases of the Small Intestine

A. Peptic Ulcer
B. Crohn Disease
C. Meckel Diverticulum
D. Malabsorption syndrome
E. Tumors of the Small Intestine

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II. Diseases of the Small Intestine

A. Peptic Ulcer of the Intestine


Most frequently in the first portion of duodenum
Is not a precursor of malignancy
Is always associated with hypersecretion of gastric acid
and pepsin
increased frequency in persons of blood group O
genetic factors?
Often complicated by hemorrhage with melena,
perforation, obstruction

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II. Diseases of the Small Intestine

A. Peptic Ulcer of the Intestine


Sometimes associated with:
Aspirin or other NSAID
Smoker: the incidence is two-fold greater
Zollinger-Ellison syndrome gastric acid hypersecretion due to
gastrin secreting islet cell tumor of the pancreas
Primary hyperparathyroidisme
Multiple Endocrine Neoplasia (MEN Wermer syndrome), an
autosomal dominant syndrome characterized by pituitary, thyroid,
parathyroid, adrenal cortical, and pancreatic islet cell adenoma, or
hyperplasias associated with hypergastrinemia and peptic ulcer

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II. Diseases of the Small Intestine
B. Crohns Disease
Chronic inflammatory condition of unknown etiology
Tends to affect young people in 2nd and 3rd decades of life
Occurs most frequently in Jewish descent
Cinical manifestations:
Abdominal pain and diarrhea
Malabsorption
Fever
Intestinal obstruction resulting from fibrous tissue
Fistulas: inter-intestine, between intestine bladder, vagina, skin

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II. Diseases of the Small Intestine

B. Crohns Disease

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Crohn Disease Ulcerative Colitis
May involve any portion of the gastrointestinal Affects only colon.
tract : ileocecal region, small intestine, colon.

Chronic inflammatory reaction extends through Inflammation and ulceration


the entire thickness of the intestinal wall. limited to mucosa and submucosa
Crypt abscess, pseudopolyp
Fistulous tracts between loops of intestines, or
between the intestine and other site; skip lesions
with mucosal cobblestone appearance.

Non-caseating granulomatous inflammation with Greatly increased incidence of


lymphocytic infiltration, fibrosis, and thickening of colon cancer in longstanding
intestinal wall. cases

Incidence of secondary malignancy is much lower


than in ulcerative colitis
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Comparison of the lesions

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II. Diseases of the Small Intestine
C. Meckel Diverticulum

Most common congenital anomaly of the small intestine


Remnant of embryonic vitelline duct distal small bowel
May contain ectopic gastric, duodenal, colon, pancreatic
tissue
Usually asymptomatic, ectopic tissue product com-
plication (peptic ulceration bleeding perforation)
Occasionally associated with: intussusception and
volvulus

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II. Diseases of the Small Intestine

D. Malabsorption syndrome
Celiac Disease

Sensitivity to gluten in cereal product


Clinically: weight loss, weakness, diarrhea with pale, bulky, frothy,
foul smelling stools
Growth retardation and general failure to thrive

Most often become symptomatic in infancy when cereals are first


added to the diet
Diagnosis biopsy blunting of small intestinal villi
10-15% small intestinal malignancy: most often enteropathy-type
T cell lymphoma

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II. Diseases of the Small Intestine

D. Malabsorption syndrome
Disorders Morphologic Features Comments
Celiac disease Flat mucosal surface with marked Gluten sensitivity
villous atrophy
Tropical sprue Micros: no change abnormalities Probable infectious origin;
similar to those of celiac disease often respond to antibiotics
Whipple disease PAS+ macrophages in mucosal Most common: small intestine;
Tropheryma whippelii EM arthralgia, cardiac & neuro. S
Disaccharidase No characteristic histologic change Sited in brush border of
deficiency mucosal cell of small intestine;
Lactase def.milk intolerance
Abetalipoproteinemia No characteristic features in the in- Hereditary deficiency of apo-
testine; circulating acanthocytes protein-B
Intestinal Generalized dilatation of the small Marked gastrointestinal pro-
lymphangiectasia intestinal lymphatics tein loss hypoproteinemia
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Celiac disease: villous atrophy, crypt hyperthrophy, lymphocyte and plasma cells
infiltrates
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Tropical sprue
Partial villous athrophy
Inflammatory cells in the lamina propria

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II. Diseases of the Small Intestine

E. Tumors of the small intestine


Make up a small percentage of the gastrointestinal tumor
Carcinoid tumor:
- most frequently in appendix (in small intestine: 30%)
- slow growing, low-grade malignancy (of appendix almost never
metastasizes
- carcinoid syndrome: caused by elaboration of vasoactive peptides
and amines, especially serotonin, manifest clinically by:
(1) cutaneous flushing
(2) watery diarrhea and abdominal cramp
(3) bronchospasm
(4) valvular lesions of the right side of the heart
Other tumors: lymphoma, adenocarcinoma (rare)

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Carcinoid; chromoganin positive

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The Spread of Tumor

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III. Diseases of the Colon

A. Hirschprung disease
B. Diverticula
C. Vascular diseases of the colon
D. Inflammatory disorders of the colon
E. Tumors

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III. Diseases of the Colon
A. Hirschprung disease
Dilatation of colon due to the absence of ganglion cells
of the submucosal and myenteric neural plexuses
Dilatation is proximal to aganglionic segment

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Aganglionic colon

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III. Diseases of the Colon

B. Diverticula
Most common in old person, and almost always multiple
Most frequently involve the sigmoid colon

Diverticulosis: multiple diverticula without inflammation


Diverticulitis:
- inflammation of diverticula, mostly in older person
- may be complicated by perforation peritonitis, abscess, bowel
stenosis (can be with lower abdominal bleeding & tenderness,
fever, leukocytosis, others)
- bright red rectal bleeding

