GASTRITIS CHRONIC, acute gastritis, peptic ulcer, duodenum and Helicobacter pylori.
Gastritis. Gastritis is a term that was once abused by ordinary people to
describe "heartburn" and, therefore, a dyspeptic syndrome (from the greek,
indigestion) today acquired new significance following the recent acquisition
gastritis antral is attributable to infection by Helicobacter pylori (HP) and is
associated duodenal ulcer. The various classifications of gastritis are those
previously used in Sydney that divided into a) acute gastritis and b) chronic
gastritis c) Special gastritis.
Acute gastritis is often the result of toxic damage and drug (NSAID gastritis)
or alcohol, or stress (see link), or respiratory failure, usually occurs in burn
patients and to the cave; frequently occurs in patients critical condition in
intensive care patients. Their most serious manifestation is gastrointestinal
bleeding, endoscopic appearance of gastric erosions will Asocio punctiform
hemorrhagic lesions or frankly hemorrhagic gastritis with erosion acute in 2 / 3
of the residual mucosa.
Chronic atrophic gastritis, which usually saves the cave is associated with the
presence of anti-parietal cells, to reduction in acid secretion and intrinsic
factor and thus pernicious anemia and other autoimmune diseases. In the form gi
chronic gastritis associated with Helicobacter pylori, the lesion is localized
in antral. The presence of H. P. can be demonstrated by bacterial culture on
antral biopsies but is usually easier to use invasive tests of urease, which is
based on the ability of HP to split urea into NH3 and CO2, by tacking a pH
indicator dye. Other times you can use non-invasive tests to assess whether the
person has benefited from the eradication therapy (see below), marked by the
test to C14, are also available tests involving the anti-HP antibodies of IgM
class ( active infection) and IgG (previous infection).
The special includes gastritis eosinophilic gastritis, gastric antrum that the
Interested, with submucosal edema and eosinophilic infiltrate and giant cells,
granulomatous gastritis that resembles that of sarcoidosis, tuberculosis and
Crohn's disease, ulcer, infiltration and thickening of mucosa and luminal
narrowing, gastritis or Menetrier ipetrofica giant folds with giant nodular or
polypoid and excessive mucus production.
Helicobacter pylori: chronic gastritis and ulcers, how and why. This stranger is
a spiral-shaped bacterium, Gram - Negative, with a width of 0.5 microns and a
length of 2 and 6.5 microns. It 'features a cover multiple unipolar and a
scourge and a powerful urease activity (on which the test al'ureasi when you
take a gastric biopsy sample is immersed in the reagent colorimetric system),
both the form and the scourge indovarsi allow the bacterium in gastric mucosa
and its urease activity allows him to create a barrier of ammonium bicarbonate
ion is essential for its colonization. The H. P. has a circulation correlated
with socio-economic development, so much so that in underdeveloped countries the
infection is present in 80-90% of subjects and up, we, with age up to 50-60%
after 70 years. The H. P. lives in the stomach and binds to gastric epithelial
cell type, but sometimes also receptor ectopic gastric epithelium of the
intestinal tract, Barrett's esophagus, Meckel's diverticula in plaques and
heterotopic gastric mucosa of the rectum. During the investigation gastroscopy,
can be seen through a) the cultivation of a piece of gastric tissue biopsy b)
urease test on gastric biopsy, are non-invasive method alternativ c) serological
test to research or IgG IgA directed against various bacterial antigens through
the Elise and) the breath test with urea: the patient swallows a tablet of urea
and, if the bacterium is present, free labeled CO2 that is collected in a breath
sample and subsequently analyzed. Why is it important to know the presence of HP?
Why H. P. is associated to chronic antral gastritis and, later, those suffering
from asthma may have recurrent ulcer, because the HP may increase levels of
gastrin and thus the production of hydrochloric acid, perhaps even through an
inhibition of somatostatin produced by antral D cells that exerts inhibitory G
podruno gastrin cells. The infection eventually, over time can lead to excessive
acid production and, consequently, damage to the duodenal mucosa, which
ultimately gives rise to a transformation in gastric intestinal metaplasia (ie
islands of gastric mucosa in the duodenum, where there should not be). Hence the
duodenum and a 'possible duodenal ulcer, treatable with classical methods.
Duodenal ulcer may also depend on other factors, for example by the use of
nonsteroidal anti-inflammatory drugs (NSAIDs), whose parent is aspirin, because
of their harmful action of prostaglandins on mucosal block, you may result in
Zollinger-Ellison syndrome or unusual events such as Crohn's disease.
All individuals infected H.P. have a histological characteristic of chronic
active gastritis (inflammation in the upper half of the gastric mucosa, with
mild atrophy and maximum activity was cavern where indovato HP) but only a
minority of them, however, will develop ulcer disease, or for immune or genetic
predisposition or more virulent strains of HP.
The symptoms of gastritis is typically characterized by slow digestion,
hardworking, epigastric pain or burning, feeling of fullness and hemorrhage (especially
in the acute form) in the case of gastric ulcer pain is exacerbated by the
ingestion of food; ulcer duodenal ulcer is, however, calmed dall'ingrestione
food, because it closes the pylorus and more acid will not flow into the
duodenum.
THERAPY.
The eradication therapy. Is, usually, the association of drugs that regulate
acid secretion and the use of two antibiotics, but encompasses several variants.
Therapy usually takes place:
a) proton pump inhibitor (omeprazole and sucedanei) 20 mg twice daily x + gx
amoxocillina tablets twice a day and / or claritromcina x 250 mg tablets twice
daily + metronidazole 400 mg tablets two x times a day. This care continues 7
days and then continue 3-5 weeks with only pump inhibitor.
b) pump inhibitor (omeprazole) + X amoxocillina 1 gram tablets twice daily or
clarithromycin 500 mg tablets twice of x, all for 15 days, with less
effectiveness for the eradication of which will be 70-80% .
Maintenance therapy. You must perform in patients who have relapses and you can
use an alternate-day pump inhibitor or ranitidine dosage children or old. Other
drugs from which the subject can benefit, especially if the disease is
associated with peptic reflux esophagitis, which is a condition in which the
lower esophageal sphincter (LES) is incontinent or the cardia malpositioned
resulting slope acid in the esophagus and a sign of regurgitation and the "shoelaces",
will be:
a) Antacids, ie preparations of aluminum hydroxide and magnesium in different
combination, taken after meals or when needed;
. B) more specific for reflux, associations of alginic acid + aluminum hydroxide
+ magnesium trisilicate + sodium bicarbonate should be given immediately after
meals and before bedtime: they form a reaction with stomach acid, alginic acid
and precipitated foaming gel in the presence of CO2 and floating on the gastric
juice, so that when reflux is a mechanical barrier to the action of the acid.
c) the old and still valid sucralfate which is a basic salt of sucrose aluminum
sulfate.
d) prostaglandin, misoprostol
e) drugs that help engines continence of SLE: eg. clebopride, cisapride,
sulpiride, they increase the tone of the LES and facilitate gastric emptying.
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