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The Oral Cavity and

Gastrointestinal Tract
ORAL CAVITY
ULCERATIVE AND INFLAMMATORY LESIONS
LEUKOPLAKIA
CANCER OF THE ORAL CAVITY AND TONGUE
SALIVARY GLAND DISEASES
Sialadenitis
Salivary gland Tumor
Esophagus

CONGENITAL ANOMALIES
Atresia and Fistules
Webs, Rings, and Stenosis
LESSIONS ASSOCIATED WITH MOTOR
DYSFUNCTION
Achlasia, Hiatal Hernia, Diverticula, Lacerations (Mallory-Weiss
Syndrome)
ESOPHAGEAL VARICES
ESOPHAGITIS
Reflux Esophagitis
Barret Esophagus
Infectious and Chemical Esophagitis
TUMORS
Benign Tumors
Malignant Tumors
Squamous Cell Carcinoma
Adenocarcinoma
Stomach
CONGENITAL ANOMALIES
Pyloric Stenosis
GASTRITIS
Chronic Gastritis
Acute Gastritis
Special Form of Gastritis
PEPTIC ULCER DISEASE
Peptic Ulcers
Acute Gastric Ulceration
MISCELANEOUS CONDITION
Hypertrophic Gastropathy
Gastric Varices
TUMORS
Benign Tumors
Gastric Carcinoma
Less Common Gastric Tumors
Small and Large Intestines
CONGENITAL ANOMALIES
Atresia and Stenosis
Merckel Diverticulum
Hirschprung Disease : Congenital Aganglionic Megacolon
ENTEROCOLITIS
Diarrhea and Dysentry
Infectious Enterocolitis
Viral Gastroenteritis
Bacterial Enterocolitis
Bacterial Overgrowth Syndrome
Parasitic Enterocolitis
Collagenous and Lymphocytic Collitis
Miscellanous Intestinal Inflammatory Disorders
Acquired Immunodeficiency Syndrome (AIDS)
Transplantation
Drug Induced Intestinal Injury
Radiation Enterocolitis
Neutropenic Enterocolitis
Diversion Colitis
Solitary Rectal Ulcer Syndrome
MALABSORBTION SYNDROMES
Celiac Disease
Tropical Sprue (Postinfectious Sprue)
Whipple Disease
Disaccharidase (Lactase) Deficiency
Abetalipoproteinemia
IDIOPATHIC INFLAMMATORY BOWEL DISEASE
Etiology and Pathogenesis
Crohn Disease
Ulcerative Colitis
VASCULAR DISORDER
Ischemic Bowel Disease
Angiodysplasia
Hemorrhoids
DIVERTICULAR DISEASE

INTESTINAL OBSTRUCTION
Hernias
Adhesions
Intussusception
Volvulus
TUMORS OF THE SMALL AND LARGE INTESTINE

Tumors of The Small Intestine


Adenomas
Adenocarcinoma
Tumors of The Colon and Rectum
Non-Neoplastic Polyps
Adenoma
Familial Syndromes
Colorectal Carcinogenesis
Colorectal Carcinoma
Carcinoid Tumors
Gastrointestinal Lymphoma
Mesenchymal Tumors
Tumors of The Anal Canal
Appendix
Acute Appendicitis
Tumors of the Appendix
Mucocele and Pseudomyxoma Peritonei
PERITONEUM

INFLAMMATION
Peritonei Infection
Sclerosing Retroperitonitis
Mesentric Cysts
TUMORS
ORAL CAVITY
Ulcerative and Inflammatory Lessions

Aphtous Ulcers (Canker Sores)


Rounded, superficial erosions, covered with a gray-white
exudate and erythematous rim
Single or in groups on the nonkeratinized oral mucosa, -sof
palate, buccolabial mucosa, floor of the mouth, and lateral
borders of the tongue
HERPESVIRUS INFECTION

Herpes Simplex Virus type 1 (HSV type 1)


Kissing
Reactivation, solitary/ multiple small vesicles containing clear
fluid appear
On the lips/ about the nasal orifices: cold sores / fever
blisters
Intraepithelial focus of intracelluler and intracelluler edema
Tzank Test
FUNGAL INFECTION

Candida Albicans
White, curdlike, circumscribed plaque
Pseudo membrane

ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)


