 Hiatal hernia:

 herniation of the stomach through an enlarged

esophageal hiatus in the diaphragm and reflux of
gastric contents
 Clinical signs of reflux -heartburn and
regurgitation
 Esophageal injury caused by the regugitation of
gastric contents into the lower esophagus.
 Decrease in the pressure of the lower esophageal
sphincter (alcohol, fatty foods, smoking, pregnancy,
estrogen therapy etc.)
 Prolonged gastric intubation
 Ingestion of irritants: alcohol, acids or alkalis, hot
fluids, smoking
 Cytotoxic anticancer therapy
 Infections: bacterial, viral (HSV, cytomegalovirus),
fungal (candidiasis, aspergillosis)
 Uremia
 Radiation
 Systemic conditions; scleroderma (CREST
syndrome), dermatologic diseases: pemphigoid
 Complication of long-standing gastroesophageal
reflux
 Distal squamous mucosa is replaced by metaplastic
columnar epithelium (gastric or intestinal type)
 Dysplasia in epithelial layer
 Complications: ulceration with bleeding, strictures,
and adenocarcinoma
 In lower 1/3 part (in association with Barrett’s
esophagus)
 25% of all esophageal cancers
 5-year survival rate 15%
 Mostly men >40
Acute mucosal inflammatory process of transient
nature. May be accompanied by hemmorhage or
erosions.
 Heavy use of NSAIDs
 Alcohol, smoking
 Cancer chemotherapeutic drugs
 Uremia
 Systemic infections (salmonellosis)
 Severe stress (burns, trauma, surgery)
 Ischemia and schock
 Acids, alkali
 Irradiation, mechanical trauma
Chronic mucosal inflammatory changes with
nonspecific, „dyspeptic” symptoms or
asymptomatic
 Chronic infections ( Helicobacter pylori)
 Immunologic (pernicious anemia)
 Alcohol, smoking
 Postsurgical (gastrectomy)
 Long use of NSAIDs
 Motor or mechanical obstruction
 Reflux of duodenal contents
 Radiation, amyloidosis, uremia
 Diffuse inflammation of mucosa of body and
fundus
 Autoantibodies to parietal cells and intrinsic
factor (pernicious anemia – decreased B 12)
 Destruction of glands and atrophy of mucosa
loss of acid production
 Association with Hashimoto thyroiditis and
Addison’s disease
 Increased risk of cancer
 Inflammatory infiltrate of lymphocytes and plasma
cells within the lamina propria
 Activity: presence of neutrophils within the
epithelial glandular layer
 Atrophy: loss in glandular structures and flattening
of the mucosa
 Metaplasia: presence of metaplastic columnar cells
and goblet cells of intestinal phenotype that
replace parts of gastric mucosa
 Dysplasia: cytologic alterations within the glandular
epithelium that may lead to in situ carcinoma
 Classification Sidney/Houston –
samples taken from 5 standarized places
(comparison between antrum and corpus)
 grading (0/+/++/+++) of 5 features:
1)„inflammation” (mononuclear infiltrate)
2) activity,
3) atrophy of glands
4) intestinal metaplasia
5) H. pylori
 S – shaped gram – negative bacteria
measuring approximately 3.5x0.5μm
 Present in high percentage of patients
 Chronic gastritis of antrum and corpus

 Acute and chronic gastritis, peptic ulcer,

carcinoma, lymphoma
 Chronic, most often solitary lesions that occur in
any portion of GT
 Distal stomach (lesser curvature near the antrum),
proximal duodenum (anterior wall), Barrett’s
esophagus, Meckel diverticulum
 Spice food, alcohol, coffee, NSAIDs,
cortycosteroids
 Men, middle aged and elderly, blood group O
(duodenal ulcer), high circulating level of
pepsinogen I (duodenal ulcer), stress, alcoholic
cirrhosis
 Round to oval, the edges are sharply punched out,
the base is gray may exhibit clotted blood and
eroded blood vessels
 On gross examination may be difficult to
distinguish chronic peptic ulcer from ulcerating
gastric carcinoma. The biopsy specimens must be
taken from the edges of any gastric ulcer
 Microscopically; superficial zone of fibrino-
purulent exudate, necrotic tissue, granulation
tissue, fibrosis in the bed of the ulcer
 Hemorrhage
 Perforation =peritonitis
 Penetration into the pancreas, liver, greater
omentum (High mortality)
 Pyloric obstruction, scaring
 Malignant transformation of gastric ulcer
 Development of combined ulcers
 Multiple „stress” ulcers
 Shock, extensive burns, severe trauma
(Curling’s ulcers)
 Increase of intracranial pressure (Cushing’s
ulcers)
 Multiple, small< 1 cm
 Carcinomas 90-95 % of all malignant tumors
 Adenomas 10-15% of all polypoid lesions
 Lymphoma 5% of all malignant lesions
 Stromal tumors
 Neuroendocrine tumors
 90-95% of all malignant tumors of the
stomach
 High incidence in Japan, South America, lower
in Europe,in USA incidence decreasing
 Early gastric carcinoma: tumor defined to
mucosa and submucosa
 Linitis plastica: diffuse infiltration of
carcinoma with rigidity of stomach walls and
desmoplasia („leather bottle”)
 Krukenberg tumor – metastasis to ovary,
mostly by peritoneum, bilateral, desmoplastic
 Diet: nitrites from nitrates (preservatives in
meats), high starch content, smoked meat,
salted pickled vegetables,fried potatos, lack of
fresh fruits and vegetables
 Host factors: chronic atrophic gastritis with
extensive intestinal metaplasia, H. Pylori,
partial gastrectomy, gastric adenomas, chronic
ulcer, ulcer scar
 Genetic: blood group A, some racial groups
(blacks, Native Americans)
feature intestinal diffuse
gross Polypoid Ulcerative,
fungating infiltrating
microscopic Well Poorly
differentiated, differentiated,
gland-foration signet–ring cells

Mucin Limited to extensive

production glands
 Lymphoma: Marginal B – cell lymphoma MALT
lymphoma

 Carcinoid (neuroendocrine tumor): rare

infiltrating tumor with metastasis

 GIST: gastrointestinal stromal tumor