Gastrointestinal tract

Alemwosen T.
 ORALCAVITY
Inflammations
Herpes simplex virus infection
- most are caused by HSV-I

- Usually trivial cold sores

- Typically occurs in children 2-4

- severe and diffuse involvement of oral mucosa, tongue and

pharyngeal mucosa may occur acute herpetic
gingivostomatitis

- xized by formation of clear vesicles

- vesicles rupture to yield extremely painful shallow ulcers

histologically intranuclear inclusions
and multinucleate giant cells
lesions resolve spontaneously within 3-
4 weeks
Aphthous ulcers ( canker sores)
very common superficial ulcerations of the oral
mucosa
more common in the first two decades
appear as single or multiple shallow hyperemic
ulcerations covered by thin exudate and rimmed by
a narrow zone of erythema
Mononuclear inflammations
lesions spontaneously resolve within a week to
10days
Rarely they persist
Oral candidiasis ( trush)
take the form of a superficial curdy, gray to
white inflammatory membrane
scraping reveals an underlying erythematous
inflammatory base
the fungus is a normal inhabitat of the oral
cavity
causes disease only in individuals who are
diabetic ,neutropenic or immunocompromised
like in AIDS
Glossitis
inflammation of the tongue
also applied to the beafy- red tongue
encountered in certain deficiency states like
vit.B12, Riboflavin, niacin, pyridoxine & iron
Xerostomia
dry mouth, a major feature of sjogren
syndrome
Hairy leukoplakia
- Uncommon oral lesion virtually restricted to
HIV patients
- appears as white confluent patches of fluffy (
hairy) hyperkeratotic thickening
- microscopically appear as piled up layers of
keratotic squames based on mucosal
acanthosis
- EBV is now accepted as a major cause
Tumors and precancerous lesions
Leukoplakia and Erythroplakia
Leukoplakia
a white plaque on the oral mucous membranes that
cannot be removed by scraping and can not be
classified clinically or microscopically as another
disease entity
clinical term
until it is proved otherwise it must be considered
precancerous
Leukoplakia. Clinical appearance of leukoplakias is highly variable and can range
from A, smooth and thin with well-demarcated borders. B, diffuse and thick. C,
irregular with a granular surface. D, diffuse and corrugated
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).
Leukoplakia with marked epithelial thickening and hyperkeratosis
Erythroplakia ( dysplastic leukoplakia)
represents a red ,velvety possibly eroded area
within the oral cavity
epithelial changes are markedly atypical
associated factors with these lesions are
Cigarettes, pipes cigars, alcohol, ill filling
denture
HPV particularly type 16 have been identified
in tobacco- related lesions
Squamous cell carcinoma
represents ~ 95% of cancers of head and neck
most common ages 50-70 yrs
commonly associated with tobacco and alcohol
HPV serotypes 6, 16, and 18 are associated
may occur anywhere in the oral cavity but favored
locations are floor of the mouth , ventral tongue , lower
lip, soft palate and base of tongue
prognosis is best with lip lesions , 5 year recurrence free
rate approaching 90%
poorest outcome is with tumors in the floor of the mouth
and base of tongue
Clinical, histologic, and molecular progression of oral cancer.
Other oral & Oropharynx Tumors

Lymphoma
Diffuse Large B-cell Lymphoma (Old age & AIDS)
MALToma
Plasmacytoma
Melanoma
Leukemic infiltrates

22
 Contd
Odontogenic cysts and tumors
Ameloblastoma
True neoplasm & arises from odontogenic
epithelium
It is commonly cystic, slow growing, and locally
destructive
Odontoma commonest lesion
Hamartomatous- extensive deposition of enamel and
dentin
Radicular cyst Cyst related to the tooth root,
usually after inflammation
Keratocyst- Cyst of dental lamina origin, lined by
stratified squames
23
 Radiographic feature
Multilocular radiolucent lesion, soap bubble / honey combed
Buccal & lingual cortical expansion
resorption of the roots of teeth

In many cases an unerupted teeth specially 3rd molar is associated with

defect

"soap bubble" appearance. "honeycombed" appearance.

A painless swelling expansion of the jaw is the usual clinical presentation

If untreated, the lesion may grow slowly to massive or grotesque proportions

Ameloblastoma

27
Keratocyst

28
 Diseases of Salivary Glands
Inflammation (Sialadenitis)
Traumatic, viral, bacterial, autoimmune origin
Mucoceles most common cystic lesion of oral cavity,
follows duct obstruction after inflammation
Mumps- most common viral sialadenitis
Sjogren syndrome- an autoimmune disease
Sialolithiasis and Chr. Nonspecific inflam
 Sialolithiasis and non specific
Sialadenitis
Most often bacterial & involves submandibular
glands
Pathogenesis:
dehydration with decreased secretory function & may
predispose to infection
Usually, secondary to ductal obstruction by stones
Unilateral involvement of single gland is the rule
SSx: painful enlargement and sometimes purulent
ductal discharge
Chronic sialadenitis

31
 Neoplasms of salivarygland
Classification
Benign Malignant
Pleomorphic adenoma Mucoepidermoid carcinoma
Warthins tumor Adenocarcinoma
Oncocytoma Acinic cell carcinoma
Basa cell adenoma Adenoid cystic carcinoma
Ductal papillomas Squamous cell carcinoma

Tumors usually occur in adults with slight female

preponderance
85% are benign and mostly in parotid
 Pleomorphic Adenoma (mixed tumors)
Represent about 60% of tumors in the parotid
Said to be of myoepithelial origin with both epithelial and
mesenchymal differentiation
Radiation exposure increases the risk
Painless, slow growing, mobile and discrete mass
Malignant transformation (2%) increases with duration
Carcinoma arising in pleomorphic adenoma is referred
as a carcinoma ex pleomorphic adenoma
pleomorphic adenoma
Pleomorphic adenoma

35
 Warthin tumor
Papillary cystadenoma lymphomatosum
Second most common, commonly in old age
Almost always arises in the parotid gland
Spaces lined by a double layer of epithelial cells resting
on a dense lymphoid stroma sometimes bearing
germinal centers
Bilateral or multicenteric
Warthins T.