LEUKOPLAKIA

whitish, well-defined mucosal patch or plaque


caused by epidermal thickening /
hyperkeratosis.
Strong associated with the use of tobacco
Banal hyperkeratosis
Erythroplasia
Leukoplakia of the tongue in a smoker. Microscopically, this lesion
showed severe dysplasia with transformation to squamous cell
carcinoma in the posterior elevated portion (arrow).
Microscopis : epithelial thickening hyperkeratosis
without dysplasia and acanthosis.
CANCERS OF THE ORAL CAVITY AND
TONGUE
Squamous Cell Carcinoma
Predominant sites :
1. Vermillion border of the lateral margins of the
lower lip
2. Floor of the mouth
3. Lateral borders of the mobile tongue

Clinical Features : Local pain, difficulty in chewing


SALIVARY GLAND DISEASE
Sialadenitis
Mumps
Autoimmune sialadenitis
Salivary Gland Tumors
Submaxillary glands is more ominous than one
in the parotids
In the parotids : mixed a tumor of salivary
gland
Pleomorphic Adenoma (Mixed Tumor
of Salivary Glands)
Encapsulated
Heterogenity, myxoid connective tissue
Malignant transformation
Warthins Tumor (Papillary Crystadenoma
Lymphomatosum, crystadenolymphoma)
Well encapsulated
1. a two tiered epithelial layer lining the
branching, cystic/ cleftlike spaces; and
2. well-developed lymphoid tissue-germinal
centres
Esophagus
Congenital anomalies
ATRESIA AND FISTULAS
WEBS
RINGS
STENOSIS
Lesion Associated with Motor
Dysfunction
ACHALASIA
HIATAL HERNIA
DIVERTICULA
LACERATIONS (MALLORY-WEISS SYNDROME)
Achalasia

Failure to relax
Morfologi :
Dilatation of the more proximal esophagus
Three major abnormalities :
Aperistalsis
Partial or incomplete relaxation of the lower esophageal
sphincter with swallowing,
Increased resting tone of the lower esophageal sphincter
Hiatal Hernia

The axial (sliding) hernia


The non-axial (paraesophageal) hernia
DIVERTICULA
Zenker diverticulum
Traction diverticulum
Epinephric diverticulum
Zenker diverticulum
May develop from disordered cricopharyngeal motor
function.
May be several centimeters long; can accumulate
food.
Dysphagia, food regurgitation, mass in the neck.
Aspiration with pneumonia is a significant risk
Traction diverticulum
( Mid-esophageal )
Possibly congenital or result of motor
dysfunction
generally asymptomatic
Epiphrenic diverticulum
May develop from discoordination of
peristalsis and lower sphincter relaxation.
Just above lower esophageal sphincter.
Nocturnal regurgitation of massive amounts of
fluid can occur.
Lacerations ( Mallory-Weiss
Syndrome )
Longitudinal tears in the esophagus at the
esophagogastric junction
In chronic alcoholics
Esophageal laceration (Mallory-Weiss tears). Gross view demonstrating
longitudinal lacerations extending from esophageal mucosa into stomach
mucosa (arrow).
Esophageal Varices
Dilated tertuous vessels
In approximately two thirds of all cirrhotic
patients and are most often associated with
alcoholic cirrhosis
Submucosa of the distal esophagus and
proximal stomach
Massive hemorrhage
Esophagitis
Inflammation of the esophageal mucosa

REFLUX ESOPHAGITIS (GASTROESOPHAGEAL


REFLUX DISEASE)
Histologic
Eosinophils, with or without neutrophils, in
the epithelial layer
Basal zone hyperplasia
Elongation of lamina propia papillae
BARRETTS ESOPHAGUS
As replacement of the normal distal stratified
squamous mucosa by abnormal metaplastic
columnar epithelium containing goblet cells
Barrett esophagus. A, B, Gross view of distal esophagus (top) and proximal stomach (bottom), showing A,
the normal gastroesophageal junction (arrow) and B, the granular zone of Barrett esophagus (arrow). C,
Endoscopic view of Barrett esophagus showing red velvety gastrointestinal mucosa extending from the
gastroesophageal orifice. Note the paler squamous esophageal mucosa.
Barrett esophagus. A, B, Gross view of distal esophagus (top) and proximal stomach (bottom), showing
A, the normal gastroesophageal junction (arrow) and B, the granular zone of Barrett esophagus (arrow).
C, Endoscopic view of Barrett esophagus showing red velvety gastrointestinal mucosa extending from
the gastroesophageal orifice. Note the paler squamous esophageal mucosa.
Barrett esophagus. A, B, Gross view of distal esophagus (top) and proximal stomach (bottom), showing A,
the normal gastroesophageal junction (arrow) and B, the granular zone of Barrett esophagus (arrow). C,
Endoscopic view of Barrett esophagus showing red velvety gastrointestinal mucosa extending from the
gastroesophageal orifice. Note the paler squamous esophageal mucosa.
Barrett esophagus. Microscopic view showing squamous mucosa and intestinal-type columnar epithelial
cells (goblet cells) in a glandular mucosa.
INFECTIOUS AND CHEMICAL
ESOPHAGITIS
Ingestion of the mucosal irritants alcohol, corrosive acids or
alkalis, hot fluids, heavy smokers
Cytotoxic anticancer therapy
Infection following bacteremia or viremia; herpes simplex
viruses and cytomegalovirus (CMV)
Fungal infection
Uremia
Tumors
Benign Tumors
Leiomyomas
Fibrovascular polyps or pedunculated lipomas
Squamous papillomas
Condyloma
Inflammatory polyp
MALIGNANT TUMORS
Squamous Cell Carcinoma
Factors Associated with the Development of Squamous Cell Carcinoma of the Esophagus

