A peptic ulcer is a sore in the lining of the
stomach or duodenum, which is a mucous lining of these organs inside to avoid
injuring the effect of digestive juices which are in permanent contact. This is
a very common disease that produces a
characteristic pain and changes in the quality
of life in those affected.
Symptoms:
Most characteristic of peptic ulcer is the onset
of pain or uncomfortable sensations in the abdominal region, which may have one
or more of the following characteristics:
·
Pain in the upper abdomen (epigastrium) which appear 30-60 minutes after
eating.
·
Night pain onset (when the stomach is empty).
·
The dull pain that radiates.
·
Pressing pain in pit.
Other symptoms of the above would result in
weight loss, loss of appetite, bloating, belching, nausea or vomiting, although
these are rare.
This pain can be associated with heartburn or
acid into the esophagus (behind the breastbone) and is often associated with a
reflux of stomach acid into the esophagus, which can be damaged by effect of
the acidity causing esophagitis.
Causes:
Numerous studies have been observed that are not
exactly the same causes which lead to a duodenal or gastric ulcer. In fact, it
seems that stomach ulcers are related to the presence in the duodenum of a
bacterium called Helicobacter pylori and duodenal ulcer associated with
excessive acidity in the stomach, although it may seem paradoxical.
Helicobacter Pylori
As it has been determined, it causes various
effects on those infected:
Higher
concentration of ammonia in the gastric mucus, about four times more than
normal; it directly damages the stomach lining, and alters the viscosity of
mucus covers and protects chelates, which makes it more vulnerable to the
effects of acid with which it is in permanent contact.
On the other hand also the infection of H. pylori
produces an abnormal elevation of gastrin, a molecule that regulates the amount
of gastric acid released in the stomach; typically, the amount of gastrin is
regulated depending on the food taken. In one infected with H. pylori, gastrin
secretion is inappropriate to a food stimulus. The basal gastrin increases by
50% and 100% postprandial. It has also been shown to reduce levels of gastrin
after eradication treatment.
Increased acid secretion:
The increase in acid secretion appears to be the
leading cause of injuries of duodenal peptic ulcer. Duodenal mucosa responds to
increased acidity to changes in the structure of the mucosa, which attempts to
become more resistant to the acid attack; its structure is changing and
increasingly resembling the gastric mucosa. More prepared to resist acid
attack. Finally, it is completely transformed into gastric mucosa, which is
called duodenal gastric metaplasia, which in turn is infected by H. pylori with
the appearance of duodenitis and duodenal ulcer.
The snuff is also a high risk factor for the
development of duodenal peptic lesions.
Anti-inflammatory
consumption:
Antiinflammatory perform their action through
numerous and complex chemical reactions, which enters regulating molecules
called prostaglandins, which promote stomach defenses against gastric acid.
Anti-inflammatory inhibit prostaglandin synthesis
(PGs) at which the stomach loses some of its ability to defend itself, to the
point that these drugs, taken continuously, without gastric protection and
uncontrolled. Very often they lead to the occurrence of digestive ulcers, or
statements under the same etiology.
In the stomach mucosa it is well prepared to
withstand a pH level of <2.5.
if the
mucosa is adapted to acidic means to display mucosal lesions it must alter some
of these defense mechanisms.
Duodenal ulcer: The mechanisms of injury to produce a gastric
ulcer are:
Anti-inflammatory drugs both orally and by other means arrive at the
gastric mucosa and do lose the outer protective coatings.
Diagnosis:
Courtship is quite characteristic symptoms of diagnosis.
It is frequently supplemented by performing a gastroscopy. For injuries, take a
biopsy of the lesions for analysis and culture for Helicobacter Pylori.
Control of Helicobacter Pylori infection can be
performed by a simple test that measures the CO2 in the breath. It is performed
by administering orally Carbon marked/Urea and blended with citric acid, if the
patient has Helicobacter pylori, urease produced by this bacterium, will be
transformed into CO2 and ammonia.
Marked Carbon / Urea Urease
+ C02 + NH3 = CURE
The CO2 released through the blood appear in the
breath through the lungs. The measurement of CO2 marking is done in two takes,
basal and half hour to take the Carbon -Urea. The test sensitivity is 90% and
is specific in over 95% of cases. This analysis can be given by controlled
infection or continue with longer treatment.
General Information on the
Treatment of Peptic Ulcer:
Antibiotic therapy is indicated for all patients with H. pylori
infection (85% of patients with gastric ulcer have it).
There
is no ideal antibiotic therapy, there are several options.
The
anti-ulcer therapy (H2-blockers-omeprazole) is recommended to relieve symptoms
and promote healing.
The
rebels ulcers require an association of secretion inhibitors with antibiotics.
In all,
ulcer patients should be mindful of the type of food they eat and stay away
from such food for better in the course of the treatment.
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