37
Mucoepidermoid carcinoma
Composed of mixtures of three cells:
squamous cells, mucus secreting cells, and intermediate cells
Occur mainly in the parotids
15% of all salivary gland tumors
Most common form of primary malignant tumor of
salivary glands
Cords, sheets, or cystic configurations of squamous,
mucous, or intermediate cells
Low grade lesions tend to be composed of largely mucus
secreting cells (cystic)
High grade tumors are composed largely of squamous
cells with only a scattering mucus secreting cells (solid)
Mucoepidermoid carcinoma

39
Mucoepidermoid carcinoma

40
 Adenoid cystic carcinoma
most common neoplasm in the minor salivary glands
Composed of small cells, having dark, compact nuclei and
scanty cytoplasm
The cells tend to be dispersed in tubular, solid, or
cribriform patterns
The spaces between tumor cells are filled with a hyaline
material
Most painful (perineural invasion) salivary gland
neoplasm
Adenoid cytic carcinoma

42
 Acinic cell tumor
Composed of cells resembling the normal serous cells
of salivary glands
Most arise in the parotid
Bilateral or multicenteric
The cells have apparent cleared cytoplasm
The cells are disposed in sheets or microcystic,
glandular, follicular, or papillary patterns
Little anaplasia and few mitoses
Acinic cell carcinoma

44
 Diseases of Esophagus
1. Atresia and Fistulas
Presents soon after birth
Atresia: A segment of esophagus represented by
only a thin, non canalized cord, connected proximally
with a blind pharyngeal pouch and distally to a pouch
leading to the stomach
It is usually associated with fistula to the bronchus or
trachea
Other associated organ malformations: hepatic,
panreastic
 Esophagus
Congenital anomalies
Atresia and fistula
A. Blind upper and lower esophageal segment
B. Fistula between blind upper segment and
trachea
C. Blind upper segment ,fistula between blind
lower segment and trachea
D. Blind upper segment only
E. Fistula between patent esophagus and
trachea
Type C is the commonest form
Tracheoesosphageal malforma.

48
 Stenosis- fibrous thickening of the esophageal
wall with atrophy of the muscularis
Fibrous thickening of the esophageal wall
Most esophageal stenosis are acquired
Mucosal webs - semicircumferential
protrusions of the mucosa into the esophageal
lumen
Rings - concentric plates of tissue protruding in
to the lumen.
Lesions associated with motor dysfunction
Achalasia
motor dysfunction: failure to relax distal
esophageal sphincter => proximal dilatation
characterized by
Aperstalisis
Partial or incomplete relaxation of the LES
Increased resting tone of the LES
Pathogenesis of primary achalasia is poorly
understood
 Achalasia
Secondary achalasia may arise in Chagas disease
in which Trypanosoma cruzi causes destruction of
the myenteric plexus
There will be progressive dilation of the
esophagus above the level of LES
Myenteric ganglia are usually absent from the
body of esophagus
Usually manifest in young adult hood
 Achalasia
Classic clinical symptom is progressive dysphagia
Regurgitation and aspiration may occur
In about 5%, possibility of developing SCC
Other complications include
candidal esophagitis
diverticula and
aspiration with pneumonia
 Hiatal hernia
characterized by separation of the diaphragmatic
crura and widening of the space between the
muscular crura and esophageal wall
Two patterns
Sliding
constitutes 95% of the cases
protrusion of the stomach above the diaphragm creating
a bell shaped dilation
Paraesophageal
a separate portion of the stomach usually along the
greater curvature enters the thorax
SSx: Heartburn; ulceration,
bleeding, perforation
 Diverticula
An outpouching of the alimentary tract that
contains all visceral layers
False diverticulum is an outpouching of mucosa
and submucosa only
Typical symptoms are dysphagia ,regurgitation
and a mass in the neck
Aspiration with resultant pneumonia is a
significant risk
 True eosophageal diverticula are usually
discovered later in life
Zenker diverticulum
Above the UES
Cricopharyngeal motor dysfunction
Traction diverticulum
Midpoint of esophagus
Scarring from mediastinium (eg.Tuberculosis
Epiphrenic diverticulum
Above the LES
incoordination of peristalsis and LES relaxation
 Laceration (Mallory-Weiss syndrome)
longitudinal tears in the esophagus at the
esophagogastric junction
Believed to be a consequence of severe
retching
Occur most commonly in alcoholics
Laceration (Mallory-Weiss syndrome)
May reach several centimeters in length
Tears may involve only the mucosa or may
penetratre deeply enough to perforate the wall
Account for 5-10% of upper GI bleeding
Boerhaave syndrome is rupture of the
esophagus and is a rare and catastrophic event
 Esophageal Varices
Tortuous dilated veins lying primarily within the submucosa of
the distal esophagus and proximal stomach
Cause: portal hypertension - cirrhosis, hepatic schistosomiasis
etc.
Clinical features
Usually produce no symptoms until they rupture
When they rupture => Massive hematemesis
Most important cause of cirrhosis associated deaths
 Esophagitis
Inflammation of esophageal mucosa
Cause: chemical, physical, biologic agents
1. Reflux esophagitis
Reflux of gastric contents into the lower esophagus
Causes: Decreased efficacy of esophageal anti-reflux
mechanisms
Sliding hiatal hernia
Inadequate clearance of refluxed material
Delayed gastric emptying
reduction in the reparative capacity of the esophageal mucosa
Reflux esophagitis
Morphology
Simple hyperemia and edematous swellings
Histology
Presence of inflammatory cells (polymorphs) in the
squamous layer
Bazal zone hyperplasia
Elongation of lamina propria papillae with congestion
Clinical features
Largely limited to adults over age 40
Dysphagia, heartburn, regurgitation (vomitting),
hematemesis, melena (tarry stool due to presence of blood)
Consequences: bleeding, ulceration, stricture, Barretts
esophagus
Reflux esophagitis