Dietary
Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)
Deficiency of trace elements (zinc, molybdenum)
Fungal contamination of foodstuffs
High content of nitrites/nitrosamines
Betel chewing
Lifestyle
Burning-hot beverages or food
Alcohol consumption
Tobacco use
Urban environment
Esophageal Disorders
Long-standing esophagitis
Achalasia
Plummer-Vinson syndrome
Genetic Predisposition
Long-standing celiac disease
Ectodermal dysplasia
Epidermolysis bullosa
Racial disposition
Morphology

(1) polypoid fungating masses that protude into the lumen


(2) necrotizing cancerous ulcerations that extend deeply and
sometimes erode into the respiratory tree, aorta, or
elsewhere
(3) diffuse infiltrative neoplasms that impart thickening and
rigidity to the wall and narrowing of the lumen

50% in the middle third


Large ulcerated squamous cell carcinoma of the esophagus.
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Adenocarcinoma
The majority of cases arise from the Barrett
mucosa
Transition from Barrett esophagus to
adenocarcinoma.
Adenocarcinoma of the esophagus. A, Gross view of an ulcerated, exophytic mass at the
gastroesophageal junction, arising from the granular mucosa of Barrett esophagus. The gray-white
esophageal mucosa is on the top, and the folds of gastric mucosa are below. (A, courtesy of Dr. James
Gulizia, Brigham and Women's Hospital, Boston, MA.) B, Microscopic view of malignant intestinal-type
glands in adenocarcinoma arising from Barrett esophagus.
Adenocarcinoma of the esophagus. A, Gross view of an ulcerated, exophytic mass at the
gastroesophageal junction, arising from the granular mucosa of Barrett esophagus. The gray-white
esophageal mucosa is on the top, and the folds of gastric mucosa are below. (A, courtesy of Dr. James
Gulizia, Brigham and Women's Hospital, Boston, MA.) B, Microscopic view of malignant intestinal-type
glands in adenocarcinoma arising from Barrett esophagus.
Stomach

Anatomy and histology of the stomach. A, Gross anatomy


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Anatomy and histology of the stomach .B, Microscopic view of
antral mucosa
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Anatomy and histology of the stomach . C, Microscopic view of
fundic mucosa.
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CONGENITAL ANOMALIES :

Pyloric stenosis
Diaphragmatic hernia
Gastric heterotopia
GASTRITIS
Inflammation of the gastric mucosa
Acute Gastritis
Chronic Gastritis
Acute Gastritis
Acute mucosal inflammatory process, usually
of a transient nature
Erosion
Pathogenesis : poorly understood
Clinical features : in alcoholics
Morphology
moderate edema and vascular congestion
- activity
-erosion
- acute erosive hemorrhagic gastritis
Acute gastritis. A, Gross view showing punctate erosions in an
otherwise unremarkable mucosa; adherent blood is dark due to
exposure to gastric acid
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Acute gastritis. B, Low-power microscopic view of focal mucosal
disruption with hemorrhage; the adjacent mucosa is normal.
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Chronic Gastritis
Chronic mucosal inflammatory changes-
mucosal atrophy and intestinal metaplasia
Pathogenesis : Helicobacter pylori
Diseases Associated with Helicobacter
pylori Infection
Disease Association

