ACUTE & CHRONIC GASTRITIS
What news about gastritis?
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by doctor
Claudio Italiano
from Italy -
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The acute gastritis is often the result of a toxic and pharmacological
damage (gastritis by NSAIDs) or alcohol, or stress, or respiratory
failure, in burns and generally is localized in antrum; frequently
occurs in hospitalized patients in serious condition of intensive terapy.
The most severe event is the serious gastrointestinal bleeding; by
endoscopy it’s possible the appearance of gastric erosions associated
to the bleeding point injuries or frankly haemorrhagic gastritis with
erosion acute in 2 / 3 of the residual mucosa.
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Gastritis. Gastritis is a term that was once used improperly by people
to indicate "heartburn" and, therefore, a dyspeptic syndrome (greek,
bad digestion); today takes on a new meaning based on the recent
acquisition that antral gastritis is attributable to infection by
Helicobacter pylori (HP) and is associated to the duodenal ulcer. The
various classifications of gastritis previously in use are those that
Sidney subdivided into a) acute gastritis b) chronic gastritis c)
special gastritis.
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The chronic atrophic gastritis, which usually saves antrum, is
associated with the presence of anti-parietal cells, and with a
reduction of acid secretion and intrinsic factor and then to pernicious
anemia and other autoimmune diseases. Already chronic gastritis is
associated with Helicobacter pylori, and the lesion is located in antral.
H.P. can be shown by examining antral biopsies and using ureasi invasive
tests, which are based on the ability of urea To split in CO2 and NH3,
making tack a pH indicator dye. Other times you can use non-invasive
test to determine whether the person has benefited from the eradication
therapy (see below), through the tests marked the C14 are also available
tests that provide the search for anti-HP class IgM ( infection in
place) and IgG (previous infection).
The special gastritis include eosinophilic gastritis, gastric antrum
interesting, with sub mucosal eosinophilic with giant cells;
granulomatous gastritis which is like a sarcoidosis, tuberculosis or
Crohn's disease, with ulcer, infiltration and thickening of mucosa and
narrowing of the lumen; Menetrier gastritis or ipetrofica giant
gastritis, with pliche giants or nodular appearance of polypoid and
excessive mucus production.
Below: vision endoscopic ulcer circumferential bulbar, courtesy of prof.
G. Urso, University of Catania.
This unknown bacterium is a spiral-shaped one, Gram - Negative, with a
width of 0.5 microns and a length of 2 and 6.5 microns. It has a
multi-coating and a unipolar scourge and a powerful ureasica activity
(on which is Based ureasic test when a gastric biopsy is immersed in
the colorimetric system responsive); Both the form and scourge enable
the bacterium to put itself in the gastric mucosa and its ureasic
activities allows him to create a barrier and ammonium bicarbonate ion,
which is essential for its colonization. The HP Has spread correlated
with socio-economic development, so much so that in underdeveloped
countries the infection is present in 80-90% of subjects and increases,
which we, with age until 50-60% after 70 years. The HP Lives in the
stomach and binds to receptor cells gastric epithelial type, but
sometimes also to receptors povrhnjice ectopic gastric intestinal tract,
of Barrett, Meckel diverticula and plaques of heterotopic gastric mucosa
rectum. During the endoscopic investigation, it can be seen through a)
cultivation of a fragment of gastric biopsy, b) ureasic test on a
gastric biopsy; alternative not invasive methods are: serological test
to seek or IgG or IgA antibodies directed to the various bacterial
antigens by ELISA and) urea marked breath test; the patient ingests a
tablet of urea marked, and if the bacterium is present, free CO2 market
that is collected in a sample of air exhaled air and then analyzed. Why
is it important to know about the presence of?
Because HP associates with chronic antral gastritis and, subsequently,
those suffering from such illnesses can have relapses ulcer; because HP
may increase the gastrina levels and thus the production of hydrochloric
acid, perhaps through a somatostatin inhibition produced by cells that
carries D antrali inhibition on G cells which produce gastrina. The
infection also can over time lead to excessive acid production and,
consequently, to a duodenal mucosa damage, which ultimately will lead to
a transformation in gastric intestinal metaplasia (ie islands of gastric
mucosa in the duodenum, where there must not to be). Hence duodenitis
and a 'possible duodenal ulcer, treatable with traditional methods. The
duodenal ulcer can also depend on other causes, for example the use of
anti-inflammatory non-steroidal drugs (NSAIDs), of which the parent is
aspirin, for their work on blocking harmful mucosal prostaglandins ; may
result in Zollinger-Ellison or unusual events such as Crohn's disease.
All individuals infected by HP have an histological characteristic of
chronic active gastritis (inflammation in the upper half of the gastric
mucosa, with mild atrophy and activities where maximum all'antrum is
localized HP), but only a minority of them, however, will develop the
disease ulcerative or for immune or genetic predisposition or more
virulent strains of HP.
The symptoms of gastritis typically are characterized by laborious and
slow digestion, pain or epigastric burning, gastric enflated feeling,
and bleeding (especially in the acute form), in the case of gastric
ulcer pain is exacerbated by food; in duodenal ulcer is, however, calmed
by food ingestion, because it closes the pyloric and don’t allow acid
flow in the duodenum.
THERAPY.
The eradication therapy. It consists, generally, the association of
drugs that regulate secretion in the use of acid and 2 antibiotics, but
includes several variations.
Typically, treatment is carried out with: A) proton pump inhibitor (omeprazole
and sucedanei) 20 mg twice daily + amoxocillina in a gx tablets twice
daily and / or claritromcina tablets of 250 mg twice daily +
metronidazole tablets of 400 mg x two times a day. This care continues 7
days and then 3-5 weeks with only pump inhibitor. B) pump inhibitor (omeprazole)
+ 1 gram tablets amoxocillina X twice than or clarithromycin 500 mg
tablets x twice of, all for 15 days, with less effective in the
eradication of which will be 70-80% .
THERAPY FOR MAINTENANCE. We must make in subjects who have relapses and
you can use a pump inhibitor or every other day doses minors or old
ranitidine. Other drugs from which the individual can benefit,
especially if the disease is associated with peptic the reflux
oesophagitis, which is the condition where the lower oesophageal
sphincter (LES) is incompetent or cardias malposizionato with consequent
rising acid in the esophagus and a sign regurgitation and lasso the
shoe, will be:
A) antacids, that is prepared based on aluminum hydroxide and magnesium
in different association, to be taken after meals or at the time of
need;
B) more specific reflux, associations alginic acid aluminum hydroxide +
+ + magnesium trisilicate sodium bicarbonate to be made immediately
after the meal and at bedtime: they form a reaction with stomach and
alginic acid precipitates in the form schiumoso gel in the presence of
CO2 and floats on the gastric juice, so when reflux is a barrier effect
of mechanical action.
C) the old and always valid sucralfate which is a basic aluminum salt
sucrose sulphate.
D) prostaglandins, misoprostol E) medicines that help the engines of
continence LES: eg. Clebopride, sulpiride; they increase the tone of
the LES and facilitate gastric emptying.