63
Epidemiology of GERD and Barretts oesophagus
increasing gastro-oesophageal reflux disease (in the UK and USA at least)
risk factors for reflux disease:
male
middle age
white
overweight
alcohol
smoking
family history
 Barretts esophagus
Def.: Glandular metaplasia after longstanding gastro-esophageal
reflux
Occurs in up to 10% of patients with GERD
Most important: risk factor for esophageal adenocarcinoma
Two criteria for diagnosis
Endoscopic evidence of columnar epithelial lining above
the gastroesophageal junction
Histologic evidence of intestinal metaplasia in the biopsy
specimen from the columnar epithelium
 Morphology
Red, velvety mucosa between the smooth, pale pink
esophageal mucosa and the light brown gastric mucosa
Definitive diagnosis made when columnar mucosa
contains intestinal goblet cells
Clinical features
Most patients between 40 and 60
Ulceration, bleeding, stricture
Development of adenocarcinoma
Baretts epithelium

70
Infectious and chemical esophagitis
Causes:
Ingestion of mucosal irritants
Cytotoxic anticancer therapy
Viral infection HSV, CMV
Fungal infection- candidiasis, mucormycosis
Uremia in renal failure
Morphology
Severe acute inflammation
Superficial necrosis
Ulceration with granulation tissue
Clinical features
Esophagus infection most often occurs in
immunosuppressed
Chemical injury in children is accidental but in adults is
suicidal attempt
These images demonstrate three types of
infective oesophagitis.

candida HSV CMV

 Eosophageal tumors
GIST
Benign
Mostly Mesenchymal
GIST
Leiomyoma
Fibroma
Lipoma
Hemangioma
Malignant
Most important:
Squ. Cell Ca
Adenocarcinoma

73
Squamous cell carcinoma
Occur in adults over 50
Has male preponderance
Has higher incidence in Iran, China, SA
Blacks
 Risk Factors for SCC of the Esophagus
Esophageal Disorders
Long-standing esophagitis
Achalasia
Plummer-Vinson syndrome (esophageal webs, microcytic hypochromic anemia, atrophic
glossitis)
Life-style
Alcohol consumption
Tobacco abuse
Hot beverage & foods
Dietary
Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)
Deficiency of trace metals (zinc, molybdenum)
Fungal contamination of foodstuffs
High content of nitrites/nitrosamines
Genetic Predisposition
Racial predisposition
Tylosis (hyperkeratosis of palms and soles)
 Squamous cell carcinoma
About 20% are located in the upper third,
50% in the middle third, and 30% in the lower third
Three morphologic patterns are described
Protruded (60%)
polypoid exophytic lesion
Flat (15%)
a diffuse infiltrative form that spreads within the wall of
the esophagus causing thickening , rigidity and narrowing
Excavated (25%)
a necrotic cancerous ulceration that excavates deeply into
surrounding structures
79
 Squamous cell carcinoma
Most are moderately to well differentiated
Local extension into adjacent mediastinal structures
occur early
Tumors in the upper third metastasize to cervical
lymph nodes
Those in the middle to mediastinal , paratracheal and
tracheobronchial nodes
Those in the lower third most often to gastric and
celiac groups of nodes
 Clinical features
Dysphagia, progressive:
Dificulty to solid diets
Difficulty to liquid diets
Obstruction
Extreme weight loss
Hemorrhage and sepsis following ulceration
Aspiration:
Food stasis
Tracheosophgeal fistula
Lymph node metastases significantly reduces five year
survival rate
Adenocarcinoma
Increasing in incidence
Associated with Barrett esophagus
Usually located in the distal esophagus and may
invade the adjacent gastric cardia
May develop nodular masses or may exhibit diffusely
infiltrative or ulcerative features
Histologically most are mucin producing glandular
tumors
Adenocarcinoma
Majority arise from the Barretts mucosa
Life time risk for cancer development in Barretts is 10%
Usually located in distal esophagus
Most are over age 40
More common in men and whites
Manifestation: Dysphagia, weight loss, bleeding, chest
pain, vomiting
Prognosis is poor like other esophageal cancers
Transition from Barrett esophagus to adenocarcinoma
Baretts:dysplasia &
carcinoma