Chronic gastritis Strong causal association

Peptic ulcer disease Strong causal association

Gastric carcinoma Strong causal association

Gastric MALT lymphoma* Definitive etiologic role

* MALT, mucosa-associated lymphoid tissue


Morphology
lymphocytes and plasma cells is present within
the lamina propria
Regenerative Change
Metaplasia intestinal metaplasia
Atrophy
Dysplasia
Chronic gastritis, showing partial replacement of the gastric mucosal epithelium by intestinal metaplasia
(upper left) and inflammation of the lamina propria (right) containing lymphocytes and plasma cells.
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Helicobacter pylori. A Steiner silver stain demonstrates the numerous darkly stained Helicobacter
organisms along the luminal surface of the gastric epithelial cells. Note that there is no tissue invasion by
bacteria.
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Reactive gastropathy. Gastric mucosa, showing hyperplasia of foveolar surface epithelial
cells, glandular regenerative changes, and smooth muscle fibers extending into lamina
propria.
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Peptic Ulcer Disease
Ulcers :
a breach in the mucosa the muscularis mucosa
into the submucosa or deeper
Peptic ulcers
chronic
most often solitary
Epidemiology : remitting, duodenal ulcers-alcoholic
cirrhosis, chronic obstructive pulmonary disease,
chronic renal failure, and hyperparathyroidism
Pathogenesis : 1. the fundamental requisite; 2. a very
strong causal association with H.pylori infection
Diagram of causes of, and defense mechanisms against, peptic ulceration. Diagram of the base of a
nonperforated peptic ulcer, demonstrating the layers of necrosis (N), inflammation (I), granulation tissue
(G), and scar (S), moving from the luminal surface at the top to the muscle wall at the bottom.
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Morphology
98% of peptic ulcers are located in the first portion of
duodenum or in the stomach, in a ratio of about 4 : 1
size and location do not differentiate a benign from a
malignant ulcer
- round
- sharply punched-out craters 2 to 4 cm in diameter
Classically, the margins of the crater are perpendicular and
there is some mild edema of the immediately adjacent
mucosa, but unlike ulcerated cancers there is no significant
elevation or beading of the edges
Peptic ulcer of the duodenum. Note that the ulcer is small (2 cm) with a sharply punched-
out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base is
clean.
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Histologic
four zones
1. necrotic fibrinoid debris
2. Neutrophils
3. granulation tissue
4. fibrous, collagenous scar
CLINICAL FEATURES
Dyspepsia
Complication : bleeding, perforation, obstruction of the
pyloric cjannel
Complications of Peptic Ulcer Disease
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
ACUTE GASTRIC ULCERATION

Focal
Stress ulcers
Clinical features :
shock (extensive burns)
Sepsis
severe burns
trauma
TUMOR
BENIGN TUMORS
Polyp :
any nodule or mass that projects above the level of
the surrounding mucosa

Hyperplastic polyps ( 80-85%)


Fundic gland polyps ( 10% )
Adenomatous polyps = Adenoma( 5 % )
Peutz-Jeghers polyps
Inflammatory fibroid polyp (eosinophilic granuloma)
By definition, an adenoma contains proliferative
dysplastic epithelium and thereby has
malignant potential
Gastric hyperplastic polyp. Low-power microscopic view of the polyp showing
hyperplastic foveolar epithelium and inflammation.

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Gastric hyperplastic polyp. Low-power microscopic view of the polyp showing
hyperplastic foveolar epithelium and inflammation.
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Inflammatory fibroid polyp; microscopic photograph showing submucosal growth of
inflamed vascularized fibromuscular tissue with prominent eosinophilic infiltrate.
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Gastric Carcinoma

Epidemiology and Classification


Japan, Columbia, Costa Rica, and Hungary
Lauren and WHO Classification
WHO Histologic Classification of Gastric Tumors
Epithelial Tumors
Intraepithelial neoplasia: adenoma
Adenocarcinoma*
Papillary adenocarcinoma
Tubular adenocarcinoma
Mucinous adenocarcinoma
Signet-ring cell carcinoma
Undifferentiated carcinoma
Adenosquamous carcinoma

Small-cell carcinoma
Carcinoid tumor

Nonepithelial Tumors
Leiomyoma
Schwannoma
Granular cell tumor
Leiomyosarcoma
Gastrointestinal stromal tumor (GIST) (gradation from benign to malignant)
Kaposi sarcoma
Others

Malignant Lymphoma

* The Laurn classification subdivides adenocarcinomas into intestinal and diffuse types
Pathogenesis
Helicobacter pylori Infection
Environtment
Host
Other Risk Factors
Factors Associated with Increased Incidence of Gastric Carcinoma

