WHAT IS PEPTIC ULCER DISEASE? Peptic ulcers are sores that develop in the lining of the stomach, lower esophagus, or small intestine. Or first few centimeters of the duodenum (duodenum ulcer). It usually penetrates through the muscularis mucosae.
From a histological perspective, an ulcer is a loss of the surface epithelium that extends deeply enough to reach the muscularis mucosae. From a clinical per perspective, an ulcer is loss of the mucosal surface visible by endoscopy. Or radiology exam. Plus diameter greater than 5mm in addition to depth.
Ulcer may range in size from several millimeters to several centimeters. Ulcer are delineated from erosions by depth of penetration. Erosion are more superficial and do not involve the muscularis mucosae. Ulcer are distinguished from erosions by size; which are small (<5mm) superficial mucosal lesions.
Because the superficial mucosa contains only capillaries, erosions usually result in clinically mild bleeding (oozing). They are unlikely to give rise to clinically significant bleeding, scaring or perforation. In contrast, ulcer may give rise to all complications.
Peptic ulcer disease (PUD) refer to the underlying tendency to develop mucosal ulcers at sites that are exposed to peptic juice (acid and pepsin). Most commonly, ulcer occurs in the duodenum and stomach. But they may also occur in the esophagus, in the small intestine, at gastroenteric anastomosis. And rarely in the areas of ectopic gastric mucosa for example meckel’s diverticula.
Causes and Pathogenesis
It appear that certain factors, namely H. pylori and NSAIDs, disrupt the normal mucosal defense and repair. This makes the mucosa more susceptible to the attack of acid. The mechanism by which H.pylori causes mucosal injury are not entirely clear, but several theories have been proposed. Urease produced by the organism catalyze urea to ammonia. The ammonia, while enabling the organism to survive in the acidic environment of the stomach, may erode the mucous barrier, leading to epithelial damage. Cytotoxin produced by H. pylori have also been implicated in host epithelial damage.
Mucolytic enzymes (eg, bacterial protease, lipase) appear to be involved in degradation of the mucous layer, making the epithelium more susceptible to acid damage.
Lastly, cytokines produced in response to inflammation may play a role in mucosal damage and subsequent ulcerogenesis. NSAIDs are likely to promote mucosal inflammation and ulcer formation through both topical and systemic effects. Because NSAIDs are weak acids and non-ionized at gastric pH. This make them to diffuse freely across the mucous barrier into gastric epithelial cells, where hydrogen ions are liberated, leading to cellular damage.
Systemic effects appear to be mediated through their ability to inhibit cyclooxygenase activity and prostaglandin production. By inhibiting prostaglandin production, NSAIDs induce several changes in the gastric microenvironment. For example; reduced gastric blood flow, reduced mucus and hydrocarbonate secretion, decrease cell repair and replication. This leads to breakdown of mucosal defence mechanism.
Most occurs in the first part of the duodenum. A chronic ulcer penetrates the mucosa and into the muscle coat leading to fibrosis. The fibrosis causes deformities such as pyloric stenosis. When an ulcer heals a scar can be observed in the mucosa. Sometimes there may be more than one duodenum ulcer. The situation in which there is both a posterior and anterior duodenum ulcer is referred to as ‘ kissing ulcer’.
Anteriorly placed ulcers tend to perforate and by contrast, posterior duodenal ulcer tend to bleed, sometimes by eroding a large vessel such as a gastroduodenal artery. Occasionally the ulceration may be so extensive that the entire duodenal cap is ulcerated and devoid mucosa.
As with duodenal ulceration, H. pylori and NSAIDs are the important aetiological factors. Gastric ulceration is also associated with smoking and other factors are of lesser importance. Gastric ulceration is substantially less common than duodenal ulceration. The sex incidence is equal and the population with gastric ulcer tends to be older.
Gastric ulcer tend to be larger. Fibrosis, when it occurs, may result in the now rarely seen hour-glass contraction of the stomach. Large chronic ulcer may erode posteriorly into the pancreases and occasionally into major vessels such as splenic artery. Less commonly, they may erode into other organs such as the transverse colon. Chronic gastric ulcer are much more common on the lesser curve, especially at the incisura angularis, than the greater curve.
Chronic duodenal ulcer are not associated with malignancy and by contrast gastric ulcer are. Widely varying estimates are made of the incidence of gastric malignancy in the gastric ulcers.
Clinical features of peptic ulcer
Usually at epigastric region, often described as gnawing and may radiate to the back. Eating may sometimes relieve the discomfort. The pain is normally intermittent rather than intractable.