87
 Rx and Px 0f esophageal cancers

Surgery is the first line treatment

Five year survival is less than 20%
Outcome is influenced by stage at diagnosis,
margin involvement and vascular invasion
Stomach
 Stomach
Congenital anomalies
Heterotopia
rests of normal tissue may be present at any site in the
GI tract
nodules of normal pancreatic tissue up to 1cm may be
present in the gastric or intestinal submucosa
Gastric heterotopia small patches of ectopic
gastric mucosa in the duodenum or in more distal
sites
 Pyloric stenosis
Aka Congenital hypertrophic pyloric stenosis
M:F 4:1
Hypertrophy or hyperplasia of muscularis propria
SSx:- Regurgitation, and persistent, projectile, nonbilious
vomiting in the second or third week of life
visible peristalsis
Firm, ovoid palpable mass in the region of pylorus
Acquired Pyloric Stenosis
Long term risk of antral gastritis or peptic ulcers
Carcinoma of pyloric region are common causes
Lymphoma of antral area
 Gastritis
Inflammation of the gastric mucosa
Acute or chronic
Acute gastritis
Acute mucosal inflammatory process , usually of
transient nature
Is frequently associated with
Heavy use of NSAIDs
Excessive alcohol consumption
Heavy smoking
Uremia
Systmic infections
Severe stress (e.g. trauma, burn, surgery)
Ischemia and shock
 Mechanisms of gastritis include
- Increased acid secretion with back-diffusion
- Decreased production of bicarbonate buffer
- Reduced blood flow
- Disruption of the adherent mucus layer
- Direct damage to the epithelium
 Morphology of Gastritis
The presence of neutrophils above the basement
membrane (within epithelium) is abnormal and signifies
active inflammation
With more severe damage, erosion and hemorrhage
develop
Erosion- loss of the superficial epithelium, generating a
defect in the mucosa that does not cross the muscularis
mucosa
Concurrent erosion and hemorrhage = acute erosive
hemorrhagic gastritis

[erosion is better than ulceration]

Clinical feature of gastritis
May be asymptomatic
May cause epigastric pain, nausea, vomiting
May present with hemorrhage, (hematemesis and/or
melena)
It is one of the major causes of hematemesis
 Chronic gastritis
Defined as the presence of chronic mucosal

inflammatory changes leading eventually to mucosal

atrophy and epithelial metaplasia usually in the
absence of erosion

Dysplasia may be seen

 Major etiologic associations of Chronic gastritis are
Chronic H.pylori infection

Autoimmune( in association with pernicious anemia)

Toxic (alcohol, cigarette )

Radiation

Postsurgical

Motor and mechanical causes

Granulomatous conditions (e.g. Crohn disease)

 H. Pylori
Most important etiologic agent
Present in 90% of patients with chronic gastritis
affecting the antrum
H.pylori is a nonsporing, gram negative rod
Specialized traits that allow H.pylori to flourish
include
Motility
Urease that produces ammonia and CO2 which buffer
HCl
Adhesin
Bacterial toxins (CagA and VacA)
 Chronic gastritis
Occurs in two patterns:
Antral type gastritis (antral)
High acid production and elevated risk for duodenal
ulcer
Lower IL-1 production (proinflammatory cytokin)
Pangastritis (body+fundus)
Multifocal atrophy
Lower gastric acid secretion, higher risk for
adenocarcinoma
Higher IL-1 production
Contd
Diagnosis of Chronic gastritis
Non invasive test
Serologic, fecal bacterial detection, urea breath
test
Invasive
gastric biopsy (Silver or Geims stain)
Treatement with antibiotics heals
 Autoimmune gastritis
10% of chronic gastritis
autoantibodies to gastric gland parietal cells , intrinsic
factor (Pernicious anemia), gastrin receptor
Gland destruction and mucosal atrophy lead to loss of
acid production(Hypo-achlorohydria)
Seen in association with other autoimmune disorders
such as Hashimotos thyroiditis
Risk of developing gastric carcinoma and carcinoid tumors
Morphology of chronic gastritis
Gross similar in all:
Reddened mucosa with thickened rugal folds
Autoimmune gastritis
Diffuse mucosal damage of the body-fundic mucosa
H.pylori
Antral and body-fundic mucosa
Micro:
Inflammatory infiltrate of lymphocytes and plasma cells
in the lamina propria
Active inflammation is signified by the presence of
neutrophils with in the glandular and surface epithelial
layer
Contd
Additional features of chronic gastritis
Regenerative change
Intestinal Metaplasia
Atrophy
Dysplasia
Clinical features of chronic gastritis
Nausea, vomiting, upper abdominal discomfort
Severe parietal cell loss: Hypochlorhydria-
Achlorohydria, hypergastrenemia
Circulating autoantibodies
 Gastric ulceration
Defined histologically as a breach in the mucosa that
extends through the muscularis mucosae into the
submucosa or deeper
Although ulcers may occur anywhere in the alimentary
tract, by far, the most common are the peptic ulcers that
occur in the duodenum and stomach
Erosion vs ulceration
 Peptic ulcer disease(PUD)
Chronic most often solitary lesions that occur in any
portion of the GI tract exposed to the aggressive action
of acid-peptic juices
Ulcer extends beyond the muscularis mucosae
Middle aged to older adults
Recurrent ulceration
Male to female ratio for duodenal ulcer is 3:1 and for
gastric ulcers is 1.5 to 2:1
PUD sites
Duodenum (1st part)
Stomach
Lower esophagus (Barretts)
Gastrojejunostomy margins
Zollinger Ellison Syndrome
Meckels diverticulum