Environmental Factors
Infection by H. pylori
Present in most cases of intestinal-type
carcinoma
Diet
Nitrites derived from nitrates (water,
preserved food)
Smoked and salted foods, pickled vegetables,
chili peppers
Lack of fresh fruit and vegetables
Low socioeconomic status
Cigarette smoking
Factors Associated with Increased Incidence of Gastric Carcinoma

Host Factors
Chronic gastritis
Hypochlorhydria: favors colonization with H. pylori
Intestinal metaplasia is a precursor lesion

Partial gastrectomy
Favors reflux of bilious, alkaline intestinal fluid

Gastric adenomas
40% harbor cancer at time of diagnosis
30% have adjacent cancer at time of diagnosis

Barrett esophagus
Increased risk of gastroesophageal junction tumors
Factors Associated with Increased Incidence of Gastric Carcinoma

Genetic Factors

Slightly increased risk with blood group A

Family history of gastric cancer

Hereditary nonpolyposis colon cancer syndrome

Familial gastric carcinoma syndrome (E-cadherin


mutation)
Morphology
Location :
pylorus and antrum 50% to 60%
cardia 25%
The lesser curvature 40%
the greater curvature in 12%
Gastric carcinoma is classified on the basis of
(1) depth of invasion
(2) macroscopic growth
(3) histologic subtype
Early gastric carcinoma : mucosa and
submucosa
Advanced gastric carcinoma : extended below
the mucosa into the muscular wall
Gasric mucosal dysplasia
Three macroscopic growth patterns

(1) exophytic
(2) flat or depressed
(3) excavated
Diagram of growth patterns and spread of gastric carcinoma. In early gastric carcinoma (A), the tumor is
confined to the mucosa and submucosa and may exhibit an exophytic, flat or depressed, or excavated
conformation. Advanced gastric carcinoma (B) extends into the muscularis propria and beyond. Linitis
plastica is an extreme form of flat or depressed advanced gastric carcinoma.

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Four macroscopic growth patterns :
Borrmanns type :

I. Polypoid carcinoma of the stomach. A large vegetating mass


without much hemorrhage or necrosis is present
II. Fungating carcinoma with extensive surface ulceration and
hemorrhage
III. Ulcerated gastric carcinoma with heaped up margins, but
without significant intraluminal growth
IV. A : The gastric wall is thickened with irregularly ulcerated
mucosa
B : Cancer involving the antrum showing a uniform
thickening of the gastric wall
Gastric carcinoma. Gross photograph showing an ill-defined,
excavated central ulcer surrounded by irregular, heaped-up borders.
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Linitis plastica
Histologic subtypes of gastric cancer
intestinal type
diffuse type
Gastric carcinoma. A, Intestinal type demonstrating gland
formation by malignant cells, which are invading the muscular wall
of the stomach
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Gastric carcinoma B, Diffuse type demonstrating signet-ring
carcinoma cells.
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signet ring cells infiltrative
Metastasis
supraclavicular lymph node ( Virchows node )
intraepithelial spreads in females is to both their
ovaries : Krukenberg tumor
Clinical features
Early : asymptomatic
Advanced : asymptomatic abdominal
discomfort or weight loss
LESS COMMON GASTRIC TUMORS

Gastric Lymphoma
* mucosa-associated lymphoid tissue (MALT lymphoma)
Gastrointestinal Stromal Tumor
Gastric Neuroendocrine Cell (Carcinoid) tumors
Lipomas
Metastatic Cancer
Gastric MALT lymphoma. Note the lymphoepithelial lesions (arrows). (Courtesy
of Dr. Melissa Li, University of Florida, Gainesville, FL.)
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Gastrointestinal stromal tumor. A, Gross photograph of
the tumor arising from the muscularis propria of the
gastric wall
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Gastrointestinal stromal tumor. B, Microscopic view of the tumor
showing spindle cell feature.
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Gastrointestinal stromal tumor. C, Immunohistochemical stain
showing the tumor cell c-KIT positivity.
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SMALL AND LARGE INTESTINES

