Department Propaedeutic of
Internal diseases with the course
of Endocrinology
Lecture №2
Theme: Actual problems
of diagnosis, treatment
and prevention of the
chronic gastritis
Chronic gastritis
- chronic inflammation of the mucous
membrane of the stomach, manifested by it's
cellular infiltration, a violation of
physiological regeneration and as a result,
atrophy of the glandular epithelium, intestinal
metaplasia, disorder of the secretory, motor
and often endocrine function of the stomach.
CLASSIFICATION OF CHRONIC
GASTRITIS ([Link], [Link], 1973)
-Type A (autoimmune gastritis), characterized by the
presence of antibodies to parietal cells, a high level of gastrin
in the blood and the predominant lesion of the stomach body;
- Type B ([Link] gastritis) develops as a result of infection
of the gastric mucosa Helicobacter pylori and bacterial
inflammation mainly of the antral part of the stomach
Type C (chemotactic) develops as a result of duodenogastric
reflux or the effects on the mucosa of certain drugs (NSAIDs)
or chemicals
Mixt gastritis (type A and B)
-
Topographically:
Gastritis of the antrum;
Gastritis of the fundus part;
Gastritis of all parts - pangastritis.
Common Sydney classification of
gastritis (1990), modified in
Houston (1994).
Type of gastritis Etiological Synonyms
factors
[Link]- H. pylori, other Superficial,
atrophic factors diffuse antral,
chronic antral,
interstitial,
follicular,
hypersecretory,
type B.
2. Atrophic: Immune Type A,
- Autoimmune mechanisms diffuse, the
body of the
stomach,
associated
with
pernicious
anemia
- Multifocal N. pylori, mixed gastritis
Features of of type A and
nutrition, B
environmental
factors
3. Special Chemical Reactive
forms: irritants, bile, reflux-gastritis,
-Chemical NSAIDs type C
-Radiation Radiation
injuries
-lymphocytic Idiopathic, veloformed
immune asociated
mechanisms, with celiac
gluten, N. disease
pylori.
-Noninfectious, Crohn's disease, Isolated
granulomatous sarcoidosis, granulomatosis
Wegener's
granulomatosis,
foreign bodies,
idiopathic.
-Eosinophilic Food allergies, Allergic
other allergens
-Other infectious Bacteria
(except H.
pylori), viruses,
fungi, parasites
Pathogenesis
H. pylori produces an urease enzyme,
that converts urea to ammonia and
carbon dioxide (СО2). They neutralize
the hydrochloric acid of gastric juice
and create around each bacterial cell a
local alkaline space.
Pain is often located in the upper-
center part of the abdomen, or in the
upper-left portion of the stomach. Pain will
often radiate to the back.
Investigations
Noninvasive testing for [Link]
1. Serological test. Anti-Helicobater pylori antibodies (IgG)
detection has sensitivity and specificity of over 90%.
2. Molecular method (material-dental plaque, fecal antigen test).
Detection of [Link] antigen in stool has sensitivity and
specificity by of over 90%.
3. 13C Urea breath test. This test is also quick, sensitive and
specific (over 90%). Positive test is indicative of active infection.
13C-labelled urea is ingested. If [Link] is present,
urea is metabolized to ammonia and carbon-labelled
carbon dioxide. The labeled carbon dioxide is then
excreted in breath as labeled carbon dioxide, which is
then collected and quantified.
Invasive testing for [Link]
1. Bacteriological: sowing a biopsy of the gastric and duodenal mucosa in
a selective culture medium followed by growth of microorganisms.
2. Histology: in the material of the biopsy of the gastric and duodenal
mucosa reveal the degree of dissemination
0-bacteria in the preparation are absent
1- weak (up to 20 microbes in sight)
2- moderate (20 to 50 in sight )
3- expressed (more than 50 microbes in sight)
3. Urease test: determination of urease activity in the biopsy specimen of
the gastric mucosa by placing it in a liquid or gelled medium containing a
substrate, a buffer and an indicator.
4. Cytological investigation of smears.
Upper GI endoscopy
Treatment
The food should be high-grade, diverse and meet the
conditions of chemical, thermal and mechanical stirring of
the gastric mucosa (exclude from the diet fried foods, fruit
juices, spices, coffee, alcohol)
Eating should be regular with a frequency of at least 4
times a day
contraindicated large breaks between meals, overeating
and dry eating
dinner should not be later than 2 hours before bedtime
Eradication of [Link]
infection
First-line therapy should be with triple therapy:
1. Omeprazole 20 mg twice gaily +
2. Clarithromycin 500 mg twice daily+
3. Amoxicillin 1000 mg twice daily or
metronidazole 500 mg twice daily
The course of therapy is 10-14 days.
Second-line therapy should use
quadruple therapy:
1. Omeprazole 20 mg twice daily +
2. Tetracycline 500 mg four times daily +
3. Metronidazole 500 mg three times daily +
4. De-nol 120 mg four times daily.
The course of therapy is 10 day.
Third-line therapy
Individual selection of drugs
based on the results of testing the
resistance of [Link] to
antibiotics
Autoimmune gastritis with B12-
deficiency anemia:
oxycobalamine (1000 mg) 0.1% - 1 ml IM daily, then for
a month 1p per week, then 1p at 2 months long.
Correction of violations of gastric secretion:
With hypo- and achlorhydria:
Inside the natural gastric juice (5 ml in ½ cup of water), the
abomin with meals.
Treatment of chemical gastritis
Reflux – gastritis: use of H2-blockers of
histamine receptors with in 1-2 weeks;
Prokinetics 3-4 times a day for 5-7 days
If necessary, the use of antacids
With chemical gastritis caused by
the intake of NSAIDs, the following
are shown:
Cancel the NSAID;
The drugs of choice is a synthetic analogue of prostaglandin
E2-misoprostol to 0.2 mg x 3 time daily at meal time and 1
tablet at bedtime.
To stop the pain and dyspeptic syndrome, H2-blockers of
histamine receptors or proton pump blockers are used for 2-
4 weeks).
In the hyperacid state:
Antisecretory drugs (H2-blockers of histamine receptors
or blockers of the proton pump), antacids.
Correction of gastric motility
- Myotropic antispasmodics (no-spa, papaverine
hydrochloride).
- M-holinoblokatory (platifillin, selective-gastrotsepin).
Correction of symptoms of
maldigestia and malabsorption:
-enzymes (pancreatin)