Transcript PATHOLOGY OF THE GASTROINTESTINAL TRACT

PATHOLOGY OF THE
GASTROINTESTINAL
TRACT
Ismail Matalka ,MRCPath
Department of Pathology
Jordan University of Science &
Technology
Irbid - Jordan
THE ALIMENTARY (DIGESTIVE) SYSTEM
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Oral cavity (including salivary glands)
Esophagus
Stomach
Small intestine
Colon
Appendix
Liver
Biliary tract
Pancreas
ANATOMY & HISTOLOGY OF
THE ORAL CAVITY
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Anatomy
– Orifice to digestive & respiratory tracts
– Lips, buccal mucosa, tongue, soft & hard
palate
– Teeth & periodontal tissue
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Histology
– Lined by nonkeratinized squamous epithelium
– Minor salivary glands & sebaceous glands in
lips & buccal mucosa
– Lymphoid tissue
DISEASES OF THE
ORAL CAVITY
Congenital anomalies, e.g. cleft lip & cleft
palate, macroglossia, branchial cleft cysts
 Inflammations: Aphthous ulcers, Herpes
stomatitis, Candidiasis ...
 Pre-malignant lesions: leukoplakia,
erythroplasia
 Tumors: Squamous cell carcinoma
 Salivary gland inflammations
 Salivary gland tumors
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ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY
APHTHOUS ULCERS (CANKER SORES)
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Extremely common, up to 40% of population
Single or multiple shallow fibrin-coated
painful ulcers of oral mucosa, usually <1 cm,
may coalesce
Unknown etiology (?viruses, hypersensitivity)
Triggered by stress, fever, menstruation,
pregnancy, certain foods; may be familial
May be associated with inflammatory bowel
disease & Behcet syndrome
Self limiting in a few weeks
ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY
HERPETIC STOMATITIS
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HSV I>>II; person to person transmission
After primary infection it is usually asymptomatic
but virus will persist in ganglia in dormant state
Reactivation: fever, sun or cold exposure, URTI, ..
Herpes labialis: cold sores or fever blisters
»Vesicular lesion, edema, degeneration of
epidermis
»Tzanck test: intranuclear inclusions & giant
cells
In immunocompromised: virulent dissiminated
infection: gingivostomatitis, encephalitis ...
ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY
FUNGAL INFECTIONS
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Candida albicans is part of normal flora (30-40%)
Oral candidiasis (moniliasis, thrush): common in:
»Diabetes mellitus
»Anemia
»Antibiotic or glucocorticoid Rx
»Immunodeficiencies & debilitating diseases
Soft white cheese-like plaques
Minimal- marked ulceration with inflammatory
exudate and fungal microorganisms
(pseudohyphae)
In vulnerable patients, disease may spread
ULCERATIVE & INFLAMMATORY LESIONS OF THE ORAL CAVITY
ACQUIRED IMMUNODEFICIENCY
SYNDROME (AIDS)
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HIV infection is associated with different lesions
in the oral cavity
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Candidiasis
Herpetic vesicles
Other oppurtunistic infections
Kaposi’s sarcoma: multifocal vascular tumor, present
in 25% of AIDS patients; HSV8
– Hairy leukoplakia: white patches with hairy surface:
» caused by EBV
» rare, but seen mainly in AIDS
» histology shows acanthosis, hyperkeratosis
PRE-MALIGNANT LESIONS OF THE ORAL CAVITY
LEUKOPLAKIA
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A clinical term used to describe a whitish welldefined mucosal patch or plaque caused by
epidermal thickening or hyperkeratosis
Older men; associated with tobacco, chronic
friction (dentures), alcohol & irritant foods; HPV
link
Microscopically, they vary from hyperkeratosis
without dysplasia to mild to severe dysplasia or
CIS
Only histologic examination distinguishes these
changes
3-6% transform into squamous cell carcinoma
PRE-MALIGNANT LESIONS OF THE ORAL CAVITY
ERYTHROPLAKIA
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Red velvety areas which may remain level with or
slightly depressed in relation to surrounding
mucosa
Greater tendency for epithelial cell atypia and
marked dysplasia than leukoplakia
Hyperkeratosis is less frequent; red color is due
to intense inflammation and vascular congestion
Higher risk (50%) of malignant transformation (the