Zollinger ellison syndrome: peptic ulceration with

gastic hypersecretion non cell tumor of pancreatic
islet.
 PUD Pathogenesis
An imbalance between gastroduodenal mucosal defence
mechansims and the damaging forces of gastric acid and
peptic enzymes
Hyperacidity is not a prerequisite
Defence mechanism
surface mucus secretion
bicarbonate secretion
mucosal blood flow
epithelial regenerative capacity
elaboration of prostaglandins
H.pylori infection & Peptic Ulcer
Not all infected develop ulcer:
Only 10-20 % of infected individuals develop
peptic ulcer
In patients with duodenal ulcer, the actual
infection by H.pylori is limited to the stomach
Infection is present in ALL patients with
duodenal ulcer and 70% of gastric ulcers
 Other Mechanisms for PUD
Zollinger Ellison syndrome
Multiple peptic ulcerations owing to excess gastrin
secretion by tumor (pancreatic gastrinoma)
Non steroidal anti-inflammatory drugs
Suppresses mucosal prostaglandin synthesis
Are also direct irritants
Cigarrette smoking impairs blood flow and healing
Alcohol if associated with cirrhosis
Corticosteroids
 Morphology of PUD
98% in first portion of the duodenum or
stomach- in a ratio of 4:1
Anterior wall of duodenum is affected more
commonly
Gastric ulcers predominantly located in the
lesser curvature
Majority are single ulcers
Gastritis usually accompany the ulcer
 Morphology of PUD
Round, oval, sharply punched out defect with relatively
straight walls
Margins usually level with the surrounding mucosa
No heaping up of margins
(heaping = malignant lesions)
Base of peptic ulcer is smooth and clean
Size and location do not differentiate a benign from
malignant ulcer
PUD, smooth base & margin
Benign gastric ulcer, PUD
Clinical features of PUD
Epigastric pain (gnawing, burning or aching)
Nausea, Vomiting, Bloating, Weight loss
The pain tends to be worse at night and occurs
usually 1 to 3 hrs after meals
Pain relieved by alkalis or food
With penetrating pains it is referred to the back
Iron deficiency anemia (with hemorrhage,
perforation)
Complication of PUD
Bleeding
Perforation
Obstruction from edema or scarring
Malignant transformation
Malignant transformation does not occur with
duodenal ulcers and is extremely rare with gastric
ulcers
Chronic gastritis is universal among patients with peptic
ulcer disease
 Acute gastric ulceration, causes
Complication of therapy with NSAIDs
May appear following severe tress:
Stress ulcers: commonly occur in patients with shock,
burns, sepsis, trauma, intracranial injury
Curling ulcer- occurring in the proximal doudenum and
associated with severe burns or trauma
Cushing ulcers gastric, duodenal, and esophageal
ulcers arising in patients with intracranial injury,
operations, or tumors
Morphology, Acute ulcer
Generally, multiple lesions located in the stomach
and duodenum
Shallow lesions, an extension of acute erosive
gastritis
Stress ulcers are usually less than 1 cm and ulcer base
is frequently stained dark brown by the acid digestion
of extruded blood
 Stomach, acute gastric ulcers
Multiple stress ulcers of the stomach highlighted by dark ingested blood on their surfaces
Hemorhagic gastritis
(Severly ill patient)
 Other lesions of the stomach

Bezoars
Hypertrophic gastropathy
Gastric varices
Tumors of the stomach
Benign tumors
Polyps any nodule or mass that projects above the
level of the surrounding mucosa
Greater than 90% are of hyperplastic nature
5-10% are adenomas which are true neoplasms
Inflammatory fibroid polyp
Adenoma contains proliferative dysplastic epithelium
and thereby has malignant potential
Can be sessile or pedunculated
 Gastric carcinoma
90-95% of malignant tumors of the stomach
Next in order are lymphoma (4%), carcinoids (3%)
and stromal tumors(2%)
Incidence varies widely being particularly high in
countries like Japan, Chile, China. .
M:F 2:1
 Three major factors are thought to affect the
genesis of gastric cancer
Environmental-
infection by H.pylori, Diet (lack of refrigration,
consumption of preserved , smoked and salted
foods , lack of fresh fruit), cigarette smoking
Host factors
chronic gastritis, infection by H. pylori ,partial
gastrectomy, gastric adenomas , Barrett esophagus
Genetic
blood type A, family history, familial gastric
carcinoma
Morphology of Gastric carcinoma
Location
Pylorus and antrum (50-60%), cardia 25%, remaining in
the body and fundus
Lesser curvature is involved in about 40% and greater
curvature in 12%
Gastric carcinoma can be classified on the basis of
Depth of invasion
Macroscopic growth pattern
Histologic subtype
Gastric carcinoma
Depth of invasion
Early carcinomas lesion confined to mucosa and
submucosa
Advanced carcinomas that has extended below
the submucosa into the muscular wall
Macroscopic growth pattern
Exophytic
Flat or depressed
Excavated
Early Carcinoma