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Diverticulosis of the Sygmoid

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III. Diseases of the Colon

C. Vascular diseases of the colon

-results in mucosal, mural, and trans mural infarction involving the wall of the intestine
-is almost always caused by arteriosclerotic occlusion (at least 2 of the major mesen-
teric vessels)
-most often affects the splenic flexures and rectosigmoid junction (watershed areas)

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Ischemic bowel disease

Almost always caused by atheroscle-


rotic occlusion

Most often affects the splenic flexure


and rectosigmoid junction (watershed

Area = relatively poor vascularized


region, between areas supplied by the

superior and inferior mesenteric artery


and internal iliac arteries

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III. Diseases of the Colon
D. Inflammatory disorders of the colon
Ulcerative Colitis
Often grouped with Crohn disease as inflammatory bowel disease; unknown
etiology; similar geographic & racial distribution family history; similar
extraintestinal manifestation: polyarthritis, uveitis & episcleritis, sclerosing
cholangitis, sacroiliitis, skin: erythema nodosum and pyoderma gangrenosum
Characteristics
- mucosal inflammation & ulceration limited to the large intestine
- confined to the mucosa & submucosa crypt abscess
- red, granular appearance of the mucosa
- pseudopolyp
- chronic diarrhea with passage of blood & mucus (bleeding is the most frequent
clinical manifestation)

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Ulcerative Colitis

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ENTERITIS TUBERCULOSA

Primer: milk + mycobacterium tuberculosa

Secunder: sputum + mycobacterium tuberculosa

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III. Diseases of the Colon: E. Tumors: Polyps
Type Comments
Non-neoplastic polyps
Hyperplastic polyp No clinical significance
Inflammatory polyp
- Lymphoid polyp Rectal mucosa; may be reactive
- Inflammatory pseudopolyp @ ulcerative colitis and others, granulation tissue
Hamartomatous polyp
- Juvenile polyp Most frequently in children
- Peutz-Jeghers polyp @ Peutz-Jeghers syndrome
Neoplastic polyps
Tubular adenoma Often multiple (hereditary multiple polyposis
syndrome) increased risk of malignancy
Tubulovillous adenoma Greater malignant potential
Villous adenoma High potential for malignant change
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Familial Adenomatous Polyposis

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Adenomatous polyp

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III. Diseases of the Colon: E. Tumors: adenocarcinoma
One of the most common neoplasm of the intestine
Peak age incidence: 6th 7th decades
Associated with increased CEA (carcinoembryonic antigen) to
follow the course of the disease
Develops through model of: adenoma carcinoma sequence
Predisposing factors:
1. Adenomatous polyp
2. Inherited multiple polyposis syndrome
3. Long-standing ulcerative colitis
4. Genetic factors: 4X increase of incidence among relatives of the cancer patients
5. A low fiber, high animal fat diet
Characteristics:
- left colon napkin-ring (annular) often producing early obstruction
- right colon polypoid chronic blood loss anemia
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Dukes Stage

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ASTLER - COLLER

Five-year survival rate


A tumor is limited in the mucosa - 100%
B1 reach the muscularis propria,
no lymphonode involvement 67%
B2 passing the muscularis propria,
no lymphonode involvement 54%
C1 reach the muscularis propria,
with lymphonode involvement 43%
C2 passing the muscularis propria,
with lymphonode involvement 22%
D metastasis very low FSR
GASTROINTESTINAL
LYMPHOMA
40% of lymphomas arise in sites other
than lymph nodes, and the gut is the most
common location
1% to 4% of all gastrointestinal
malignancies are lymphoma
MALT lymphoma is a sporadic lymphoma,
which arises from the B cells of MALT
(mucosa-associated lymphoid tissue)

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In the earliest histologic lesions, atypical
lymphoid cells may be seen infiltrating the
mucosa, with effacement and loss of
glands and massive expansion of
lymphoid tissue
monotonous infiltrate of malignant cells,
consisting of a mixture of small
lymphocytes and immunoblasts in varying
proportions
Most gut lymphomas are of B-cell type
(over 95%)
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IV. Diseases of the Appendix

A.Inflammatory diseases
1. Acute appendicitis
2. Chronic appendicitis

B.Tumors of the appendix


The most common : carcinoid
tumor

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At the earliest stages, only a scant neutrophilic exudate may be
found throughout the mucosa, submucosa, and muscularis propria.
Subserosal vessels are congested, and often there is a
modest perivascular neutrophilic infiltrate.
The inflammatory reaction transforms the normal glistening serosa
into a dull, granular, red membrane; this transformation signifies
early acute appendicitis for the operating surgeon.
At a later stage, a prominent neutrophilic exudate generates a
fibrinopurulent reaction over the serosa .
As the inflammatory process worsens, there is abscess formation
within the wall, along with ulcerations and foci of suppurative
necrosis in the mucosa. This state constitutes acute suppurative
appendicitis. Further appendiceal compromise leads to large areas
of hemorrhagic green ulceration of the mucosa and green-black
gangrenous necrosis through the wall, extending to the serosa,
creating acute gangrenous appendicitis, which is quickly followed
by rupture and suppurative peritonitis.
The histologic criterion for the diagnosis of acute appendicitis is
neutrophilic infiltration of the muscularis propria

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APPENDICITIS

SIMPLE ACUTE SUPPURATIVE GANGREN

CHRONIC APENDICITIS

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