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The Digestive SystemPeptic ulcer Synonyms : Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs, A
peptic ulcer is a mucosal lesion of the stomach or duodenum (duodenal ulcer is
4 times more common) which extends into the submucosa or even deeper. Peptic
ulcer is very common in Western communities, affecting approximately 10% of
all adult males. Incidence is much higher among males than females. In
simple words there are two main types of peptic ulcer: one associated with
long-term treatment with nonsteroidal
anti-inflammatory drugs (NSAIDs) with or without corticosteroids (e.g., in
management of chronic joint problems such as rheumatoid arthritis) and the
other one associated with Helicobacter pylori infection. First type of
peptic ulcer is seen in the stomach and its development is well understood.
Chronic use of NSAIDs suppresses mucosal prostaglandin synthesis and may produce
direct irritation and damage of the gastric mucosa (especially aspirin -
acetylsalicylic acid). Corticosteroids
in high doses and with repeated use promote ulcer formation, because they also
suppress production of protective prostaglandins in the stomach.
However there is less complete knowledge of the pathogenesis of Helicobacter
pylori-associated peptic ulcer. This ulcer can develop both in the
stomach and duodenum. It has been found that 95-100% of patients with duodenal
ulcer and 75-85% of patients with gastric ulcer harbour the organism. It is very unlikely that persons without H. pylori
will ever develop duodenal ulcer. On the other hand, only 15-20% of persons infected
with H. pylori will develop an ulcer in their lifetimes, implying that
additional pathogenic factors must be involved. This gram negative
microorganism is a worldwide pathogen that has the highest infection rates in
developing countries, where it is probably spread by the faecal-oral (H.
pylori can be
cultured from the stools in most infected persons) or
oral-oral route (e.g., sharing cutlery and glasses/cups, eating from the same
dish, kissing). In Western countries H. pylori affects about 20% of persons below the age
of 40 years, and 50% of those above the age of 60 years. It is uncommon in
young children. Low socio-economic status favours H. pylori infection. In
developing countries most adults are infected. H. pylori is normally found in the deep portions of the mucus gel layer that coats the gastric mucosa and in most cases does not invade it (the notion of non-invasiveness has recently been challenged). Once H. pylori is safely embedded in the mucus, it is able to fight the stomach acid that does reach it with an enzyme it possesses called urease. Urease converts urea, of which there is an abundant supply in the stomach (from saliva and gastric juices), into bicarbonate and ammonia, which are strong bases. This creates a cloud of acid neutralizing chemicals around the H. pylori, protecting it from the acid in the stomach. The reaction of urea hydrolysis (urea is broken down to ammonia and carbon dioxide) is shown below. The mechanism by which H. pylori causes a peptic ulcer is very complex.
The organism produces a variety of proteins such as chemotactic factors (they
attract inflammatory cells), certain proteases and phospholipases enzymes,
which mediate its damaging effects on the mucosa and initiate chronic
inflammatory changes. However body’s natural defences such as leukocytes, killer T cells,
and other infection fighting agents cannot reach the bacterium in the mucus
layer of the stomach because they cannot easily get through stomach lining.