risk corresponds to the degree of atypia)
Erythroleukoplakia: speckled leukoplakia; mixture
of erythroplasia and leukoplakia
MALIGNANT TUMORS OF THE ORAL CAVITY
SQUAMOUS CELL CARCINOMA
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Represent 90% of oral cavity malignancies (3% of all
malignant tumors); M>F
Lip>ant. floor of mouth>tongue>palate
Etiology: smoking, smokeless tobacco, protracted
irritation (e.g. dentures), chronic dental & oral infections,
sunlight, heat, alcohol, atrophy, HPV
Plaque, mucosal thickening or ulcer
Invasive &/or in situ carcinoma; well differentiated to
undifferentiated
Spread to local LN (submandibular, high jugular…)
Px: depends on location (e.g. lip), grade, stage
50% lead to death in 5 years ;overall 5 YS without L.N mets
is 40% after chemo & radio ;and 20% with L.N mets
DISEASES OF THE
SALIVARY GLANDS
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Inflammation
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Viral sialadenitis
Bacterial sialadenitis
Autoimmune sialadenitis
Sialolithiasis
Tumors
– Benign
» Pleomorhpic adnoma (mixed tumor)
» Warthin’s tumor
– Malignant
» Carcinoma ex-pleomorphic adenoma
» Mucoepidermoid carcinoma
» Adenoid cystic carcinoma
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Mickulicz’s syndrome
INFLAMMATIONS OF THE SALIVARY GLANDS
VIRAL SIALADENITIS
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Most common cause is mumps, which usually
affects the parotid gland (epidemic parotitis)
70% bilateral parotid; 20% unilateral; 10% others
Mumps is an acute contagious childhood disease
Paramyxovirus, acquired by respiratory droplets
Usually self limited, but may lead to
complications, which are commoner in adults:
– Pancreatitis
– Orchitis: usually unilateral; rarely leads to
infertility
– CNS inflammation: rare but serious
INFLAMMATIONS OF THE SALIVARY GLANDS
AUTOIMMUNE SIALADENITIS
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Sjogren’s syndrome: inflammation of salivary
glands & mucus-secreting glands of nasal
mucosa (resulting in dry mouth or xerostomia)
and lacrimal glands (resulting in dry eyes or
keratoconjunctivitis sicca)
90% are females; parotid enlargment in 50%
May be primary or secondary (60%) to othe
autoimmune disease (RA, SLE, polymyositis ..)
Lymphocytic infiltration & fibrosis
RF, ANAs +/-; anti-ribonucleoprotein SS-A & B
Abs
High risk to develop lymphomas
INFLAMMATIONS OF THE SALIVARY GLANDS
SIALOLITHIASIS & NONSPECIFIC
SIALADENITIS
Bacterial
 Secondary to ductal obstruction by stones
(sialolithiasis) in major excretory duct
 Usually unilateral
 Pathogenesis: impacted food debris &
edema around orifice following injury
 Ductal dilatation, periductal inflammation,
secondary bacterial invasion & suppuration
 Predisposing factors: Hx of major surgery,
dehydration, long-term phenothiazines Rx
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SALIVERAY GLANDS
TUMORS
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Relatively uncommon; 2% of tumors in humans
80% of tumors occur in parotid gland
Equal M:F ratio; all ages [6th - 7th decade]
Most of these neoplasms are benign: 70-80% of
parotid tumors and only 50% of submaxillary
tumors
c/o: mass at angle of jaw
Wide histologic variations
– Benign: Pleomorphic adenoma, Warthin’s
tumor
– Malignant: Carcinoma ex-pleomorphic
adenoma, mucoepidermoid carcinoma, adenoid
cystic carcinoma
TUMORS OF THE SALIVARY GLANDS
PLEOMORPHIC ADENOMA
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aka: mixed tumor: Most common tumor (6580%) of the salivary glands
Slowly growing well-demarcated, mostly
arising from superficial parotid
Pathology: heterogeneous histology with
epithelial elements, myxoid stroma, often
containing chondroid foci or, rarely, bone
Px: recurrence after surgery: 10%
Malignant transformation: 15% in parotid, 40%
in submandibular gland
TUMORS OF THE SALIVARY GLANDS
WARTHIN’S TUMOR
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aka: Papillary cystadenoma lymphomatosum
Benign slowly growing tumors
5-10% of all parotid tumors; extremely rare in
other salivery glands
Pathology: composed of cystic spaces lined
by tall columnar cells overlying abundant
lymphoid tissue
Histogenesis: vestigial embryonic remnnants
of branchial cleft origin?