A, Normal small-bowel histology, showing mucosal


villi and crypts, lined by columnar cells
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B, Normal colon histology, showing flat mucosal
surface and abundant vertically oriented crypts.
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Congenital Anomalies
In the small intestine
Atresia or stenosis
Duplication
Meckels diverticulum
Omphalocele
In the large intestine
Malrotation
Hirschsprung disease
Congenital Aganglionic Megacolon Hirschsprung
Disease

an aganglionic segment is left that lakcs both


Meissners submucosal and Auerbachs
myenteric plexuses
ENTEROCOLITIS
DIARRHEA AND DYSENTERY
Diarrhea is elusive, an increase in stool mass, stool
frequency, or stool fluidity
Dysentery is low-volume, painful, bloody diarrhea
Categorized : secretory diarrhea, osmotic
diarrhea, exudative diseases, deranged motility,
and malabsorption
Major Causes of Diarrheal Illnesses
Secretory Diarrhea
Infectious: viral damage to mucosal epithelium
Rotavirus
Caliciviruses
Enteric adenoviruses
Astroviruses
Infectious: enterotoxin mediated
Vibrio cholerae
Escherichia coli
Bacillus cereus
Clostridium perfringens
Neoplastic
Tumor elaboration of peptides, serotonin, prostaglandins
Villous adenoma in distal colon (nonhormone mediated)
Excess laxative use
Major Causes of Diarrheal Illnesses
Osmotic Diarrhea
Disaccharidase (lactase) deficiencies
Lactulose therapy (for hepatic encephalopathy, constipation)
Prescribed gut lavage for diagnostic procedures
Antacids (MgSO4 and other magnesium salts)
Primary bile acid malabsorption
Exudative Diseases
Infectious: bacterial damage to mucosal epithelium
Shigella
Salmonella
Campylobacter
Entamoeba histolytica
Idiopathic inflammatory bowel disease
Typhlitis (neutropenic colitis in the immunosuppressed)
Major Causes of Diarrheal Illnesses

Malabsorption
Defective intraluminal digestion
Primary mucosal cell abnormalities
Reduced small intestinal surface area
Lymphatic obstruction
Infectious: impaired mucosal cell absorption
Giardia lamblia infection
Major Causes of Diarrheal Illnesses
Deranged Motility
Decreased intestinal transit time

Surgical reduction of gut length


Neural dysfunction, including irritable bowel syndrome
Hyperthyroidism
Diabetic neuropathy
Carcinoid syndrome
Decreased motility (increased intestinal transit time)

Small intestinal diverticula


Surgical creation of a "blind" intestinal loop
Bacterial overgrowth in the small intestine
INFECTIOUS ENTEROCOLITIS
Viral Gastroenterocolitis
Bacterial Enterocolitis : Eschericia coli, Salmonella,
Shigella, Campylobacter, Yersinia enterocolitica,
Vibrio cholerae, Clostridium difficile, Clostridium
perfringens, and Mycobacterium tuberculosis
Protozoal Infection : Entamoeba histolytica &
Giardia lamblia
Entamoeba histolytica in colon. High-power view of the organisms. Note some
of the organisms ingesting red blood cells.
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Giardia lamblia. Trophozoite (arrow) of the organism immediately adjacent to
the duodenal surface epithelium.
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Shigella enterocolitis. Segment of colon showing pale, granular, inflamed mucosa with
patches of coagulated exudate.
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Antibiotic-Associated Colitis
(Pseudomembranous Colitis)

Caused by toxins of Clostridium difficile


Acute
Plaque-like adhesion
Pseudomembranous colitis from C. difficile infection. A, Gross photograph
showing plaques of yellow fibrin and inflammatory debris adherent to a
reddened colonic mucosa. B, Low-power micrograph showing superficial
erosion of the mucosa and an adherent pseudomembrane of fibrin, mucus,
and inflammatory debris.
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Pseudomembranous colitis from C. difficile infection. A, Gross photograph showing
plaques of yellow fibrin and inflammatory debris adherent to a reddened colonic mucosa.
B, Low-power micrograph showing superficial erosion of the mucosa and an adherent
pseudomembrane of fibrin, mucus, and inflammatory debris.
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Necrotizing Enterocolitis
particularly devasting in the neonate
Acute necrotizing inflammation
severe consequence of transmural necrosis of
intestinal segments
Necrotizing enterocolitis. A, Postmortem examination in a severe case of NEC shows the entire small
bowel is markedly distended with a perilously thin wall (usually this implies impending perforation).
B, The congested portion of the ileum corresponds to areas of hemorrhagic infarction and
transmural necrosis microscopically. Submucosal gas bubbles (pneumatosis intestinalis) can be
seen in several areas (arrows).
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Necrotizing enterocolitis. A, Postmortem examination in a severe case of NEC shows the entire small
bowel is markedly distended with a perilously thin wall (usually this implies impending perforation). B,
The congested portion of the ileum corresponds to areas of hemorrhagic infarction and transmural
necrosis microscopically. Submucosal gas bubbles (pneumatosis intestinalis) can be seen in several
areas (arrows).
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Malabsorption Syndromes