Extra nutrients are sent to reinforce the white cells, and the H. pylori can
feed on this. It may not be H. pylori itself which causes peptic ulcer, but
instead the inflammation of the stomach lining (the response to H. pylori)
through release of various toxic materials from inflammatory cells such as
free oxygen radicals and hydrolytic enzymes. It has been suggested that H. pylori can indirectly
stimulate gastrin release and consequently gastric acid production, which
could be interpreted as a stomach’s attempt to fight the bacteria. Normal mucosa is able to resist the corrosive action
of gastric acid and pepsin. Protective
mechanisms that prevent the mucosa from being digested include the
following:
Secretion
of mucus by surface epithelial cells that form a protective barrier
Secretion
of bicarbonate into the mucus, to create a buffered surface micro-environment
and neutralise gastric acid that comes dangerously close to the mucosa
Secretion
of acid and pepsin-containing fluid from the gastric pits as ‘jets?/i>
through the surface mucous layer, which enters the lumen directly without
contacting surface epithelial cells
Rapid
gastric epithelial turnover and regeneration (normally 3-5 days)
Quick
mucosal blood flow, to sweep away hydrogen ions that have back-diffused into
the mucosa from the lumen and to sustain the high cellular regenerative
activity
Mucosal
secretion of prostaglandins (especially PGE2,
PGI2),
which increase production of alkaline mucus and increase blood flow Other events may act alone or together with H. pylori
to promote peptic ulceration. Cigarette
smoking may impair mucosal blood flow and healing (it does not increase
gastric acid secretion) but current knowledge argues against any significant
role of smoking in pathogenesis of peptic ulcer. Alcohol and coffee have not
been proved to directly cause peptic ulceration, although they can stimulate
gastric acid secretion. Finally, it appears that personality and psychological
stress are important contributing factors. Patients with peptic ulcers
often have a family history of the
disease; this is particularly so with duodenal ulcers. Chronic
gastric ulcers are usually situated on the lesser
curve near the junction between the body and antral mucosa. Chronic
duodenal ulcers are usually in the first part of the duodenum. Gastric and
duodenal ulcers coexist in 10% of all patients with peptic ulcers. If left
untreated peptic ulcer disease is a chronic
condition with a natural history of spontaneous relapses and remissions
lasting for decades if not for life. Although they are different diseases,
duodenal and gastric ulcers share common symptoms. Clinical features: < BACK TO TOP >
Recurrent
abdominal pain localised in the epigastrium is the most frequent symptom.
The
pain is often described as sharp, burning or gnawing, but it may be ill
defined, boring or aching.
It
occurs intermittently during the day, often when the stomach is empty, and
the patient can usually obtain relief by eating (“hunger
pain?.
If the
pain wakes the patient from sleep it is known as “night
pain?/i>.
The
pain is also relieved by milk or antacids and by vomiting (many patients
self-induce vomiting in order to obtain pain relief).
Characteristically
the pain occurs in episodes, lasting 1-3 weeks at a time, 3-4 times a year;
seasonal variations are noted in temperate climates.
Waterbrash
(excessive salivation), heartburn and loss of appetite are frequently
reported.
Nausea
and vomiting suggest gastric ulcer; in duodenal ulcers they indicate the
possibility of gastric outlet obstruction by scarring. Differences between gastric and duodenal
ulcer:
Gastric
ulcer tends to occur over age 40, and affects the sexes equally, while
duodenal ulcer occurs predominantly in male subjects between the ages of 20
and 40.
In
gastric ulcer, episodes tend to last longer and the pain may occur daily for
long periods of time. The pain of gastric ulcer is not consistently relieved by antacids and may be provoked rather than relieved by food; heartburn and night pain are less common, and anorexia and nausea are more common in gastric ulcer. Diagnosis: < BACK TO TOP >
History
provides important clues although it is usually very difficult, if not
impossible, to distinguish between gastric and duodenal ulcer on clinical
grounds alone.
On
physical examination, epigastric tenderness is the most frequent finding. The
area of tenderness is usually in the midline, often midway between the
umbilicus and the xiphoid process.
The
diagnosis can be confirmed by barium meal examination
(less reliable and consequently less used) or at endoscopy.
Endoscopy
(gastroduodenoscopy) is the preferred investigation because it is more
accurate and offers biopsy. Histologic examination of a tissue sample can
rule out malignancy, which is very useful in gastric ulcers (gastric
carcinoma can resemble a benign gastric ulcer).
Serologic tests for Helicobacter pylori based on ELISA (enzyme-linked
immunosorbent assay) technique can detect IgA and IgG antibodies against the
bacteria. The main problem with this technique is that it doesn’t
differentiate between active and past infection (antibodies can be found for
up to 3 years after successful eradication of H. pylori).