Rx: cured by surgical excision
PATHOLOGY OF THE SALIVARY GLANDS
MICKULICZ’S SYNDROME
Combination of salivary and lacrimal
glands enlargement with xerostomia
 May be due to many causes:
– Sarcoidosis
– Leukemia/lymphoma
– Sjogren’s syndrome
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THE ALIMENTARY (DIGESTIVE) SYSTEM
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

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Oral cavity (including salivary glands)
Esophagus
Stomach
Small intestine
Colon
Appendix
Liver
Biliary tract
Pancreas
DISEASES OF
THE ESOPHAGUS
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Congenital anatomic disorders
– Agenesis, atresia, fistula, stenosis
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Acquired anatomic/motor disorders
– Stenosis, webs & rings, HH, achalasia, ...
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Inflammations
– Reflux esophagitis
Barrett’s esophagus
 Vascular diseases
 Tumors
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CLINICAL FEATURES OF
DISEASES OF THE ESOPHAGUS
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Different esophageal diseases share a limited number
of symptoms:
– Dysphagia: difficulty in swallowing
» deranged esophageal motor function
» narrowing or obstruction of lumen
– Heartburn: retrosternal burning pain
» regurgitation of gastric contents
– Hematemesis: vomiting of blood
– Melena: blood in stools
» severe inflammation, ulceration or laceration
– Respiratory symptoms: dyspnea, cough,..
» aspiration
PATHOLOGY OF THE ESOPHAGUS
CONGENITAL ANATOMIC DISORDERS
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Present at birth with vomiting, aspiration
(pneumonia, asphyxia), gastric distention
Agenesis: absence of esophagus. Very rare
Atresia: failure of development of a segment of
esophagus, which is replaced by a thin noncanalized cord (absence of lumen) with formation
of upper & lower pouches; associated with
tracheo-esophageal fistula
Stenosis: developmental defect resulting in partial
obstruction or narrowing of the esophageal lumen
Rx: Urgent medical & surgical intervention
PATHOLOGY OF THE ESOPHAGUS
ACQUIRED ANATOMIC DISORDERS
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Stenosis : caustic strictures ,post-surgical ,inflammatory,
tumours , autoimmune diseases ( Scleroderma ) .
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Webs & Rings : Mucosal webs or mucosal and submucosal
concentric ring partially occluding the esophagus .
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Diverticula : outpouching of the esophageal wall
ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUS
HIATAL HERNIA
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Protrusion of a dilated sac-like segment of
stomach above the diaphragm
Separation of the diaphragmatic crura
Incidence: 1-20% of adults; increase with age
Mostly asymptomatic
c/o heartburn & regurgitation of gastric juices in
9% due to LES incompetence; related to position;
symptoms are accentuated by positions favoring
reflux
Patients with severe reflux esophagitis usually
have HH; however, HH & reflux are not the same
condition
TYPES OF
HIATAL HERNIA
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2 anatomic patterns:
– Sliding (axial): 95% of cases; bell-shaped dilation; due
to congenital short esophagus, strictures, spasm or
long-standing fibrous scarring of esophagus, resulting
in traction on stomach
– paraesophageal (non-axial or rolling): segement of
cardiac stomach dissects alongside esophagus
through a defect. May follow traumatic rupture of
diaphragm; may strangulate and infarct
ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUS
ACHALASIA
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Failure to relax, i.e., incomplete relaxation of LES
in response to swallowing, producing functional
obstruction & dilation of more proximal
esophagus
c/o progressive dysphagia to liquids and solid
food, nocturnal regurgitation & aspiration of
undigested food, aspiration pneumonia
Abnormal manometric studies: aperistalsis, partial
relaxation of LES, & increased basal tone of LES
Pathology: deranged innervation of LES; absent
myenteric ganglia in the body of esophagus;
normal, hypertrophic , or thining of muscles;
associated mucosal inflammation, ulcer or fibrosis
TYPES OF
ACHALASIA
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Two main types:
– Primary (sporadic): Commoner. Unknown cause
? Autoimmune. ? Previous viral infection.
– Secondary:
» Chaga’s disease: Tryponosoma cruzi infection causing
destruction of myenteric plexus ganglion cells in the GIT &
ureter; megaduodenum, megacolon, megaureter
» Diabetes (Autonomic neuropathy); vagus nerve injury ..