Advanced carcinoma
Morphologic types of
Carcinoma Stomach

Fungating

Ulcerating

Diffuse
Gastric Ca: Linitis plastica
Gastric carcinoma
Histologic subtype
Intestinal type
composed of neoplastic intestinal glands resembling
those of colonic adenocarcinoma
Diffuse type
composed of gastric type mucus cells which do not
form glands but permeate the wall as scattered
individual cells or clusters
These cells contain abundant mucin and form signet
ring configuration
Gastric carcinoma ..ctd
For obscure reasons gastric carcinomas frequently
metastasize to supraclavicular LN (Virchows node)
A notable site of visceral metastasis is to one or both
ovaries - Krukenberg tumor
Sister Mary Joseph nodule: The tumor can also
metastasize to the periumblical region
Clinical feature
Wt. loss , abdominal pain ,anorexia ,vomiting ,
altered bowel habit , anemia , hemorrhage ,
dysphagia . .
Less common gastric tumors
Gastric lymphoma
represent 5% of all gastric malignancies
related to H. Pylori
GI neuroendocrine cell tumors ( carcinoids)
Mesenchymal tumors
Leiomyoma , leiomyosarcoma , . .
GI stromal tumors (GIST)
Small and Large intestines
Congenital anomalies
Duplication
Malrotation
Omphalocele failure of formation of
abdominal musculature with herniation of
abdominal contents into a membraneous sac
Gastroschisis portion of the abdominal wall
fails to form altogether with extrusion of the
intestine
Atresia and stenosis
Meckel Diverticulum
- failure of the vitelline duct ,which connects the lumen
of the developing gut to the Yolk sac produce a Meckel
Diverticulum
- is a true diverticulum and lies usually 85cm from the
ileocecal valve
- heterotopic rests of gastric mucosa (or pancreatic
tissue) are found in about 50%
- occur in 2% of the population but most remain
asymptomatic
- when peptic ulceration occurs in the small intestinal
mucosa adjacent to the gastric mucosa bleeding occur
A
C
Congenital aganglionic Megacolon
(Hirschsprung disease)
Characterized by the absence of ganglionic
cells in large bowel leading to functional
obstruction and colonic dilation proximal to
the affected segment
Histologically there is absence of ganglionic
cells in the muscle wall(Auerbach plexus) and
submucosa (Meissner plexus)
 Most cases involve the rectum and sigmoid only

Proximal to the aganglionic segment , the colon

undergoes progressive dilation and hypertrophy

Dilation may achieve large sizes (15-20cm)

Clinical features

M:F 4:1

10% occur in children with Down syndrome

 Usually manifest in the immediate neonatal
period by failure to pass meconium followed
by obstructive constipation

Acquired magacolon can occur at any age and

results from Chagas disease, organic
obstruction of bowel , toxic megacolon
complicating UC or CD, functional
psychosomatic disorder
Enterocolitis

Diarrhoea and dysentry

Diarrhoea an increase in stool mass, stool

frequency or stool fluidity is perceived as
diarrhoea by most patients

The principal mechanisms of diarrhoea are

Secretory diarroea intestinal fluid secretion

Osmotic diarrhoea osmotic forces exerted by

luminal solutes leads to diarrhoea

 Exudative diseases mucosal destruction leads

to output of purulent bloody stool

Malabsorption improper absorption of gut

nutrients produce voluminous bulky stool

Deranged motility improper gut

neuromuscular function may produce

increased stool
Infectious enterocolitis
Viral gastroenteritis
Rota virus is the most common cause

Clinically has incubation period of about 2

days followed by vomiting and diarrhoea for
days
 Mostly in children

Norwalk virus cause the majority of cases of

non-bacterial food-borne epidemic
gastroenteritis in older children and adults

It has incubation period of 1-2days followed

by 12-60hrs of nausea vomiting watery
diarrhoea and abdominal pain
Bacterial enterocolitis
Pathogenetic mechanisms
Ingestion of preformed toxin present in contaminated

food (S.aureus, Vibrios, C.perfringens)

Infection by toxigenic organisms which proliferate

within the gut lumen and elaborate an enterotoxin

Infection by enteroinvasive organisms which

proliferate invade and destroy mucosal epithelial cells

 In case of infection key bacterial properties are
1. Ability to adhere and replicate
2. Ability to elaborate enterotoxins
3. The capacity to invade
Adherence is usually mediated by adhesins
Enterotoxins are polypeptides that cause
diarroea e.g. V.cholerae
Invasion e.g. enteroinvasive E.coli and shigella
possess a virulence plasmid that confers
capacity for invasion of the epithelium
Morphology
Most bacterial infections exhibit a general non
specific pattern of damage to the surface
epithelium

Decrease epithelial cell maturation

Increased mitotic rate (regenerative changes)

Hyperemia and edema of lamina propria

Neutrophilic infiltration
Clinical features
Ingestion of preformed bacterial toxins
symptoms develop within hours ,explosive
diarrhoea, acute abdominal distress . . .

Infection with enteric pathogens : after incubation

period of several hours to days diarrhoea ,
dehydration . ..