Rapid urease test is based on H. pylori urease
production and can be done to detect the bacteria in biopsy specimens (tissue
samples) in few minutes. The test is inexpensive with a sensitivity of at
least 90%. The main drawback is that it requires endoscopy. Urea breath test is non-invasive and does not require tissue sampling. The test also may be used to demonstrate that H. pylori has been eliminated by treatment with antibiotics. The urea breath test is based on the ability of H. pylori to break down urea, a waste product of protein metabolism normally eliminated in the urine. For the test, patients swallow a capsule containing urea (NH4OCN) made from a radioactive isotope of carbon. If H. pylori is present in the stomach, the urea is broken up into ammonia and carbon (as carbon dioxide). The carbon dioxide is absorbed across the lining of the stomach and into the blood. It is then excreted from the lungs in the breath. Samples of exhaled breath are collected after 30 minutes, and their radioactivity is measured. If the isotope is detected in the breath, it means that H. pylori is present in the stomach. If the isotope is not found, H. pylori is not present. When the H. pylori is effectively treated (eradicated) by antibiotics, the test changes from positive (isotope present) to negative (isotope absent). The urea breath test has a sensitivity of 90-95%. The amount of radioactive exposure from the test is less than one will normally receive in one day from nature. Management < BACK TO TOP >
The aims: to relieve symptoms and induce ulcer healing in the short term, and to
prevent relapse in the long term.
Cigarette
smoking should be strongly discouraged, aspirin and NSAIDs should be avoided
if possible; alternatively a selective COX-2 inhibitor celecoxib [Celebrex]
can be tried if NSAID treatment is essential.
Alcohol
and coffee in moderation are not harmful, and no special dietary advice is
required apart from the avoidance of food that appears to exacerbate the
problems.
Antacids
neutralise gastric acid and are widely used for self-medication. Liquid
preparations are probably more effective than tablets.
Classic
treatment is with histamine H2-antagonists (cimetidine [Tagamet], ranitidine [Zantac], nizatidine [Tazac]
and famotidine [Pepcidine, Amfamox]) and proton pump inhibitors (omeprazole [Losec],
lansprazole [Zoton] and pentoprazole [Somac]) to decrease the production of
gastric acid.
It is
now recommended that drugs to eradicate H. pylori should be included from the
very beginning.
Drugs
active against H. pylori are colloidal bismuth compounds, antibiotics
amoxycillin [Amoxil, Cilamox, Moxacin], clarithromycin [Klacid], tetracycline
[Achromycin, Tetrex] and metronidazole [Flagyl, Metrogyl, Metrozine].
A
popular approach is ‘triple therapy?composed of bismuth, tetracycline
and metronidazole for 2 weeks [Helidac] (H2-antagonist or a proton pump inhibitor is usually added for 6 weeks).
This treatment eradicates H. pylori with 80% success rate, but up to 30% of
patients complain of troublesome nausea and vomiting, as well as darkening of
the tongue and stool and constipation (bismuth is likely to be responsible
since it has to be chewed first and then swallowed).
Other
regimes have been suggested, such as omeprazole,
amoxycillin and clarithromycin [Klacid Hp 7, Losec Hp 7], omeprazole,
amoxycillin and metronidazole [Losec Helicopak], and ranitidine,
clarithromycin and amoxycillin [Pylorid-KA] for only one week with
even better results (more than 90% success).
Eradication
of H. pylori is confirmed by urea breath tests.
Recurrence
rates of peptic ulcer are very low if H. pylori is successfully eradicated
(reinfection probably does not occur), otherwise they can be up to 80% with
the classic treatment.
Surgical
treatment is reserved for non-responding ulcers which cause significant
morbidity, and today is rarely attempted due to efficient drug therapy. If it
has to be carried out, surgical choices are partial gastrectomy (Billroth I
procedure- gastroduodenostomy, Billroth II procedure - gastrojejunostomy) and
vagotomy (selective when only the branches of the vagus that supply the
stomach are cut, and supraselective where vagal innervation of the pylorus is
preserved). Complications:
Upper
gastrointestinal haemorrhage, with vomiting of fresh blood or ‘coffee
grounds?material, or the passage of black, tarry stools (melaena).
Sometimes with more subtle blood loss, iron deficiency anaemia can be the
only sign of chronic bleeding.
Acute
perforation of a peptic ulcer with constant more severe pain and a rigid,
board-like abdomen (guarding), usually with generalised rebound tenderness
(peritonitis). This complication warrants emergency surgery to prevent the
development of life-threatening bacterial infection. Gastric outlet obstruction in long standing cases due to formation of fibrous strictures leads to impairment of gastric emptying and frequent vomiting. It requires some form of surgical treatment. Prognosis < BACK TO TOP >
Nutrition < BACK TO TOP > Nutrition that alleviate or prevent Peptic ulcer :- Herbs < BACK TO TOP > Herbs that alleviate or prevent Peptic ulcer :- (source : -) | |
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