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Peptic Ulcer Disease
Author:
Musab T. Ejami, MBBS, Faculty Of
medicine, University Of Al-Zaiem Al-Azhari
INTRODUCTION:
The term ulcer means: discontinuation of the epithelium, the term peptic
ulcer refers to an ulceration of the lower oesophagus, stomach or
duodenum, in the jejunum (after surgical anastnmosis of the stomach or
rarely in the ileum adjacent to Meckel’s diverticulum which contains
ectopic gastric mucosa.
EPIDEMIOLOGY:
* Duodenal ulcers (DUs) are 2-3 times more common than gastric ulcers (GUs).
* 15% of the population in the UK suffers from DUs.
* They are common in males more than females.
AETIOLOGY:
It was long believed that ulcers are a result of increased acid
secretion in response to chronic stress and inflammation of the mucosa
secondary to ingestion of spicy food. It is now known that this is not
the case, and the prime cause of peptic ulcer is an infection with
Helicobacter Pylori, which is responsible for almost all cases of
duodenal ulcers, and about 70% of cases of gastric ulcers, it was
estimated that more than 20% of gastric ulcers may also be caused by
NSAID. Other causes and factors that may be involved include:
* Zollinger-Ellison syndrome.
* Smoking.
* Hereditary and genetic susceptibility.
PATHOPHYSIOLOGY:
1- HELICOBACTER PYLORI (H.PYLORI):
The main cause of ulcer is imbalance between acid secretion and mucosal
defense. H.Pylori causes ulcer by either increasing acid secretion (as
in DUs) or by decreasing the mucosal defense (GUs).
Duodenal ulcers:
The organism colonizes only gastric type epithelium, and is found in the
duodenum only in association with patches of gastric mucosa. The
mechanism by which this happen is as follows;
* Once infected, the bacteria lies deep within mucosal layer of the
antrum closely adherent to the epithelial surface, a location that keeps
it way from the immune system and the acidity of the stomach, in
addition the bacteria buffers any drop in the PH through the unique
enzyme urease that produces ammonia from urea and raises the PH around
the organism.
* The D cells of the antrum are destroyed by the bacteria, and hence the
reserve for somatostatin (a gastrin inhibiting enzyme) is depleted.
* Thus G cells are stimulated hypergastrenemia follows, which in turn
causes a rise in the parietal cells mass and activity and increased acid
secretion.
* The intestinal epithelium of the duodenum is sensitive to acid, thus
the excessive irritation of acid eventually leads to metaplasia,
converting intestinal-type epithelium to gastric type epithelium.
* Here H.Pylori can finally colonize the duodenum and lead to further
damage and eventually ulceration.
Gastric Ulcers:
The role of H.Pylori here is less clear than DUs, but it is proposed
that it decrease the mucosal defense which normally protects the gastric
cells from increased acidity. Normally, mucus, bicarbonate and
prostaglandins (specially of the E series) are secreted by the gastric
cells to buffer and counter act the acidity, H.Pylori seems to produce a
local inflammatory response that lead to production of cytokines, all of
which destroy these defense barriers.
2- NON STEROIDAL ANTI-INFLAMMATORY DRUGS:
NSAID act by inhibiting the cyclo-oxegenase activity. Cyclo-oxygenase
enzymes are important for the production of prostaglandins that protect
the gastric epithelium. Most NSAID are non-selective, they block both
COX1 and COX2 receptors, the former which is found primary in the
stomach. The new generations of NSAID which are selective to COX2
receptors (e.g. etodaloc) may have less GIT toxicity.
3- ZOLLINGER-ELLISON SYNDROME:
results from a tumor of the G- cells of the pancreas (gastronoma) that
results in high levels of circulating gastrin, triggering high acid
secretion leading to ulcers (mostly in the duodenum).
CLINICAL FEATURES:
The most common presentation is through recurrent abdominal pain, which
has the following characteristics:
* Site: epigastric area, it’s said that if the patient points to it with
2 or 3 fingers as a site of pain this has a high discriminatory value
for diagnosis (pointing sign).