Insideous infection : e.g. yersinia and

mycobacterium
Antibiotic associated colitis
(pseudomembraneous colitis)
Acute colitis characterized by formation of an
adherent inflammatory exudate
(pseudomembrane) overlying site of mucosal
injury
Usually caused by two protein exotoxins
(A&B) of C.difficile ,a normal gut comensal
Disease occurs in patients with a background
of chronic enteric disease after a course of
broad spectrum antibiotic therapy
A, Gross photograph showing plaques of yellow fibrin and
inflammatory debris adherent to a reddened colonic mucosa.
B, Low-power micrograph showing superficial mucosal erosion,
an adherent pseudomembrane of fibrin, and inflammatory debris.
 Thought to result due to the flourish of toxin
forming strains after alteration of normal
intestinal floura
Parasites and protozoa
E.histolytica
G.lamblia
AIDS
-diarrheal illness occur in 30-60% of HIV
infected pts
-most cases are due to microorganisms
-AIDS enteropathy is thought to represent
some proportion
Malabsorption syndrome
Malabsorption is characterized by suboptimal
absorption of fats, fat-soluble and other
vitamins ,proteins ,carbohydrates
,electrolytes minerals and water
Results from disturbance of
Intraluminal digestion
Terminal digestion
Transepithelial transport
Consequences of malabsorption affect many
organ systems
Alimentary tract diarrhea , flatus, abdominal
pain, weight loss. . .
Hematopoetic system anemia from
,pyridoxine ,folate, VB12 ,deficiency ,
bleeding from v.k deficiency
Musculoekeletal system osteopenia and
tetany from calcium, Mg . . .deficiency
Epidermis purpura and petechiae from
vitamin K deficiency, edema from protein ,
dermatitis from vit. A, Zink deficiency
 Nervous system peripheral neuropathy
from vitamin A and B12 deficiency
Features
Steatorrhea passage of abnormally bulky,
frothy , greasy stool is a prominent feature
Other features are wt loss, abdominal
distension, borborygmi
Celiac sprue
Rare chronic disease
Characteristic mucosal lesion of the small
intestine and impaired absorption which
improves on withdrawal of wheat and related
grains
A.k.a. glutein sensitive enteropathy , non-
tropical sprue
Mucosa appears flat or scalloped or may be
visually normal
 Biopsy show diffuse enteritis with marked
atrophy or total loss of villi
Clinical manifestations include diarrhea ,
flatulence, wt. loss and fatigue
There is a long term risk of malignant disease
(more than half of these are intestinal
lymphomas)
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. B, A normal
mucosal biopsy.
Tropical Sprue(post infectious sprue)
Occurs almost exclusively in people living in
or visiting the tropics

May occur in endemic form and epidemic

outbreaks have occurred

No specific causal agent has been associated

but bacterial overgrowth by enterotoxigenic
organisms(e.g. E. coli and Hemophylus has
been implicated)
 Intestinal changes are extremely variable
ranging from near normal to severe diffuse
enteritis

Clinically malabsorption becomes apparent

within days or a week of an acute enteric
infection in visistors to endemic locales

Mainstay of treatment is broadspectrum

antibiotics
Whipple isease
Systemic disease which may involve any
organ of the body but principally affects the
intestine ,CNS and joints

Cause is gram-positive actinomycete

Tropheryma Whippeli

Hallmark of Whipple disease is a small

intestinal mucosa laden with distended
macrophages in the lamina propria
 The macrophages contain PAS positive
granule and rod-shaped bacilli by
electronmicroscopy

More common in whites in their thirties to

fourties

M:F 10:1

Usually present with diarrhea and wt loss

sometimes of years duration
Whipple disease. A, Note foamy macrophages in the lamina
propria. B, PAS stain showing the positive granules in the
foamy macrophages
Disaccharidase(Lactase ) deficiency

The acquired one is more common

Incomplete breakdown of the disacchride

lactose into glucose and galactose leads to
osmotic diarrhea
IDIOPATHIC INFLAMMATORY BOWEL DISEASE
Crohn disease and ulcerative colitis
A set of chronic inflammatory conditions
resulting from inappropriate and persistent
activations of mucosal immune system, driven
by the presence of normal intraluminal flora.
Both are chronic, relapsing inflammatory
disorders of obscure origin.
IDIOPATHIC INFLAMMATORY BOWEL DISEASE
Crohn disease and ulcerative colitis
CD is an autoimmune disease that can affect any
portion of the GIT but often involves the distal
small intestine and colon.
UC is a chronic inflammatory disorder limited to
the colon and rectum.
Both exhibit extraintestinal inflammatory
manifestations.
IDIOPATHIC INFLAMMATORY BOWEL DISEASE
Crohn disease and ulcerative colitis
Etiology and pathogenesis
Two basic pathogenic abnormalities
1. Strong immune response against normal flora
2. Defects in epithelial barrier function
Genetic predisposition
Infections cause
- Incriminated agents include Chlamydia, atypical
bacteria and mycobacteria
Abnormal Host immunreactivity
Inflammation as the final common pathway
CROHN DISEASE
a.k.a terminal ileitis ,regional enteritis ,
granulomatous colitis
- When fully developed it is characterized
pathologically by
1. sharply delimited and typically transmural
involvement of the bowel by an inflammatory
process with mucosal damage
2. the presence of non caseating granuloma
3. fissuring with formation of fistulas
Epidemiology
occurs at any age, but peak is teens and
twenties with a minor peak in fifties and sixties
Females are slightly more affected
Smoking is a strong exogenous risk factor
Morphology
Small intestine alone -40%
Small intestine + colon -30%
Colon alone -30%
 may involve duodenum, stomach, esophagus
and even mouth but very rarely

the intestinal wall is rubbery and thick

which is the result of edema inflammation
fibrosis and hypertrophy

classic feature is the sharp demarcation of

diseased bowel segments from adjacent
uninvolved bowel
 When multiple bowel segments are involved the
intervening bowel is essentially normal ( skip
lesions) and the mucosa acquires a coarsely
textured cobblestone appearance

linear ulcers develop

narrow fissures develop between the folds of

the mucosa often penetrating deeply leading to
fistula or sinus tract formation
The characteristic histologic changes include :-
Mucosal inflammation