Celiac disease
Tropical Sprue (Postinfectious Sprue)
Whipple Disease
Disaccharidase (Lactase) Deficiency
Abetalipoproteinemia
Celiac disease (gluten-sensitive enteropathy). A, A peroral
jejunal biopsy specimen of diseased mucosa shows diffuse
severe atrophy and blunting of villi, with a chronic
inflammatory infiltrate of the lamina propria
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Celiac disease (gluten-sensitive enteropathy). B, A
normal mucosal biopsy.
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Whipple disease. A, Note foamy macrophages in the
lamina propria
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Whipple disease B, PAS stain showing the positive
granules in the foamy macrophages.
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Idiopathic Inflammatory Bowel Disease
( IBD )
Crohns disease ( CD ) and ulcerative colitis (
UC )
CD : granulomatous disease; autoimmune
disease
UC : non-granulomatous disease limited to the
colon, chronic inflammatory disease
CROHNS DISEASE

Segmental transmural fibrosis and thickening


of therminal ileum terminal ileitis
Morphology :
(1) sharply delimited and typically transmural involvement
(2) noncaseating granulomas in 40% to 60% of cases
(3) fissuring with formation of fistulae
Creeping fat
String sign
Skip lesions regional enteritis
Microscopic examination :
(1) mucosal inflammation crypt abcesses;
(2) ulceration; and
(3) chronic mucosal damage
(4) transmural inflammation
(5) noncaseating granuloma
(6) other mural change
Crohn disease of the colon. A noncaseating granuloma is present in
the lamina propria of an uninvolved region of colonic mucosa (arrow).
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ULCERATIVE COLITIS

Ulceroinflammatory colon the mucosa


and submucosa
Begins in the rectum
In UC, well formed granulomas are absent
UC does not exhibit skip lesions
The mucosal ulcers in UC rarely extend below the
submucosa, and there is surprisingly little fibrosis
Mural thickening does not occur in UC, and the
serosal surface is usually completely normal
Patients with UC are the greater risk for carcinoma
Morphology
pancolitis
pseudopolyps
toxic megacolon
Ulcerative colitis. Ulcerated hemorrhagic surface with knobby
pseudopolyps.
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Inflammation --- chronic mucosal damage --- ulceration
(similar colonic CD)
A diffuse, predominantly mononuclear inflammatory
infiltrate in the lamina propria is almost universically
present
Further destruction of the mucosa leads to outrigth
ulceration, extending into the submucosa and something
leaving only the raw, exposed muscularis propria
Granulation tissue fills in the ulcers creaters
Ulcerative colitis. Microscopic view of the mucosa,
showing diffuse active inflammation with crypt abscess
and glandular architectural distortion.
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Vascular Disorders

ISCHEMIC BOWEL DISEASE


The predisposing conditions :
Arterial thrombosis
Arterial embolism
Venous thrombosis
Non occlusive ischemia
Miscellaneous
Morphology
Transmural infarction
Gangrene
Perforation
Mural & Mucosal Infarction
Inflammation pseudomembrane
Chronic vascular insufficiency
a chronic inflammatory and ulcerative
condition, mimicking idiopathic inflammatory
bowel disease
Chronic Ischemia
Chronic ischemia of the colon, resulting in chronic mucosal damage
and a stricture.
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ANGIODYSPLASIA

Tortous dilatations of submucosal and


mucosal blood vessels
Most often in the caecum or right colon
HEMORRHOIDS
Variceal dilatation of the anal and perianal
submucosal venous plexuses
Above the anorectal line and are covered by
rectal mucosa (internal hemorrhoids)
Below the anorectal line and are covered by
anal mucosa (external hemorrhoids)
Diverticular Disease
a diverticulum is a blind pouch leading off the
alimentary tract, lined by mucosa, that
communicates with the lumen of the gut
Intestinal Obstruction

Hernias

Intestinal adhesions

Intussusception

Volvulus
Major Causes of Intestinal Obstruction
Mechanical Obstruction
Adhesions
Hernias, internal or external
Volvulus
Intussusception
Tumors
Inflammatory strictures
Obstructive gallstones, fecaliths, foreign bodies
Congenital strictures; atresias
Congenital bands
Meconium in mucoviscoidosis
Imperforate anus
Pseudo-obstruction
Paralytic ileus (e.g., postoperative)
Vascular-bowel infarction
Myopathies and neuropathies (e.g., Hirschsprung)
Schematic depicting the four major causes of intestinal obstruction:
(1) Herniation of a segment in the umbilical or inguinal regions; (2)
adhesion between loops of intestine; (3) intussusception; (4)
volvulus formation.
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Tumors of The Colon And Rectum

