PEPTIC ULCER [Symptoms/ Causes/ Pathogenesis/ Complications]
Peptic ulcer disease presents as duodenal ulcer or gastric ulcer. During the last few disease, the incidence of peptic ulcer disease has decreased in India. In one study, prevalence of duodenal ulcer was 12% in 1998, but it declined to 3% in 2008. During the same period, gastric ulcer prevalence declined from 4.5% to2.7%
Symptoms
*Burning stomach pain. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain that improves with eating, with a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache
CAUSES OF PEPTIC ULCE
*H. pylori infection
*NSAIDs
*Alcohol
*Cigarette smoking
*Psychogenic stress
PATHOGENESIS
It is a physiological marvel that gastric juice can easily digest the swallowed pieces of meat but normally, it has no corrosive action on the gastric mucosa itself. Several factor seem to be involved in the protection of gastric mucosa from autodigestion. These factor, collectively known as gastric mucosal barrier, include:
A. Mucus secreted by surface epithelial cells and mucus neck glands which forms a water insoluble visco-elastic gel with poor diffusion coefficient for H+
B. Bicarbonate secreted by surface epithelial cells into boundary zone between the epithelial cells and the mucus layer. The secretion of mucus and bicarbonate is believed to be medicated through prostaglandins.
C. Tight junction between the adjacent cells of gastric surface epithelium
D. Rapid turnover of surface epithelial cells, and rich blood supply.
E. Prostaglandins. Endogenous prostaglandins stimulate secretion is gastric mucus as well as gastric and duodenal mucosal bicarbonate. Prostaglandins also participate in the maintenance of gastric mucosal blood flow and integrity of mucosal barrier and promote epithelial cell renewal in response to mucosal injury.
Under normal condition, a physiologic balance exists between peptic acid secretion and gastro-duodenal mucosal defence. Mucosal injury may leads to peptic ulcer when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as H. pylori, NSAIDs, alcohol, cigarette smoking, psychogenic stress can alter the mucosal defence and allow back diffusion of hydrogen ions and subsequent epithelial cell injury.
Mechanisms of injury differ distinctly between duodenal and gastric ulcers. Duodenal ulcer is essentially a H. pylori-related disease and is caused mainly by an increase in acid and pepsin load, and gastric metaplasia in the duodenal cap. Gastric ulcer is most commonly associated with NSAID ingestion, although H. pylori infection might also be present. Chronic, superficial and atrophic gastritis predominate in patients with gastric ulcer, When even normal acid levels can be associated with mucosal ulceration.
1.Role of Helicobacter pylori
Helicobacter pylori is a bacillus responsible foe one of the most common infections found in humans worldwide. H. pylori inhabit the mucus adjacent to the gastric mucosa. Helicobacter pylori bacteria colonize the stomach and induce chronic gastritis. H. pylori is able to survive the highly acidic environment of the stomach because it protects itself by release of an enzyme urease, that splits blood urea and produces ammonia. The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the side of H. pylori colonization.
In those with duodenal ulcer, H. pylori colonizes the antrum. The inflammatory response to the bacteria cause destruction of somatostatin-producing D cells in the pylorus. Consequently, the G cells in the antrum secrete more of the hormone gastrin, Which travels the bloodstream to the fundus and body of the stomach. Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen. Chronically increased gastrin levels eventually causes the number of parietal cells to also increase, further escalating the amount of acid secreted. The increased acid load damages the duodenum, and ulceration may eventually result.
In contrast, in gastric ulcers, H. pylori colonize the corpus of the stomach Where the acid -secreting parietal cells are located. However, chronic inflammation induced by the bacteria leads to reduction of acid production, and eventually atrophy of the stomach lining. Gastric atrophy may lead to gastric ulcer and increases the risk for stomach cancer.
2. Non-Steroidal Anti-Inflammatory Drugs
Non- steroidal anti-inflammation drugs (NSAIDs) including low-dose aspirin are some of the most commonly used medicines. They are associated with gastrointestinal mucosal injury. Endoscopic studies have shown a prevalence rate of 14-25% of gastric and duodenal ulcers in NSAID user, NSAID acts as anti-inflammation agents by inhibition of prostaglandin (PG) synthesis. As discussed earlier, prostaglandins are important components of gastric mucosal barrier. Inhibition of PG synthesis breaks gastric mucosal barrier leading to peptic ulcers.
3. Smoking
Cigarette smoking appears to be a risk factor for the development, maintenance, and recurrence of peptic ulcer disease. Smokers are about two times as likely to develop ulcer disease as non-smokers. Smoking predisposes to peptic ulcer by 1) Acceleration of gastric emptying of liquids, 2) Promotion of duodeno-gastric reflux, 3) Reduction in mucosal blood flow, and 4) Inhibition of mucosal prostaglandin production. Cigarette smoking not only causes ulcer bleeding, stomach obstruction and perforation. Since cessation of smoking is associated with the promopt recovery of the respective functions, smokers will benefit immediately by stopping or reducing cigarette consumption. Cigarette smoking is also a leading cause of failure of medicinal treatment of peptic ulcer.
4.Role of stress
The development of acute gastric ulcers as a result of severe stress after major surgery or extensive burns is well known. Reduced gastric blood flow coupled with raised plasma cortisol levels seem to be primarily responsible for such ulcers.
Till1980s, psychological stress was considered the chief cause of duodenal ulcer. The high stung type "A" individuals were considered special candidates foe the development of duodenal ulcer. In 1990s, after the discovery of H. pylori, it began to be believed that psychogenic factors play no role in the development of chronic peptic ulcer disease. Over the years, it is now being appreciated that psychogenic stress acts ass a co-factor with H. pylori in the production of hyperacidity leading to duodenal ulcer.
Risk Factors
*alcohol
*spicy food
Alone, these factors do not cause ulcers, but they can make them worse and more difficult to heal.
Complications
Left untreated, peptic ulcers can result in serious complications;
*Internal bleeding, Bleeding can occur ass slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion. Severe blood loss may cause black or bloody vomit or black or bloody stools.
*Infection, Peptic ulcers can perforate the wall of stomach putting at risk of serious infection called peritonitis.
*Obstruction to the passage of food.
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