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Esophageal squamous cell carcinoma in 5%
usually in younger age than in patients without
this disease
ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUS
LACERATIONS
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aka: Mallory-Weiss syndrome
Longitudinal tears at the esophago-gastric
junction
Encountered in alcoholics, after bout of severe
retching or vomiting
Pathogenesis: inadequate relaxation of LES
muscle during vomiting
May occur in patients without hx of vomiting
HH is found in 75% of patients with MWS
Linear irregular lacerations, few mm-cm in length
Involve mucosa or deeply penetrate & perforate
wall
5-10% of all cases of massive hemetemesis;
however, the majority do not cause profuse
bleeding
VASCULAR LESIONS OF THE ESOPHAGUS
VARICES
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Due to portal hypertension, which leads to
formation of portal-systemic collateral bypass
channels
Collateral veins will develop in the region of lower
esophagus when portal flow is diverted through
the coronary veins of stomach into the plexus of
esophageal submucosal veins into azygous veins
Most common cause of portal hypertension is
liver cirrhosis
Rare causes: portal vein thrombosis, hepatic vein
thrombosis (Budd-Chiari syndrome),
pylephlebitis, tumor compression or invasion into
major portal radicals
VASCULAR LESIONS OF THE ESOPHAGUS
ESOPHAGEAL VARICES
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Tortuous dilated veins directly beneath mucosa
or in periesophageal tissue. Overlying mucosa
may be normal or eroded & inflammed; +/thrombosis
Asymptomatic until they rupture when massive
hemetemesis results; rupture may be
spontaneous or secondary to vomiting;
hemorrhage rarely subsides spontaneously; 40%
die after 1st episode
70% of survivors will rebleed within 1 year;
mortality rate 40%
Develops in 2/3 of cirrhotic patients; accounts for
50% of deaths in liver cirrhosis
INFLAMMATIONS OF THE ESOPHAGUS
ESOPHAGITIS
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Caused by multiple factors:
– 1. Reflux of gastric contents (reflux esophagitis)
– 2. Ingestion of irritants (alcohol, corrosive acids,
alkali, excessive hot fluids like tea, heavy smoking)
– 3. Bacteremia & viremia with direct infection of
esophageal wall or contiguous structures (HSV,
CMV)
– 4. Fungal infections in immunocompromised
patients (Candidasis, mucormycosis, aspergillosis)
– 5. Systemic desquamative skin diseases
(pemphigoid)
– 6. Graft-versus-host disease
– 7. Radiation; cytotoxic therapy; uremia
INFLAMMATIONS OF THE ESOPHAGUS
REFLUX ESOPHAGITIS
Gastroesophageal Reflux Disease ( GORD )
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Reflux of gastric contents is commonest cause of
esophagitis
Pathogenesis:
– Frequent & protracted reflux due to incompetence of
LES & decreased efficacy of other antireflux
mechanisms (diaphragm, cardio-esophageal angle,
pressure on intraabdominal esophagus)
– Disordered esophageal motility: gastric contents
remains longer in contact with mucosa
– Elevated acid peptic levels of regurgitated fluid and
duodenal bile acids & lysolecithin
– Impaired reparative capacity of the esophageal mucosa
CLINICAL FEATURES OF
REFLUX ESOPHAGITIS
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Predisposing factors:
– Fat, chocolate, alcohol, smoking …
– Hiatal hernia
– Pregnancy
– Drugs
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Consequences of reflux:
– If occasional: no consequences
– It recurrent & persistent: inflammation,
ulceration, bleeding, stricture, Barrett’s
esophagus, dysplasia ..