Non Neoplastic Polyps


Adenomas
Familial Syndromes
Colorectal Carcinogenesis
Colorectal Carcinoma
Carcinoids Tumors
Non-neoplastic colonic polyps. A, Hyperplastic polyp; high-power
view showing the serrated profile of the epithelial layer.
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Non-neoplastic colonic polyps. B, Peutz-Jeghers polyp; low-
power view showing the splaying of smooth muscle into the
superficial portion of the pedunculated polyp.
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Adenomas
(adenomatous polyps)

3 subtypes epithelial
Tubular adenomas
Villous adenomas
Tubulovillous adenomas
Familial Syndromes

Familial Adenomatous Polyposis (FAP) Syndrome


Hereditary Nonpolyposis Colorectal Cancer
(HNPCC) Syndrome
Colorectal
Carcinogenesis
Molecular Carcinogenesis
First pathway
(APC/Beta-caterin pathway)
- Loss of Adenomatous Polyposis Coli (APC) gene
- Mutation of K-RAS
- Loss of SMADA-5
- Loss of p53
- Activation of Telomerase
Second pathway
Microsatellite Instability Pathway
- DNA mismatch repair genes
Schematic of the morphologic and molecular changes in the adenoma-carcinoma sequence. It is postulated that loss of
one normal copy of the tumor suppressor gatekeeper gene APC occurs early. Indeed, individuals may be born with one
mutant allele of APC, rendering them extremely likely to develop colon cancer. This is the "first hit," according to
Knudson's hypothesis. The loss of the normal copy of the APC gene follows ("second hit"). Mutations of the oncogene
K-RAS seem to occur next. Additional mutations or losses of heterozygosity inactivate the tumor suppressor gene p53
(on chromosome 17p) and SMAD2 and SMAD4 on chromosome 18q, leading finally to the emergence of carcinoma, in
which additional mutations occur. It is important to note that while there seems to be a temporal sequence of changes,
as shown, the accumulation of mutations, rather than their occurrence in a specific order, is more important.
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Colorectal Carcinoma
Epidemiology
Etiology
Pathogenesis
Morphology

Distribution:
rectosigmoid colon 55%
proximal colon
polypoid, exophytic
distal colon
annulair, encircling napkin-ring constriction of
the bowel
signet ring appearance
Clinical Features:
The single most important prognostic
indicator of colorectal carcinoma is the extent
of the tumor at the time of diagnosis, the so
called stage
Dukes and Kirklin................................
................ Aster and Coller ................
...... American Joint Commision on Cancer
Table 17-14. TNM Classification of Carcinoma of the Colon and Rectum

Tumor Stage Histologic Features of the Neoplasm

Tis Carcinoma in situ (high-grade dysplasia) or intramucosal carcinoma


(lamina propria invasion)
T1 Tumor invades submucosa

T2 Extending into the muscularis propria but not penetrating through it

T3 Penetrating through the muscularis propria into subserosa

T4 Tumor directly invades other organs or structures

Nx Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis in 1 to 3 lymph nodes

N2 Metastasis in 4 or more lymph nodes

Mx Distant metastasis cannot be assessed

M0 No distant metastasis

M1 Distant metastasis
Pathologic staging of colorectal cancer. Staging is based on the depth of tumor invasion.

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Carcinoid Tumors
GASTROINTESTINAL LYMPHOMA

MESENCHYMAL TUMORS
Leiomyomas and Leiomyosarcomas

TUMORS OF THE ANAL CANALS


Carcinomas
APPENDIX

Acute appendicitis
Early acute appendicitis
Acute suppurative appendicitis
Acute gangrenous appendicitis
Tumors of the appendix
Carcinoid
Mucocele
Pseodomyxoma Peritonei
MIKROSKOPIK :
JARINGAN SEMBAB : OEDEMA
PELEBARAN PEMBULUH
DARAH/VASODILATASI
INFILTRASI SEL RADANG PMN
NEKROSIS LIQUEFACTIVE/PUS
lymphocytic and plasma cell infiltrate in the
lamina propria
(1) intestinal metaplasia
(2) proliferation of lymphoid tissue

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