One of the classical features of untreated peptic ulceration is periodicity. Symptoms may disappear for weeks or months to return again. This periodicity may be related to the spontaneous healing of the ulcer.
whilst this occurs, it is not notable feature unless the stenosis has occurred.
Alteration in weight:
Weight loss or, sometimes weight gain may occur. Patients with gastric ulceration are often underweight but this may precede the occurrence of the ulcer.
All peptic ulcer may bleed. The bleeding may be chronic and presentation with anaemia is not uncommon.
Examination of the patient may reveal epigastric tenderness but except in extreme cases( for instance gastric outlet obstruction) there is unlikely to be much else to find.
Investigation of the patient with suspected peptic ulcer disease
Identification of H. pylori infection.
- None-endoscopic tests.
- 1)Serological: Presence or absence of immunoglobulin G (IgG) antibody to H.pylori infection.
- 2)Non endoscopic urease test (NUTS): The urea breath or blood test are noninvasive and unlikely antibody tests, identify only patients with active H.pylori infection.
- 3) Fecal antigens test: The fecal antigens test (FAT) utilizes polyclonal anti-H. pylori to capture antibody absorbed to microwells.
- Endoscopic test: In patient with a peptic ulcer disease diagnosed by endoscopy, biopsies can be performed to look for evidence of H. pylori.
- Rapid urease testing: H. pylorus produces large amounts of the enzyme urease, which cleaves urea to ammonia and bicarbonate leading to pH change in the microenvironment of the organism.
- Histology: Routine hemotoxyline and eosin staining typically allows recognition of the organism by an experienced pathologist.
- Culture: Although H.pylori can be cultured from gastric biopsies, the process is slow, complicated. It needs special culture media and expensive.
Other conditions that may give rise to similar peptic ulcer disease.
- Gallstone disease and its complications,
- Gastroesophageal reflux disease
- Chronic pancreatitis,
- Cancer of the stomach and pancreas
- Postgastrectomy gastritis
- And rarely disease of transverse colon
Treatment of peptic ulcer disease:
The vast majority of uncomplicated peptic ulcer disease are treated medically. Surgical treatment was aimed principally at 1)reducing gastric acid secretion. 2) And in case of gastric ulceration, removing the diseased mucosa is advised. When originally devised medical treatment also aimed to reduce gastric acid secretion. This involves use of highly successful H2 receptor antagonist and subsequently proton pump inhibitors. This has now largely given way to eradication therapy.
It involves modification of patient’s lifestyle, particularly the cessation of cigarette smoking.
PPI based triple therapies are effective in eradicating H.pylori infection and it well tolerated by patients. These regiment consist of of a PPI in combination with two antibiotic (amoxicillin,clarithromycin or metronidazole). Medication are given twice daily for for periods of 7-14 days. Particularly notable are the combination of PPI, clarithromycin and either amoxicillin or metronidazole, which have consistently achieves eradication rates of >80%.
Surgical treatments as follow:
Duodenal ulcer surgery-rationale;
This is achieved by diversion of the acid away from the duodenum. It reduces the secretory potential of the stomach or both.
- Billroth II gastrectomy
- Truncal vagotomy and drainage
- selective vagotomy and drainage
- Highly selective vagotomy
- Complication arising from peptic ulcer disease:
The complications of peptic ulcer disease are principally;
- Penetration and
- Obstruction in that order.
Hemorrhage is common and perforation is the most lethal.
Classically, hematemesis is more common in gastric ulcers and malena in duodenal ulcers. Sometime combination of hematemesis and malena may occur with either ulcer when bleeding is brisk. Ulcer hemorrhage may be recognized clinically in five patterns of increasing severity and clinical importance.
- occult blood in the stool with or without anemia.
- coffee grounds emesis
- sudden collapse and shock or fecal dysfunction in a vital organ ( eg cerebrovascular accident, coronary ischemia),with or without obvious hemorrhage.
Ulcer perforation is usually a dramatic event, the onset of which may be accompanied by severe generalized abdominal pain. There is loss of bowel sounds and board-like rigidity of the abdominal wall.
Unlike perforation, ulcer penetration into an adjacent viscus. such as liver, pancreas or biliary system, is rarely dramatic. Rather,it presents with gradual exacerbation of pain, loss of rhythmicity, increase in local tenderness. Most common manifestation is pancreatitis .
Patient may present with gastric outlet obstruction of two types. The first is due to edema and inflammation surrounding an acute ulcer, especially in the antrum or pyloric channel. Second is due to chronic, permanent scarring with fibrosis and outlet narrowing.
Though intensive medical therapy may reverse the first type, it cannot resolve the second.