PATHOLOGY OF
ESOPHAGITIS
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Pathologic findings:
– Depend on the cause, duration & severity
– Hyperemia, edema, wall thickening, pseudomembrane formation, necrosis & ulceration
– Fibrosis & stricture formation may follow
– Candidal esophagitis: gray-white inflammatory
pseudomembranes
– Viral esophagitis: intranuclear inclusions
– Reflux esophagitis: basal zone hyperplasia &
presence of intra-epithelial eosinophils &/or PMNs
PRE-MALIGNANT LESIONS OF THE ESOPHAGUS
BARRETT’S ESOPHAGUS
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Condition in which a gastric or intestinal type of
mucosa (i.e., metaplasia) lines the distal esophagus
above the LES
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Mostly acquired & in adults, but may be seen in
children, and rarely congenital in origin
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Complication of long-standing reflux
inflammation and ulceration of squamous mucosa
healing by re-epithelialization & ingrowth of
pluripotential stem cells which differentiate into
gastric or intestinal epithelium
CLINICAL FEATURES OF
BARRETT’S ESOPHAGUS
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Clinical symptoms:
– Dysphagia, retrosternal pain, hemetemesis, melena
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Secondary complications:
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Barrett’s ulcers
Strictures
Dysplasia
Adenocarcinoma: 8-10% of patients develop Ca
(patients with Barrett’s esophagus have 30-100X
higher risk than general population)
Barrett’s esophagus is the only recognized
precursor of esophageal adenocarcinoma
ESOPHAGEAL
TUMORS
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Benign tumors are rare: leiomyoma is the
most common, and is usually small,
asymptomatic and discovered incidentally
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Malignant tumors: Esophageal cancer is the
7th most common tumor in humans
– More common in males (M:F=3:1)
– Great variation in geograhic distribution
– Commonest types: Squamous cell carcinoma
and adenocarcinoma
TUMORS OF THE ESOPHAGUS
SQUAMOUS CELL CARCINOMA
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80-85% of esophageal cancers
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10% of all GIT cancers; higher contribution to mortality
(asymptomatic with late diagnosis)
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Patients: most patients are adults >50 yrs; M>F
– Higher incidence in certain countries (Iran, China..)
– Higher incidence in blacks than whites
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Etiology & pathogenesis: multifactorial with environmental
& dietary factors acting synergistically
RISK FACTORS FOR ESOPHAGEAL
SQUAMOUS CELL CARCINOMA
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Associated factors:
– 1) Dietary:
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Fungal contamination of food (Aspergillus)
High content of nitrites/nitrosamines
Deficiency of vitamins (A, C, riboflavin, thiamin, ..)
Deficiency of trace metals (zinc, molybdenum)
– 2) Esophageal disease: achalasia, reflux
esophagitis , strictures, Plummer-Vinson syndrome
– 3) Lifestyle: Alcohol & tobacco abuse
– 4) Racial or genetic predisposition: blacks; celiac
disease, Tylosis, ...
- 5) ? HPV in squamous cell carcinoma
- 6) p16/INK4 tumor supressor gene & EGF receptor
abnormalities. p53 mutations in 50% .
PATHOLOGY & CLINICAL FEATURES OF ESOPHAGEAL
SQUAMOUS CELL CARCINOMA
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Pathology:
– 50% in mid 1/3; 30% in lower 1/3; 20% in upper 1/3
– Starts as in situ lesion; thickening of mucosa
– Polypoid fungating (60%); ulcer (25%); diffuse
(15%)
– Grade: Most are well to moderately differentiated
– Stage: I (<5 cm), II (>5 cm; resectable LN), III (>10
cm; extension to adjacent tissue; inoperable); IV
(perforation; metastasis)
Clinical feature: symptoms are gradual & late;
include dysphagia, extreme weight loss, aspiration,
hemorrhage & sepsis
Rx: surgery & radiotherapy
Px: 70% die within 1 yr; 5 yrs survival 5-10%
TUMORS OF THE ESOPHAGUS
ADENOCARCINOMA
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5-10% of esophageal cancers; rising incidence
Middle or lower third; may extend to stomach
Vast majority arise from Barrett’s esophagus
Most are adults >40 yrs; M:F=5:1; v. rare in blacks
Mass or nodular elevation of mucosa; frequently
multicentric
Histologic types: intestinal, diffuse (signet cell) or
adenosquamous
Grade: most are moderately to poorly
differentiated
Stage: similar to squamous cell carcinoma
c/o: progressive dysphagia; long standing
symptoms
Barrett’s &Adenocarcinoma
Progression of low grade dysplasia is very
low
 Progression of high grade dysplasia is about
10% or more per year
 Overall risk is 30-fold to more than 100fold above normal
 P53 mutations
 Alterations in HER-2 and B-catenin
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DISEASES OF THE
STOMACH
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Congenital anomalies
– Diaphragmatic hernia & pyloric stenosis
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Inflammations
– Gastritis
– Acute erosions & ulcerations
– Peptic ulcer
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Tumors
– Polyps
– Adenocarcinoma
– Lymphoma
CONGENITAL ANOMALIES OF THE STOMACH
DIAPHRAGMATIC HERNIA
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Weakness or partial-to-total absence of a
region of the diaphragm, permitting abdominal
contents to herniate into the thorax
Defect does not involve the hiatal orifice (vs.
