Chronic Gastritis.

Ulcer of Stomach
and Duodenum.
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Chronic
Gastritis.
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 Gastritis
 Is inflammation of the gastric mucosa
 Is clinical and morphological diagnosis
 Is a histological diagnosis nowadays, although
it can sometimes be recognised at endoscopy.
 Is not a single disease but rather a group of
disorders that all induce inflammatory changes
in the gastric mucosa but that differ in their
clinical features, histologic characteristics, and
causative mechanisms.

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 Sydney Classification
of Gastritis, 1990
TYPE
 Acute
 Chronic
 Uncommon forms

AETIOLOGY
 Infectious – H.Pylori (HP)
 Non-infectious (alcohol, NSAID,
autoimmune,…)
 Unknown factors 4
 Sydney Classification
of Gastritis, 1990
TOPOGRAPHY
 Antral-predominant
 Body-predomonant
 Pangastritis

MORPHOLOGY
 Inflammation (activity)
 Atrophy
 Intestinal metaplasia
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 Endoscopic classification
 Superficial gastritis
 Atrophic gastritis

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 Chronic Gastritis
 Type A (autoimmune) – 5-20%
 Type B (HP) – up to 80%
 Type AB
 Indeterminant type

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 Type A gastritis
 Rare
 Antibodies to parietal cells and to intrinsic
factor have been shown to be cytotoxic for
gastric mucosal cells
 Parietal cells are invariably destroyed
atrophy
 Parietal cells inability to secrete
hydrochloric acid achlorhydria
 It results in malabsorption of vitamin B12 8

anemia progression
 Type A gastritis
 Not young age
 No complains – during many years,
but:
 Nausea
 Epigastrium discomfort
 Appetite lowering
 Air belching
 Abdominal fullness or early satiety
 Tendency to diarrhea
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 Type A gastritis
 Inspection:
 - anemia signs (pallor of mucous and skin)
 - flatting of papillas (bald tongue)
 - diffusive epigastral abdominal tenderness
 Common blood test – normal or anemia
 Gastrinemia
 Endoscopic investigation:
 - pallor of mucous
 - hypotonic and hypokinetic stomach wall
 Histology:
 - parietal cells atrophy
 - intestinal metaplasia 10

 - minimal inflammation
 Type A gastritis
Treatment:
 Diet № 2
 Replaceable therapy
 – natural gastric juice
 - “acidin-pepsin”, “Pepsidil”,..
 Increasing of gastric secretion (Euphyllin)
 Vitamins (e.g. B12)

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 Type B gastritis
Synonyms:
 Antral-Predominant Gastritis
 HP Gastritis
 Environmental Gastritis

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Some factors influence the
virulence of HP

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 Type B gastritis
 Since young age
 Often – with duodenitis
 Increasing of gastric secretion

 Epigastrium discomfort and pain

 Reluctance to eat due to anticipate
discomfort
 Nausea
 Appetite lowering sometime
 Air belching sometime 16
 Type B gastritis
 Inspection:
 - tongue: white fur and enlargement with
dental pits in sides
 - local epigastral abdominal tenderness in
the pyloroduodenal part
 Endoscopic investigation:
 - hyperemia and oedema of mucous
 - folder’s hyperplasia
 - pylorospasm
 Histology:
 - inflammation (lymphocytes, plasmocytes)

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- HP
Methods for the diagnosis of HP
Non-invasive:
 Serological (population studies)
 Urea breath test (high sensitivity and
specificity)
Invasive:
 Histology (antral biopsy)
 Rapid urease tests (“Pyloritek”)
 Microbiological culture (“Gold standart”)
defines anbiotic sensitivity 18
 Treatment
 Diet № 1
 Antibiotics for HP (eradication therapy)
– in ulcer only
 Antacids (Maalox, Almagel,
Phosphalugel)
 H2-receptors antagonists (Cimetidine,
Famotidine, Ranitidine)
 Proton pump inhibitors (PPIs) –
Omeprazole, Lansoprazole)
 Prokinetic agents (Metoclopramide,
Domperodone) 19
 Ulcer of
Stomach and
Duodenum
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 Ulcers
 peptic ulcer (язвенная болезнь)
 symptomatic ulcers

 A peptic ulcer is
 a mucosal lesion of the stomach or
duodenum
 Anatomical and clinical conception

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 Aetiology
 HP
 Nervous stress
 Food taking regimen violating
 Smoking
 Gene-factors (1 blood group)
 Immunological theory
 Severe inner diseases
 Old age
 NSAIDs taking
 Gastrinoma
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 Pathogenesis
of peptic ulcer

 Balance disturbance between

aggressive factors and defense
mucosal factors.

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 Aggressive factors
 Gastric acid
 Pepsins

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 Protective mucosal factors
 Gastric mucus
 Bicarbonate
 Prostaglandins

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 Duodenal ulcer
 The prevalence of DU is estimated to range
from 6 to 15 % of Western populations
 The frequency of DU has been decreasing in
the United States and England, especially in
males.
 Current estimates suggest that
approximately 10 % of the population has
clinical evidence of DU at some time in their
lives.
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Pathogenesis of DU

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 Clinical features of DU
 Recurrent abdominal pain - sharp,
burning, or gnawing
 Pain occurs 90 min to 3 h after eating and
frequently awakens the patient at night
(“hungry pain”)
 Localisation - epigastrium and right
hypochondrium
 Irradiation – lower part of interscapular
space (X-XII thor.vert.) 30
 Clinical features of DU
 During spring and autumn (season’s
character of the pain)
 Episodic occurrence
 Vomiting "coffee grounds" material
 Black, tarry stools
 Weakness and fatigue (silent
bleeding)
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 Physical examination
 See gastritis Type B
 May be forced position – “posture of
shoemaker”
 Epigastric tenderness is the most frequent
finding

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 DIAGNOSIS
 Barium examination of the upper GI
tract (X-ray)
 Endoscopic examination of the upper
GI tract
 In most patients with typical DUs,
specific diagnostic testing for H. pylori
may be unnecessary because the
organism can be assumed to be
present
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 Complications
 Penetration (often posteriorly into the
pancreas)
 Pylorostenosis = gastric outlet obstruction
 Perforation
 Bleeding

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 Treatment
 Diet 1
 Eradication of HP (so-called
( triple therapy)
 H2 receptor antagonist
 Antacids
 Anticholinergic Agents (now rare)
 Coating Agents (sucralfate
( and Colloidal
bismuth compounds)
 Prostaglandins
 Proton Pump Inhibitors
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 Ulcer of Stomach
 The incidence of GU peaks in the sixth
decade, approximately 10 years later than
for DU
 Slightly more than half of GUs occur in
males
 The precise incidence of GU is not known,
since many GUs are asymptomatic
 Why some persons infected with H. pylori
develop DU and others develop GU (in the
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absence of NSAID use) is not clear.

 Clinical features of GU
compare to DU
 Epigastric pain, but the pattern is less
characteristic
 The pain may be precipitated or
accentuated by food
 Nausea and vomiting without
pylorostenosis
 Weight loss
 Complication – see DU + tendency to be
malignant (> 3 cm in diameter)
 Treatment – see DU + surgical in
complications 38
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