* Nature: burning, boring pain some patients describe it as discomfort
or indigestion, some may relate the nature of pain to food by saying:
“hunger pain”.
* Aggravating & reliving factors: classically food aggravates gastric
ulcers, thus they are afraid to eat and they appear thin due to weight
loss, the pain is relived by vomiting. Duodenal ulcers cause hunger
pain, the pain is abolished by eating, patients with DUs typically wake
at night because of the pain and they tend to eat biscuits and milk to
relive it. Antacids also relive both types of pain.
* Associated symptoms: include vomiting (may be self induced to relief
the pain, a daily persistent vomiting points towards Gastric Outlet
obstruction), nausea, anorexia (true anorexia indicates malignancy
rather than peptic ulcer, gastric ulcers patients are afraid to eat
although they wish to – false anorexia-) waterbrash, heartburn.
* The pain is Episodic: that may last for weeks with an interval which
is symptom-free.
INVESTIGATIONS:
* ENDOSCOPY: for exclusion of GORD and Cancer, a biopsy may help further
in the diagnosis.
* BARIUM MEAL (DOUBLE CONTRAST): for seaing the lesion, this is now
mostly replaced by endoscope which is more acuurate and alows biopsy.
* ACID-SECRETION & SERUM GASTRIN MEASURMENT: used only in diagnosing Z-E
syndrome.
* SCREENING FOR H.PYLORI: the most used method is urea breath test, the
test is based on the organsims ability to do prodce urease, which splits
radio-active given urea to the patient to ammonia and CO2, if
radio-active CO2 resulting is collected, the test is positive. This is
not perforemd routinely, though its promising tool for identifying those
with H. Pylori infection, the main disadvanteg is that screening
identifies only infected individauls, but not those with actual active
ulcer disease. Other screening tools where also developed (see table).
TREATMENT:
treatment of peptic ulcer was highly controversial, surgical procedures
like vagotomy (which where based on the old theories) where the prime
treatment, now it came more to conscious that Peptic Ulcer disease is a
medical condition requiring medical treatment, and surgery should be
reserved for complications and non-responding cases.
1- MEDICAL TREATMENT:
(a) If the ulcer was associated with H.Pylori, then eradication therapy
or should be administered, current regimes consist of 2 types of
antibiotics + a proton-pump inhibitor (PPI-based triple therapy),
examples
* Omeprazole 2mg twice daily + Metrinadazole 400 mg twice daily +
calrithrpmycin 250 mg twice daily.
* Omeprazole 2mg twice daily + Metrinadazole 400 mg twice daily + 1 g
amoxycillin mg twice daily.
(b) If the cause was NSAID or other cause rather than H.Pylori, then the
acid suppression and avoidance of NSAIDs would be appropriate, the
following agents may be given:
* PPI: Opemarozole or lasnoprazole or pantoprazole.
* H2-receptor antagonist: like cimitidne, rantidine and famotidine.
* Misoprostol.
(c) Other measures may include:
* Stop smoking.
* Careful diet, avoid alcohol and acid substance.
Follow-up:
* DUs: clinical resolution of the symptoms.
* GUs: Endoscopy after 6 month 2 exclude malignancy, especially in those
above 45.
2- SURGICAL TREATMENT:
There are 2 types of operations performed:
* Gastrectomy: which could be total or partial, partial procedures where
used using Billroth 1 or Billroth 2 techniques.
* Vagotomy: division of the vagus nerve which stimulate acid secretion,
this could be (a) truncal (b) Selective (c) highly selective.
Long term complications of surgery:
* Recurrent ulcer.
* Dumping effect.
* Diarrhea.
* Blind loop syndrome.
* Nutritional complications ( iron-deficiency anemia, megaloblastic
anemia, osteomalacia
COMPLICATIONS OF PEPTIC ULCER:
* Hemorrhage
* Perforation
* Pyloric outlet obstruction
See Figure For surgery:
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