HH)
Hernia wall often be composed of peritoneum
& pleura
Portion of stomach, small intestine or liver
may protrude into hernial pouch
Symptoms depend on size: Asymptomatic to
acute respiratory distress in newborn
Rare
CONGENITAL ANOMALIES OF THE STOMACH
PYLORIC STENOSIS
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Familial condition (multifactorial inheritance)
Patients: 1:300-900 live births; M:F=3:1
Pathology: Hypertrophy & hyperplasia of circular
muscle of muscularis propria of pylorus;
narrowing of lumen leads to mucosal edema and
inflammation
c/o: regurgitation & persistent projectile vomiting
usually appear in 2nd-3rd week of life.
o/e: visible peristalsis & firm ovoid palpable mass
in abdomen
Rx: Pyloromyotomy
INFLAMMATIONS OF THE STOMACH
GASTRITIS
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Inflammation of the gastric mucosa
Overused term and underdiagnosed condition
Classification:
– 1) Acute gastritis
– 2) Chronic gastritis: most cases; prevalence
exceeds 50% in adults >50 yrs; usually
asymptomatic or cause few symptoms (upper
abdominal discomfort, nausea and vomiting)
» Helicobacter pylori associated gastritis: main
cause
» Autoimmune (atrophic) gastritis
» Hypertrophic gastritis (gastropathy)
» Granulomatous gastritis; eosinophilic gastritis
INFLAMMATIONS OF THE STOMACH
ACUTE GASTRITIS
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Acute mucosal inflammation, usually of transient
nature
May be accompanied by hemorrhage & erosions
Pathology: spectrum of severity: acute simple
gastritis, acute hemorrhagic gastritis, acute
erosive gastritis, acute stress gastritis &
perforated acute ulcer
Pathogenesis is poorly understood: multifactorial
due to loss of balance between:
– gastric acidity: stimulation of acid secretion by H+
back-diffusion, decreased bicarbonate buffer
production
– mucosal resistance: reduced mucosal blood flow,
mucosal cell disruption or direct epithelial damage
RISK FACTORS & CLINICAL FEATURES OF
ACUTE GASTRITIS
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Frequently associated with:
– Heavy use of NSAIDs, especially aspirin (up to
25%)
– Excessive alcohol consumption
– Heavy smoking
– Severe stress, e.g. trauma, burns, surgery
– Ischemia and shock; suicidal attempts with
acids/alkali
– Mechanical trauma (NG tube); post-gastrectomy
– Chemotherapeutic Rx; uremia; systemic infections
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Clinical features depend on severity:
asymptomatic or variable epigastric pain, nausea,
vomiting, hemetemesis (particularly alcoholics),
melena & fatal blood loss
INFLAMMATIONS OF THE STOMACH
CHRONIC HELICOBACTER PYLORI
GASTRITIS
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Commonest form of gastritis
H. pylori is a widespread noninvasive curved
gram -ve rod, which is present in gastric
mucosal surface of 50% of adults >50 yrs old
Infection may be acquired in childhood
Most infected individuals have gastritis but
are asymptomatic
Pathogenesis: Directly by bacterial enzymes
& toxins, and indirectly by recruitment of
PMNs which release noxious chemicals
PATHOLOGY & CLINICAL FEATURES OF
CHRONIC HELICOBACTER PYLORI GASTRITIS
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Appearance: Hyperemic edematous gastric
mucosa
Pathology:
– Lymphocytic & plasma cell infiltrate in lamina
propria, accompanied by PMNs inflammation
of neck region of mucosal pits (cryptitis and
crypt abscess)
– Proliferation of lymphoid tissue
Clinical features are variable
Rx: anti-acid drugs and antibiotics
Px: Relapses are associated with reappearance
of H. pylori; peptic ulcer disease; association
with gastric lymphoma
Table 17-2. 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
Clinical significance of Helicobacter
associated chronic gastritis
Most common cause of chronic gastritis and
peptic ulcer disease.
 Long term risk for gastric carcinoma (5 fold
risk). gastric atrophy, intestinal metaplasia,
and dysplasia role.
 Long term risk for gastric MALTlymphoma.
 ?Future possible prophylactic vaccines