Chronic mucosal damage

Ulceration

Trans mural inflammation affecting all layers

Non caseating granulomas

Clinical features
Variable but disease usually begins with
intermittent attacks of mild diarrhea, fever
and abdominal pain

In some patients the onset is more abrupt

with acute right lower quadrant pain, fever
and diarrhea
Crohn disease of the ileum showing narrowing of the lumen, bowel wall
thickening, serosal extension of mesenteric fat ("creeping fat"), and linear
ulceration of the mucosal surface (arrowheads).
CD of the colon showing a
deep fissure extending into the
muscle wall, a second, shallow
ulcer (upper right), and relative
preservation of the intervening
mucosa
Non-caseating granuloma
 Complications include strictures, fistulas
malabsorption.
Extra intestinal manifestations include
migratory poly arthritis, sacroilitis, ankylosing
spondylitis, erythema nodosum, uveitis.
There is an increased incidence of cancer of the
Gl tract ,but is considerably less than ulcerative
colitis.
ULCERATIVE COLITIS
An ulceroinflammatory disease limited to the
colon and affecting only the mucosa and
submucosa except in the most severe cases
incidence is slightly greater than Crohn disease
onset peaks between 20 and 25 years
UC involves the rectum and extends proximally
in a retrograde fashion to involve the entire colon
in the more severe cases
 It is a disease of continuity and skip lesions like
crohn disease are not found

In10% of patients the distal ileum may develop

mild mucosal inflammation ( backwash ileitis)

Isolated islands of regenerating mucosa bulge

upward to create pseudopolyps

Mural thickening does not occur in UC and the

serosal surface is usually completely normal
Clinical features
present as a relapsing disorder marked by
attacks of bloody mucoid diarrhea that may
persist for days, weeks or months, then subside
& recur

abdominal pain and in minority constipation

the most feared long term complication of UC is

cancer
Comparison of the distribution patterns of Crohn disease and ulcerative
colitis, and the different conformations of the ulcers and wall thickenings
Hemorrhoids
variceal dilations of the anal and perianal
venous plexuses
common problems which develop secondary
to persistently elevated venous pressure
within the hemorrhoidal plexus
most frequent predisposing influences are
constipation with straining at stool and the
venous stasis of pregnancy
much more importantly but rarely develop as
result of portal hypertension
 they may develop in the inferior
hemorrhoidal plexus located below anorectal
line external hemorrhoid
they may also develop in the superior
hemorroial plexus and produce internal
hemorroids
commonly both are affected
secondary effects include thrombosis,
ulceration, fissure formation and infarction
with strangulation
INTESTINAL OBSTRUCTION
Although any part of the gut may be
involved, because of its narrow lumen, the
small bowel is most commonly affected. Four
entities-hernias, intestinal adhesions,
intussusception, and volvulus-account for at
least 80% of the cases
c/m :- abdominal distension, abdominal pain,
vomiting, failure to pass feces and flatus..

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
Other causes of obstruction
Inflammatory strictures
Obstructive gallstones, fecalith, foreign body
Congenital strictures, atresias
Bands
Imperforate anus
Pseudo-obstruction
Paralytic ileus
Vascular-bowel in farction
Myopathies and neuropathies ( eg
Hirschsprung)
Toxic Megacolon
Hernias

A weakness or defect in the wall of the

peritoneal cavity, may permit protrusion of a
pouch like, serosa-lined sac of peritoneum,
called a hernial sac
The usual sites are anteriorly at the inguinal and
femoral canals, at the umbilicus, and in
surgical scars.
Rarely retroperitoneal herniation- ligament of
Treitz
 segments of viscera frequently intrude and
become trapped in them (external herniation)
most frequent intruders are small bowel loops,
but portions of omentum or large bowel also
may become trapped.
It may lead to permanent
trapping(incarceration) and infarction of the
trapped segment(strangulation)
 Surgical procedures, infection, and even
endometriosis often cause localized or general
peritoneal inflammation (peritonitis). With
healing, adhesions may develop between bowel
segments or the abdominal wall and the
operative site. These fibrous bridges can create
closed loops through which the intestines may
slide and become trapped (internal herniation).
The sequence of events is much the same as with
external hernias.
 Intussusception denotes telescoping of a
proximal segment of bowel into the immediately
distal segment. In children, intussusception
sometimes occurs without apparent anatomic
basis, perhaps related to excessive peristaltic
activity. In adults, such telescoping often points
to an intraluminal mass (e.g., tumor) that
becomes trapped by a peristaltic wave and pulls
its point of attachment along with it into the
distal segment.
 Not only does intestinal obstruction ensue,
but the vascular supply may be so
compromised as to cause infarction of the
trapped segment.
 Volvulus refers to twisting of a loop of bowel
or other structure (e.g., ovary) about its base
of attachment, constricting the venous
outflow and sometimes the arterial supply as
well. Volvulus affects the small bowel most
often and rarely the redundant sigmoid.
Intestinal obstruction and infarction may
follow.